dysautonomia Archives - Page 2 of 4

Migraine Energy Metabolism: Connecting Some Dots

Published on October 10, 2023

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I have been reading some of the fascinating posts by Angela Stanton PhD concerning her research in migraine headaches. I regard the substance of her discussions as somewhat like dots on a chart that need to be connected. I learned a great deal about the chemistry involved in migraine. One of her comments that involves ion homeostasis in brain metabolism is fascinating. She noted that “serotonin is created by a normally functioning brain. Why it decreases or increases in the brains of migraineurs has always puzzled me. Should we not try to find out why?” That simple three letter word is the heart and soul of research and I believe that I may be able to add some information that might provide an answer.

Ehlers Danlos and Migraine

In one of Angela’s posts she discusses a subject which has been of interest to me for many years, the overlap of symptoms in disease. She noted that 60% of migraineurs have one type of Ehlers Danlos syndrome (EDS) and 43% of EDS have minor changes in DNA (SNPs) found in migraineurs. She concludes that they must be related. Over 70% of migraineurs have Raynaud’s disease and there is an overlap with EDS and Raynaud’s. Therefore, she concludes that these three diseases are variants. In fact, there is an association between EDS, Postural Othostatic Tachycardia Syndrome (POTS) and a group of conditions known as mast cell disorders. EDS-HT, (one of the manifestations of this disease), is considered to be a multisystemic disorder, involving cardiovascular, autonomic nervous system, gastrointestinal, hematologic, ocular, gynecologic, neurologic and psychiatric manifestations, including joint hypermobility. Many non-musculoskeletal complaints in EDS-HT appear to be related to dysautonomia, consisting of cardiovascular and sudomotor dysfunction. Many of the clinical features of patients with mitral valve prolapse can logically be attributed to abnormal autonomic function. Myxomatous degeneration of valve leaflets with varying degree of severity is reported in the common condition of mitral valve prolapse.

A woman, with what was described as a “new” type of EDS, died after rupture of a thoracic aortic aneurysm. Autopsy revealed myxomatous degeneration and elongation of the mitral and tricuspid valves. Patients with POTS, a relatively common autonomic disorder, may have EDS, mitral valve prolapse, or chronic fatigue syndrome and are sensitive to various forms of stress, as depicted in the clinical treatment of a dental patient affected by the syndrome. Dysautonomia has been described in the pathogenesis of migraine, featured by nausea, vomiting, diarrhea, polyuria, eyelid edema, conjunctival injection, lacrimation, nasal congestion and ptosis. In general, there is an imbalance between sympathetic and parasympathetic tone.

Energy Metabolism and Migraine

Technological studies have confirmed the presence of deficient energy production together with an increment of energy consumption in migraine patients. An energy demand over a certain threshold creates metabolic and biochemical preconditions for the onset of the migraine attack. Common migraine triggers are capable of generating oxidative stress and its association with thiamine homeostasis suggests that thiamine may act as a site-directed antioxidant. It strongly suggests that migraine is a reflection of an inefficient use of brain oxygen. An intermediate consumption of oxygen between deficiency and excess appears to be a necessity at all times. In fact,” moderation in all things” is an important proverb

Backing up energy deficiency, two cases of chronic migraine responded clinically to intravenous administration of thiamine. However, the authors are in error when they state in the abstract that “nausea, vomiting and anorexia of migraine may lead to mild to moderate thiamine deficiency”. An otherwise healthy 30-year-old male acquired gastrointestinal beriberi after one session of heavy drinking. Nausea, vomiting and anorexia relentlessly progressed. He had undergone 11 emergency room visits, 3 hospital admissions and laparoscopy within 2 months but the gastrointestinal symptoms continued to progress, unrecognized for what these symptoms represented. When he eventually developed external ophthalmoplegia (eye divergence), he received an intravenous injection of thiamine which reversed both the neurologic and gastrointestinal symptoms within hours.

In other words it is important to be aware that nausea, vomiting and anorexia are primary symptoms of beriberi due to pseudohypoxia in the brainstem where the vomiting center is located. Chronic migraine has a well documented association with insulin resistance and metabolic syndrome. The hypothalamus may play a role. One of Angela’s comments concerns ion homeostasis in migraines. Thiamine triphosphate (TTP) can be found in most tissues at very low levels. However, organs and muscles that generate electrical impulses are particularly rich in this compound. Furthermore, TTP increases chloride (ion) uptake in membrane vesicles prepared from rat brain, suggesting that it could play an important role in the regulation of chloride permeability. Although this research was published in 1991, the exact role of TTP is still unknown. It has been hypothesized that thiamine and magnesium deficiency are keys to disease.

Angela wondered why serotonin might be increased or decreased in migraineurs. I strongly suspect that it is due to brain thiamine deficiency as the ultimate underlying cause of the migraine. In a review of thiamine metabolism, it was pointed out that metabolites could be high or low according to the degree of the deficiency. Victims of beriberi were found to have either a low or a high potassium according to the stage of the disease. If they were found to have a low acid content in the stomach, treatment with thiamine resulted in a high acid content before it became normal. If the stomach acid was high it would become low before it became normal. Since low and/or high potassium levels may be found in the blood of critically ill patients, thiamine deficiency should be a serious consideration in the emergency room or ICU Thiamine deficiency may be the answer for the fluctuations of serotonin observed in migraine.

Redefining Disease Models

According to the present medical model, each disease is described as a constellation of symptoms, physical signs and laboratory studies, each with a separate etiology. The overlap discussed by Angela suggests that the various conditions nominated have a common cause and that they are indeed nothing more than variations. If energy metabolism is the culprit, it would make sense of the infinite variations according to the degree and distribution of cellular energy deficiency. EDS-HT, described above is reported as a multi-system disease, exhibiting cardiovascular, autonomic gastrointestinal, hematologic, ocular, gynecological and psychiatric symptoms as well as the joint mobility. It seems to be impossible to explain this multiplicity without invoking energy deficiency as the cause. People with prolapsed mitral valve and a patient with a “new” form of EDS, reportedly have myxomatous degeneration as part of their pathology and it is tempting to suggest that such an important loss of structure might well be because of energy deficit.

The controls of the autonomic nervous system are located in the lower part of the brain that is particularly sensitive to thiamine deficiency and beriberi is a prototype for thiamine deficiency in its early stages. Dysautonomia is frequently reported as part of many different diseases, offering energy deficiency as the etiology in common. Yes, it is true that thiamine is not the only substance that enables the production of ATP. Nevertheless, it seems to dominate the overall picture of energy metabolism. It has long been considered the essential focus in the cause of beriberi, even though all the B complex vitamins are found in the rice polishings. Milling and the consumption of white rice was the prime etiology of the disease when it was common in rice consuming cultures.

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This article was published originally on June 22, 2020.

An Artist’s Decades Long Dysautonomia Treated With Thiamine

by Lynne Campbell

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.

We Need Your Help

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

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Image: Original painting by the author.

This article was published originally on April 19, 2021.

Medication and Vaccine Adverse Reactions and the Orexin – Hypocretin Neurons

by Chandler Marrs, PhD

Published on June 1, 2023

15336 views

A paper published in Science Translational Medicine, provides preliminary evidence that the H1N1 Flu Vaccine Pandemrix can evoke immune system mediated damage to the orexin – hypocretin neurons and induce narcolepsy in individuals with a particular genetic variant. The orexin – hypocretin neurons were only recently discovered in the mid 1990s, by two separate research groups, hence, the two names for the same molecule. For this paper, we’ll be utilizing the orexin nomenclature.

Initially, the orexin neurons were thought to be involved only in feeding behavior, as damage elicited hypophagia in animals. Soon it was learned that more severe damage to the orexin neurons induced narcolepsy and the orexin system became a key focus in narcolepsy related research. With time, however, it became quite clear that these neurons were involved in regulating a myriad of hormone and neurotransmitter systems and their consequent behaviors. Narcolepsy or rather the ability to sustain wakefulness, is but one of the many functions regulated by the orexin system.

In a previous paper, I touched briefly on the possibility that the orexin neurons might be damaged and have diminished functionality in individuals suffering from post Gardasil side effects. In particular, I suspected these neurons were indicated in post-Gardasil hypersomnia, a derivative of narcolepsy. That may be only the tip of the iceberg. As I soon learned, the hypocretin/orexin neurons are brain energy sensors and may be involved in array of post medication or vaccine adverse reactions. Indeed, they may be central to the ensuing state of sickness behaviors that emanate once an organism becomes overwhelmed.

The Orexin – Hypocretin Basics

Orexin nuclei are located in the lateral hypothalamus, the section of the hypothalamus that is most known for regulating feeding, arousal and motivation. The hypothalamus is the master regulator for all hormone systems and hormone related activity including feeding, sleeping, reproduction, fight, flight, energy usage – basically every aspect of human and animal survival. It sits at the interface between the central nervous system functioning and the endocrine system functioning.

From the lateral hypothalamus, orexin neurons project across the entire brain with its two receptors (OXA and OXB) differentially distributed throughout the central nervous system and even in the body, including in the kidney, adrenals, thyroid, testis, ovaries and small intestine. The orexin neurons also modulate local networks of adjacent neurons within the hypothalamus that in turn influence a myriad of behaviors.

The most densely innervated brain regions include the thalamus, the locus coeruleus, dorsal raphe nucleus, accounting for the hormone’s role in arousal, feeding and energy management. At the most basic level, release of the orexin induces wakefulness. 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 also located in the amygdala, the ventral tegmental area (VTA) and throughout the limbic system, accounting for its role in emotion and the reward system. Orexin directly activates dopamine in the VTA. The VTA is the reward, addiction, and in many ways, the pleasure center of the brain. All drugs of addiction, all pleasurable activities, activate dopamine in the VTA. Through the release of dopamine, here and elsewhere, orexin modulates the motivation to sustain pleasurable activities. When orexin is diminished, not only does dopamine diminish, but the motivation to sustain behaviors decreases and dysphoria increases.

That’s not all. Orexin influences the release of many other neurotransmitters and hormones, several of which are co-located on the orexin neurons themselves. For example, the neuropeptide dynorphin is co-located on orexin neurons. Dynorphin is an endogenous opioid involved in the perception of pain and analgesia. It has dual actions that can both elicit analgesia or pain depending upon dose and length of exposure. Stress activates dynorphin. Dynorphin then inhibits orexin firing by as much as 50%. Illness is a stressor, a vaccine is a stressor, either could activate dynorphin and inhibit orexin. After the initial activation of dynorphin, and the ensuing decrease in orexin, the presence of chronic stressors and chronic pain could begin a continuous feedback loop of diminished arousal, and increasing pain.

Other Neurochemical Connections

Consistent with orexin’s role in arousal, orexin neurons contain glutamate vesicles. Glutamate is the brain’s primary excitatory neurotransmitter. Drugs that increase glutamate, also increase orexin. Drugs that block glutamate, via its NMDA receptor, decrease orexin. Common migraine medications block glutamate and thereby may also diminish orexin.
Serotonin and norepinephrine decrease hypocretin/orexin firing (suggesting if one is concerned with hypersomnia, anti-depressants might not be a good option).
As one might expect, orexin neurons are inhibited by GABAα agonists – sedatives. From a women’s health perspective, consider that cycling hormones would also affect orexin neurons through the GABAα pathway. Progesterone is a GABAα agonist – a sedative, while DHEA and its sulfated partner DHEAS are GABAα antagonists, anxiolytics that block GABAα, reduce sedation, and thereby increase anxiety and wakefulness. There may be a cyclical nature to orexin firing that has yet to be investigated.
The hypocretin/orexin neurons also influence galanin, a GI and CNS hormone that seems to inhibit the activity of a variety of other neurons in those regions.

These are but a few of the brain systems that the orexin neurons touch in some way or another. Damage to this system would have serious health consequences by initiating a cascade of biochemical changes within the brain and body. Many of which, we have yet to fully understand.

How Might the Orexin Neurons Become Inhibited?

Quite easily, apparently. In addition to the orexin’s vast interconnected pathways with a myriad of neurotransmitters and neuropeptides, the orexin neurons act as energy and activity sensors with some unique intracellular mechanics that make them especially sensitive to the changing dynamics of the extracellular milieu. Disruptions in ATP, glucose and temperature, elicit reactions in orexin functioning.

Orexin neurons require as much as 5-6X the amount of intracellular ATP to maintain firing, and to maintain a state of wakefulness or arousal. This extreme sensitivity to reduced ATP makes the orexin neurons uniquely positioned to sense and monitor brain energy resources, early, before ATP levels become critical in other areas of the brain. The orexin neurons cease firing when ATP stores become low, thereby allowing the reallocation energy, perhaps to those cells required for survival, breathing and heart rate. As Hans Selye observed many decades ago, one of the first, and indeed, most consistent of the sickness behaviors, no matter the disease, is lethargy, fatigue and sleepiness. Orexin is at the center of this behavior.

Orexin neurons react to extracellular glucose levels, though perhaps not as one might expect. When extracellular glucose levels are high, orexin neurons stop firing via what is called an inward rectifying potassium (K+) channel that is ATP dependent. That means that when extracellular glucose is high, intracellular ATP is allocated to open K+ channels and flood the cell with the inhibitory K+ ions. K+ hyperpolarizes the cell, prohibiting it from firing. This mechanism reminds me of Dr. Peter Attia’s talk about the nature of Type 2 Diabetes and our approach to treatment. He proposes that the body’s metabolic response – the conservation of energy – to Type 2 Diabetes is not something aberrant but is exactly as it should be with a disease state. We’re just not treating the correct disease state.

Another way we can shut down the orexin neurons is via increased temperature. The orexin neurons are very sensitive thermosensors. Increased temperatures shut down orexin firing via the inward K+ flow. Again, this is consistent with sickness behaviors and the reallocation of resources.

Orexin – Hypocretin Neurons in Migraine and Seizures

Diminished orexin has been linked to migraine and seizure activity. With migraines specifically, orexin may contribute to the early warning, hours to days, of impending cortical disruption via changes in feeding and sleep patterns that often precede migraine onset. Orexin may also be linked to the pre-migraine aura mediated by changes in brain electrical activity that prelude the migraine pain itself by minutes, called cortical spreading depression or more appropriately, cortical spreading depolarization – the massive spreading change in ion balance of the neurons. Initially the wave is excitatory, neurons are firing, but that is soon followed by a period of neural silence. Finally, orexin is also connected to the vasodilation of the trigeminal nerve, the nerve responsible for migraine pain. These findings have led some to call orexin a migraine generator.

Diminished cerebral spinal concentrations of oxerin have been found in patients generalized tonic-clonic seizures. Conversely, in rodent studies, injections of orexin elicit seizure activity. Despite the somewhat contradictory findings in seizure activity versus migraine activity, it is likely that the orexin system is involved both disease processes.

Pulling it all Together: Orexins Monitor and Mark Disruptions in Brain Homeostasis

Here’s where it gets really interesting. Although some have argued orexin, particularly diminished orexin functioning, is the cause and culprit of disruptions in brain homeostasis, leading to narcolepsy, excessive sleepiness, migraine, seizures and other diseases, I think this system represents merely a marker of a disease process. I think the orexin system is the stopgap, the final barrier of disrupted cellular energetics, of mitochondrial function. Mitochondrial ATP is the key.

When we consider orexin’s role in migraine, in particular, we see clearly how environmental changes (diet, stress, illness, medication/toxin exposure) can lead to changes in the extracellular milieu where orexins reside. The orexin sensors adjust to these changes, mostly by reducing neural firing in attempt to counteract damages. The reduction in orexin then elicits the premonitory phases of the impending brain disruptions, sleep and hypophagia – the sickness behaviors. If it progresses, the massive waves of electrical disruption ensue, and migraine, perhaps even seizures are evoked. When the extracellular environment become chronically disrupted, so too does the diminishment of orexin activity, thereby initiating a perpetuating loop of dysregulated brain activity. We can hypothesize that similar progressions exist with disease processes marked by aberrant electrical activity, such as epilepsy.

We know that mitochondrial dysfunction is often generated by genetic polymorphisms and can predispose individuals to an array of seemingly unrelated conditions like migraine and fibromyalgia, dysautonomias and cognitive deficits. At the root of the dysfunction is a error of some sort in mitochondrial energy processing – ATP.

What has become increasingly clear, is that the production of cellular energy, can be disrupted environmentally, by diet, illness and exposures, if co-factors necessary for the production ATP like thiamine are diminished. It is via diminished ATP production, that I think some medications and vaccines evoke adverse reactions in some individuals. The orexin system, because it is so exquisitely sensitive to changes in cellular energy, is our warning system; first by subtle changes in neurochemistry, then by changes in arousal and feeding behavior, and finally, by an all-out reallocation of resources – excessive sleeping. If ATP remains deficient chronically, and an individual is so disposed, then the cortical misfiring we see in migraine and seizure ensues, along with autonomic dysregulation and the syndromes associated therewith. It is not the orexin – hypocretin system that is at root of many of these diseases, but rather, the causes are deeper yet and reside with mitochondrial health.

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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 January 29, 2014.

Dysautonomia and Chronic Illness Post Brain Surgery

by Silvi Si

Published on April 19, 2023

10287 views

I wanted to share my experience going through thiamine paradox and my journey to heal. I am 27 year old girl from Italy and have been suffering from various health problems since I was 14 including a brain tumor that necessitated surgery, followed by Epstein Barr Virus, Hashimoto’s thyroiditis, multiple parasitic infections, antibiotic reactions, extreme and chronic fatigue, fibromyalgia, dysautonomia, SIBO, and gastroparesis. I have begun thiamine therapy six months ago and while some of my symptoms have improved, others have remained or worsened. I am not sure what to do next and am writing this in the hope that someone will have some answers.

Dysautonomia and Illnesses Post Brain Surgery

In 2008, I underwent neurosurgery to remove a benign tumor in my temporal lobe. It was very large, near the hypothalamus and on the optic tract. After that surgery, I was in sympathetic mode for about a year and a half. It was intense. I was always alarmed and anxious with school performance anxiety. I was exhausted, but at the same time, I had the energy to do more than I could afford. Furthermore, I gained 20kg in 6 months despite eating well. This was traumatic for me. Even though I did everything I could to not gain weight, the weight still went up. I felt powerless and I was pissed off. I did a thousand diets and I still fight to lose weight. I have been on a diet ever since.

In 2010, I got an Epstein-Barr viral (EBV) infection. Next, I developed Hashimoto thyroiditis and lost a lot of hair. My beautiful hair that was soft and silky, became sparse, few and very thin. I also had pain in my neck for two years. After that EBV infection, I started to feel tired all the time, but still managed to go out and go to school

In 2011, after a month and a half of pain in the lower back and abdomen, I had a fecal analysis done and found that I had parasitic infection called blastocystis hominis. The doctor gave me metronidazole (Flagyl) in a very high dosage. When the pain in my right leg appeared, the suspicion that it was appendicitis became certain and they operated on me. The surgeon told me my appendix was was 12 centimeters, inflamed and had two abscesses.

In 2012, I had some months of extreme fatigue and abdominal pain. The seizures I had before my brain surgery returned, as did my inability to study due to lack of concentration. I then discovered that I had another parasitic infection, this time giardia. I was treated with Flagyl again. After Flagyl, I was infection-free for 6-7 months.

In March of 2013, I developed an acute onset case of what the doctor’s called a severe case of chronic fatigue, fibromyalgia, and dysautonomia. I had brain fog and was unable to focus. I had tingling in my neck arms. I started gaining again. I have episodes of dysautonomia with vagal crises that include palpitations and tachycardia so strong that even moving around in bed accelerates my heartbeat. Add to all of this a plethora of other minor symptoms. In particular, I have become unbearably cold. Previously, I was the the person who was always in half sleeves. I have also mood swings that sometimes make me feel crazy (such as unexplained nervousness attacks). I felt I had no energy in my muscles and that I could not do anything. Even though and above all I was a girl full of energy and always very cheerful.

Failed Attempts at Healing

Since then, I have done many different types of therapies (homeopathy, mineral and vitamin integrations, neural therapy, micotherapy, osteopathy) with small and short improvements. In 2017, I did probably one of the stupidest things I’ve ever done before, I fasted for 16 days. I was convinced of the idea that it could cure my thyroiditis. After that, I started not digesting well, so much so that if I ate a little more than I should, I was throwing up, and the cold in my body became even more unbearable.
A few years later in 2019, after years of GI problems, that included gastroparesis/delayed stomach emptying, bloating and pain, I was diagnosed with SIBO (sulfur). I was given Rifaximin. I also tried a herbal therapy for SIBO, and for candida, which I also had, and NAC. Nothing worked.

Where I Am Now

I still have most of these conditions. Some symptoms have passed but new ones have emerged. Overall, I am better than in 2013 when CFS started and I just couldn’t get out of bed.

A few months ago, I discovered Dr. Lonsdale’s work on thiamine deficiency and I bought his and Dr. Marrs’ book: Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition. I believe many of health issues involve thiamine deficiency.

I began with 15mg thiamine HCL injections daily for about two weeks and then increased it to 30mg per day. I also take B complex, magnesium, seleniomethionine, molybdenum, vitamin C, vitamin D, omega 3, zinc and copper because they were low in my blood exam. The first month I also took SAMe with many benefits, but now it seems to make things worse.

I eat only organic food. I don’t eat sugar, processed food, junk food, gluten, milk or dairy products, or alcohol. I have only one or two espressos per day and I eat a lot of apples because they are low in oxalates.

Thiamine Reaction or Something Else?

When I woke up on day 2 of thiamine, I saw that my eyes were swollen like balloons, there were some itchy blisters on my eyelids and around the eyes. In the morning other blisters appeared on my elbow and behind my neck under my hair. The morning of day 4, I woke up with a skin rash near the hip.

At the beginning, I had thought these reactions were relative to the thiamine, but I later realized that the hives and swelling were linked to the inositol hexanicotinate, a niacin substitute in the B complex. I have no problems with niacin though, just the inositol hexanicotinate form. From that episode forward, I began taking all the B vitamins separately.

After 2 months of thiamine HCL, I added allithiamine. I began with 1 pill, 50mgs, and I added another 50 mg pill every week, until I reached 300mg. Initially, all the symptoms I had at the beginning of the disease reappeared: severe myalgic attacks in the leg or abdomen, abdominal pain, other pains and unbearable cold in the whole body, especially in the hands. The chills are so severe that I am often shaking. It is so severe that it paralyzes me. This shaking disappeared in a few weeks, but sensation of being cold still persists. And I am still very tired.

After Six Months of Thiamine Therapy

There are some improvements from since I started with allithiamine. For example, my fatigue has improved. Although I always have chronic fatigue, there are times when I feel better for a few hours. Before starting the thiamine, I had frequent attacks of voracious hunger during which I never felt full. I’ve always tried to ignore them, because if I’m not on a strict diet, I am gaining weight. Since taking thiamine, this happens much more rarely and my sense of fullness has improved. Finally, I have fewer nervous attacks. My digestive system seems to be little better. What I am currently taking:

Allithiamine – 300mg
Riboflavin – 320mg
Niacin – 100mg
Pantothenic acid – 200mg
Pyridoxine – 20mg
Myo inositol – 2gr
Biotin – 5000mcg,
B12 – until a few months ago. It was low and now it is high.
Zinc – 30mg
Copper – 2mg
Omega 3
Inulin – 2gr
Keppra – 250mg x2 a day
Molybdenum – 200mcg
Seleniomethionine – 200mcg
NAC – 1200mg
Magnesium malate – 1800mg
Magnesium citrate – 1500mg
Vit C – 2gr x5 a day
Lysin 1gr
Vit D – 10000 UI
M2MK7 – 100mcg
DHEA – 50mg
Maca powder – 5gr
CoQ10 – 100mg
LDN therapy – since March 2020

I still have the symptoms of the paradox effect. It has been almost 6 months since I started thiamine, how is it possible? The worst symptoms now are fatigue, frozen hands, shivering. Is the thiamine not working or is something else going on? Could it be that the thiamine revealed some other deficiency that is causing me this reaction? I’d like to know whether I should continue to take it.

A warm hug from Italy.

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This article was published originally on May 17, 2021.

Progressive Deterioration of Health With Severe Nutrient Deficiency

by TJ

Published on February 2, 2023

10186 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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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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Burning Out From Worsening Dysautonomia

by Tony Maestro

Published on July 27, 2022

5995 views

Longstanding Symptoms of Dysautonomia

I am a 34-year-old male with symptoms of dysautonomia including small fiber neuropathy (SFN), postural orthostatic tachycardia syndrome (POTS), fatigue, insomnia, and problems with attention. I have had some of these symptoms for as long as I can remember but they have become worse after contracting COVID in December of 2021. I suspect I have issues with thiamine and possibly other nutrients.

History of Heavy Medication Use and Poor Diet

At around age 19, I felt what could be described as intracranial hypertension. I had multiple MRIs and CAT scans, but everything came back normal. At age 22, I began exhibiting signs of fatigue and insomnia coupled with anxiety. I most likely have some form of hypermobility too.

I was diagnosed with ADD and anxiety in my teens and prescribed Adderall and Prozac at the time. I was on those medications from the age of 16-25 years old. Then again from the age of 27-32 years old, I was given Adderall. I smoked and chewed tobacco until age 30 and was on and off hydrocortisone for poor adrenal function too. Evidently, adrenals can “fatigue” or become dysfunctional under high amounts of stress, even though blood cortisol was normal, saliva cortisol levels would always be low. Only functional doctors buy into this diagnosis.

I had strep and sinus infections a lot in my teens and early twenties and have probably had 40-50 doses of various antibiotics over the years. During this time, I worked out regularly with weight training and ice hockey. I was pretty competitive growing up. I would train 4-5 times a week and wake up early every Saturday to play hockey. I still work out around 5 days a week, mostly weight training now.

As a child and teenager, my diet was filled with carbs and crappy junk food like waffles and cereals and breads, and sweets. At around age 25, I began to eat a more healthy, paleo diet. I also began to avoid gluten. My diet currently consists of mostly carnivore/keto. I consume no alcohol at all. I did have a 10-year marijuana habit, from age 15-25, but I quit cold turkey years ago. I am currently taking Klonopin and have begun supplementing bone broth and a multivitamin. I have been taking 1mg per/day of Klonopin for a decade now. This may be affecting my symptoms.

Along Came COVID

In December of 2021, I got COVID and since then I have felt even worse. The COVID was mild. I took Ivermectin for 10 days and seemed to recover from the virus but all of my symptoms of dysautonomia have worsened.

Given my history, I am looking for advice on how to repair the damage I have done to myself with the poor diet, medications, and drugs. I have read about thiamine deficiency and it fits many of my symptoms but I am unsure how and where to begin. What else may be required?

We Need Your Help

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

Yes, I would like to support Hormones Matter.

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Thiamine for Fibromyalgia, CFS/ME, Chronic Lyme, and SIBO-C

by AMZ

Published on June 7, 2022

37030 views

The Road to Thiamine

In August 2020, I was at my wits end. I had developed gastroparesis in March 2020, after 10 days of metronidazole (Flagyl), for a H. Pylori infection and SIBO-C symptoms. After seven days, I developed the symptoms usually associated with the intake of this drug – nausea, confusion, anxiety, paranoid thinking and mild gastroparesis symptoms. I no longer had bowel movements initiated by my body and had to use enemas twice a week. This state continued and worsened until the end of July 2020, when I also had a surgery for stage 4 endometriosis.

I managed to stay alive those months by eating an elemental diet (90%) and a few bits of solid food such as white rice, goat cheese, or lean meat. After the surgery, however, my gastroparesis got worse. I contacted my family doctor at the end of August and told her that I could no longer eat any solid food without severe nausea and that I need to be in a hospital to be fed intravenously or with a gastric tube. She agreed that my situation demanded immediate attention and she wrote me the referral for an inpatient hospital admission.

I was lucky though that at that exact time, I stumbled upon the low oxalate diet mentioned by a member of a Facebook group. I joined the Trying Low Oxalate (TLO) group on Facebook and read what researcher Susan Owens wrote about oxalates. I started implementing it and realized that small portions of low oxalate food every 2-3 hours were accepted by my body. In a few weeks my gastroparesis symptoms were reduced and my belly pain diminished.

From the Low-Oxalate Diet to Discovering Beriberi Disease

At some point in September 2020, while researching oxalates, I found Elliot Overton’s videos on oxalates and I listened to them. I also read his articles on this website where he talks about allithiamine, a thiamine supplement that contains something called TTFD, as being something radically different in terms of its unparalleled effects on the human body. I was skeptical, because I had spent about 20,000 euro on supplements in the previous four years, each of them being promoted as health-inducing by big names in the field of chronic Lyme disease, MTHFR, CFS/ME, SIBO and so on, while their effects on my health were only partial and temporary at best.

I decided that this would be the last supplement I’d buy. The worse would be losing 40 euros and I had already spent too much on worthless treatments. I took 150 mg allithiamine + magnesium + B2 + B3 for 3 weeks and I was less tired, could move more around the house, and overall was feeling much better, even my extreme light sensitivity was subsiding. Then I stopped taking it, not sure it was doing anything. That’s when I knew that it had worked and that I needed it badly. I took the same dosage for another 2 weeks. The next three weeks I had to wait to receive it from the USA, and I was again completely bed ridden.

However, I used this time to read most of Dr. Derrick Lonsdale’s book on thiamine deficiency. I became convinced that I had dry beriberi and that most of my neurological symptoms were caused by thiamine deficiency. I also noticed that the dosage is highly individual and some individuals needed very high doses of thiamine per day in order to function.

I now understood, why 2015 was the year I became bedridden for most than 90% of the time: I spent 6 months in a very hot Asian country, as part of my master degree studies. The energy requirement to deal with the hot weather and the demanding job depleted my already low thiamine levels. At that time, I was on my way to diabetes as well. I had fasting blood sugar levels of 120 mg/dl. I could no longer assimilate/use carbs in the quantities my body required (70% of the daily caloric intake) and I was always hungry and always thirsty. Looking back on my childhood and my ever-declining health from 2008 onwards, it was clear to me that I had problems with thiamine.

The Astonishing Effects of Thiamine

In December 2020, I increased my thiamine dosage to 300 mg per day and I was astonished at the changes I experienced – an 80% reduction across all my symptoms and some even completely disappear.

Mid-January, I decided to increase my allithiamine dosage to 450-600 mg because I felt like my improvements were stagnating. I also noticed that during the days I was more physically active (meaning: I cooked food for longer that 10-15 minutes, my energy levels were higher when I was taking more allithiamine and I didn’t experience the typical post-exertional malaise I was used to in the past). I also noticed that taking allithiamine alone in high doses doesn’t work so well and that the active B complex capsules and the B3 I was taking did have an important part to play in how I felt.

In the beginning of February, I was craving sugars so badly, that I gave in and bought a cake for my birthday. I ate two slices and discovered that my mental confusion, the brain fog and generally poor cognitive skills improved “overnight”. I was astonished, since I had been led to believe that “carbs are bad”, “sugar is bad” and “gluten is bad” and that the problem was with the food itself rather than with my body missing some vital nutrients. I didn’t experience any side effects from the gluten either, even though my food intolerance test shows a mild reaction to gluten containing cereals.

By February 20th, this high-dose allithiamine ‘protocol’ and the ability to eat carbs again, eliminated all of my symptoms of SIBO-C/IBS-D/slow transit constipation, endometriosis, CFS/ME, fibromyalgia, constant complicated migraine with aura, severe food intolerances, including a reversal of my poor cognitive skills. I was able to discuss highly philosophical concepts again, for one hour, without suffering from headaches and insomnia.

Early Metabolic and Mitochondrial Myopathies

On February 21^st, I decided to go for a walk. I walked in total that day 500 meters AND walked up four flights of stairs, because I live on the 4th floor without an elevator. By the end of that day, my disease returned and I became bedridden again. I could not believe it. This was the only thing I did differently. I just walked slowly.

And so I searched the internet for “genetic muscle disease”, because my sister shares the same pattern of symptoms. A new world opened before my eyes. I found out that in the medical literature, exercise intolerance, post-exertional malaise and chronic fatigue are well known facts and are described in conditions known as “myopathies”. That there are several causes for myopathy and that they can be acquired (vitamin D or B1 deficiency, toxic substances impacting the mitochondria, vaccines and so on) or inherited. It was also interesting to find out that while doctors manifestly despise and disbelieve CFS/ME symptoms, they are not utterly unknown and unheard of or the product of “sick” minds.

When I read this paper, although old and maybe not completely accurate in the diagnostics, I understood everything about my health issues.

I remembered my mother telling me that my pediatrician said he suspected muscular dystrophy when I was one years old, because I could not gain weight. I weighed only 7 kg at the age of one year, but he wasn’t convinced and so no tests were done in communist Romania. In addition to being overly thin, throughout my childhood, I always had this “limit” that I couldn’t go past when walking uphill or if I ran up a few flights of stairs, no matter how fit and in shape I was. Otherwise, I would develop muscle weakness such that my muscles felt like jelly. I would become completely out of breath, which I now know is air hunger. I couldn’t climb slightly steeper slopes without stopping 2/3 of the way up. My heart would beat very hard and very fast. I would feel like I was out of air and collapse. I first experienced this at the age of 5-6 and these symptoms have been the main feature of my physical distress since.

Because of these symptoms, I have led a predominantly sedentary lifestyle with occasional physical activity, never daily, apart from sitting in a chair at school. I didn’t play with classmates for more than 5 minutes. I couldn’t participate in physical education classes. Any prolonged daily physical activity led to general weakness, muscle cramps, prolonged muscle “fever”, and so I avoided them.

Now, I know why. Since reading this article, I was able to present my entire medical history to a neurologist and my symptoms were instantly recognized as those of an inherited mitochondrial or metabolic myopathy. I am currently waiting for the results of the genetic tests ordered by the neurologist, which will make it possible to get the right types of treatments when in a medical setting.

Before Thiamine: A Long History of Unexplained Health Issues

In addition to the problems with gaining weight and inability to be active, I had enuresis until 9 years old, along with frequent dental infections, and otitis. I had pain in my throat every winter, all winter and low blood pressure all the time. At 14 years of age, I weighed about 43-45 kg. I remained at that weight until age 27. I had a skeletal appearance. I also had, and continue to have, very flexible joints. For example, my right thumb is stuck at 90 degrees, which I have to press in the middle to release. I can feel the bone repositioning and going into the joint. This happens at least once a week.

My diet was ovo-lacto-vegetarian diet, with 70% of the calories coming from carbohydrates from when I was able to eat until 2015. In 2015, I could no longer process carbohydrate due to severe thiamine deficiency.

Since the age of 18, I have had quasi-constant back pain in the thoracic area. I have stretch marks on thighs, but have had no sudden weight gain/loss. Among the various diagnoses I had received before the age of 18 years old:

Idiopathic scoliosis – age 18. No treatment.
Iron deficiency anemia – at 18. Treatment with iron-containing supplements. No result.
Frequent treatments for infections (antibiotics)
Fasting hypoglycemia (until 2015).

The Fibromyalgia Pit

In 2008, my “fibromyalgia” symptoms began, although looking back at my history, many of these symptoms were there all along. I made a big change in my physical activity levels and this began my 12 year decline in health. In 2008, I started my philosophy studies at the university and decided to get more “in shape” by walking daily to and from the university. A total of 6 km per day.

Constant fatigue, no energy.
Worsened back pain.
Weak leg muscles at the end of the day.
Frequent nightmares from which I could never wake up. I felt like I couldn’t find my way out of sleep. After waking up, I would sit down and after 10 minutes I found that my head had fallen on my chest and I had fallen asleep involuntarily, suddenly.
Sensations of waves of vibrations passing through me from head to toe, followed by the sensation of violent “coming out” of the body and out-of-body experiences.
Heightened menstrual symptoms.
Fairly frequent headaches.

Over the summer, I recovered completely as I resumed my predominantly sedentary lifestyle. Then, in the fall, I began walking to and from university again, and my symptoms just got worse. This cycle continued for the next few years. My symptom list expanded to include:

Migrating joint pains.
Frequent knee tendinitis.
Pain in the heels.
Generalized pain, muscles, joints, bones.
Frequent headaches.
Sleep disturbance with insomnia beginning at 2-3am every night.
Frequent thirst, increased water intake (3-4 l/day).
Frequent urination, especially at night (woken 2-3 times).
Bumping my hands on doors/door frames.
Unstable ankles.
Painful “dry” rubbing sensation in hip/femur joint.
Prolonged angry spells.
Memory problems (gaps).
Difficulty learning new languages.

I underwent a number of tests including, blood tests, X-ray + MRI of the spine, and a neurological consultation. All that came back was high cholesterol (180 LDL, 60 HDL), low calcium, iron deficiency anemia, scoliosis, and hypoglycemia. No treatment was offered.

From February 2010-August 2010 I had a scholarship in Portugal. Philology studies interrupted. I was using public transport to go to classes, which were about only 3 hours a day. I required bed rest outside classes with only the occasional walk. I had a complete remission of all symptoms in July 2010 when I returned home and resumed my sedentary lifestyle. This was the last complete remission.

From August 2010 – December 2010, I resumed day courses at both universities and resumed the walking.

All of my symptoms were aggravated enough that by December I was bedridden. I stopped attending classes due to back pain in sitting position. I wrote two dissertations lying in bed. Once again, I sought medical advice and had a number of tests and consultations with specialists. I was diagnosed with peripheral polyneuropathy and “stress intolerance”, fibromyalgia. The treatment offered included:

Medical gymnastics: aerobics, yoga and meditation presumably to get me in shape and calm me down.
Calcium and iron supplementation, gabapentin, and low-dose mirtazapine.

The physical activity worsened symptoms, as it always does. The mirtazapine improved my sleep. I took it for 2 weeks and then stopped because I was gaining weight extremely fast.

From 2011 – October 2012, I was almost completely bedridden. I had to take a year off because I couldn’t learn anything, my head hurt if I tried. The physical symptoms improved after about a year, as did the deep and total fatigue. I tried to get my driver’s license in 2012, but failed. I couldn’t remember the maneuvers and the order in which to perform them. I couldn’t concentrate consistently on what was happening on the road. There was too much information to process very quickly.

From 2012-2015, I was getting my master’s in France. This aggravated all of my symptoms of exertion, both physical and intellectual. In 2013, I underwent general anesthesia for a laparoscopic surgery due to endometriosis, after which something changed in my body and I never fully recovered to previous levels of health. I took another year break between the two years of master’s studies. I couldn’t learn anymore. Symptoms relieved a bit by this break. After three months in Thailand for a mandatory internship, in one of the most polluted cities in the world, I got sick and developed persistent headache, with very severe cognitive difficulties. At this point, 90% of my time was spent in bed.

A general anesthetic in the autumn of 2015 for a nose tumor biopsy was the “coup de grâce”. Since then, I only partially recovered a few hours after a fluid infusion in the emergency ward and a magnesium infusion during a hospital stay in Charites Berlin in 2016. Other improvements: daily infusions of 1-2 hours with vitamins or ceftriaxone.

How I Feel Since Discovering Thiamine

In order to recover from the crash I experienced in February, I increased my B1 (TTFD) intake mid-March and made sure I was eating carbs every three hours, including during the night. I need about 70% of my total caloric intake to come from carbs.

I am currently taking 1200 mg B1 as TTFD, divided in 4 doses, 600-1200 mg magnesium, 500 mg B2/riboflavin, 3 capsules of an active, methylated B vitamin complex, 80-200 mg Nicotinamide 3X per day and 1-2 capsules of a multi-mineral and a multi-vitamin. I make sure I eat enough proteins, especially from pork meat, because it contains high amounts of BCAAs and helps me rebuild muscles.

I walked again the last week of April 2021, 500m in one day, because of a doctor’s appointment. I did not experience a crash that day or the following days. I did not have to spend weeks recovering from very light physical activity.

I can now use my eye muscles again, and read or talk with people online. I can cook one hour every day without worsening my condition.

After 5 years of constant insomnia, only slightly and temporarily alleviated by supplements, I can finally sleep 7.5 hours every night again. I no longer wake up 4-5 times a night.

My wounds are healing and my skin is no longer extremely dry and cracked.

My endometriosis, SIBO-C, gastroparesis, food intolerances, “fibromyalgia” pain, muscle pain due to hypermobility, are all gone.

And to think that all of this was possible because of vitamin B1 or thiamine, in the form of TTFD and that I almost didn’t buy it, because I no longer believed in that ONE supplement that would help me!

I will always be grateful for the work Dr. Derrick Lonsdale, MD, researcher Chandler Marrs, PhD and Elliot Overton, Dip CNM CFMP, have done so far in understanding, treating and educating others about chronic illnesses. More than anything, more than any physical improvement I experienced so far thanks to their work, what I gained was truth. Truth about a missing link, multiple diseases being present at one time and about why I have been sick my entire life.

Physical Symptoms and Diagnoses Prior to Taking Thiamine

Fibromyalgia and polyneuropathy diagnostic and mild, intermittent IBS-C since 2010;
Endometriosis symptoms aggravating every year, two surgeries, stage 4 endometriosis in 2020;
Surgeries under general anesthesia severely worsened my illness and set my energy levels even lower than they were before;
CFS/ME symptoms, hyperglycemia/pre-diabetes, constant 2-3 hours of insomnia per night and constant 24/7 headache since 2015, following an infection and during my stay in a very hot climate;
POTS, Dysautonomia, Post Exertional Malaise Symptoms from minor activities, starting with 2016;
Increased food intolerances (gluten, dairy, sugar/sweets, histamine, FODMAPs, oxalates, Sulphur-rich foods), to the point of eating only 6 foods since 2018;
Chronic Lyme disease diagnostic based on positive ELISA and WB test for IgM, three months in a row, in 2017;
Weight gain and inability to lose weight after heavy antibiotic treatment, skin dryness, cracking, wounds not healing even for 1.5 years, intolerance to B vitamins and hormonal preparations, since 2017;
Complicated migraine symptoms and aura, light intolerance, SIBO-C and IBS-D, slow intestinal transit, following a 4 month period of intermittent fasting that made me lose 14 kg, living in bed with a sleep mask on my eyes 24/7, severe muscle weakness, since 2018;
Two weeks recovery time after taking a 10 minute shower;
Gastroparesis, living on an elemental diet, in 2020;
All my symptoms worsened monthly, before and during my period.

Treatments Tried Prior to Thiamine

Gluten, dairy, sugar/sweets, FODMAPs, histamine, oxalate, Sulphur-rich foods/supplements free diets; AIP, SCD, Wahl’s protocol, candida diets; high dose I.V. vitamins and antibiotics, oral vitamins and antibiotics, liver supplements and herbs, natural antibiotics (S. Buhner’s protocol), MTHFR supplements, alkalizing diet, essential oils, MCAS/MCAD treatment, SIBO/dysbiosis diets and protocols, insomnia supplements, and any other combination of supplements touted as helpful for such symptoms.

And this is just what I remember top of my head. Their effect was, at best: preventing further deterioration of my body, but healing was not present.

Additional Literature

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Image by Gordon Johnson from Pixabay.

This case story was published originally on May 11, 2021.

The Appalling State of American Health

by Derrick Lonsdale MD, FACN, CNS

Published on March 1, 2022

7388 views

Mental Illness As Brain Energy Deficiency

The February 3 issue of Time magazine had an entry entitled “When Every Day is a Mental Health Day”. The Blue Cross Blue Shield Association reportedly found that in people between the ages of 24 and 39 in 2020, depression is the fastest-growing health condition. Fainting attacks, known as syncope, reportedly occur in 15-39% of the general population when they suddenly stand up from a chair.

It was also reported from Kaiser Permanente that “depression is a leading cause of illness among young people and anxiety is on the rise. Suicide ranks third as a cause of death for 15 to 19 year olds”. It is interesting that a picture of a young woman is shown whose anxiety level is described as medium-high. Her favorite pick-me-ups are described as “hugs, candy, conversation”. This is the cryptic message that invokes the methods which she uses to calm herself in the face of stress. Yes indeed, it is true that candy is often used as a kind of solace for the misfortune of stress.

I will show that far from helping an individual to adapt to stress, candy is often the underlying cause of the depression and anxiety that represents maladaptation to the stresses of daily life.

Stress: Anything That Demands a Physical or Mental Response

I turn to the work of Hans Selye who proposed that human diseases were the “diseases of adaptation”. Hans Selye was a Hungarian medical student. He was in a class where the professor was bringing patients into the classroom to describe the disease that was diagnosed in each of these individuals. Selye was not listening to the professor. He was engaged in looking at the facial expressions of each of the patients as they were brought in. He came to the conclusion that the facial expression was similar from patient to patient, irrespective of the disease that was being described, that they were all suffering from the stress of the disease, irrespective of its diagnostic category. He immigrated to Canada and set up an institution in Montréal to study the effects of stress. Of course, he was unable to study this in humans so he inflicted physical trauma to rats by the thousand and did laboratory studies to show the effects. He found that the laboratory showed changes in the blood that were similar to those found in human beings afflicted with chronic illness. He formulated his findings under the heading of “the General Adaptation Syndrome” and labeled human disease as “the diseases of adaptation”. The remarkable conclusion was that the resistance to whatever was responsible for causing the disease (stress) required huge amounts of energy in the brain for the process of adaptation. I am suggesting that the vulnerability of the American population is because so many people are unable to adapt to the everyday incidents encountered in just living.

This of course makes a world of sense because infections, trauma and prolonged mental pressures such as ugly divorce or business assignments (stress) are known to initiate disease and sometimes even death. At the time of Selye little was known about the way that the body manufactures the energy derived from food so his conclusion was the mark of genius. He actually did recognize his own genius and firmly believed that he would be the central figure in 21^st century medicine. I believe that he could have been right but his work has been largely ignored for at least two reasons. The cruelty to animals got him into trouble with the antivivisection league and the pharmaceutical industry captured the field.

Energy and Illness

We now know a great deal about the way this energy is produced and consumed in the body to produce function. The conclusions of Selye now make perfect sense in analyzing the cause of human disease. The only change that I would make would be to call human diseases “the diseases of maladaptation” because Selye pointed out that succumbing to stress was nothing more than the failure of energy production in adapting to whatever form of stress was being imposed. In order to understand this, you have to remember that infection, trauma, and problems involving mental work all come under the dominant heading of stress and that they all demand consumption of mental energy in the solution by adaptation.

Thus, we can begin to see that disease, irrespective of diagnosis, is nothing more than a combination of genetic risk coupled with a failure to meet the energy demands required. The initiation can be represented by the integrative action of one or more of three interlocking circles labelled Genetics/ Sress/Nutrition. There is now evidence that most genetically determined disease, including cancer, does not usually produce disease on its own. For example, diabetes is genetically determined but does not develop until middle age and often following a “stress event” such as an infection, trauma or a prolonged and nasty divorce. We have to recognize that the body’s ability to manufacture sufficient energy to meet whatever stress is imposed comes from the quality of the food. A relatively new science is called epigenetics and is the study of how our genes can be affected by nutrition and lifestyle.

I know that I am repeating myself (for emphasis) when I write that the ability to adapt to any form of physical or mental stress depends on brain/body energy and that if bad news, injury, infection or a nasty divorce, has to be faced in the modern world, Selye would point to the need for brain energy in meeting and adapting to that stress. Of course, if we are healthy, the adaptation is automatic and we don’t even think about it. In short, we adapt. That has given rise to the idea of “good, and bad, stress”. However, if a person becomes sick at such a time we are most unlikely to think of it as mild to moderate brain energy deficiency. Without this, the brain “complains by initiating symptoms”. In other words, individuals developing mental disease have biochemical deviations in their ability to adapt. Depression and anxiety are merely examples of the way in which the brain shows energy failure, the result of simply being alive. Note that depression and anxiety are perfectly normal as we adapt to the appropriate stimulus. They are abnormal when they exist chronically for no apparent reason or stimulus. The underlying mechanism has been exaggerated and is a reflection of abnormal brain function.

The January 2020 issue of National Geographic magazine states that “stress plays a major role in many illnesses that kill us. It also drives unhealthy eating, poor sleep, alcohol and drug misuse, and other bad habits. Modern medicine really sucks (their word) at preventing chronic disease”. In the same issue, “food allergies have become so widespread that many schools restrict what kind of lunch kids can bring from home for fear of setting off a classmate’s allergic reaction. Oddly enough, allergy is a brain sensitivity, resulting in abnormal organ action, so it is in reality brain related. For example, a woman who was known to be allergic to rose pollen enters a room where there is a bowl of roses. She succumbs to an attack of asthma that requires hospitalization, only to find later that the roses were artificial. The point is that the asthma could be initiated by more than one sensory input.

In the United States 5.6 million children suffer from food allergies. This translates to two or three in every classroom”. I will illustrate the unifying concept of energy deficiency by discussing a number of diagnoses in which the medical literature supports it.

Energy and Brain Autonomic Function: Parkinson’s and Alzheimer’s Diseases

The classic prototype for dysautonomia is beriberi, the vitamin B1 deficiency disease. Although this is not by any means the only cause of energy deficiency in the brain, it acts as a model for clinical expression. To put it as simply as possible, it represents an unbalanced ratio between calories ingested and the density of the micronutrients contained in the food source that catalyze the complex mechanisms of energy production. For example and contrast, the diet in Okinawa, Japan, that boasts a high concentration of centenarians, is nutritionally dense, meaning that it contains the vitamins and essential minerals that enable the calories to be burned (oxidized). It is also calorically poor, while in the US it is the reverse and where chronic disease is common. It has been shown in animal studies that a calorie poor diet correlates with the prolongation of youthful activity and even life itself.

In this presentation, I will try to show that brain energy deficiency is the major cause of disease. Because the controls of the autonomic nervous system in the lower part of the brain are quickly affected by energy deficiency, (the commonest cause in America is TD) it is not surprising that dysautonomia is common and occurs as part of other diagnostic categories. What I mean by that is that many diseases have been described in the medical literature associated with dysautonomia. For example, Parkinson’s and Alzheimer’s diseases are in a group of conditions that have a causative relationship. Both are associated with dysautonomia.

Megadose thiamine treatment has been reported to be successful in Parkinson’s disease.This information comes from a physician in Italy and it amply supports the concept that this chronic disease is caused by brain energy deficiency. The importance of the word megadose means that thiamine is not simply replacing a dietary vitamin deficiency. It is being used as a drug. The multiple actions of thiamine are all known to be essential in energy synthesis. If two diseases such as Parkinson’s and Alzheimer’s have a common cause, you might well be asking how is it that they are different in character? I think that this is an extremely important point. The disease in the brain depends on the distribution of the deficiency and hence the function of the affected cells. There is always symptom overlap in the two diseases. Variations in the presentation of disease can be extraordinarily variable.

Panic Disorder, Autonomic Dysregulation, and Energy

Supposedly psychological in nature, it is really a sympathetically initiated fight-or-flight reflex, originating because of brain oxygen, or oxidation, deficiency. The association between panic disorder and cardiovascular disease has been extensively studied. Some of these studies have shown anxiety disorder co-existing with or increasing the risk of heart disease. Heart disease almost always occurs in vitamin B1 deficiency beriberi, because the heart functions continuously throughout life and requires a continuous supply of energy. But heart disease occasionally does not occur, depending on the severity and the cellular distribution of the deficiency.

Recent interest has focused on whether some modern heart disease is caused by energy deficiency. What is confusing to people is that tachycardia (accelerated heart), occurring for no specific reason, is caused by an erratic signal from the brain via the autonomic nervous system. If the heart muscle is also deficient, the autonomic signal may result (for example) in atrial fibrillation. The treatment would therefore be energy stimulus in both brain and heart. This is why beriberi, the disease that is the well accepted result of vitamin B1 deficiency, causes defective function in the controls of the autonomic nervous system and the heart as the commonest result of this disease.

It also raises eyebrows when I say that beriberi is common in America, but is unfortunately not recognized by physicians whose overall philosophy is that “any sort of vitamin deficiency simply never occurs in America because of vitamin enrichment of foods by the food industry”. The trouble with that philosophy is that the extraordinary ingestion of empty calories in this population overwhelms the vitamin dependent machinery that oxidizes the calories. The best analogy that I can offer is a choked car engine. The input of gasoline must match the capacity of the spark plug to initiate gasoline ignition.

Overall, results suggest that rates of epilepsy are elevated among individuals with panic disorder and that panic attacks are elevated among individuals with epilepsy. An article reviewing the causes of epilepsy includes recent reports on the effects of inefficient cellular use of oxygen as a causative factor. Hyperventilation (over breathing) occurred in 25% of a group of patients with a relatively common form of dysautonomia (POTS) associated with fainting attacks. The authors hypothesized that the hyperventilation in this condition arises because of brain hypoxia.

This is supported by the fact that people prone to panic disorder are known to develop one of their attacks when situated on the top of a mountain. One of my patients was an elderly lady who indulged in square dancing once every two weeks. Invariably she would develop a feverish illness lasting several days after returning home. Without going into the complex details I was able to conclude that her energy requirement was increased by the physical effort required for square dancing. Because her energy synthesis mechanism was depleted from thiamine deficiency, these episodes of fever were exactly similar to the condition called mountain sickness. With megadose thiamine she was able to continue her square dancing without suffering these repeated illnesses. This patient’s problem could not have been addressed by the orthodox assumption that each episode of illness was due to an infection; Because of a rigid concept that these recurrent episodes were only the result of an infection, we tend to forget that the “illness” is really an exhibition of the complex mechanisms of defense organized by the brain. Lacking in a full complement of energy, its organizational capacity is depleted.

Many examples of manuscripts appearing in the medical literature describe the presence of multiple diseases occurring in a single patient. We suggest that this stretches credibility because we cannot predict the incidence of one disease in a person, let alone the incidence of two or three at the same time. Rather we should be seeking a single causative factor to explain all the symptoms. In the reports of multiple conditions occurring in one individual, one of them is invariably described as dysautonomia, strongly suggesting that the cause in common is brain energy deficiency affecting the controlling mechanisms.

Energy Deficiency and Health Across Generations

Mental illness, including depression, anxiety and bipolar disorder, accounts for a significant proportion of global disability and poses a substantial social, economic and health burden. Treatment is presently dominated by pharmacotherapy that averts less than half of the disease burden and is purely treatment of symptoms. In the January 2020 issue of the National Geographic under the heading of “A World of Pain”, a case is described of a pregnancy in which the patient called Karen “begins bleeding profusely so is taken to the operating room, where doctors perform a hysterectomy. After the operation, she suffers multiple organ failure and has a cardiac arrest from which she does not recover. Karen dies of pre-eclampsia”. This is a high blood pressure disorder that is unfortunately all too common in pregnancy. I recently learned from a book written by an American Ob/Gyn specialist that this kind of tragedy could be completely prevented by the initiation of a megadose of thiamine routinely given daily during the pregnancy. It is indeed stunning to claim that pregnancy complications are all manifestations of beriberi and that this cheap and simple ingestion can prevent all pregnancy complications, a fact that most people would find hard to believe.

But this also makes sense. The food that the mother ingests must be able to provide the energy, not only for herself but for the rapidly growing infant that she has to support. It is no surprise to me that dietary indiscretion by the mother, such as the use of alcohol and the lunacy of smoking, provides a legacy to her yet unborn child that adds to the burden of child development both before and after birth. It is now well known that sudden death syndrome in infants can be a legacy of the pregnancy. Breast milk thiamine deficiency has long been known to be responsible for sudden death in a breast fed infant and breast fed infants are associated with a higher risk of autism in our modern world.

What about other nutrient deficiencies as a cause of disease? People suffering from depression, schizophrenia and dementia often have measurably lower levels of serum folate compared to people not experiencing psychiatric disorder. Even the use of methyl folate, an important part of the chemistry of folate, as a stand-alone monotherapy has been observed to exert antidepressant properties. Earlier in this presentation, I mentioned that sugar was the cause of anxiety, not a treatment for it. The fact is that the processing of sugar is extremely complex and can initiate energy deficiency in the brain. Obviously, energy deficiency represents a threat to the organism and so there is an automatic initiation of the sympathetic nervous system that results in the fight-or-flight reflex. In other words, under these circumstances the initiation of this reflex is because the sugar has caused thiamine deficient pseudo-hypoxia. The obvious safety measure, automatically governed by the brain, is to alert the organism to the perceived danger, however that interpretation or brain misinterpretation might arise.

Brain Energy Deficiency and Violence

There is a link between mental illness and firearm violence, reported to be a significant and preventable public health crisis. Hypoxia and hypercapnia (too much carbon dioxide in the blood from inadequate breathing) excite the sympathetic branch of the autonomic nervous system. Excitation of this system generates the fight-or-flight reflex that is associated with aggression. Pseudohypoxia (imitates true hypoxia) is caused in the brain by thiamine deficiency. Therefore, there should be a serious look at the diet history of gun violence perpetrators.

Early Diet and Behavior

Many years ago, when I was in practice as a pediatrician, I saw many children who were brought because of emotional disease such as hyperactivity, learning disability, unusual temper tantrums and sleep problems. The current and false explanation for this was poor parenting, but on discussion with the parents I found that in almost every case the parenting was perfectly healthy. The diet of these children was appalling, however, very high in empty calories, particularly as those from sweets and I began to keep records of the dietary mayhem that was so common. In many cases I measured the intake of carbonated beverages in gallons per week. When I instructed the parents concerning an appropriate diet for their children, the emotional symptoms disappeared. This was so impressive and the children’s response to drugs so unpredictable, I decided to practice what has become known as Alternative Complementary Medicine. Please note that complementary is spelled with an ‘e’ not an ‘i’ and it indicates that it strives to take the best of orthodox medicine and complement it with the use of nutrients that represent the elements essential to energy metabolism. The two physician organizations that have developed are the American College of Advancement in Medicine (ACAM) and the International College of Integrative Medicine (ICIM).

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Photo by karatara: https://www.pexels.com/photo/male-statue-decor-931317/.

This article was published originally on February 24, 2020.

dysautonomia - Page 2

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