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A Case of Classic Beriberi in America

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thiamine deficiency beriberi in america

A desperate mother sent me an email about her 23-year-old son and it was easy to recognize that this young man had full-blown beriberi. You may or may not know that beriberi is well known as a vitamin B1 deficiency disease. Because the medical profession is convinced that this disease never occurs in America, it is usually not recognized for what it is. He had seen many physicians without success. I want to record the majority of his symptoms to show that they are surprisingly common and are usually ascribed to a “more modern” diagnosis. I have christened beriberi as the “great imitator” and I am sure that the reader will readily recognize the common nature of these symptoms, presented below in the form of a Table. It is important also to understand that these symptoms can occur for other reasons, but thiamine deficiency is widespread.

 

collapsing fatigue confusion
panic attacks loss of balance
blurred vision cluster headaches
hair loss jaundice at birth
infantile colic migraines
poor intestinal motility bloating
severe calf pain joint pains
weakness salt craving
cold extremities chemical sensitivity
POTS severe pain sensitivity

 

I want now to describe some of the features reported by this mother that were extremely important major clues. She described her son, when in good health, as 6’2”,  175 pounds, extremely athletic with “amazing hand-eye coordination and finishing college with high honors”.

As a result of his undiagnosed illness, his weight had dropped to 133 pounds. Because thiamine governs energy metabolism, an intelligent brain consumes a great deal. Of course, compromised energy production can occur for reasons other than thiamine deficiency. But there were very strong clues for beriberi. The mother described how her son

“…went out drinking with friends. The next day he could barely sit up in the car or stand. We were all commenting on why he was having such an extreme hangover”.

Alcohol would certainly exaggerate an existing thiamine deficiency. It is a well-known association. The symptoms were intermittent, rising and falling “for no apparent reason”. For example, she said that he was

“able to play sports, then lose his balance, become weak and complain of blurred vision”.

The reason for this is because the physical activity was demanding energy that could not be supplied because of the thiamine deficiency. He had jaundice at birth, now known to be because of inefficient oxygen utilization. This would indicate poor maternal diet in pregnancy or a genetic mechanism involving thiamine absorption. So-called panic attacks are common in the modern world and are absolute indicators of poor oxygen utilization in the brain. Under these conditions the reflex known as fight-or-flight would be initiated and this is what is being called panic attacks. The blurred vision would go along with this too.

Beriberi Is a Form of Dysautonomia

We have two nervous systems. One maintains what we call willpower and is known as the voluntary system. The other one is known as autonomic and is entirely automatic and outside willpower. This system controls all the organs within the body. It explains why there are so many symptoms involving many parts of the body. This is because of the loss of signaling power between the organs and the brain. A lot of energy is required to run this system and explains why the autonomic nervous system is affected in beriberi. POTS is one variety of dysautonomia. This young man craved salt and that too is a form of dysautonomia is known as cerebral salt wasting syndrome, explaining the natural craving.

Thiamine deficiency beriberi in America

Is There a Help From the Laboratory?

The answer to this is no, as long as physicians refuse to recognize that beriberi is common in America. This unfortunate young man was diagnosed almost certainly as psychosomatic. The disease has a very long morbidity with symptoms shifting up and down according to the state of energy metabolism on a day-to-day, week-to-week and month-to-month basis. The laboratory has to look for it because the standard tests done only provide distant clues. It is the absence of the abnormal results that make it easy to conclude that this is “a psychologic disease”. For example, it was reported that this young man had an elevated vitamin B12 and a mildly elevated CRP. I cannot give the complex details here, but both are peculiarly related to energy metabolism and require understanding in order to fit them into the pattern of diagnostic clues. I have reported these facts elsewhere.

What Is the Hope of Normal Health in This Person?

It stands to reason that the first thing is proper diagnosis and a knowledge of the widespread symptomatology, including their fluctuation. As long as he continues to take alcohol and sugar, he will never get his health back even if he supplements with thiamine. He is in danger of developing the classical brain disease known as Wernicke’s Encephalopathy. This state of the disease almost certainly involves cellular damage that cannot be repaired. It is therefore very urgent to understand the self-responsibility that is required. He has to learn that alcohol is potentially lethal for him. There is undoubtedly a genetic relationship between alcoholism and sugar craving and it is probably true that a search for the genetic relationship would at least be helpful in understanding the nature of this disease.

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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 August 9, 2017. 

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When Glaucoma Is More Than an Eye Disease

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glaucoma dysautonomia

Dr. Marrs and I are very much on the same plane of thinking. We both believe that much of the illness in America is not being recognized for what it really represents, hence the publication of our book:  Thiamine Deficiency Disease, Dysautonomia and High Calorie Malnutrition. I want to give you an illustration of a typical situation where the patient is falling through the cracks of modern medicine. I live in a retirement home and one of my friends who is resident here told me the following story, believing that his medical history was a reflection of how well he had been treated.

Open Angle Glaucoma: A Marker of Autonomic System Dysfunction

His story begins in his forties with a burgeoning glaucoma in the left eye. He told me that the surgeon had to make a cut in his eye to let the fluid out and he later required a corneal transplant. At the time he was smoking a pack a day of cigarettes. He continued by telling me that he periodically had cardiac palpitations and in his fifties he had cardiac bypass surgery and was being treated with aspirin. He still experiences heart palpitations. At present, he has periods where he is unable to catch his breath, sometimes for half an hour or so. As he was telling me his story, I could clearly see that all of these events might easily be put together with one underlying cause. Ophthalmologists (eye specialists) know perfectly well that one type of glaucoma known as “open angle” is not a disease of the eye. It is a disease of the autonomic nervous system (ANS), so let me try to explain this.

The eye-ball is filled with fluid that has entry and exit portals, allowing for the circulation of nutrient bearing fluid throughout the eye. Entrance and exit are controlled by a branch of the ANS. If the exit mechanism fails, the fluid cannot leave the eye and the pressure builds up. The exit is in an angle representing the detailed way in which the eyeball is constructed, hence the termination “open angle”. The key to relieving the fluid buildup is by fixing the neurological control of the entrance and exit of fluid.

The trouble with this is that the pressure can build up slowly and even the vaguest eye symptoms are unlikely. Even when visual limits are first noted, the disease is usually quite advanced. Increased blood pressure or family history of glaucoma may be an indication for an eye examination on a regular basis. The next thing to be understood is that the ANS is not symmetrical. In other words the right half of the body is controlled differently from the left half, thus explaining why the glaucoma can be in only one eye. In my view, in an ideal medical situation, the eye doctor should have advised the patient of the underlying cause and referred him for further evaluation. The patient should have been informed that the “pack a day” of cigarettes was the underlying cause of the glaucoma. He is unlikely to have suspected the connection.

Other Symptoms of Autonomic Disruption: Sleep Apnea, Dyspnea and Heart Palpitations

Evidence for the ANS association has been shown by the fact that sleep apnea (repeated temporary cessation of automatic breathing in sleep), surprisingly common in the United States, is prevalent in primary open-angle glaucoma patients. Although this would be a potential clue for an eye examination, there was no history of sleep apnea indicated by my friend. This disease develops because of defective control mechanisms in the brainstem and automatic breathing, particularly necessary in sleep, is mediated through the ANS. The complaint of cardiac palpitations also indicates abnormal activity of the ANS, because the speed and regularity of the heart is controlled by this system. Finally, his difficulty in breathing with the technical name of dyspnea is typical of heart and lung disease. His previous history of heart palpitations suggests that this is heart-related. I would suggest that his health is in a precarious state and I think that he might wind up eventually by being treated with nasally administered oxygen, as I see repeatedly in other elderly residents. I often wonder whether the oxygen is really giving benefit if the catalysts that enable cells to use it are in insufficient supply, because they are never given a thought.

Disparate Symptoms within the Framework of Dysautonomia

Most people know that we have two nervous systems. One is known as voluntary and the other that takes care of all automatic mechanisms in the body, is called the ANS. This is the nervous system with which we are concerned here. The brain may be thought of as having two primary sections. The upper part thinks while the lower part automates by signals to and from all the organs in the body through the wiring of the ANS and a bunch of glands known as the endocrine system. Another illustration of asymmetry, as indicated in this case of glaucoma, is the fact that nerves from the ANS deliver a different signal to the heart from the right side of the body versus the left side. One controls the strength of contraction of the heart while the other controls the speed at which it beats. Therefore, it is not too difficult to understand that heart palpitations are a function of this nervous control and that their cause is the same one that gave rise to glaucoma, faulty action of the ANS. Finally, the difficulty in breathing is because of defective metabolism in the brainstem where automatic breathing is controlled. That is why glaucoma and sleep apnea sometimes occur together as we have stated.

Why the Autonomic System Becomes Disturbed? Poor Oxidative Metabolism

The lower part of the brain, known as the limbic system, is a complex of cells that come together in the operation of the ANS and endocrine system. The metabolism of these cells is inordinately dependent on a high rate of oxygen utilization. Because of this, they are very sensitive to thiamine deficiency, resulting in what is sometimes referred to as brain pseudohypoxia (false lack of oxygen). The lack of energy in these cells produces abnormal function in the ANS.

The toxic effect of smoking results in slowly producing damage in oxidative metabolism. This may give rise only to minor changes in mental or physical fitness, sometimes for years, but the metabolic inefficiency eventually affects the ANS, often initiating serious disease, as in this case. Although smoking is generally thought of as the commonest cause of lung cancer, it has a much wider danger of triggering virtually any disease because of its role in reducing cellular energy. There is circumstantial evidence that many, if not all, diseases are the result of oxidative dysfunction. Zbinden published a paper in which he found 696 papers that described treatment of 242 different diseases, other than beriberi, with thiamine, providing a variable degree of success.

We can now see why the patient described above had a series of events that could be ascribed to an underlying cause in common, inefficient oxidation. In fact, the symptoms of beriberi, none of which are pathognomonic (strong indicators of that disease exclusively), are so prolific that it can be looked at as the great imitator of disease. Chronic fatigue, heart palpitations, insomnia, abdominal bloating, constipation, panic attacks and many other symptoms, so often regarded erroneously as psychological or referred to as Chronic Fatigue Syndrome are common in America today. The official medical denial of it as an acceptable solution leave the unfortunate patient in limbo without the necessary, relatively simple treatment that is so effective.

The Problems with Compartmentalized Medicine

It seems to me that the patient that I have described represents a failure of perspective in modern medicine. The glaucoma is treated as an eye disease and changes in heart function are seen as diseases of the heart, whereas the two have an identical underlying cause, chiefly in the brain. The patient can be seen as slipping through the cracks in perspective and it carries with it a serious indictment of the present medical model. The surgical approach to the glaucoma was unavoidable and saved the patient’s eye. We know that that kind of glaucoma can build up slowly without the patient being aware.

My point is this: I would be willing to bet that the patient had other trivial symptoms at the time of his glaucoma that would be a reflection of abnormal ANS activity. They could have been so trivial that they weren’t even mentioned to the physician and long forgotten by the patient when serious disease made its appearance. Although the glaucoma could not have been predicted even under those circumstances, at least it would not have been a surprise to the ophthalmologist. In an ideal doctor/patient relationship, the ophthalmologist would be aware of the ANS connection and refer the patient to a colleague who understands this underlying cause. The later development of heart palpitations might have been seen differently as dysfunction in the ANS. Modern heart disease and thiamine deficiency have recently been connected.

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 showing acute angle-closure glaucoma which is a sudden elevation in intraocular pressure that occurs when the iris blocks the eye’s drainage channel—the trabecular meshwork.”

Image credit: Jonathan Trobe, M.D., CC BY 3.0, via Wikimedia Commons.

This article was published originally on August 22, 2019.

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Migraine Energy Metabolism: Connecting Some Dots

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migraine, brain energy, thiamine

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.

We Need Your Help

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

Yes, I would like to support Hormones Matter. 

Image by Chen from Pixabay.

This article was published originally on June 22, 2020.

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An Artist’s Decades Long Dysautonomia Treated With Thiamine

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artist with thiamine deficiency

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.

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Medication and Vaccine Adverse Reactions and the Orexin – Hypocretin Neurons

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orexin hypocretin neurons brain energy

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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This article was published originally on January 29, 2014.

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Dysautonomia and Chronic Illness Post Brain Surgery

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Dysautonomia

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

Yes, I would like to support Hormones Matter. 

This article was published originally on May 17, 2021.

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Progressive Deterioration of Health With Severe Nutrient Deficiency

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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 20th, 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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Burning Out From Worsening Dysautonomia

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dysautonomia

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. 

Photo by Gift Habeshaw on Unsplash.

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