beriberi Archives - Hormones Matter

Dysautonomia and Hypoxia

Published on April 15, 2024

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Every profession has its jargon that enables its practitioners to communicate relatively easily but is incomprehensible to those outside the indicated profession. This is most true in the medical profession, so I am about to explain a disease condition that has become extraordinarily common. I will begin by defining the word dysautonomia. “Dys” is a prefix meaning abnormal and “autonomia” refers to the autonomic nervous system. The autonomic system is the part of the nervous system that controls autonomic functions and behaviors that ensure survival. This includes, heart rate, respiration, digestion, temperature, even libido.

The autonomic system operates largely involuntarily and without conscious consideration. Many people are not aware that we have two types of nervous system. The one that we all understand is called “voluntary”, enabling us to carry out willed actions. This nervous system is controlled by the upper part of the brain known as the cortex, the latest part to be evolved, capable of thought and giving us those human abilities that are unique within the animal kingdom. In contrast, the lower part of the brain controls an involuntary “messenger system” that enables us automatically to adapt to the conditions of environment that we meet on a daily basis throughout life. The messenger system does not think. It acts automatically. The autonomic system is a “three channel system” that sends and receives signals to and from all parts of the body.

The Three Channels of the Autonomic System

The first channel connects with a bunch of glands known as the endocrine system. These are the glands that produce hormones, messengers borne by the blood to the body organs. This is a complex messenger system that adjusts, influences and modifies behavior. The other two channels are known as the sympathetic and parasympathetic systems. Between them, they provide direct communication that enables a given organ to react and participate in the symphony of adaptation. All work in a coordinated manner. Thus, the action of the autonomic nervous system, either by direct communication with an organ or by means of releasing a hormone, activate or deactivate all the organs in the body selectively.

Sympathetic System. This is best thought of as the action stimulating mechanism. Its best known reflex is known as “fight-or-flight”, activated by any form of mental or physical stress or threatened danger. It will accelerate the heart, deactivate the intestine, produce a sense of anxiety or panic, dilate the pupils in the eyes and raise the blood pressure, all things that you desire to happen if you are either fighting or fleeing from an enemy. It is designed for short-term action and consumes energy at an accelerated rate, particularly in the brain. It is important to note that this is a reflex, not a thought process. It is activated by a visual, auditory or tactile stimulus that is interpreted as danger. I think of this as a “stress input” that is answered by either physical or mental action in some form of self-preservation.

Reading a telegram that provides bad news triggers an emotional reflex that does not necessarily require physical action but is an obvious source of stress and the mental response is sympathetic and energy consuming. It may well induce accelerated heart rate, pallor and pupillary dilatation as a modification of a fight-or-flight reflex. Emotions are reflex, engineered by the lower brain and programmed according to the nature of the incoming stimulus perception. This in turn stimulates the thought processes of the higher brain that is capable of modifying the reaction. Sympathetic action of this nature is also activated by the release of adrenaline from its appropriate gland “and gives rise to what is sometimes called the ”adrenaline rush”.

Parasympathetic System. This is best thought of as “the rest-and-be-thankful” mechanism. It will decelerate the heart, activate the intestine, produce a sense of peace, constrict pupils of the eye and lower blood pressure, the very opposite of that produced by the other system. Our primitive ancestor could now roll a stone over the mouth of his cave and carry out the functions of the body after he has escaped from danger. He can now sleep, eat, indulge in bowel activity and experience a sense of peace. This also is not a thought process.

Dysautonomia: Autonomic Chaos

It is obvious that if the sympathetic and parasympathetic systems were activated together there would be chaos. Reflex sympathetic action under normal circumstances is balanced by a withdrawal of the parasympathetic action and vice versa. Thus, for example, accelerated heart rate is partly produced by withdrawal of the parasympathetic at the same time as it is accelerated by the sympathetic. This coordination is computed by the lower part of the brain. Under normal circumstances its action is modified by the upper brain that provides willpower under what might be called “advice and consent”. On the other hand, under urgent necessity, when danger is life threatening, the sympathetic system takes over the action completely, explaining why a soldier in battle may not be consciously aware that he has lost a finger until the action is completed.

If the reflex coordinated mechanism of the autonomic system is lost for any reason, it is referred to as dysautonomia. A medical textbook entitled “Dysautonomia” was edited by Sir Roger Bannister, then a London physician who was the first athlete to run the four-minute mile. The book describes many examples of this condition and deals with the genetic aspect. It never addresses the subject of nutrition, an oversight that introduces the clinical blindness of the modern physician to nutritional deficiency disease. This is in spite of the fact that the best example of dysautonomia is beriberi, long known to be caused by deficiency of thiamine (vitamin B1) by the ingestion of empty carbohydrate calories.

Hypoxia and Pseudo-hypoxia in Dysautonomia

The word hypoxia refers to lack of oxygen. Its most devastating effect is in the brain and particularly the lower brain that never sleeps. This is because the cells in that part of the brain have a heavy requirement for oxygen. As we all know, oxygen is delivered to all the 70 to 100 trillion body cells by the bloodstream and they consume it in the synthesis of energy. This consumption of oxygen is in turn dependent on the presence of thiamine and other vitamins. A deficiency of thiamine therefore produces the same clinical effect as hypoxia. For this reason, its deficiency causes what is sometimes known as pseudo-hypoxia (pseudo meaning false).

Since the lower brain controls the autonomic nervous system, we can now see how thiamine deficiency results in dysautonomia. Of course, as we all know, a complete lack of oxygen means death. We are here discussing the effects of a mild to moderate hypoxia or pseudo-hypoxia. The so-called TIA (transient ischemic attack) is an example of hypoxia because of a temporary failure of blood delivery to the brain. In most cases it is probably a brief contraction in the muscular wall of a major artery resulting in constriction of the artery. The irony is that I believe a common mechanism for TIA may involve arterial artery spasm from magnesium deficiency. It might well be obviated by taking a supplement of magnesium as a preventive. Thiamine and magnesium deficiency both produce the same effect by preventing the consumption of oxygen, thus stopping energy synthesis: hence the term pseudo.

Clinical Effects of Pseudo-hypoxia

There are many papers published in the medical literature in which a particular disease (for example lung cancer) is associated with dysautonomia. Each one of these manuscripts offers a case report in which the cause of this interesting but baffling association is unknown. My hypothesis is that pseudo-hypoxia gives rise to the dysautonomia whose symptoms are not recognized for what they represent, are ignored, or treated symptomatically and lead eventually to more cellular damage within a body organ that becomes an organic disease. If recognized in the early stages, diet correction and a few supplementary vitamins are all that is needed. If not, it is hypothesized that symptoms increase and reflect irreparable cellular damage. The constellation of symptoms is then referred to as disease A or B, e.g. Parkinson’s or Alzheimer’s.

It has now been shown that a common condition called “panic attacks” can be induced in a patient by the inhalation of air enriched with about 30% carbon dioxide, producing hypoxia. Therefore, this condition has nothing to do with Freudian psychology. It is a purely biochemical phenomenon, induced by hypoxia or pseudo-hypoxia. I recently met a friend with a story that I hear repeatedly. He was suddenly overcome by faintness while at work. It was associated with dizziness, lack of control and unconsciousness. He was conveyed by ambulance to the nearest emergency room where all the tests were negative and he was allowed to go home. Almost automatically this is referred to as psychosomatic disease as though the unfortunate patient is imagining or even inventing the obvious brain caused symptoms. There is little doubt that this represents a temporary period of hypoxia or pseudo-hypoxia that is extremely threatening to the individual for his or her future, since it indicates a state in the brain that can result in a recurrence, perhaps of greater severity.

I learned later that this friend had received heart surgery many years before this incident. Since the primary organs affected by the pseudo-hypoxia of beriberi are the brain, the nervous system and the heart, perhaps pseudo-hypoxia was the underlying cause of the heart problem that led to surgery. I doubt that it was ever considered. The trouble is that I cannot tell a friend that perhaps all he has to do is to take a few vitamin supplements. He simply would not believe me. My credibility would be lost, possibly with the loss of friendship and my proffered advice, like the proverbial seed falling on stony ground. The concept is “outside the box” and does not conform to the medical model that exists in the minds of all of us.

What is particularly important to understand is that mild to moderate hypoxia or pseudo-hypoxia is itself a form of stress and triggers the fight-or-flight reflex. This is quite logical since a decreased oxygen concentration is dangerous and even life-threatening. Under these conditions the lower brain is more easily activated and the resulting action fails to heed the advice and consent provided by the upper brain. Thus, a child or adolescent consuming empty calories, will be thiamine deficient and his brain susceptible to periods of pseudo-hypoxia, particularly when experiencing other energy demanding stressors. The hypoxia will affect autonomic regulation, which will manifest in a number of seemingly unrelated symptoms, that include digestive issues, attentional deficits, unexplained aches and pains and perhaps most notably in children, behavioral difficulties represented by extreme emotional lability. The easiest way to produce pseudo-hypoxia is by the widespread consumption of carbohydrate and fatty foods (e.g. doughnuts) representing empty calories, so commonly associated with the consumption of high sugar content beverages. Sugary foods are not only devoid necessary nutrients, but the sugar itself forces what thiamine stores that exist out of the cells. Could high calorie malnutrition be responsible for some of the otherwise inexplicable violence reported almost daily in the news media? It is biochemically possible. Perhaps an easier question to answer, could thiamine deficiency and the resultant hypoxia be responsible for the myriad of autonomically controlled systems currently labeled dysautonomia? Possibly.

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This article was published originally on February 13, 2017.

Familial Beriberi: Discovering Lifelong, Genetic, Thiamine Deficiency

by KY

Published on February 22, 2024

13210 views

Familial Beriberi - genetic thiamine deficiency

In 2017, at the age of 52, I had an unexpected call from my new doctor informing me “I know what’s wrong with you! Come to my office now!” Lifelong increasing chronic fatigue and untreatable Hashimoto’s thyroiditis were my chief complaints.

Past doctors prescribed high dose thyroid medication, which made me feel worse. An autoimmune diet kept me trim but provided no energy. I read adenosine triphosphate (ATP) is required for thyroid production, though ATP isn’t discussed in treatment. Baggage from Effexor and an adverse childhood were also contributors to my health.

Desperate, every relevant supplement and thyroid medication on the market, I tried. Only two were effective. GABA relaxed me, and d-ribose cured my depression 100%. I became bubbly. My personality changed, but after four weeks they both stopped working. Amour thyroid lifted my brain fog for a week. Then, I had side effects. Eventually, I would learn that I, and many members of my family, across several generations, had beriberi or thiamine deficiency. In my case, I had a defect in a key thiamine transporter that made getting sufficient thiamine from diet all but impossible. Unfortunately, I did not learn this crucial information, until I was in my fifties, after years of illness and suffering.

Women’s Issues and Unrelated Problems Begin

While my problems began decades earlier, they seemed to hit a crescendo as I hit menopause. The HRT patch relieved hot flashes, only to fuel a fruit-sized fibroid that split in half with one part covering my rectum. A GP prescribed colon therapy causing severe leg cramps and constipation. A fibroid ablation enabled normal bowel function. Afterward, ozone baths caused my bowel function to stop and I developed air hunger. An ENT said, “you don’t have sleep apnea, there’s another system in your body that is causing air hunger.” He recommends a university clinic over going to different specialists. I pursued genetics.

Starting to connect my cognitive decline, prediabetes, and depression in my grandparents to myself, I went to the MTHFR expert that wrote the report. Her extensive 15-page genetic/supplement report offered no results. After failed treatments from endocrinologists, functional doctors, and big-name clinics like Mercola, I took a chance on Orthomolecular Medicine.

Discovering a Familial History of Beriberi

On the day I was diagnosed with thyroid treatment failure, I found a nutrient interaction article and had a light bulb moment, I’m missing a nutrient for thyroid production. I went to the author, the late Dr. Richard Kunin, San Francisco’s legendary go-to doctor for solving mystery illnesses through nutrients. He was a pioneer in antioxidant therapies, utilizing diet, nutrient and genetic testing since the seventies. His orthomolecular research was the first to verify the use of a mineral therapy in a drug-induced disease.

When his door flung open, I saw wisdom. A rare commodity. Here was this brilliant doctor and a poster of his early collaborator Linus Pauling, staring down at me. Dr. Pauling coined the term orthomolecular meaning “the right molecule in the right amounts.” A doctor like this comes once in a lifetime and I handed him my three-inch binder.

A true scientist, he was able to assess my biochemical individuality, in two sessions.

In the doctor’s intake, the first clue is asking what my parents ate. They ate both Chinese and Western foods, which seemed like no big deal. After lab results, he searches through 300 genes, to find the biggest picture, the gene. Instead of trying to treat multiple gene defects with a supplement. He addresses the root cause first.

He announces, “You’re deficient in thiamine,” and gives me the SNP, called Transporter 2 (SLC19A3) which provides instructions for making a protein called the thiamine transporter, which moves thiamine into cells. Over time, the transporter dissolves.

I had thiamine and asparagine deficiency and riboflavin and glutathione borderline deficiency. The thiamine or vitamin B1 deficiency caused the other deficiencies, but he stays on point and discusses thiamine and only thiamine. He prefaces the session with a history of beriberi and birds fed white rice. Looking back, it’s rudimentary B1 history, but as a patient stuck in the Hashimoto’s/Adrenal Fatigue paradigm for so long, my mind went blank. I remained silent, I didn’t know if I could die from it.

To make matters more confusing. I had stopped taking thiamine after an OATS showed B1 adequacy.

When he told me I can’t convert energy from food, I thought how absurd. He reminded me “the bottom line is how well you absorb the thiamine; not how much I tell you to take”. A Meyer’s Cocktail IV is an initial part of treatment. The next step is collecting data to prove the relevance of thiamine as an essential nutrient required to make energy.

When I Added Thiamine, My Body Began To Recharge

For the first time, I saw a difference in labs and body function. At 300 mg of HCL, my increasing A1C levels fell below the prediabetes range. I almost took metformin at one point, recommended by an integrative doctor. I felt the effects of B1 utilizing B6, through a lucid dream. Treating methylation since 2006, he says “B1 is the gateway to methylation.” With before and after data, he points out B1 upregulating the folate cycling. My energy was increasing. Muscular problems resolved, elevated branched chain aminos were absorbing and TMJ and bruxism disappeared. This was just the beginning. familial beriberi - thiamine deficiency

I found the thiamine experts, Dr. Derrick Lonsdale and Dr. Chandler Marrs during my titration period. Nuances of thiamine used as a drug to make ATP are available with a detailed overview of beriberi, throughout Hormones Matter. Post to post, the doctors’ addressed every missing piece to my complex puzzle and more. They prompted me to take a closer look inside my dad’s past, one he rarely spoke of, and connections were made.

While titrating up, I had a short bout of diarrhea in the middle of the night. When I decreased the dose, I developed POTS for the first time, the room would spin 24/7 whenever I stood up. My GP referred me to the ER. I was unaware that I was having a paradox reaction. I just upped the thiamine, POTS, and diarrhea resolved.

Chronic TD is called beriberi means “I can’t, I can’t” in Singhalese. The problem is Chinese typically under 80, have never heard of beriberi, and in the US, beriberi is known but assigned as a disease that does not exist anymore or a condition only seen in alcoholics and bariatric patients. Genetic beriberi is passed through families, causing the inability to absorb thiamine from foods.

Beriberi In Two Families Going Back Three Generations

My family history revealed apparent genetics expressing as neuropsychiatric disorders and other conditions that appeared unrelated. Thiamine deficiency (TD) is not easily identified, due to its polysymptomatic nature. Besides the brain, the heart, muscle skeletal, digestive system, and autonomic nervous systems (ANS) need thiamine to function.

My maternal side lived in prosperity and ate a traditional Chinese diet and tropical delicacies. There were 7 members, including my grandfather that had Alzheimer’s (AD) and one family member had Parkinson’s. My grandmother had TD from kidney dialysis. There was TD in AIDS. Untreated hyperthyroidism resulted in cardiac failure mortality at 58. An alcoholic uncle had deficits, anxiety, cancer, and AD. An anorexic cousin refuses whole meals, develops a damaged digestive tract, severe IBS-C, chemical sensitivities, and major depressive disorder.

My paternal side lived in poverty. White rice was a diet staple. There was an aunt that died from child mortality in China from starvation.

After migrating to the US, food scarcity persisted. My grandfather had obesity and type 2 diabetes. My grandmother had sadness after her husband sold their daughter’s papers in China, never to see them again. At 61, my 4’10” grandmother fell over and died from beriberi.

Her wake was the first time my dad went to a restaurant at age 16. He often licked food and preserved it for later. Falsely accused of stealing, the detention center fed him regular meals. Five siblings had short stature and high IQs. His Chinese brother pictured right, was saved by the U.S. Army from malnutrition and assigned to be the radar instructor. There was bullying, anger, and irritation in the three boys. One, a bar owner exhibited extreme behavior like bringing a gun over a trivial conflict that would leave in-laws aghast.

Ocular diseases, restless leg syndrome, circadian rhythm disorder, cancer, some OCD and hypermobility, and osteoporosis appear. There was TD from chemotherapy. Two aunts left behind in China lived to be centurions and a daughter has fibromyalgia, depression, and other deficits.

Connect the lineage with a pregnancy gone wrong.

Genetics and a Traumatic Pregnancy Sets the Stage for Life

Pregnancy, a hypermetabolic state, requires sufficient thiamine for the development of a healthy child. My mom, a robust woman, was overmedicated and bedridden for a month post-pregnancy. She recovered but my brother was permanently disabled. My brother was born with uncontrollable hyperactivity and oppositional disorder. Our theory was his oxygen supply was cut off to his brain, but it was thiamine deficiency.

Two years later I was born. As a young child, I was hypoactive and didn’t move much. In grade school hearing loss was detected. Early memories included some clumsiness and not having the strength to swing on monkey bars like other children. My first feelings of frustration were over homework, especially math. My overall health waxed and waned and would not draw attention until high school when tiredness, poor memory and learning disabilities appeared. I was bullied by my older brother.

Nine years later my younger brother was born, bruxism as a baby, was his first sign of thiamine deficiency.

The next generation, symptoms of thiamine deficiency show in a gifted child.

Neurological deficits ranging from severe to minor were a sign of impaired methylation since birth.
My mom’s prenatal diet was traditional and American, and we were bottle-fed. This was in the ’60s when women were weaned off breastfeeding.

Now connect the genetics, the pregnancy and untreated thiamine deficiency in a parent and sibling.

A Genius Mind Uses More Energy and Requires More Thiamine

My dad invented the on-line TV guide in the eighties. In a constant state of fight-or-flight, working through the middle of the night on patents, sugary snacks were comfort foods to compensate for early years of food deprivation. The “night owl” term we used was circadian rhythm dysfunction. Thiamine is an overlooked nutrient required for sleep and the breakdown of cortisol.

When my brother’s hyperactivity was unmanageable, breaking things, beating the ADD out of my brother was habitual. A dysfunctional limbic system causes knee-jerk reactions to uncontrollable rage. I just learned that my seemingly nice uncle, an alcoholic, frequently tried to beat the homosexuality out of his young child.

A psychologist thought violence only happens in alcoholics. I think this limited view needs to be updated to include excess processed food intake. I remember “children should be seen and not heard” commercials as a child when hitting and spanking was more accepted.

In 1983, Dr. Kunin cited Dr. Lonsdale’s research that describes the B vitamin link with violence in Mega Nutrition for Women, “patients whose violent behavior was inexplicable by conventional medical diagnosis were found to be deficient in one or more B vitamins, notably B1, B3, and B6”.

During the Covid-19 shutdown, I thought of TD when incidences of abuse spiked, homelessness and random violence spread, and middle-class families now become dependent on food banks.

Poor Health After Antibiotics

As a young teen, I lost my glow, I looked tired, and my skin had a jaundiced yellow-greenish tint. In high school, after a round of tetracycline for transient acne, I was never the same. My metabolism stopped and I gained 40 lbs. I also have leptin deficiency and so I am always hungry. Napping after school was an everyday event. My limited thyroid test given showed normal thyroid-stimulating hormone (TSH). I was also constipated but didn’t know it until middle-aged after I was diagnosed with Hashimoto’s. In my 20’s I took antibiotics for chronic strep throat. Uninterested in nutrient dense foods, I subscribed to carb loading and high-intensity aerobic activity, the trend of the day.

Changes in My 30’s and the Promise of Modern Medicine

When my dad had side effects from sleep medication, he did his research, bought supplements for every system in the body, and stopped going to doctors. He got the family off of rice and put us on B vitamins. Uneducated in vitamins, I gave up on them too soon. I wasn’t taking enough! My mom’s acupuncturist treated my ADD, but I strayed when a well-meaning friend steered me towards pharmacology, and I took Effexor. The damage showed up over the next decade when increased nervous system and mitochondrial dysfunction begin.

Loud bar music in the back of my unit initiated chronic insomnia in my forties. I had open mouth breathing. Elevated cortisol and night sweats woke me at least 8 times a night. If I was mad, I’d have an instant hot flash and sizzle like a red bull. I lost my sex drive. After quitting Effexor, elevated thyroid TBO antibodies appeared. Later diagnosed with sensorineural hearing loss, the psychiatrist prescribed sound therapy but the condition isn’t curable.

Musculature problems began, I had an unrelenting frozen shoulder from a gym accident, and at one point, I had ataxia and couldn’t walk straight. After a trip, while in Hurricane Ivan, I was unable to walk for a month with ataxia. I once met an advanced multiple sclerosis patient, that experienced the exact same symptom from Ivan. The cause was thiamine deficiency in the cerebellum, the part of the brain that controls movement and walking.

For work, I illustrated 300 skylines from around the world and market them on Etsy. My fine motor skills and artistry remain superior, but my spatial organization was nonexistent. I was very messy. Taking GABA hampered work stress, but I couldn’t cycle it from thiamine deficiency. Managing inventory and college students wore me out. One told me “You can’t retain what I tell you”. Finding my car in large parking lots was often challenging. The hippocampus circuitry requires thiamine for short-term memory function.

Orthomolecular psychiatry has proven to treat and manage these types of disorders with nutrients and diet, as the first line of defense. There was no need for antidepressants.

After My Diagnosis, I Learned My Parents Were Already Taking Thiamine

When I told my dad about my thiamine deficiency, he pulled out a bottle of thiamine labeled anti-beriberi. He was taking B1 for cardiac support. The heart and brain consume a vast amount of energy and require thiamine to meet the demand. My mom took benfotiamine successfully for shingles, a neuropathic pain.

When I told my original acupuncturist, about my diagnosis he said, “I already know you have beriberi, just take B vitamins and lots of them. You don’t need my herbs.” He had been treating me for dysautonomia, twenty years before I developed POTS. I detested the point because his needling pressure hurt. No questions asked; he needles points by observation and pulse, Western characterization in diseases have no significance.

Part of the treatment for dysautonomia is a needle to the center of the philtrum, this point prevents fainting. Another needle is inserted into the center of the forehead and one on top of the head for balance. Traditional Chinese Medicine (TCM) healers identify liver and lung channels weakness two decades before western medicine.

The New Doctor Damaged My Health In Only Eight Months

Twenty nineteen was a bad year. Dr. Kunin sees Vitamin C deficiency and signs of anemia and then retired. I stopped getting IVs. I would still nap after taking them. My trusted acupuncturist, also a nutritionist moved. I began dry coughing a lot, which later I learned was a sign of TD. Then I met the worst doctor ever.

I showed her, Thiamine Deficiency, Dysautonomia, and High Calorie Malnutrition and she handed it back to me and said “Oh, another patient brought this in the office.” I interviewed another doctor and told him I have TD and he replied with, “what’s your point!” and referred me to a doctor out of state.

I settled on the first doctor, and everything started wrong. She put me on a high-dose thyroid medication without titrating, and Low Dose Naltrexone (LDN), which gave me a stomachache. She wanted me back on LDN after I told her I had side effects. She recommends NAD instead of Meyer’s Cocktails which includes thiamine.

By the time I realized I was in a hyperthyroid state, the damage had begun. A cascade of beriberi symptoms begins. When one symptom would go away, another would begin. The neuropathy was more long-term. I had resting tachycardia, lactic acidosis after five days of yoga stretch that caused feet neuropathy and then trigger finger. All the doctor could say was “I had candida overgrowth”. The cause of candida was that I had a weakened immune system from TD. I watched videos on lactic acidosis to explain it to her.

When I saw an eleven year old’s homework on glycolysis it made me wonder how much doctors remember from medical school.” I tested the doctor and asked her “What does pyruvate convert to?” She answered incorrectly.

I was developing non-alcoholic Wernicke’s encephalopathy (WE), acute short-term memory loss. I almost walked out of a restaurant thinking I paid the bill. I couldn’t remember putting a credit card back in my wallet and arguing with the clerk after she had handed it back to me. Once I read, “if you think you’re deficient in thiamine, get an IV right away.” After a series of Myers Cocktails with phosphatidylcholine, the progression stopped.

Another doctor got me off the thyroid meds, yet wet and dry beriberi symptoms continued. My left-hand lost circulation and turned hard and purple. The back of my neck hardened and my backside turned into butter. I had unintentional weight loss and my hand reflexes slowed. My minerals were becoming unbalanced. I contacted a refeeding syndrome clinic, for a consult, but was turned away because I wasn’t anorexic. A few months later I traveled to Hawaii and made a mistake.

Orthomolecular Medicine Rescues Me Again

Accidentally packing thiamine HCL instead of TTFD, the HCL initiated my paradox reaction and I had diarrhea several times the first night. Every day I napped from the sun’s UV rays. Excruciating muscle cramps sent me to Dr. Pritam Tapryal, Honolulu’s IV doctor specializing in chronic fatigue syndrome. Thiamine handouts, a stockpile of capsules and vials of B1 were waiting for me.

He calculates that I needed 600 mg of IV thiamine based on the length of time I had been feeling unwell. With an iron load before the second IV, I felt a surge of energy – I got ATP! My vagus nerve stimulated peristalsis and excess fermentation stuck in my body for three months finally released. Elevated liver enzyme activity and low blood pressure normalized. Afterward, I found a doctor willing to provide high dose thiamine therapy at home.

I went back to the doctor that said “what’s your point” when I told him I had thiamine deficiency and requested 600 mg of parenteral B1 instead of 100 mg. A bit taken back, he shows compassion and custom orders 500 mg of B1 in a Myers Cocktail, after I explained my recent experience. The IV manager thought I was an ICU patient, but I wasn’t. It was the dose I felt best on.

High Dose IV Thiamine Therapy: From A Patient’s Perspective

A series of high-dose thiamine (HDT) IV treatments, turned into an epigenetic treatment going on two years and two months. I’ve taken 100,000 mg of parental thiamine to this date. Infusions continued to sustain therapeutic effects and increased thyroid production. Unknown cause of malabsorption required ongoing infusions. Resolved through extensive pre-and post-labs.

I self-directed my treatment and gauged myself. I found thiamine articles from all over the world, but high-dose thiamine information was limited to WE treatment only. I received no medical advice on thiamine therapy from allopathic doctors that had clinical nutrition education, or from a young orthomolecular doctor or GP. Familial beriberi - thiamine deficiency

I had two to three IVs per week the first year that included 500 mg of thiamine. The longest time without an IV was three weeks at the beginning of 2020 and eleven days at the end of 2021. Below is a 12-month summary, from a 55-year-old woman with unrecognized lifelong thiamine deficiency from a SLC19A3 gene defect.

Journal From Long Term, IV, High Dose Thiamine Therapy

My high-dose thiamine regimen began 11/21/2019. This is the Meyers Cocktail titration period:

2 infusions of 200 mg of thiamine in 2 weeks in end of Nov. to Dec.
5 infusions 300 mg of thiamine in 2.5 weeks Dec. to Mid Dec
2 infusions 400 mg of thiamine in 2 weeks Mid Dec. to January.
500 mg of thiamine 2 to 3 times a week were taken in the middle of January.

11/2019 Concerned about anaphylaxis. Only a few teeny bumps around lips developed and disappeared after the first day. Visual clarity is the first sign of improvement.

12/2020 – Foot neuropathy and trigger finger for 4 months, resolved with 7 IV’s spread out over 4.5 weeks. The IV thiamine doses were 300 mg or 200 mg. Dexa scan shows osteopenia in lower back and femur and only 3 lbs. of lean muscle mass, muscle wasting, a hallmark symptom of beriberi.

OATS test taken a day after HDT infusion – tested B1 borderline deficient. Borderline and deficient in minerals and vitamins except manganese, doctor thought something was wrong with lab.

1/2020 – Right mucosal lining was demyelinating and slightly bleeding for a month, saw glitter. Zonulin levels over 800, the doctor told me not to be concerned, but I was. Slight rectal bleeding.

An unintentional fast in cold weather caused syncope. Broke out in an intense sweat, became faint and lost appetite. Leaned against buildings every few feet to get home, no thiamine in am. Sitting on bench resolved symptoms. MCV increases to 100, normal range is up to 95.

Tested negative for panel of inborn errors of metabolism. Autoimmune panel negative except – Arthritis – equivocal, Thyroiditis- out of range, Epstein Barr – negative.

2/2020 – New formulation of phosphatidylcholine, with small amount of dextrose without B1 was a mistake.

On three-week break, nighttime driving vision had decreased. Resumed Meyer’s Cocktail after break, fatigued, fell asleep in IV chair after IV. Reduced thyroid medication from I grain a week, increased after break to 3.5 grains a week. A1C 4.8 increased to 5.2 after break.

Right quadrant of my upper teeth dropped down. Oral surgeon said “not pathogenic of disease”.

Last visit with Dr. Kunin. Concerned I looked just as depressed as when we first met. I was happy to see him, unable to express it. Continue a more DIY approach and TCM, “the Chinese have found ways to treat that western medicine has not figured out, and one day technology will be so advanced doctors won’t be necessary”. He handed me the keys and said, “Figure it out on your own.”

3/2020 – Introduced high fat diet. Lost 3 lbs.in a week. Severe leg cramps from foot to shin. During an IV, felt leg cramping. Normal cholesterol increased from 260 to 400. Stopped diet. No B1 in fat.

4/2020 – Lowered stress from semi-retirement and resting. IBS starts to resolve for the first time at 55. Felt extreme chill one day. Took injectables at another doctor’s office due to shut down. I took 100 mg B1 in a B complex in intramuscular (IM) with B12 to ease B1 ‘pinch’, plus IM biotin for a month. Not as effective as HDT infusions. Combination of B1 with complex and biotin had best results.

5/2020 – Meyer’s Cocktail and 350 mg of NAD back-to-back infusions lifted brain fog profoundly. Able to do tasks I couldn’t perform prior. I cried with joy, my cells were not permanently damaged from past use of Effexor and antibiotics. Unable to replicate treatment. Oral Inositol reduced elevated triglycerides dramatically, then stopped working. IBS came back off and on.

6/2020 – Tested borderline low on calcium, choline, magnesium, B5, B12, Vit C, K2, zinc on a three month average. GI lab shows mal-digestion, metabolic imbalance, and dysbiosis. Stomach pain from psyllium and flax, phytobezoar build up, rash on neck since 2019 getting worse, insomnia resolved.

7/2020 – Severe anemia showing and severe muscle weakness. I couldn’t lift a 5 lb. weight. Acute memory loss, almost walked out of lab before taking the lab. Waking up early in am in summer at 8:00. Hemoglobin normal and then drops frequently, IV doctor sees bleeding. Ophthalmologist finds arcus build up from high cholesterol, strong arteries, and recommends latanoprost for glaucoma after field test.

8/2020 – Decreased parenteral 500 mg B1 to 300 mg to test if high dose thiamine is depleting B12. Began coughing after 7 days. Post NAD IV lab tested B12 deficiency, causing hemoglobin and T3 deficiency. Acupuncture treatment creates switch sensations throughout body allowing oxygen flow, heart channel under arm point pulsated – oxygen and lung channels communicate. Leg bruising – Vitamin C deficiency. Insomnia came back when B1 parental dose decreased, never resolved fully after increasing B1.

9/2020 – ANS dysfunction – uncontrollable body flipping in bed two nights in a row, movements like a fish out of water. Resumed 500 mg of prenatal B1 after two weeks at 300 mg. Ophthalmologist said “you look more alert”, compared to two months ago. Started IM Mic-B and hydroxocobalamin, 5 days a week. IBS-C decreased with B12 IM. Coughing on Lipothiamine, switched permanently to Allithiamine, cough resolved. Normal zonulin levels return, reduced gut inflammation. GI didn’t order endoscopy after I told him something hit my stomach when walking and had rectal bleeding. He wrote IBS on notes. Stopped EDTA IVs for cadmium after a few treatments, when urine began foaming.

10/2020 – Latent deficiencies appear: B12, CoQ10 malabsorption. B1 not absorbing. Vitamin C deficiency appears, lifelong subclinical scurvy, bleeding gums, gingivitis, pilaris keratosis, bruising, poor iron absorption, rectal bleeding, low tyrosine. Sick people are low in B vitamins and Vitamin C. Repeated thiamine depletions cause heavy Vitamin C deficiency in lung, kidney, thymus, and liver.

Tested positive for Intrinsic Factor AB, Pernicious Anemia (PA). Hematologist defensive when I asked him if TD can cause anemia, cancelled next appt., told me to see a GI. Doctors booked from Covid-19 delays.

Oral surgeon cleared teeth shifting. Orthodontist ordered aligners, short teeth roots in scan.

Trialed compounded thiamine cream from Lee Silsby pharmacy and replaced TTFD.

11/2020 – Stomach pain increasing after meal. Twelve days in, I thought I was going blind. The thiamine cream wasn’t absorbing. Indoor and night vision blurry. Back to TTFD and Myers Cocktail together. My vision came back, but not as clear before getting blurry. Mild paradox reaction, a bowel movement in the middle of the night.

12/2020 – Endoscopy shows chronic gastritis, h. pylori and peptic ulcers. A combination of a lack of nutrients cause ulcers, including B1. Refused triple therapy (antibiotics and PPI). Treated with cabbage, herbals, mastic gum. ION Panel indicated GSH and potassium deficiency, lactic acidosis (TD), ketosis, oxidative stress, transmitter deficiencies and metabolic syndrome.

Elliot Overton of EO Nutrition interprets mitochondria in battleship mode, suspects mold toxicity. Unseen mold or water damage. Incontinence and frequent urination. Second ophthalmologist told me don’t take latanoprost. MCV high still high with regular IM B12, since 10/20. With small veins and bursting arteries, it’s difficult to maintain IV’s.

In 2020, my health was like my dad’s. My hearing and vision deteriorated, I was unable to hear people speak with masks on and had difficulties focusing on conversation in noisy rooms. Gingivitis developed into periodontal disease; teeth aligners require lifetime use. My dad is deaf in one ear, and now going blind in the second eye and had the periodontal disease the same year and wears dentures.

Observations at 43,500 mg IV Thiamine After 13 Months

Intravenous therapy can target issues in ways oral thiamine cannot reach.

Improved thyroid production, A1C, insomnia, IBS and CFS, overall energy level partially improved. Foot neuropathy and trigger finger resolved. Cocktails with phosphatidylcholine, iron, and NAD, had increased effects, latent deficiencies appear, no nutrient depletions from high-dose thiamine.

Infection, gastritis, ulcers during treatment caused malabsorption. Reducing thiamine caused insomnia to reoccur and acute vision reduction, increased ANS dysfunction caused temporary uncontrollable body movements. Increased dose of 300 mg to 500 mg of B1 resolved uncontrollable body movements and regained vision.

I saw one patient vomit, and a patient have nausea during 300 mg B1 Meyers Cocktail.

ROS from unknown cause extends treatment into 2021.

High Dose Thiamine IV Therapy, Toxins, Diet, Labs, and Gigong

In 2021, I tapered to two IVs a week and increased the 500 mg to 600 mg mid-year. Hot flashes returned after 5 years of remission causing a three-month setback. Insomnia made me delirious and had to take naps. PEMF bio-mat calms the nervous system to assist in sleep, without it I’ll wake up a few times during the night. For over 10 years, I wake up and urinate once a night. My eyes became blurry and I walked slowly like an old lady for a short period. Daily clear phlegm wants to come out since 2020 when I eat.

In spring my bloodwork showed Stachybotrys and Aspergillus mold. I found growth on papers in a storage box against a wall with the laundry room on another side. Condensation went through the wall.

With my gut healing and IV therapy, my TBO antibodies levels reduced significantly. The increased T3 raised my steroid hormones. Reducing thyroid medication again was a real possibility. IBS-C was resolved by mega-dosing powder magnesium with fiber, B1 and B12. I once had an offer to see the world authority on IBS-C, though all I needed was a good form of high-dose magnesium. I was feeling better until I experienced unexpected setbacks.

Everything Changed With Two Major Endocrine Disruptors

Microscopic brick debris during construction flew under my windows. Debris flew inside over 50 ft. and landed everywhere, never thought my eyes and lungs could clear it. Due to an HLA-DQB1 gene defect, I’m unable to break down mycotoxins (mold). Mold is an anti-thiamine factor and it oxidizes B1 and B12.

When inflammation started to calm down, my hallway went under remodeling, and material debris and paint fumes went under my door. The chemicals shut down my thyroid. Antibodies rose from 180 to 535. Inflammatory markers that were improving became elevated and deficient. My killer cell function, HNK1 (CD57) level was 50 and now 18. The doctor thinks I have Lyme. I’m testing for MARCoNS, a staph infection that resides deep in the nasal passage, due to sinus inflammation from the biotoxins.

After trialing Cholestyramine for mold binding, it made me constipated. My acupuncturist gave me a two-hour treatment to undo the damage. To detox, I use an FIR infrared sauna on the mat. I’m getting an ERMI test kit to test other rooms, an air test hardly detected mold.

HDT Isn’t a Standalone Treatment

With the amount of IVs I took, I tested questionable foods. A few small gluten-free snacks put me into a comatose within 20 minutes. Less than two ounces of coffee initiated leg/foot cramping. I never had this problem a few years ago. Removal of processed carbs is the only way I can maintain my thiamine storage.

Staying in mild ketosis, on a paleo diet is optimal for me. When I tried high-fat and vegan diets, they caused deficiencies. I have a nonfunctional gene cluster FADS1/FADS2, that requires the consumption of EPA and DHA found in seafood. Drinking concoctions of vegetables and minerals activate B vitamins throughout the day. TD causes nitric oxide deficiency and I replete myself with nitric oxide greens. My one kryptonite food is liver, it elevates my copper. Using food as medicine supports my overall immune function as I recover from Chronic Inflammatory Response Syndrome.

My hydrochloric acid is deficient from TD, and I have low gastrin. I’ve taken 13,000 mg of Pepsin Betaine and feel no sensation. Apple cider vinegar doesn’t seem to work. My amino supplements aren’t absorbing. I also have oxalates, Elliot recommends more B6 and I’ve increased molybdenum to meet my sulfur intake.

I take a blend of B1 that includes: 900 mg Allithiamine, 300 mg benfotiamine and 500 mg thiamine HCL. Over 900 mg Allithiamine and sulfur come up. Before a Meyers Cocktail, I’ll soak in magnesium salts. I’ve increased all the B’s and take them with other essential nutrients throughout the day in moderate to high doses. I require biotin intramuscularly every few weeks, otherwise my nails chip, this started last year. My transporter may be dissolving.

Utilizing Biomarkers and Managing Nutrients

Every six weeks I rotate biochem panels and adjust diet and supplements. My weaknesses this year have been lipids, omegas, aminos, and inflammatory markers. My B12 continues to pool due to suboptimal thiamine levels unable to utilize B12, so I stopped testing. I inject 35 mg of hydroxocobalamin a week, plus sublingual, and hemoglobin is always on the lowest end of normal after I had pernicious anemia. Mold is the suspect cause. I may also have scar tissue from ulcers and scurvy of the colon. The GI doctor recommends an endoscopy once every three years when there’s been a problem.

I’ve found nutrient panels reliable when B1 is extremely deficient. On two occasions my lactate tested normal. Then I had beriberi symptoms after I took the labs on the same day. This was from eating beans and walking in sun, which forced me to sleep. My citric acid markers were normal on an ION panel and I was in ketosis, but the clinician didn’t know I had POTS on the morning of the lab. This was from a three-day fast suggested by a doctor. Thiamine deficiency can worsen on a dime.

Diagnosed with TD on a SpectraCell micronutrient panel, I had long-term B1 deficiency. Normal B1 levels are misleading on my labs once there’s been intake. The Vibrant America panel showed B1 malabsorption at 35,000 mg of parenteral B1. I’ll continue with this panel and monitor nutrients connected to B1.

My doctor’s friend offered me the two-part transketolase lab for research, but my doctor forgot to arrange the sampling. I was upset at the time, but it doesn’t matter now. I manage myself by how I feel. With Excel journaling, the more elements I add, the more clarity I receive. Observing physical changes are equally valuable to the labs.

A Revisit to Energy Medicine That Compliments Nutritional Balancing

I recently discovered group Primordial Qigong. I haven’t found any other modality that has the same restorative benefits that give energy instead of using energy. Movements connect the body, mind, and soul with the focus on living in the present. Gentle stimulation of systems and body parts creates rejuvenation from within. Who doesn’t want that?

Dysautonomia, the fainting prevention point, is taught in practice. The bank of hands faced together inverted pushed downwards from the forehead over the philtrum encourages balance. Made for masses with no resources, it only requires continuity. This is a welcoming alternative compared to the nutrient-depleting therapies, recommended by for-profit western doctors that made my health worse when they didn’t know what they were dealing with.

At 100,000 mg Of IV Thiamine – It Feels Like I’m on a Train I Can’t Get Off

Overall, the quality of my life has improved. I no longer need to lie down and sleep during the day, even if I feel tired. I’m more active in mind and body. I can sit up and read, wake up earlier, and exercise. My processing speed and speech are faster. The left side of my brain is strengthened. I did audits on my condo association to trace missing dues and one over BlueCross when many claims were unpaid. My brain fog had been too severe to do this previously.

Neuropsychiatric issues appear in less frequency. I still experience forgetfulness and minor learning impairments. Irritation is manageable. I believe some brain function is permanently damaged along with hearing loss. Considering my long-standing history, I’m pleased with the results even though it is only a partial recovery.

Since my body called out for a high dose, there’s a chance I can regress. At 11 days off the IVs, I was deficient in Co2. I don’t know if the thiamine coenzymes can function without high-dose therapy because of my genetic liability. I’m patiently waiting to see how my body changes after the toxins are eliminated and figure out how to taper down from the IVs.

Final Thoughts

Thanks to Dr. Marrs and writers on HM for elucidating thiamine awareness, I learned how to use thiamine as a drug at a time when I needed it most.

Through luck, I found nutritional clinicians that made a significant difference in my health. Educated in Dr. Lonsdale’s thiamine research, they applied his nutrient-based knowledge into their practices. Understanding that beriberi still exists today and is not an ancient scourge from yesterday, is critical.

By assimilating the genetic impact of beriberi and orthomolecular dosing, I’m regaining health in my late fifties. However, no patient should have to spend a lifetime finding a treatment based on luck. There’s no reason to it’s all here: Thiamine Deficiency, Dysautonomia and High Calorie Malnutrition, Derrick Lonsdale and Chandler Marrs; www.orthomolecularmedicine.org

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This article was published originally on February 14, 2022.

Beriberi is Alive and Well in America

by Derrick Lonsdale MD, FACN, CNS

Published on February 15, 2024

13369 views

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

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

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

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

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

Additional Cases of Thiamine Deficiency

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

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

Ondine’s Curse

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

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

The Complexity of Treating Vitamin Deficiencies

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

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

Common Presentations of Thiamine Deficiency: The Walking Sick

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

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

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

This article was published originally on April 11, 2019.

SIDS and Vaccination

by Derrick Lonsdale MD, FACN, CNS

Published on December 4, 2023

8024 views

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

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

What History Tells Us about SIDS

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

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

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

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

Predicting SIDS

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

SIDS, Thiamine and Brain Development

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

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

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

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

Does Thiamine Deficiency Underlie Post Vaccination SIDS?

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

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

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

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

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

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

From the Legs to the Heart: Historical Descriptions of Beriberi

by Chandler Marrs, PhD

Published on August 2, 2023

7292 views

Over recent weeks, I have been working on a paper involving thiamine deficiency diseases and have been looking into the historical descriptions. I was aware of the history emanating from Japan and the stories of Kanehiro Takaki, the Japanese naval medical officer who first connected the symptoms of beriberi to diet at the turn of the 20th century, and of the subsequent research that isolated the thiamine in the bran of the rice, which had been removed to make it appear more palatable. I was also well aware of the history of Wernicke’s and Korsakoff’s syndromes and the neuropsychiatric manifestations of alcohol-induced thiamine deficiency. Although, when the symptoms were first observed, they had not yet been connected to thiamine. What I wasn’t aware of was the long and rich history of writing about beriberi in China. There is some evidence that the recognition of beriberi dates back to 1st century China, although much of the writing on this topic has been lost and so it is difficult to confirm. Nevertheless, from the 7th century onward, beriberi in its various manifestations was written about extensively in medical texts. I thought I would share some of the descriptions here.

From the Legs to the Heart

The thiamine deficiency disease we call beriberi was called jiaoqi by Chinese physicians and was written about extensively from the 7th century onward both by independent physicians and in texts sponsored by the Chinese government. Jiaoqi, which means ‘leg-qi’, described the nerve, muscle, and/or circulatory (edema) related leg symptoms that would come to be associated with dry and wet beriberi respectively, centuries later.

What I found particularly interesting, was the recognition of both the subtle progression of symptoms and the variety of symptoms by which the illness could manifest. Beriberi, as it is currently described in western texts, is emblematic of the end stages of disease. For the Chinese, and for anyone who has read either our book or our articles published here on thiamine deficiency, the disease process begins years before. It is insidious in its trajectory and complicated in its presentation. The seventh century Chinese physicians recognized this.

When they get this illness, many people do not immediately feel it. Some first have no other disorder and then suddenly get [this one]; some contract it after suffering multiple other illnesses. In the beginning, the symptoms are trivial; the patient eats, drinks, and amuses himself the same as ever, and his physical strength is the same as before. At this time one must observe the illness carefully…
Its symptoms: numbness from the knee to the foot, sometimes aching, sometimes a creeping sensation like insects crawling around. In some cases, the area from the toes to the knee and calf is especially sensitive to cold. In some cases, the lower leg is bent and weak and [the patient] cannot walk. In some cases, the lower legs have slight swelling, extreme sensitivity to cold, or pain. In some cases [the lower legs] are relaxed and do not obey [the patient’s intentions], or twitch acutely. There are some whose condition is dire [yet] they can still eat and drink; [but] there are some who cannot eat, or who vomit upon seeing food and drink and can’t stand the smell of food. Some [patients] feel a thing like fingers, dispatched from the meaty part of the calf, which travels upward and attacks the qi of the heart system. Some have spasms over the entire body. Some have a serious fever and headache. Some people’s brains and hearts rush and throb [as though frightened], and they do not want to see light in the places where they sleep. Some patients have a bitter pain in their bellies and simultaneously have diarrhea; in some, their language is sloppy and error-filled and they easily forget or mistake things. Some have cloudy eyes and a confused aura. All of these are signs of the illness… When one first contracts this illness, one should treat it quickly. It is different from ordinary illnesses.

Japanese physicians, who followed many of the teachings of Chinese medicine, also wrote copiously about this disease through the 12^th century and again from the 17^th century onward. Only they called it kakke. Kakke is the phonetic equivalent of the Chinese word jiaoqi but means beriberi. Early Japanese researchers also noted that symptoms of kakke began in the legs with the ‘swollenness’ of the lower limbs first, followed by swelling in the abdomen and heart as it progressed indicating wet beriberi and the appearance of emaciation, dry skin, and lower abdomen numbness demarking dry beriberi. In both cases, it was recognized that if the disease process reached the organs, especially the heart (Shoshin) death was imminent.

Jumping continents and a few centuries, a Dutch physician in the East Indies wrote about the neuropathy, ataxia, muscle wasting, and general fatigue and malaise associated with beriberi and its onset associated with alcoholic intake.

The inhabitants of the East Indies are much afflicted with a troublesome disease they call Beriberii (a word signifying sheep). The disease has probably received this denomination on account of those who are seized with it, from a tottering of the knees, and particular manner of walking, exhibit to the fancy a representation of that animal… Among the chief symptoms of this disease is lassitude of the whole body. The motion and sensation, especially of the feet and hands are depraved; and for the most part, titillation is felt in the parts, familiar to what seizes them in cold countries in the winter; but with this difference, the sensation the Barbiers [a paralytic disease of the east thought to be beriberi] is more painful…In general, the disease invades slowly but upon drinking a large draught of Palma Indica when he is heated, the attack of it is sometimes extremely sudden…” pp. 1-3.

All of this has become part of what we now know to be thiamine deficiency-induced diseases. To think, these observations were made centuries ago and still hold today is quite remarkable.

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This article was published originally on July 21, 2021.

From Mother to Daughter: The Legacy of Undiagnosed Vitamin Deficiencies

by B. Figueroa

Published on July 10, 2023

14207 views

This is a story of a mother with undiagnosed vitamin B deficiencies who gave birth to a daughter who was also born with undiagnosed vitamin B deficiencies. In the eyes of conventional doctors and labs, there was not much wrong with us, but we knew that life was harder than it should be. We lived managing debilitating dizziness, daily migraines, fibromyalgia pain, chronic fatigue, allergies, hormonal changes, anxiety, and depression. Until we discovered that we were both hypermobile with histamine issues, hypoglycemic, and had many vitamin B deficiencies. The biggest challenge was for my daughter to start taking thiamine (vitamin B1). Her heart rate was all over the place and she had such a bad paradoxical reaction to thiamine that we believe she had been living with undiagnosed beriberi along with POTS.

Mom’s Health Marked by Asthma, Anxiety, Migraines, and a Difficult Pregnancy

All I remember as a child is being afraid to talk in school even if I knew the answer to a question. I had allergies and could not exercise due to asthma. During college, I had to read over and over the same thing because I could not concentrate. I worked extremely hard because the fear of failure was too much to bear. I started to have hormonal imbalances and missing periods. I successfully finished college and moved away to another state. That is when migraines started. Later, I became pregnant with my first child and started having blood clots. Anxiety and depression would come and go with hormonal changes.

When I was pregnant with my second child, my daughter, I was sick every morning with nausea. After 6 months of pregnancy, I had gained only 6 pounds. Ultrasounds showed that the baby was growing normally, but I was losing weight. At that point, I also could see blood clots on my leg. I was placed on bed rest. By the 8^th month, my water broke and my daughter was born. She was jaundiced and placed under UV light for a week. I also stayed in the hospital for a week dehydrated, with blood clots, and with the “baby blues”. We left the hospital after a week, and she had a “normal” development. However, you could see that she was a baby that would not go with anyone, not even the people close to us, indicating some anxiety.

Daughter’s Early Health Issues: Selective Mutism, Asthma, Concentration Issues

When my daughter turned four years old, we moved out of state and that is when she stopped talking outside the house. I later found out that it is called selective mutism, a form of severe social anxiety. She started seeing a school counselor to try to help with her anxiety and self-esteem issues. I brought a girl scout group to my house so that she could start having friends and talk to others in her area of comfort. She also developed asthma and needed nebulizer/albuterol treatments frequently and daily QVAR for prevention. She was given Singulair, but it made her very depressed. Her grades in all classes were all over, from A to D. She would spend the whole time after school trying to complete homework, but she couldn’t. Her teacher told me that she really did not have that much homework. I would ask her to watch the dog eating and to take her outside as soon as the dog finished but she would be wandering around the kitchen and could not pay attention to the dog. Her neurologist gave her Strattera and that helped a little. Her EGG also showed some abnormal activity. The doctor recommended anti-seizure medicine and said that she was probably having mal-petit seizures. I refused medication based on how she reacted to Singulair and because the doctors were using words like “probably” and “just in case”. I kept an eye on her and noticed when she ate ice cream and got asthma. I had her stop sugars and dairy. Soon after that, a teacher called me, excited to tell me that my daughter was talking at school. She also was able to stop all asthma medication except for 2 weeks every year when seasonal allergies would hit. At this point, it had been already four years since she stopped talking outside our house. She started excelling in all classes and we were able to stop Strattera. However, the continuous anxiety remained.

The Teenage Years: Continuous Migraine, More Medications, and No Answers

At 16 years old, she got a cold that turned into asthma with a continuous headache that just would not go away. She started waking up every day with a migraine, depressed with no energy. We had to wait three months to see a pediatric neurologist. Meanwhile, I would take her to my chiropractor early in the morning, give her an Excedrin, and she would go to school whenever she felt better. She began drinking at least 2 cups of coffee every day to help with the pain. Sometimes she would go to school at 11am, sometimes at 1pm. Even if there was just one class left, she would go to school. At this point, she felt that she wouldn’t have a future.

When we finally went to the neurologist, he recommended amitriptyline. I had been on amitriptyline and woke up one day not knowing which year or season was, but I was told that the issue was the high dose given to me (125mg), after decades of it increasing it every year. I agreed as long as it was a low dose. Amitriptyline lessened the continuous headache, but it was not really gone, and she still needed some Excedrin. She started daily aspirin as well. She was just getting by day to day trying to manage her pain and mood and trying to have a normal teenage life.

Increasing Weakness When Outdoors: Untangling Root Causes

She became very weak whenever we would go to the beach or to a park. We would have to drag her indoors and give her water. On some occasions, she would say that she could not see. Somehow, she successfully managed to graduate from high school. We started seeing functional doctors. We found that she had some variants related to mitochondria dysfunction, but we really didn’t know how to address this. We also found out that she had Hashimoto’s and antibodies against intrinsic factors, which was indicative of pernicious anemia. We knew right there, that she had issues that conventional doctors had missed.

We also did a Dutch test and found that all of her hormones were high. The functional doctors suggested sublingual B12, folinic acid, and a B complex. She said the vitamins made her feel awake for the first time. However, chronic fatigue was still a major struggle for her. Eventually, she had to stop folinic acid because it made her depressed and unmotivated. Meanwhile, she managed her anxiety with herbs, but it was a real struggle. She also continued to have asthma requiring albuterol every fall season. She chose a very challenging career in cell biology with biochemistry. She went through college with many cups of coffee just to control migraines, have energy, and be alert.

Discovering Her POTS Symptoms

The summer of 2019, before her senior year of college, the nurse checked her vitals as part of her new summer internship. The nurse thought the pulse monitor was broken because her heart rate was 120 sitting down. After a few minutes, it went down to 99, so the nurse dismissed it. When she told me that, I started paying attention to her heart rate. We went to her physician and neurologist and in both instances, her heart rate was 100, just sitting down waiting for the doctor. I asked if it was normal, and they said that it was in the upper range but not a concern. I was still concerned and made an appointment with a cardiologist but also bought her an iwatch. She noticed right away how her standing heart rate would be over 100, and by only taking a few steps, her heart rate would go even higher and she would become fatigued and even dizzy. From the heart rate monitor on her iwatch, we could see how quickly her heart rate would climb upon standing and then slow a bit when sitting.

That is when I remember that I have read about POTS and hypermobile people. I remember that when she was a child, the neurologist had said that she was hypermobile, but never said that it could be a problem for her. It just seemed like a fun thing to have. I started asking in health groups and someone mentioned that her medications could also cause high heart rate. I searched and amitriptyline did have that side effect. That is when my daughter showed me that her resting heart rate was in the 90s and it would fluctuate from 29 to 205 without exercising. When we went to the cardiologist and explained all of this, he said that he did not even know how to diagnose POTS because it is rare. He did testing and said that the heart was fine but there was some inefficiency due to some valve leaking but that it usually does not cause symptoms. I asked about amitriptyline and he confirmed that it could raise heart rate. At that point, she stopped amitriptyline and her maximum heart rate was 180 instead of 205.

She went back to her last year of college when Covid hit. She came back home and we could see the lack of energy and how much doing any little thing or stress would crash her for days. Since I needed glutathione for chemical sensitivities, I decided to see if it would help her. Glutathione with co-factors helped her recover, instead of crashing for days, she would recover the next day. That is when she told me that every time she walked to school, she felt that she would pass out. When she gets up in the morning, she ends up lying on the floor because of dizziness. Despite her dizziness, daily muscle pain, daily migraines, and chronic fatigue, she had big dreams. She just kept pushing through day by day, with coffee, herbs, and whatever it took, but she knew that something had to change. She successfully graduated in May, Magna Cum Laude, and she had a couple of months to deal with her health before she would leave to start her graduate studies and research job. That is when I found people that knew about Dr. Marrs’ work and thiamine, and her life finally changed.

Introducing Thiamine and Other Micronutrients: Navigating the Paradox

A functional doctor recommended magnesium and niacin for her migraines and they significantly helped. This gave the functional doctor the idea to try tocotrienols. High doses of tocotrienols worked better for reducing her migraine pain than amitriptyline and aspirin combined. Then she started taking high doses of B6. This helped her muscle pain and improved her mobility. Despite being hypermobile, easy stretches gave her intense muscle cramps prior to starting B6. Guided by very knowledgeable researchers belonging to Dr. Marrs’ Facebook group, Understanding Mitochondrial Nutrients, we started Allithiamine. The first thing she said was “wait, the sun does not hurt?”. I asked her what she meant. She explained that all her life, being in the sun gave her pain in her eyes and forehead and that she couldn’t understand why people wanted to be outside. No wonder she never wanted to go outside. She also said her migraines were gone. We have waited 4 years to hear that!

After just a couple of days, she started having a lot of nausea and lower-intensity migraines returned. The researchers knew right away that she needed more potassium. She started to eat apricots, coconut water, or orange juice every time she had nausea and it helped. However, it was happening every hour so we decided to try a different Thiamine. We tried half Lipothiamine and Benfotiamine but she didn’t feel as much benefit and still gave her issues. We went back to 1/10 of Allithiamine. Chatting with the researchers, one asked if she also experienced blinding episodes. Yes! Finally, someone that knew about that! They recommended B2 and we started it. That’s when we discovered that her pain in the sun and dizziness were caused by a B2 deficiency. She continued waking up with crashes needing potassium every hour. She did not sleep that week. The researchers suggested taking cofactors including the rest of the B vitamins, phosphate salts, phospholipids, and beef organs. Beef organs and phospholipids helped with energy and bloating, phosphate salts helped with nausea and irritability.

Then researchers suggested that she needed to stabilize sugars and have more meat. That is when we realized that she had some type of hypoglycemia. We had noticed that she would get very tired and got shaky hands if she didn’t eat. Functional doctors had mentioned that she may have reactive hypoglycemia since she had a fasting glucose of 70. She started having more meat to stabilize her sugars and removed all packaged foods, sugars, grains, and starches. She started having just fresh meat, veggies, rice, beans, nuts, and berries. She felt that she was so much better with beef that she started using it for potassium between meals and bedtime.

She was able to increase allithiamine little by little. She would mix a little bit with orange juice since it tasted so awful. Little by little, she started having fewer crashes and feeling better. It took a month for her to be able to tolerate one capsule of Allithiamine. She was sleeping more but not the whole night. That is when our functional doctor suggested supporting adrenals. That really helped but then she began having stomach pain and nausea after eating beef and developed frequent diarrhea. Chicken always increased her hunger and reduced her energy compared to beef and but now she was afraid of having beef. She stopped all sources of beef and phospholipids.

We consulted a very good functional doctor. She did Nutraeval and confirmed that all her B vitamins were low or deficient and recommended TUDCA and Calcium D Glucarate along with trying lamb and bison first. Both helped in reducing bloating/nausea and she was able to start eating lamb and bison along with reintroducing a minimal amount of carbs. Soon after, she was eating beef again with no pain. After starting TUDCA, her bilirubin levels were normal for the first time in her life. We continued to work with the functional doctor to fix other deficiencies.

Recovery from Multiple Nutrient Deficiencies and the Prospect of a Normal Life

After Allithiamine and vitamin B2, we worked with our functional doctor to balance the remaining B vitamins. She is now able to go out in the sun without bothering her eyes and without passing out. She gained weight after starting the B vitamins and began looking healthier, compared to how skinny and underdeveloped she looked before. She also learned how to manage electrolytes. She sometimes needs more sodium, but other times needs more potassium. She feels sick when electrolytes get out of balance. Although she still had some continuous pressure in her head, she no longer needs any amitriptyline, aspirin, or Excedrin for pain. One thing that remained problematic was folate deficiency. She still became depressed with folinic acid, so she tried methylfolate instead. She felt so unmotivated that preferred not to have it, but she realized that it was key to something that she struggled with all her life: anxiety. She figured that she could have methylfolate every other day, so that she could have less anxiety.

Now, for the first time, she began to have a normal life. She can now exercise daily without dizziness and her heart rate skyrocketing. Her heart rate in general is more normal, doesn’t go down to 29 or up to 205. She had not had any asthma requiring albuterol. She started driving without having to deal with anxiety and panic attacks. She was able to walk to her office without fainting. She now can now live alone dealing with the stress of having a full-time job, graduate classes, cooking her food, and exercise every day! She is not cured completely but for a person that once thought she couldn’t have a future, she is doing pretty darned good!

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

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This article was published originally on July 22, 2021.

Health Requires Energy. Energy Requires Nutrients.

by Derrick Lonsdale MD, FACN, CNS

Published on June 27, 2023

11477 views

A Fundamental Issue

I was horrified to watch the “60 Minutes” program Sunday, April 12th, 2020 on television that dealt with the colossal number of Americans suffering from obesity, chronic fatigue and diabetes, both types I and II. About half of the program dealt with the essential consumption of natural food, reminding us that Hippocrates, 400 BCE said “let food be your medicine and let medicine be your food”. This must have been said thousands of times but everything in our modern civilization is totally destructive to the whole idea. I have seen so many hundreds, if not thousands, of people whose illness was caused by themselves. It was treatable by making sure that each individual understood the fundamental issue. So before I illustrate a typical illness situation within my experience, I will try to state what I mean by describing what I consider to be the “fundamental issue”.

“We behave according to what we eat”.

I have stated this so many times but unfortunately the American medical profession is the major inhibitor to its clinical success. When a suffering patient with many symptoms arising from what I call “dietary mayhem”, goes to his or her physician, they simply do not recognize the clinical expression of the popular high calorie malnutrition. The many symptoms are usually referred to as psychosomatic and the unfortunate patient is told that “it is all in your head”. I have witnessed this so many times; I cannot understand why the physicians don’t pay a little more attention to what the patient is trying to tell them. Often the patient has discovered the real cause of the problem but find that her words are considered to be the voice of ignorance and delusion.

Food and Energy

Our food consists of fuel that must be burned (oxidized) to liberate energy. In any text this element of the food is described as “calories”. The energy quality of our food intake is measured in kilocalories and a single one is defined as “the energy needed to raise the temperature of 1 kg of water through 1°C”. Notice the use of the word energy, the result of oxidation. Now, as everyone knows, vitamins and minerals, known as non-caloric nutrients, are vital to the release of energy from the caloric elements. To understand how this combination of chemicals works, there must be a ratio of calories to the noncaloric elements. That is why high calorie foods without vitamins or minerals are known as empty calories. It is the consumption of empty calories across America that has given rise to the idea of high calorie malnutrition. I have actually seen a written statement that this is an oxymoron. “How can excess of calories be considered a form of malnutrition?” It seems that few people understand this vital ratio and they seem to think that as long as you are consuming calories, you will flourish. Also, the food industry fills the grocery store with cartons of temptation and seems to have no regard for the well-being of its consumers. They keep using the term “all natural” so much, it becomes meaningless.

A Typical Case of Energy Deficiency

I was a pediatrician at Cleveland Clinic and one of my interests was sudden infant death (SIDS). So one day I was having lunch with one of the surgeons who practised ear nose and throat surgery. He told me that he had been called to the medical ICU because a woman had stopped breathing and he had performed a tracheostomy. He was intrigued by the reason for this disaster and, knowing my interest, he suggested that I should take a look. Pediatricians are assumed to be familiar with diseases of children but ignorant of adult disease and I knew that I was not welcome. I found a 50-year-old woman who was grossly edematous and unconscious. Without considering the technical details, I proved that she had the vitamin B1 deficiency disease beriberi. With injections of thiamine she became conscious and the edema disappeared. During her recovery she developed a progressive anemia, thought to be evidence of internal bleeding, but all the tests were negative. I took some urine from her and subjected it to a special type of test. It showed that she was deficient in folate, another B vitamin. It is important to note that she did not develop folate deficiency until she began her recovery from thiamine, it was masked by cellular energy deficiency. When she began to receive folate there was an immediate recovery from the anemia but she had been given at least one injection of thiamine by then.

She was discharged from hospital, wheelchair bound, taking both thiamine and folate. When she returned as an outpatient, I found that she had a skin rash and that her legs were, if anything, weaker. It had long been known that anemia would develop from either folate or B12 deficiency, but the folate deficient variety required B12 supplementation as well as folate. If B12 was not provided, the patient would develop paralysis of the legs and I had forgotten this. Also, it is not well-known that vitamin B12 deficiency can cause a skin rash. I gave her an injection of B12 and the rash disappeared. However, for a few days she had muscle aches and fever that I did not understand at that time. Looking back I would now assume that this was what we call “paradox” on Hormones Matter. To those that may not have read about this it is the temporary worsening effect by introducing an essential nutrient to someone who has long been deficient in that nutrient. One of the things that had probably been a serious indictment on self cause was that she was a chronic cigarette smoker, a well-known habit that damages oxidation.

Energy Metabolism

Can we extrapolate from this case any general ideas about how medical treatment should advance? Perhaps the general opinion would be that this is a rare and unusual case, an outlier from the “usual and customary diagnosis”. But if we consider the facts; long-term cigarette smoking, dietary indiscretion and genetic risks appear to be quite common. I treated a 12-year old girl with a conventional diagnosis of Juvenile Rheumatoid Arthritis, using a nutritional supplement. Without discussing the technicalities of laboratory evidence, it was clear that defective energy metabolism was the underlying cause. The combination of genetic risk, failure to adapt to any form of stress (infection, trauma, chronic useless brain activity etc) and inadequate energy metabolism are the three factors that either collectively or singly lead to breakdown of health. As Selye predicted, energy for adaptation is the essential ingredient.

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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 April 22, 2020.

Thiamine Deficiency and Dependency Syndromes: Case Reports

by Derrick Lonsdale MD, FACN, CNS

Published on January 31, 2023

27424 views

I have been studying thiamine metabolism since 1969 when I published the first case of thiamine dependency: Intermittent cerebellar ataxia associated with hyperpyruvic acidemia, hyperalaninemia, and hyperalaninuria. The case involved a 6-year old boy experiencing recurrent episodes of cerebellar ataxia (a brain disease resulting in complete loss of a sense of balance). These episodes, occurring intermittently, were naturally self-limiting without any treatment and were triggered by inoculation, mild head trauma, or a simple infection such as a cold. In other words, his episodes of ataxia were repeatedly initiated by an environmental factor. I have called each of these variable factors a “stressor”. Our studies showed that one of these stressors would unmask the true underlying latent thiamine dependency, falsely giving the impression that the stressor was the primary cause. This may be the principle of post vaccination disease in some cases. It may also be too easy to explain symptoms arising from trauma or infection as primary cause. These recurrent ataxic episodes were prevented from occurring by giving him mega-doses of a thiamine supplement.

Cerebellar Ataxia of Metabolic Origins?

When ataxia, as in this child, or other symptoms, occur intermittently, as they did in many other patients whom I would treat across my career, it is difficult to identify the true cause. The studies performed by neurologists, neurosurgeons and others inevitably would be normal, causing diagnostic confusion. In other patients with less serious symptoms, they are considered to be somehow feigned or of psychological origin. Symptoms that appear and disappear in a seemingly random manner and are not supported by conventional laboratory data are often explained this way. Please be aware that ataxia should never be regarded as psychosomatic. The point is that less serious symptoms that cause deviant behavior may not be recognized as biochemical changes in the brain.

With the present medical model, it is difficult to understand and accept that a stress factor can initiate the symptoms of a metabolically caused disease that has been relatively innocuous or silent until the stress is imposed. Let me give you another example.

Loss of Consciousness, Edema, Joint Pain: Rheumatic Disease or Metabolic Disorder

Since I was working at a multi-specialty clinic I was sitting having lunch with an ear, nose, throat (ENT) surgeon who knew of my interest in sudden death in infants (Treatment of threatened SIDS with megadose thiamine hydrochloride). He had been called to put in a tracheostomy to a middle-aged woman who had suddenly stopped breathing. Unlikely as it sounds, he suggested that I should go and look at the situation unofficially.

In the hierarchy of specialization, a pediatrician is not supposed to know anything about adult conditions, so I was not welcome. Because the internists who were taking care of her were rheumatologists, it was considered to be some kind of rheumatic disease, because of aches and pains in joints and limbs. She had had periods of unconsciousness over many years and her body was profoundly swollen, the hallmark of beriberi. Without going into details I was able to prove that this was indeed beriberi.

When I approached the rheumatologist who was her primary physician, I could not convince her of what appeared to her as too bizarre to contemplate. Notwithstanding, I had the cooperation with the nurses who followed my directions. When the patient was given injections of thiamine, she recovered consciousness and the gross body edema disappeared.

So fixed in the mind of many physicians is the concept that a vitamin related emergency simply does not occur, it was called “spontaneous remission” by my colleagues and “had nothing to do with vitamin therapy”. When I asked the rheumatologist whether we could conference the patient, she ignored the request. Well, this was not the end of the story.

Resolving One Deficiency Often Unmasks Another

After she started the injections of thiamine, with recovery of the nervous system, she began to develop a progressive anemia. It was considered by the internists to be internal bleeding and a thorough search produced only negative results. So ingrained is the negative attitude to vitamin therapy, I was even in fear that I might be blamed for causing the anemia. In the meantime, I took a specimen of urine and found a substance in the urine that suggested a deficiency of folic acid. Readers will remember that folic acid is a member of the B group of vitamins, as is thiamine. A blood test proved that she was indeed deficient in folic acid. When this vitamin was given to her, the anemia rapidly disappeared. This, believe it or not, still did not interest my colleagues.

She was discharged from the hospital, receiving supplements of thiamine and folic acid and her nervous system gradually improved. Some months later she developed a rash of a type that had been reported a few months previously as due to vitamin B12 deficiency. She was given an injection of vitamin B12 and over the next few days suffered slight fever and variable joint pains. These were symptoms with which she was familiar and had been responsible for the diagnosis of rheumatic disease. This sometimes happens temporarily with vitamin therapy, but often enough that I refer to it as “paradox”, meaning that things seem to be worse before they get better. Note that this paradox is not the same as side effects from a drug. The symptoms that cause a patient to see a doctor are temporarily exacerbated. With our present model the patient concludes that this is side effects from the vitamin(s) being used. I had to learn that paradox was the best sign that improvement would follow with persistence. She then continued on the thiamine, folic acid and vitamin B12.

The Role of Lifestyle and Diet Disease Expression – Oft Ignored Stressors

The fact that this woman was a chronic beer drinker and smoker had been ignored. They were, if you will, the “stressors” that were the dominant cause, perhaps impacting on genetic risk factors. The relationship between alcohol and thiamine deficiency is well known and so she had induced her own disease. Since there was a profound ignorance concerning vitamin deficiency diseases, the beriberi had been referred to by her internists as “rheumatic” in nature. This is because joint and limb pain, usually not recognized for what the pains represent, are often associated with compromised oxidative metabolism, either in the limb itself or in the brain where the pain is interpreted.

Defective oxidative metabolism caused in this patient’s case by thiamine deficiency, causes exaggerated brain perception. The brain induced a pain that gave the false impression that the disease originated in the joints and other parts of the body. Even if the origin of the pain is truly from a joint or muscle, defective oxidative metabolism in the brain will exaggerate the sense of pain perceived by the patient. Although this “phantom” pain is known as “hyperalgesia”, the mechanism is not well known as being due to compromised oxidation in the pain perception brain centers. Thiamine deficiency was responsible for the hyperalgesia experienced by the case of a patient with eosinophilic esophagitis that was posted recently on this website.

Beyond Thiamine: Multi-Nutrient Deficiencies

What interested me in the woman with beriberi was that folic acid deficiency was not revealed until her metabolism had been accelerated by the pharmacological use of thiamine. The folic acid deficiency then became clinically expressed as her metabolism “woke up”. It had been well known for some time that folic acid produced anemia would have to be treated with both folic acid and vitamin B12.

In the case of folic acid deficient Pernicious Anemia, if vitamin B12 was not given at the same time, the patient would develop a disease known as subacute combined degeneration of the spinal cord. Because I had forgotten this fact, I had neglected to give her vitamin B12 until it was finally expressed clinically in the form of a rash. Associating a skin rash with a vitamin deficiency is certainly not commonly accepted as a possible indicator of an underlying cause by physicians.

Vitamin Deficiency Versus Dependency

Returning to the case of the 6-year old boy discussed above, we learned over time that his health was dependent on high doses of thiamine to function. Believe it or not, this child required 600 mg of thiamine a day in order to prevent his episodes of illness. If he began to notice the beginning of an infection he would double the dose. The recommended daily allowance for thiamine is between one and 1.5 mg a day. Here, and in many other cases, huge doses of the vitamin are required in order to accomplish the physiologic effect. This represents what I call vitamin dependency.

Thiamine and magnesium, like many other vitamins, are known as cofactors to enzymes. An enzyme without its cofactor works inefficiently if it works at all. The “magic” of evolution has “invented” this cooperative action which is in itself under genetic control. In technical terms, the vitamin has to “bond” with the enzyme. If this bonding mechanism is genetically compromised, the concentration of the corresponding cofactor has to be increased enormously by supplementation in order to prevent the inevitable symptoms. You can see that this requires a clinical perspective tied to unusual biochemical knowledge. This is in complete contrast to what is usually regarded as vitamin deficiency, arising from insufficient concentrations in the diet.

What is perhaps not known sufficiently is that prolonged vitamin deficiency appears to affect this bonding mechanism. For example, it has long been known that to cure chronic beriberi, megadoses of thiamine are required for months. I have concluded that the megadoses of thiamine given by supplementation to a patient with long term symptoms arising from unrecognized deficiency appears to re-activate the inefficient enzyme. It is as though the enzyme has to be repeatedly exposed to megadoses of its cofactor to stimulate it and restore its lost function.

This may mean that even if the bonding mechanism is normal in chronic deficiency, enzyme function has simply decayed from lack of stimulation. This may explain why genetically determined dependency and long term dietary deficiency will produce the same clinical effect. The dosing of vitamins, if the clinical effects of deficiency are recognized, is not well understood in traditional western medicine. When insufficient doses are given and the symptoms fail to abate, the practitioner views it as evidence that supplements do not work.

Biochemical Diagnoses are Complex

I want the general public to begin to understand the principles that underlie the complexity of biochemical diagnosis. Perhaps a reader might find that a case like this is a reminder of a loved one whose illness was never understood after seeing many different specialists, all of whom were like the blind men and the elephant. Each was confined to his specialist status but none of them could see the overall big picture.

Reading these cases, you might easily come to the conclusion that they represent a rarity. Chronically unrecognized thiamine deficiency is common. Dependency is not uncommon. It is not as rare as is presently thought. Believe me, cases like these are surprisingly common and are responsible for a great deal of diagnostic confusion.

Vitamins are essential to consumption of oxygen in all life processes. To go against the principles of diet dictated by Mother Nature is a risk to life and limb that is not worth the derived pleasure. When limb pain is experienced without an obvious trauma, it is difficult to accept that it is because of inefficient use of oxidation in the brain, but that is exactly what we found.

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