thiamine deficiency

Diet Induced Pseudo-Hypoxia and Hypertension

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

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

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

Understanding the Autonomic Nervous System

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

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

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

Chronic Activation of the Sympathetic Nervous System

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

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

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

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

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

Hypothesis: High Calorie Malnutrition Induces Chronic Sympathetic Overdrive

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

Spontaneously Hypertensive Rats

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

Conclusion: Diet Matters

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

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

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Western Medicine: A House Built on Sand

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Let Food Be Medicine

At the risk of repeating myself too much as in former pages of this website, I want to return to discussing in some depth the fallacies incorporated in our present approach to health and disease. You may or may not remember that I have stated a number of times that Hippocrates (400 BCE) uttered the formula “Let food be thy medicine and medicine thy food”. Having been construed as the “father of modern medicine”, it has seemed to me for a long time that he has been ignored as a “parent”.

For centuries, there was no idea about disease. The early Egyptians bored holes in people’s heads “to let out the evil spirits”. Throughout medieval history the only treatment seems to have been “bloodletting”. In our modern world, horns from the rhinoceros are regarded so highly for their medical properties, that this wonderful animal is reaching the point of annihilation. Pharmaceutical drugs, with the exception of antibiotics, only treat symptoms. I ask you, does this make any sense at all in the light of what Hippocrates suggested?

Because humanity tends to follow a collective pattern and only rarely listens to an idea derived from rational deduction, I view medicine as like a traveler on a road without a known destination. In my imagination, he comes to a fork in the road, but the signpost records information on only one fork. It reads “kill the enemy”, reminding me of the story of Semmelweiss, a lone thinker in his time and who “gave thought to the message on the signpost”. Most physicians are familiar with this story but it is worth repeating.

Semmelweiss was a physician who lived at a time before microorganisms had been discovered. He presided over an obstetric ward where there were 10 beds on one side and 10 beds on the other. The physicians would deliver their patients without changing their clothes or washing their hands. As we would expect today, the death rate from infection was extremely high. Semmelweiss said to himself, “they must be bringing [the enemy] in on their hands” and he devised the first known clinical experiment. He made it a rule for the physicians on one side of the ward to wash their hands in chlorinated lime before they delivered their patient. The physicians on the other side of the ward continued to deliver their patients in the same old way. As we would easily recognize today, it did not require a statistician to see the difference between the incidences of infections on the two sides of the ward. Irrespective of the fact that this was a dramatic discovery that later had obvious meaning, Semmelweiss was accused by the medical authorities of the day of being non-scientific because he could not explain what it was that was supposed to be on the hands of the physicians. Of course the medical establishment had no idea that their model for disease was catastrophically wrong, although collectively certain that their philosophy bore all the hallmarks of scientific truth. Semmelweiss had offended the medical establishment and they threw him out of the hospital. He died a pauper in a mental hospital.

The First Medical Paradigm: Kill the Enemy

When microorganisms were discovered to be responsible for infections, it fulfilled the message on the signpost and it became the first paradigm in medicine. Kill the bacteria: kill the virus: kill the cancer cell, but try not to kill the patient. If we look at the history of this time, we find that a lot of patients were killed in the concerted attempts to find ways and means of killing the enemy. We all remember the discovery of penicillin and how it led to the antibiotic era, still the major therapeutic methodology, even though we know that it is running into bacterial resistance and has never been a good idea for viruses or cancer cells.

Although the germ theory had been around for a long time, Louis Pasteur, Ferdinand Cohn and Robert Koch were able to prove it and are regarded as the founders of microbiology. However, Pasteur was said to have uttered the words on his deathbed “I was wrong: the microbe (germ) is nothing. The terrain (the interior of the human body) is everything”. Perhaps he had unknowingly voiced the principles of the next paradigm in medicine.

The Second Medical Paradigm: Genetic Determinism

The monk, Mendel, by his work on the segregation of peas, formulated what came to be known as the genetic mechanisms of Mendelian inheritance and the discovery of DNA modeled the next stage in our collective development. The fact that each of us is built from a complex code that dictates who we are was a remarkable advance. The fact that the construction of the code sometimes contained mistakes (mutations) led us to explaining many diseases and for a long time we believed that the genes were fixed entities, dictating their inexorable commands throughout life. However, the newest science of epigenetics has shown us that the DNA that makes up our genes can sometimes be manipulated by nutrition and lifestyle, as well as by artificial means in the laboratory.

Health: The Ability to Respond Effectively to a Hostile Environment

We are surrounded by germs that exist everywhere, many of which cause disease as we are all too well aware. Nevertheless, whatever evolutionary mystery guides our development, we are all equipped with an extraordinarily complex, genetically determined, defense system. We now know that this is organized and directed by the brain. Assuming that the genetic determinations of the terrain are completely intact, we can be reasonably assured that we can defend ourselves from any germ that Mother Nature can throw at us. Built in mechanisms in the brain require a huge amount of energy when it goes into action directing the traffic of the immune system. It is a crisis and can be likened to a war between the body and the attacking organisms. Thus, if Pasteur may have stated the next paradigm in medicine, what does it mean?

As an example, a typical microbial attack causes a common disease that goes by the name of febrile lymphadenopathy (strep throat). The throat becomes inflamed, perhaps because the increased blood supply brings in white blood cells, acting in defense. An increase in circulating white cells also occurs, bringing a brigade of defensive soldiers. The glands in the neck become swollen because they catch the germs that get into the lymph system.  Lastly, the increased temperature of the body is also part of the defense. Germs are programmed to have their most intense virulence at 37°C, the normal body temperature. If this temperature is increased, the attacking germ does not have its maximum efficiency. In other words, what we are looking at as the illness is really the act of brain/body defensive interaction. Besides attempting to kill the attacking germ as safely as possible, should we not be assisting the defense? The answer calls into question the relationship between genetic intactness and the required energy to drive the complex defensive action. Perhaps a genetic mistake (mutation) can sometimes be manipulated by an epigenetic approach through nutrients, just as advised by Hippocrates.

Disease: The Inability to Adapt to the Environment

If we look at health as the ability to respond effectively and adapt to environmental, mental and physical stressors, it is possible to re-conceptualize illness by the manner in which that response is carried out. A healthy individual will respond to stressors without problem, because of an efficiently effective mobilization of energy dependent mechanisms. In contrast, individuals who are not healthy will respond in one of two ways. Either the defense mechanisms will be incomplete or absent or over-reactive and inconsistent. Listed below are examples of both. Note that this is in line with the ancient philosophy of Yin and Yang or, in modern terms “everything in moderation”. Too much of anything is as bad as too little.

Exhausted Defense Systems

When I was a resident in my English teaching hospital, before the antibiotic era, I admitted a patient with pneumonia who was known to have chronic tuberculosis. He was seen to be “unconsciously picking at thin air with his fingers” and the physician for whom I was resident pointed out that it was a classic example of “a sick brain” and that he would die. He never had any fever, elevation of white blood cells or any other marker of an infection but at autopsy, his body was riddled with small staphylococcal abscesses. He had lived in the east end of London, notorious for poverty and malnutrition at that time. In fact, as an organism, he never showed the slightest sign of a defense. His “sick brain” was completely disabled in any attempt to organize his defense.

Excessive or Aberrant Defense Mechanisms

Many years ago I was confronted with two six-year-old unrelated boys who for several years had each experienced repeated episodes of febrile lymphadenopathy. Both boys had been treated elsewhere as episodes of infection. In each case the swollen glands in the neck were enormous. One of the boys had been admitted to a hospital for a gland to be removed surgically for study. It had been found that the gland was just enlarged but had a perfectly normal anatomy, only contributing to the mystery. One of the curious parts of the history was that each of these boys had been indulged with sweets. Because I was well aware that sweet indulgence could induce vitamin B1 (thiamine) deficiency, I tested them and found that both were indeed deficient in this vitamin. Treatment with large doses of thiamine completely prevented any further attacks. The mothers of the boys were advised to prohibit their sweet indulgence. I needed some evidence and asked one of the mothers to stop giving thiamine to her son. Three weeks later he experienced a nightmare, sleep walking and another episode of lymphadenopathy that quickly resolved with thiamine.  A nightmare and sleep walking supported the contention that the brain was involved in the action. In addition, his recurrent illnesses had been associated with increased concentrations of two B vitamins, folate and B12, both of which decreased into the acceptably normal range with thiamine treatment. Of course, this added complexity to an explanation.

What I had already learned about thiamine deficiency is that it makes the part of the brain that controls automatic mechanisms much more sensitive. One or more reflexes are activated unnecessarily. No reflex activation is as bad as too much. Thus, the “trigger-happy” defense mechanisms were being activated falsely. Thiamine is perhaps the most important chemical compound derived from diet that presides over the intricacies of energy metabolism. All that was required was an improved energy input to the brain. Folate and B12 are vitamins that work in energy consuming mechanisms and I hypothesized that their respective functions were stalled for lack of energy, causing their accumulation in the blood. Whatever the explanation, the facts were as described. It is interesting that the high levels of folate and B12 had been found at the hospital where a lymph node had been removed. The mother had been accused of giving too many vitamins to her child. She had told me that she did not understand this explanation because she had not given any vitamins to him. I had measured them solely to verify this finding.

The Treatment of Disease Should Begin with Host Defenses

We exist in a hostile environment. Each day throughout life we live in anticipation of potential attack. A physical attack may be an injury, an infection or an ingested toxin. A mental attack, divorce, grieving, loneliness, generally referred to as “stress” may be virtually anything that causes the brain to go into increased action. In facing both physical and mental forces, it is the brain that organizes the defense and it demands an increase in energy output that depends solely on the ability to burn fuel. The fuel burning process is governed by a combination of genetically determined ability and the nature of the fuel. Thus, the treatment of all disease is dependent on this combination being effective. It can be seen as obvious that killing the enemy is insufficient. As our culture exists at the present time, trying to get people to understand the necessity of perfect nutrition is a pipe dream. This particularly applies to youth and the artificiality of the food industry. However, our culture is also virtually brainwashed to accept tablets as a means of treating anything.

In our recently published book “Thiamine Deficiency, Dysautonomia and High Calorie Malnutrition“, Dr. Marrs and I have shown that thiamine deficiency is extraordinarily common and that supplementary thiamine and magnesium together balance the ratio of empty calories to the required concentration of cofactors necessary for their oxidation. The question remains, would vitamin supplementation, just as artificial, be a more successful sell as a preventive measure? We have shown that the symptoms derived from prolonged high calorie malnutrition can last for years as an unrecognized polysymptomatic illness that haunts many physicians’ offices. Early recognition represents an easy cure. There is a good deal of evidence that ignoring the symptoms and the persistence of high calorie malnutrition creates a gradual deterioration that then turns up as chronic disease. Some drugs, metronidazole being an example, will precipitate thiamine deficiency, so we have to recognize the precarious nature of the present medical approach in the use of drugs whose action in treating disease is often unknown. Although recognition of the artificiality of thiamine supplementation is implicit in this proposal, it is better than allowing a common example of continued morbidity to exist.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Photo by Phil Hearing on Unsplash.

This article was published originally on July 19, 2018. 

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Familial Beriberi: Discovering Lifelong, Genetic, Thiamine Deficiency

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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. 

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Beriberi is Alive and Well in America

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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.

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Depression, Anxiety, and the Chronically Hypoxic Brain

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I couldn’t help noticing the Wall Street Journal of Thursday, June 7, in which a column reported a completely unexpected suicide. The title of the column was “Kate Spade’s Family Recounts Her Battle With Depression”. It was reported that “Ms. Spade had suffered from depression and anxiety, and was being treated with medication and therapy. Depression and anxiety disorders occur simultaneously in about 25% of general practice patients. In the abstract, the author says “about 85% of patients with depression have anxiety and 90% of patients with anxiety have depression. Benzodiazepines may help alleviate insomnia and anxiety but not depression”. It must be obvious that the general impression is that these are two different expressions of psychological disarray that require different drugs to treat them. Evidently, Ms. Spade had left a suicide note indicating that she had been under mental stress from her marriage. There were other stresses reported. She had been living separately from her husband for 10 months and had been seeking help for the past five years.

The incongruity requires explanation. Here was a 55-year-old woman who was highly successful in the eyes of the world and her suicide appears to be completely incongruous, as indeed most suicides are. There should be a logical explanation for such an anachronism. The instinct for life is incredibly strong for us and indeed for all creatures in the animal kingdom. I offer my explanation here, based on the contention that the human brain is an electrochemical machine and that its functions are highly dependent on an adequate supply of energy. This does not take into account the concept of a soul that must remain one of the great mysteries of life.

Revisiting Freud: The Ego and the Id

According to Sigmund Freud, the id is the subconscious mind supervised by the ego and what he called the super-ego. All are built upon the presupposed existence of conscious and unconscious thoughts. Modern research has failed to find individual areas in the human brain dealing with the control of specific action. Its function is now regarded as an integrated organ, all parts of which share that action. However, much of this activity is entirely automatic and below conscious level. All brains in higher members of the animal kingdom are built on the same anatomical principle, presumably reflecting a “oneness” in design. If we are to accept evolution as the driving force, the brain of each animal has been developed to service that animal in its natural niche. The niche of Homo sapiens appears to be that of the dominant species and it has evolved from a more primitive state to a more sophisticated one, gradually introducing increased complexity. Brain action would be expected to become more and more sophisticated over time, perhaps making us more cooperative.

We have no idea what is in store for us with continued evolution, but it has long seemed to me that we are still relatively primitive at the philosophical level. Under stressful conditions, the actions of the human brain are much less predictable. However we consider the distribution of brain function, it is an electrochemical machine and a great deal of its activity is unconscious and purely automatic. Body organs signal the brain that then gives instructions to them via the autonomic and endocrine systems. It is therefore convenient to accept the ego and the id, each with its separate functions, however, they are controlled, by the conscious and unconscious mind. Some of the net behavior might be perceived as actions of the automatic component, governed and permitted by the conscious component. It has been suggested that human beings are built as “mean fighting machines equipped for self-interest”.

The Nervous System

Many posts on this website describe the difference between the so-called voluntary and the autonomic nervous systems. The term “voluntary” indicates that we can think and move at will and its actions are dictated by the conscious mind. The autonomic nervous system is almost completely automatic and governs many purely reflex actions, the fight-or-flight reflex being the best known. Hunger and thirst are self-preservatives. The sex drive preserves the continued existence of the species. Yes, these reflexes give us a sense of pleasure, which is the driving incentive and the brain provides us with sensory mechanisms that provide that pleasure. Everything is tied together by a complex code known as DNA, whose individual characteristics describe the physical profile and personality of each animal including humans. From a purely philosophical point of view, it calls into question whether we truly have free will or whether we are programmed by the environment in which we find ourselves. If all components fit together as designed, we can say that the “blueprint” for each person dictates the nature of the personality and reflects his/her mental and physical health. Our training to meet life starts in infancy and is in the hands of parents.

Of Stress and Stressors

Stress is a physical or mental event to which each of us has to adapt. As I have mentioned in other posts on this website, a Canadian researcher by the name of Hans Selye studied the effect of physical stress in animals for many years. He came to the conclusion that virtually any form of stress demanded an increase in the supply of cellular energy, much like the engine of a car climbing a hill. A stressed animal had to adapt to the injuries applied by Selye. He called it the “General Adaptation Syndrome”. He used many different methods to induce stress because he wondered whether there were different responses, depending on the nature of the stressor. He found that the stress response was uniformly identical across species and was able to divide the General Adaptation Syndrome into several predictable phases, each of which was repeatable in each experiment. Not surprisingly, his studies included an array of sequential biochemical changes in the body fluids. I found these changes to be similar to the laboratory changes seen in chronically sick patients. One of his students was able to produce the syndrome by first making the animal deficient in the vitamin thiamine, thus supporting the role of energy deficiency as the causative factor. Selye suggested that human health broke down as a result of energy failure, particularly in the brain, leading to what he called “the diseases of adaptation”. It is probably true that some form of life stress is absolutely necessary for a person to contemplate suicide. Therefore, it seems necessary to discuss the mechanisms by which the brain responds to stress.

The Biological Brain

Whether we like to recognize it or not, the brain is an electrochemical machine whose functions, like any machine, require energy. The fact that the brain requires 20% of the total oxygen inhaled is an absolute indication of its energy requirement. There is much evidence that even a mild reduction influences brain activity and this will be reflected in some kind of change in thought processes and the consequent behavior resulting from it. Nutrition affects mood. A deficiency of many vitamins is associated with psychological symptoms. In some elderly patients, folate deficiency is associated with depression. Iron deficiency is associated with apathy, depression, and rapid fatigue when exercising. In several studies, an improvement in thiamine status was associated with improved mood. One of the major manifestations of obstructive sleep apnea is profound and repeated (episodic) hypoxia (insufficient oxygen) during sleep. This increase in activity in the sympathetic nervous system affects blood pressure. Thiamine deficiency induces gene expression similar to that observed in hypoxia and has been referred to as causing pseudo-hypoxia. Magnesium and thiamine deficiency have both been implicated in depression.

Hypoxia and Pseudohypoxia in Depression and Anxiety

During many years of medical practice, I found that a mild degree of thiamine deficiency was responsible for symptoms that are often regarded as psychological. Chronic anxiety and depression were regularly alleviated by getting people to understand the importance of an appropriate diet, together with the administration of supplementary vitamins, the most important of which were thiamine and magnesium. I could never understand how a patient could be actually blamed for producing symptoms beyond the comprehension of the physician. Abnormal thoughts, emotions, and all forms of mental activity are produced by electrochemical reactions that are exaggerated by a mild degree of hypoxia or pseudo-hypoxia.

Anxiety and depression are perfectly normal emotional reactions but when they are sustained for absolutely no reason, it is because of this biochemically initiated exaggeration. In particular, the sympathetic branch of the autonomic nervous system is easily activated because any degree of oxygen lack is obviously dangerous to the organism and a fight-or-flight reflex reaction would be initiated by the perception of danger. This reflex, because of its nature, might give rise to aggressive behavior when a nursed a grievance explodes into violence. The widespread intake of empty calories, particularly in the form of sugary and fatty substances, is responsible for polysymptomatic disease in millions. Such individuals cannot handle the normal stresses of life and are much more easily imbued with a sense of hopelessness. Suicide seems to be the only option. The idea that dietary excesses might be responsible for depression and suicidal ideation is not a presently acceptable concept, but the biochemical results of alcohol and sugar ingestion are identical in the part of the brain that has to deal with these inbuilt vital reflexes.

We Need Your Help

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

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This article was published originally on June 20, 2018. 

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Are Thiamine Deficiency Symptoms Too Narrowly Focused?

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Much of our understanding regarding thiamine deficiency comes from early reports of illness from far-off lands, case reports that suggest rarity, and from rodent studies. While all of these are useful, none easily translate to the realities of this disease process on the ground, in the clinician’s office, or in the hospital. Do we really know what thiamine deficiency, or more appropriately, thiamine insufficiency looks like in everyday practice? Would we recognize it in the patients who walk through the doors of any medical facility? Probably not. And that is a problem.

We tend to think about nutrient deficiencies as emerging only in populations affected by starvation or absence-based malnutrition. This interpretation evolved from the early descriptions of beriberi, where the individuals most afflicted included Japanese sailors, Pacific Island communities, and regions afflicted by food scarcity. Later, alcoholics were added to the list of potential populations affected by thiamine deficiency. More recently, post gastric bypass patients, hyper-emetic pregnant women, and patients with critical illnesses were identified as at risk for deficiency. With each set of populations though, we are given the impression that thiamine deficiency is rare but easily recognized. It is neither, but the lens through which we view this disease process was focused generations ago on only the most severe examples, and that lens has remained ever since.

The Legacy of Early Scientists

The typical descriptions of thiamine deficiency disease, come from the perspective of the early investigators who described these conditions and have changed very little in decades since. Definitions of beriberi, which in Japanese means I cannot, I cannot, was, and still is, largely focused on the progression to heart failure in later stage deficiency. Here, there are two primary types of beriberi: wet beriberi, which is defined as high output cardiac failure with edema, and dry beriberi described as the central and peripheral nervous system and cardiovascular disturbances without edema. In recent years, gastrointestinal beriberi and neuritic beriberi have been added but they remain poorly recognized.

Likewise, our understanding of Wernicke’s encephalopathy (WE), a disease process that was first described by Carl Wernicke in 1881 and later associated with alcoholism and thiamine deficiency, is still described using Wernicke’s original triad of symptoms: mental confusion, ocular abnormalities, and ataxia. This despite the fact that 1) these symptoms represent a later stage manifestation of the disease process, where the deficiency is sufficient to produce brain damage and 2) these symptoms infrequently present, either alone or in combination, in most cases of WE. In fact, one study found that 80% of cases WE were identified only postmortem, meaning they were missed entirely while the patient was alive. Of those, only 16% had documentation of all three symptoms, 44% had one or two of the classic triad symptoms and 19% had none at all. This suggests that the classic triad, while a brilliant original observation, requires adjustment.

Korsakoff’s syndrome, a later stage and more severe form of thiamine deficient brain damage that includes neuropsychiatric and neurocognitive manifestations like confabulation, psychosis, and significant memory deficits, shares a similar lack of diagnostic clarity and is often mistaken for more traditionally defined psychiatric cases and dementias. Like Wernicke’s syndrome, Korsakoff’s is named after the scientist who first reported it in the late 19th century, a Russian by the name of Sergei Korsakoff. Like Wernicke’s, the lens through which we view this disorder owes largely to the original descriptions. Both syndromes are now combined as Wernicke-Korsakoff syndrome (WKS). For that reason, there are no clear data on the prevalence of Korsakoff’s syndrome or on how many patients progress through the different stages of brain damage associated with thiamine deficiency.

Those Rare Cases of Thiamine Deficiency

Modern case reports reinforce these legacy definitions of thiamine disease and continue to portray thiamine deficiency as a rare manifestation of severe illness. The literature is replete with cases of patients who demonstrate none of the classic symptoms associated with thiamine deficiency and yet are clearly deficient. Likewise, in each of these reports, the development of thiamine deficiency is considered rare. Indeed, the rareness of this condition is almost always explicitly emphasized in the text with statements like:

  • A severe depletion is not commonly seen, except in cases of inadequate nutrition and/or alcoholism.”
  • Cardiac beriberi, or heart failure due to thiamine deficiency, is considered rare in the developed world.”
  • Thiamine deficiency is rare in developed countries and is most commonly associated with chronic alcoholism. The other predisposing conditions include chronic dietary deprivation and impaired absorption or intake of dietary nutrients.
  • Nowadays, in the developed world it is relatively rare.

Next time you are reading a case study, or really, any report on thiamine deficiency, note the remarks of rarity. What if thiamine deficiency is not rare, but simply under-recognized? If we rarely consider it based on the lack of matching symptoms, how do we know what the real prevalence is?

Of Rodents and Men

The rodent research, although more adept at addressing the progression of deficiency symptoms across time, is still problematic. Aside from the obvious differences between rodents and humans, the highly controlled and contrived experimental conditions under which this research occurs in no way reflects the messiness of life. Rarely are we exposed to an absolute deprivation of a single nutrient, unless under some sort of duress or a medical error. More frequently, the progression to thiamine deficiency is an extended process of months to decades, where exposure to thiamine or anti-thiamine factors varies across time, and as a result, so too does the expression of illness.

From the rodent research, we do know, however, that there is a clear progression of symptoms across the period of deprivation. Here, among the first manifestations of thiamine deficiency are hair loss, apathy, and anorexia. These symptoms emerge within two weeks of thiamine deprivation. At about 4 weeks, neurological symptoms emerge, and death by cardiac arrest occurs at about 6 weeks.

Whatever the problems there are translating patterns gathered from animal research to those of human studies, and there are many, at least with these studies we can see the early indicators of problems. If a patient were to complain of new-onset hair loss, apathy, or anorexia, or even newly emerging neurological symptoms, more often than not, the symptoms would be dismissed as stress-related and relegated to the category of psychosomatically induced. An antidepressant or anxiolytic would be prescribed and that would be the end of it. Thiamine or other nutrient deficiencies would not be considered until a much later stage, if at all.

The Progression of Symptoms in Human Females

From some highly unethical studies conducted on female psychiatric patients in the late 1930s and early 1940s, we know that the human progression of thiamine deficiency does indeed mirror what is illustrated by animal research somewhat. The early symptoms are so benign that most would miss them. Similarly, as the symptoms build over time, although they worsen considerably, they remain more general than specific and might easily be ascribed to other conditions if one were not trained to consider thiamine.

A few notes about the studies. There were three in total, two with four women each and one with 11 women maintained on a diet of .15mg of thiamine per day for 147 days, .45mg of thiamine for 88 days, and 11 women at ~.15 – .2mg thiamine per day plus 1mg of thiamine given intermittently for up to 196 days, respectively. In the third study, where additional thiamine was provided, when averaged, the total thiamine consumed was ~.175mg per 1000 calories of food or .35mg for a 2000 calorie per day diet. Also, in this study, 5 of the 11 women were maintained on the diet for an undisclosed period before resuming a normal diet, while the remaining 6 were kept on the diet for as long as 196 days. This is approximately 30% of the recommended daily allowance needed to stave off deficiency symptoms and syndromes.

Before each study period, the women were provided a normal ‘healthy’ diet for up to 52 days. It is not clear what that constituted. Upon beginning the study, the diets became quite unhealthy, consisting of food products using white flour, sugar, tapioca, corn starch, polished rice, raisins, egg white, cottage cheese, American cream cheese, butter, hydrogenated fat, tea, and cocoa. Additional B vitamins, as well as some fat-soluble vitamins, were provided via supplement, even though thiamine was all but eliminated.

Below is a compilation of the observed symptoms in two of the case descriptions provided.

  • First few weeks: emotional instability, irritability, moodiness, anxiety, agitation, depression, reduced activity, and numerous, often vague, somatic complaints. Weakness and anorexia begin to present.
  • 30 days: anorexia, weight loss, epigastric distress, increasing weakness, periodic vomiting
  • 50 days: nausea and vomiting after meals, progressive weakness from low energy to bedridden, sometimes constipation
  • 70 days: constant nausea, severe weakness, apathy, confusion, numbness, and tingling in extremities
  • 90 days: inability to read or focus, aberrant to absent sensory recognition, tender calves, inability to stand from squatting position, hypoactive Achilles tendon reflex, nausea continues progressing to regular vomiting after meals
  • 110 days: appetite fails, apathy, vagueness and confusion, low blood pressure and heart rate at rest, rapid increase upon ordinary exertion, aberrant and absent sensory perceptions, aberrant and reduced reflexes, reduced flexion of ankles and knees, ataxia, inability to stand on toes.
  • 120 days: impaired pain perception on legs, loss of patellar and Achilles reflex, weakness in abduction, adduction, and flexion of thighs, weakness in the legs with limited ability to extend legs with quadriceps, inability to stand or walk without support, ankle and knee clonus absent, Babinski response absent.

One of these two subjects developed severe neurological defects at 120 days and so the experiment was stopped. The researchers noted that appetite had completely failed and remarked that ‘inanition seemed imminent. They also remarked that with 60-80mg of thiamine given orally and parenterally many, but not all, of the deficits. Appetite returned and strength was regained within the first week, and within 30 days, the less severely ill of the two women was mostly recovered. At 60 days, she was fully recovered. For the other women, recovery was incomplete, even after 120 days of treatment.  Of note, it was the younger and more active woman who suffered the most serious neurological deficits and who was unable to fully recover.

In the 88-day study, the most common and debilitating symptoms included vomiting and subsequent anorexia. The authors note:

We nevertheless are impressed by the degree of debility induced by the isolated withdrawal of thiamine. Fatigue, lassitude, and loss of interest in food developed early and increased progressively as the period of deficiency extended, to the point of intolerance for food. So great was this intolerance that uncontrollable vomiting, even after tube feeding and parenteral injection of solutions of sodium chloride and dextrose, automatically brought the observations to a close.

Also observed in this study, was an association between pre-deficiency energy levels and severity of illness propagated by the deficiency.

The time of development of symptoms and the time of development of severe symptoms differed among the subjects and seemed to be related to physical activity. The subjects who were more active showed symptoms earlier and were more seriously affected later than others who from the beginning were less energetic.

A few additional observations:

  • When thiamine was added intermittently, even though the total levels were still considerably below normal, symptoms improved for a period of a few days to a week. This happened repeatedly. The improvement was so noticeable that some of the women begged to remain on the higher levels of thiamine.
  • Pyruvate and lactic acid levels were higher throughout the period of thiamine deprivation but peaked differentially by individual, by duration of thiamine deficit, and across time, relative to when dextrose was given.
  • Pyruvate and lactic acid levels increased variably after meals and when dextrose was given but returned to the pre-meal/pre-dextrose basal rate within 120 minutes.

Finally, the most notable symptoms in each of the studies involved gastric distress, with vomiting, severe constipation, severe food intolerance, and anorexia. This, of course, was in addition to a decline in energy, polyneuropathy, changes in blood pressure, heart rate, and rhythm, and a decline in cognitive capacity.

So What Does Thiamine Deficiency Look Like?

Everything. And nothing. It is non-specific. It is the sickness behaviors of which Selye writes that underlie all illnesses. Thiamine deficiency looks like every other non-specific illness until it becomes severe enough to approximate some of the more well-recognized aspects of beriberi or WKS. Even in its most severe stages, however, the symptoms could easily be ascribed to other types of illness. Making matters more difficult, unlike the research presented above where thiamine is restricted consistently across time, in modern, developed countries, thiamine is rarely restricted so consistently. Thiamine consumption waxes and wanes across time, as does the demand. It is that mismatch between consumption or availability and needs that initiates the molecular events, deep in the mitochondria where thiamine is critical, that is responsible for the bevy of symptoms attributable to thiamine deficiency. This means that if we rely on the conventional diagnostic parameters, defined generations ago, we are all but guaranteed to miss it. Instead, we ought to be considering thiamine and other nutrient deficiencies in all cases of illness, whatever their manifestation, but that demands an entirely new lens through which to view health and disease; a lens that is quite at odds with the current model of medicine.

We Need Your Help

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

Yes, I would like to support Hormones Matter. 

This article was published originally on April 29, 2021. 

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SIDS and Vaccination

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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:

  1. 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.
  2. 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.
  3. 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:

  1. Genetic risk, “e.g. a high brain energy requirement”
  2. A non specific stress factor, “e.g. vaccination”
  3. 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.

 

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My Decade of 24/7 Depression

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I am a 60 year old female who has been experiencing severe depression with anhedonia for over a decade. I often feel oxygen and energy deprivation in my head more often when I lie down. I have a lot of short term memory problems and executive functioning issues that began around age 50. Sometimes I feel the earth move under my feet and I am occasionally dizzy and have double vision. If I look intently at things, it appears as though they are moving. I also have some visual tracking issues. This is partly do being blind focally in one eye and floaters in both, but I suspect there is more too it. I have endured restless leg syndrome for years, which has been significantly less for the last few weeks after beginning thiamine, as have some of my other symptoms, but the depression, anhedonia and general loss of motivation and lack of joy remains. I have begun using a variety of supplements but feel as though I am still missing something. I am sharing my story in the hopes that someone can offer some help.

Childhood Through Early Adulthood

Since childhood, I have felt physically crappy. I was never able to breathe through my nose. I had asthma and constant, intense itching in my ears, nose, throat, head, and eyes. Insomnia plagued me as a child due to anxiety, along with the inability to breathe and the intense itching in my head. Regularly, and especially at night, I fantasized of putting an icepick into my ear to scratch the horrible itch in the center of my head. All day, everyday, I choked on the constant snot that continuously poured out of my nose and clogged my throat. I choked often on my food being a total mouth breather. I needed a box of Kleenex’s to get through a day. Despite it constantly running, I could not breathe through my nose at all. Encumbering as all this was, I still managed to feel somewhat hopeful, played outdoors, had friends, and attended school most days.

I chose to leave home quite young (at 15 years old) because of family dysfunction. By 16, I stopped consuming liquid dairy, thus leading to a nose-breathing liberation. I still was plagued with sinus issues but could breathe occasionally through my nose to some degree for the first time ever.

As a youth, I experimented with drugs, but never really took anything regularly as the hangovers were horrible and weakening for me. I did a fair amount of drinking in twenties as well but paid the price health wise, and since have not had a drink in many years.

In my twenties, I became aware of sugar causing severe hypoglycemia in me, caused huge mood swings and vision loss. I also self-diagnosed myself with hypothyroidism. I went to see doctors assuming this was causing my miscarriages but the doctors invalidated me at every turn, insisting I was fine. So my Hashimoto’s went untreated for many years until I discovered I could treat it with over-the-counter desiccated thyroid.

Even with all of this going on, I just kept dragging myself along through life on what felt like sheer willpower alone. During this time (my 20’s), I ate more vegetables (fresh organic) and less meat, I had a lot of stomach pain that plagued me on top of everything else, even though my diet was quite good and full of organic vegetables grown nearby. I wasn’t a trying to be a vegetarian, I always thought of myself a bit more of a carnivore, but being that I lived among vegetarians I didn’t eat meat on a daily basis. I noticed that when I did eat meat, I felt a little better. I wish I had taken it more seriously then, but I was still in my optimistic youth, and every day was a new day where I thought I was going to magically feel better.

Lifelong Anxiety and Stage Fright

Prior to the depression, I was a violinist, but one who suffered from lifelong, crippling stage fright. As a child I couldn’t sleep at all for days prior to an audition or performance, which was often. This continued my whole life. Nevertheless, I was able to push through and have performed and recorded many pieces with many different people through the years. Over time though, I began to avoid auditions, and mostly, only performed solo for strangers like at weddings and parties where there weren’t high expectations. Many times, I convinced myself to get over this anxiety, I just had to do it, to get out there and perform. This never worked. I never got over it. Oddly enough, no one realized what I was going through while I played.

I took immediate release Adderall 40-60mg 2-4 x a week for about 5 years in my late 40s to early 50s. It was prescribed for ADHD and for stage fright during violin performances. It also helped with motivation. I have always had a pretty scattered ADHD type personality and felt that I was a high functioning autistic person.

I take trazodone to help sleep when I can afford to get it, but it doesn’t always work. So lately I have been taking a break. Sometimes I will take an over the counter antihistamine/cold medicine like Tylenol when I am desperate to sleep, like when I’m caring for mother. It is a last resort though. I prefer not take anything being it makes me a little nauseous and I worry about liver damage.

I tried Wellbutrin for depression for several months about a year and a half ago, but felt nothing. I tried Prozac for four weeks in my 40s and also felt nothing.

Mumps and Loss of Vision in One Eye

I got the mumps in my forties. This was the closest I ever felt to death in my life. I subsequently lost vision in my right eye. When I lost my vision, it was assumed that I had ocular histoplasmosis but a few years prior to that I had lost vision in one eye for a few months to an unusual eye condition called MEWDS, (multiple evanescent white dot syndrome). MEWDS can be induced by a virus, perhaps having the mumps virus had something to do with it. I also wonder if I was actually type 2 diabetic off and on in my life, or at least borderline, and if that cost me my eye.

Debilitating Depression

After a lifetime of feeling crappy, multiple miscarriages, carpal tunnel, loss of vision in one eye, foot, back, and joint pains, continuous often intense neck pain that has been there since my twenties, along with severe insomnia and allergies, I arrived at 50 years old and began a quick descent into an abyss of deep and unexpected depression and anhedonia. I have been stuck here and have wanted to die 24/7 for 10 years, but haven’t because I do not want to hurt my grown son, and I am sharing the out of state caretaking of my mother and stepfather with dementia with my brother. I have been desperately trying for the last decade to recover my health. To that end, I have taken many supplements but none have really noticeably worked.

Attempts to Recover

Seven years ago, I took to injecting B12 after self-diagnosed pernicious anemia, but never felt a noticeable difference. I was extremely fatigued. I also injected a B complex regularly for several weeks or more without noticing a difference. I still feel a lot of fatigue but with the loss of motivation I think it is possibly more mental than physical.

Ten months ago, I began a strictly carnivore diet. Carnivore has helped inflammation. My bowels are way better and my lifelong mouth ulcers stopped immediately. There have been many other small wins. Unfortunately though, it means  next to nothing to me because it has not fixed my depression, my enjoyment, or will to live. These are the core symptoms that I need to fix. I don’t understand why others get over their depression and insomnia and I cannot seem too. I also still loose lots of hair, but this has been going on for about 7 years. This is traumatic for me (constantly).

About three months ago, I experienced tachycardia plus dizzy spells for several days. The doctors said my iron was fine but I upped my heme iron and b12 and I think it helped. I eat a lot of liver/meat so it surprises me that I would ever be low in b12 or iron. I still feel a little floaty at times, but my heart rates are more normalized.

Recently, I discovered the literature and videos on high dose thiamine. I was very excited, and finally, once again hopeful.

I have taken both TTFD and benfotiamine for a couple weeks now and am not really noticing any changes paradoxically or feeling better. I recently added the HCL too. I have tried upping my doses significantly to where I was taking over 2000mg of Benfotiamine, 400mmg of TTFD and 400mg of thiamine HCL for several weeks. But I have since lowered it considerably. I also take magnesium (100mg), glutathione, riboflavin (100mg) the other B vitamins via yeast, B12 with intrinsic factor (500mg), and electrolytes, and I eat head to tail carnivore including bone broth. I take a substantial amount of more than 400mg of desiccated thyroid as well for the Hashimoto’s disease.

I started taking high dose niacin, perhaps a week ago and I think it kind of helped the thiamine. I felt a certain weight in my head lessen. It was not so much emotionally noticeable but like a bunch of swelling must have loosened. Then two nights ago, my body, legs, and some in arms, swelled up horribly. It was very itchy, painful and lumpy; like I had gained 20 pounds overnight. I haven’t had a history of noticeable edema. This scared me and I decided it was lymphedema, so I began doing lymph draining exercises. I finally felt it was not expanding any longer and perhaps even subsiding a day and half later. I felt hopeful that the brain inflammation FINALLY made a breakthrough, and my body was dealing with the toxicity that had been stuck in there, but I’m not sure what caused the sudden swelling. I also noticed during the swelling that I was urinating less, no matter my fluid intake. Perhaps my body was trying to dilute the toxicity and thus the necessary accumulation. I didn’t take the niacin or thiamine for the next two days. Then yesterday, I took a 1 gram niacin dose and felt a decline in the swelling, and later, around 3 am, I took another niacin, which somehow helped my body hurt less and I could relax. Now a few weeks later, the swelling has decreased considerably. I think it’s going to take some time to feel the results of brain regeneration and habitual behavior, but I don’t feel that feeling of a huge lump of coal stuck in my head anymore. I am currently taking 300mg of benfotiamine, 100 thiamine HCL and 100 allithiamine along with my minerals, electrolytes and vitamins. I also added oregano oil protocol that I heard could help with Hashimoto’s.

Please Help

I used to be highly creative and performed violin for a living, whereas now I cannot find any hope or inspiration to play or do anything and haven’t in years. I desperately want to clear the fog from my brain and regain my will. It is as if I am overwhelmed and underwhelmed at that same time. It is difficult to describe, except that I am miserable. What am I missing? Please any advice appreciated. Thank you!

We Need Your Help

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

Yes, I would like to support Hormones Matter.   

Photo by Annie Spratt on Unsplash.

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