thiamine deficiency - Page 7

A Case of Classic Beriberi in America

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

 

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

 

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

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

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

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

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

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

Beriberi Is a Form of Dysautonomia

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

Thiamine deficiency beriberi in America

Is There a Help From the Laboratory?

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

What Is the Hope of Normal Health in This Person?

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

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

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This article was published originally on August 9, 2017. 

Treating Sensory Processing Disorder in Children

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On Tuesday, August 16, 2016, I read an article in the Wall Street Journal with this title: Treating Children for Sensory Processing Disorder. Since I have treated hundreds of these children, I am posting here some of the facts that I have learned. First of all let me provide some extracts from this article that is all about a diagnosis of “Sensory Processing Disorder” (SPD). The article says that SPD is believed to affect 5% to 16% of children in the United States.

I want to make it clear what we are talking about. This article describes a three-year-old child who, when accompanying his mother to the grocery store would have meltdowns. His mother was quoted as saying “he would literally bite me throughout the grocery store”. An occupational therapist determined that he had SPD: “a condition in which the body and brain have difficulty processing and responding to sensory stimuli in the environment”. The article goes on to say that “some people with SPD are hypersensitive to loud noises or different textured foods. Others may be agitated by the touch of a clothing tag”. The Director of Occupational Therapy (DOT) research at Cincinnati Children’s Hospital Medical Center was reported as saying

Occupational therapists treat dozens of SPD patients every week. It can affect just one sense, such as hearing, touch or taste, or multiple senses. Sensory processing problems can also affect the body’s vestibular system, creating difficulties with balance, or the proprioceptive system, leading to problems with clumsiness and body positioning.

The DOT “has worked with some children with SPD who are academically gifted and don’t have autism or ADHD. It is clear from the article that the method of treatment, entitled “sensory integration”, looks upon SPD as abnormal psychological behavior. This is  in spite of the fact that a professor of radiology and bioengineering at University of California, San Francisco stated that studies showed that children with SPD had less developed white matter mostly in the back of their brain, compared with typically developing children. This posterior region of the brain is where a lot of sensory processing takes place. This is a major clue as we shall see shortly.

Beyond the Bad Parenting Theory of Sensory Processing Disorder

Now I ask you dear reader, is it common sense to claim that this kind of disorder in 5% to 16% of our children is purely psychological from bad parenting, acceptably normal in a young child, or caused by genetic changes? Since the Wall Street Journal article claims that “adults can have SPD”, it is clearly not confined to children. To believe that any of these facts, or all of them together, can result in so much willful behavioral deviation is a reduction to absurdity. It is absolutely certain that Mother Nature never makes that kind of genetically determined mistake in so many individuals.

The article in the Wall Street Journal reports that “a common treatment at Cincinnati Children’s is called sensory integration, involving three sessions a week for about six weeks”. The founder of the STAR Institute for sensory processing disorder in Denver involves an intensive treatment program of some 31-hour sessions nearly every day for several weeks. The cost is about $175 per session.

When I was a consultant pediatrician at Cleveland Clinic Foundation, I saw many children who were referred because of “emotional problems”. The accepted cause at that time (and still is by many pediatricians) was lack of good parenting. In discussions with parents, I found that bad parenting was rare, but lousy diet was common, particularly because of the enormous overload of sugar, often started in infancy. In fact, sugar was used as an inducement to good behavior, not recognizing the fact that the sugar was the cause of the bad behavior in the first place. By doing a blood test on these children I repeatedly found evidence of thiamine deficiency. To me, the extension of the absurdity is that there is no mention at all in this article about the role of nutrition. I have posted a number of articles on this website concerning vitamins, particularly  vitamin B1 (thiamine). I have pointed out many times that overloading the diet with empty calories, particularly from sugar, automatically induces thiamine deficiency relative to the excessive calories. The scientific evidence for this has been known since 1936. Any attempt to depict thiamine deficiency by measuring its blood level in a person eating “empty calories” will be doomed to failure. The concentration of thiamine in the blood is only normal in relation to a normal calorie content of the diet. It is the calorie/thiamine ratio that counts.

Sugar, Thiamine, and SPD

By pointing out to the parents that they had to get rid of the sugar and providing the child with a supplement of thiamine and magnesium, all the symptoms of “psychological misbehavior”, no matter what pretty name was given to it, quickly resolved. For literally a few dollars and cents, this form of treatment is overwhelmingly simple and effective. The “posterior region of the brain where a lot of sensory processing takes place” is peculiarly sensitive to thiamine deficiency. It will affect balance and in its extreme form, can affect brainstem mechanisms where the control of heart rate and breathing is automatically conducted. This is why an excess of sugar is incredibly dangerous, not because the sugar is a poison in its own right, but because of the secondary effect on energy metabolism in that part of the brain that is essential to life itself.

What seems to be poorly understood is that thiamine deficiency produces the same effect in the brain as lack of oxygen and sensory perception becomes exaggerated. Pain is felt more intensely and may give rise to a phenomenon known as “hyperalgesia”(acute pain perception). Sound and light may be so much more perceived that the sufferer puts hands over his ears or closes his eyes, because the perception is offensive. Touch is grossly exaggerated and may even give rise to screaming by the child when being physically examined by a physician. Because of this poor understanding, the behavior of the child is regarded as “psychological”. Under such circumstances a mild injury to an ankle may give rise to severe pain in the leg. It used to be known as “acute sympathetic dystrophy”. The name has been changed to “acute regional pain syndrome” or “complex regional pain syndrome“. Let it be clearly understood that no matter what kind of injury, obvious inflammatory reaction or source of discomfort occurs in the body, the pain is perceived by the brain. If the mechanism of sensory perception is exaggerated, the pain will be more intense.

Conclusion

It is becoming abundantly clear that a diagnosis of sensory integration, ADD, ADHD, OCD and many other diagnostic refinements are not separate diseases at all. Like variations on a symphonic theme in music, the biochemical changes in the brain are responsible for creating the symptomatic expressions on a completely variable basis. It also explains in practical terms why many of the so-called SPD children in the Wall Street Journal article “were unusually gifted”. Like different models of cars with different horsepower, surely the more intelligent brain requires efficient energy metabolism to meet its “gifted” requirements. For those interested in further details of this concept, turn to the post on “Eosinophilic Esophagitis” on this website. There you will find that the unfortunate patient described with this disease was misdiagnosed for many years as psychosomatic. I will go further than this and say that if the symptoms that are commonly represented by changes in brain processing are neglected, and the malnutrition continues, we can expect damaging changes to take place. I would expect this to lead to a whole series of diseases that also go by different diagnostic nomenclatures, Parkinson’s disease, Alzheimer disease and various forms of dementia that represent the end point damage that has accrued over years. Are we collectively insane?

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

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This article was published originally on August 24, 2016. 

Vitamin Therapy Paradox: Getting Worse Before Getting Better

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Does modern medicine accept the idea of vitamin therapy? The answer is a resounding no!  It has only been a little over 100 years since vitamins were synthesized. Of course, as everybody knows, all of these chemical substances were found to exist in natural food. They were very much part of the mystery of evolution. Essential to all animal life, they were there for the picking. Later, it was also found that a number of essential minerals were required. Both the vitamins and minerals need to be present in minute doses, covered under the eponym of recommended daily allowance (RDA). All we had to do was to obey the rules set out by Mother Nature. Our ancestors were classified as “hunter gatherers”. They hunted animals and gathered the bounty of nature. Yes, we were primitive savages and life was not the ideal by any means, but the food contained all that was necessary for life.

An Evolutionary Imperative To Eat Real Food

To ascertain what kind of food is required by an animal, you simply look at the teeth. We have front teeth called incisors for cutting, the pointed teeth called canine for tearing meat and the back teeth molars, used for grinding. Cows and horses are vegetarian and only have molar grinders. Human beings are omnivores (all foods edible) meaning that we are designed to eat meat, fruit and vegetables. Some of the vitamins are recycled through eating other animals. Others are recycled by being returned to the soil and passing into plants. That is why I have said to many people in answering the question as to what diet they should pursue, eat only nature made food and leave the man made food alone. Well, of course, you know that we didn’t do that.

We now have a food industry and it is quite unbelievable, at least to me, to see some of the stuff that passes as food, based solely on taste and appearance. Sometimes I find a person with these typical symptoms who is very careful with diet and does not practice taste hedonism, but because farming practices have changed in modern times, the produce does not have the same kind of non-caloric nutrient content. It may not be coincidental that such persons are almost invariably intelligent and physically and mentally active. It is reasonable to assume that their nutritional demand exceeds supply and they need non-caloric nutrients.

Sugar and the Vitamin Paradox

Now let me turn to the reason that I used “vitamin paradox” in the title. Anyone that wants to follow my reasoning can look back at previous posts on this website. You will find that there is a significant emphasis on the calamity of sugar ingestion and its association with vitamins, particularly thiamine. I am sure that I will look like a broken record to many people, but here is what happens to your health. Although it is obvious that all the vitamins and essential minerals are required, I am taking the example of thiamine because of its close association with the wide consumption of things called “goodies” or “sweets”.

All simple carbohydrate foods are broken down in the body to glucose. Research has shown that overloading the metabolism with sugar overwhelms the capacity of cellular machinery to burn (oxidize) it by producing a relative deficiency of thiamine, the vital catalyst that ignites (oxidizes) glucose to synthesize cellular energy for function. Recently it has been found that thiamine is required for the oxidation of fats, making the doughnut a perfect example of high calorie malnutrition. This is so important in the brain that I simply cannot overstate it.

High Calorie Malnutrition, Oxygen Deprivation and Brain Function

High calorie malnutrition is exactly equivalent to a mild degree of oxygen deprivation, so it is sometimes referred to as pseudo-hypoxia (false oxygen deprivation). If this is induced by poor diet where the pleasure of taste (hedonism) overrides appropriate nutrition, a curious thing happens! The lower part of the brain that deals automatically with your ability to adapt to a hostile environment becomes much more susceptible in its responsiveness.

I will give you one example: panic attacks, so extraordinarily common in our culture, are simply fight-or-flight reflexes that are triggered by pseudo-hypoxia. Messages go out to the body from this part of the brain, falsely initiated as though you were actually being “chased by a tiger”. Such an affected person will begin to experience the following symptoms as examples: palpitations of the heart, unusual sweating, a sense of anxiety or panic, irritable bowel syndrome, manifestations of allergy, emotional lability (emotions out of control) etc.  He or she will go to the doctor who will do a series of tests. If they are all normal, you will then be told that this is “all in your head” (psychosomatic). On the other hand, the doctor might find evidence for “mitral valve prolapse” (MVP), now known to be an early sign of “wear and tear” damage in the heart and the focus becomes “heart disease”(often used to explain heart palpitations) rather than its original cause, associated with nervous system dysfunction. I have seen MVP disappear in people from correcting their nutrition. It is rare for a patient to be asked about diet and rarer still to question the possibility of a vitamin deficiency.

Vitamin Deficiency: The Walking Sick

This kind of health situation may go one for a long time. The patient has symptoms but is not really a sick person. I refer to people like this as the “walking  sick”. Life continues as usual, but medications have failed to relieve the symptoms, or worse yet have introduced side effects. Over time, the loss of metabolic efficiency gradually leads to damage in cellular machinery (e.g. MVP) because the energy need to drive daily function is not being met. Thiamine activates the most important enzyme in energy synthesis and, in the early stages of nutritional deprivation, a thiamine plus multivitamin supplement would quickly abolish the symptoms. If neglected and the marginal malnutrition continues, it will be gradually more difficult to repair the damage.

Vitamin Therapy With Chronic Deficiency: Expect a Decline Before Improving

Physicians who practice Alternative Medicine have found that it is possible sometimes to retrieve function at this late stage of development by the use of a course of vitamins given intravenously. They have also learned that the symptoms of the patient actually get worse (paradox) in the initial stages of intravenous treatment but begin to get better following an unpredictable period of worsening. Naturally, the patient concludes that the treatment is bad or that it is causing side effects as in the use of vitamins. That is why I have christened it paradox, meaning that the unexpected happens.

Over the years of administering intravenous vitamin therapy for all kinds of conditions, irrespective of conventional diagnosis, I quickly learned to inform a patient about paradox before instituting treatment. Surprisingly, this paradoxical response usually heralds a good outcome. I do have some ideas about the cause of paradox, but it is so technical that I cannot attempt it here, perhaps in future posts. Intravenous vitamins are tremendously effective in the improvement of most chronic diseases, an effect that is almost impossible to achieve with the standard treatment of drugs as used in modern medicine today.

Thiamine Deficiency in Modern Medical Practice

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Modern medical practices are plagued with patients who present with chronic, complex, and seemingly treatment resistant illness; illnesses that defy most laboratory testing and abound current diagnostic categories. Some data suggest that 25-75% of symptoms experienced by these patients fall under the umbrella of ‘medically unexplained symptoms’.

What if some of those symptoms were not only explainable but treatable and the expression of these illnesses manifested not from some complicated new disease but from a simple but forgotten nutrient deficiency? What if this nutrient was uniquely critical to mitochondrial competence such that its insufficiency would derail energetic capacity, affect cellular function broadly and diversely, and produce many of the symptoms currently ascribed as medically unexplained? Wouldn’t this be worthy of investigation in your patient population?

That nutrient is thiamine or vitamin B1 and it is essential to mitochondrial energetics – the conversion of food into adenosine triphosphate (ATP). This process is the backbone of all health, and absent sufficient thiamine, it grinds to a halt producing many of the diseases processes vexing modern medicine.

Thiamine is a critical and rate-limiting cofactor to five key enzymes involved in this process, including those at the entry points for the glucose, fatty acid, and amino acid pathways. It has a very short half-life (1-12 hours), limited storage capacity, and is susceptible to depletion and degradation by a number of products that epitomize modern life.

When thiamine is insufficient to overcome these variables, oxidative metabolism falters and the ability to generate molecular energy declines. Over time, aerobic respiration turns anaerobic, oxidative stress increases, and cellular, tissue, and organ function dependent upon steady state energetics deteriorates.

Anaerobic glycolysis, the telltale sign of everything from general metabolic dysfunction to cancer, is, at its root, an adaptive response to insufficient micronutrients like thiamine. Replenish thiamine, recover mitochondrial capacity, and aerobic metabolism and health improve.

Critically Ill Versus Walking Sick: Gradations of Insufficient Thiamine

Conventionally, thiamine deficiency syndromes have been described relative to overt, and often later stage illness in the hospital setting. The most common designations include: Wernicke’s encephalopathy marked by nystagmus, ataxia, and cognitive deficits; wet beriberi or high output cardiac failure with edema and dry beriberi, central and peripheral nervous system and cardiovascular disturbances without edema. More recently, sensorimotor polyneuropathy or neuritic beriberi, gastrointestinal dysmotility syndromes, and the dysautonomias have been included in the spectrum, but recognition is lagging.

These designations give the false illusion of a disease process that happens acutely and one that can be categorized by the afflicted organ system. Neither is accurate. While overt thiamine deficiency is certainly a medical emergency and may sometimes develop acutely, the vast majority of cases represent a culmination of years, if not decades, of insufficient thiamine intake relative to need. Until fulminant, these disease processes are marked by low mortality, but high, chronic, and polysymptomatic morbidity. This suggests ample opportunity to treat and prevent more serious illness, improve the patient’s quality of life, and possibly even regain health. Even in overt and emergent cases, where symptomology is obvious, resolution is possible with thiamine repletion.

Thiamine Depleting Factors

Thiamine deficiency is most commonly associated with food insecurity and chronic alcoholism; a narrow view that risks missing early signals of accruing disease across patient populations. Contributors to this deficiency are far more prevalent in first world countries with westernized food production than is recognized. Among the key dietary contributors to insufficient thiamine:

  • Alcohol
  • Tobacco
  • High carbohydrate, highly processed foods
  • Coffee, tea, energy drinks

Additionally, the regular use of common medications and/or exposures to environmental chemicals independently and synergistically provoke thiamine deficiency. Every medication and environmental chemical depletes thiamine directly or indirectly by a number of mechanisms including blocking thiamine uptake, increasing its degradation, preventing synthesis in gut microbiota, increasing excretion and/or by inducing mitochondrial damage by other means that then necessitates a higher thiamine intake to compensate. Some of the most commonly used medications are the biggest offenders:

Sadly, poor dietary habits trigger thiamine insufficiency independently, leading to the prescription of many of these medications, which then further derail thiamine status and mitochondrial capacity. It is an illness spiral that can only be resolved by addressing diet and mitochondrial nutrients like thiamine.

Genetic Contributors to Thiamine Deficiency

While thiamine deficiency diseases are predominantly attributable to diet and lifestyle variables, a number of common genetic polymorphisms in the solute carriers responsible for thiamine uptake, and in enzyme activity involved in thiamine metabolism, increase the demand for thiamine intake. In these cases, disease expression, particularly later in life, represents a latent genetic vulnerability triggered by environmental or lifestyle stressors. Many medication and vaccine reactions fall into this category.

Prevalence Across Patient Groups

Inasmuch as thiamine status is not regularly evaluated in clinical care, it is difficult to know how pervasive thiamine deficiency is within the general population. Moreover, there are no universally accepted cutoffs demarking the progression from suboptimal to frank deficiency. Of the data that do exist, it is likely far more common than recognized across a broad swathe of patient populations.

Strikingly, diabetes confers one of the largest risks for thiamine deficiency across patient populations. This is largely do to metabolic derangements (to be discussed in a subsequent post) initiated by the hyperglycemia. These include the increased excretion of thiamine, and interestingly, the endogenous production of the anti-thiamine molecule oxythiamine.

Thiamine Testing

Laboratory assessment of thiamine status varies in sensitivity and specificity, with some tests carrying a high false negative rate (standard serum and plasma), particularly when thiamine status is marginal and with recent intake of thiamine. The two most sensitive tests are whole blood HPLC and the erythrocyte transketolase activity/thiamine pyrophosphate effect combination, neither of which is readily available. Urinary organic acid tests, while indirect, may provide useful patterns for determining the need for thiamine and other mitochondrial nutrients.

How To Recognize Thiamine Insufficiency

In light of the difficulties associated with laboratory testing, clinical acumen is required. Given its role in energy metabolism, lack of energy, in multiple manifestations, is a cardinal indicator of insufficiency.

  • Chronic fatigue, muscle weakness, or pain
  • Hypersomnia or anorexia
  • Dysautonomic reactions – exaggerated, ill-timed, or inadequate autonomic responses to stressors, most notably in the brain, heart and/or GI system

Office observations to support thiamine insufficiency:

  • Subtle changes in gait, stability, muscle tone, speech, decrements cognitive or affective acuity or stability
  • Asymmetrical pulse pressure, postural hyper- or hypotension, general tachycardia (early stage), bradycardia (later stage)

Standard labs pointing to problems with energy metabolism:

How to Treat

While clinical practice guidelines exist for overt thiamine deficiency in hospital, which include the use of IV thiamine and additional nutrients at a range of doses dependent upon severity, there are no established guidelines for out-patient thiamine deficiency or insufficiency syndromes. This is partly due to its lack of recognition and partly due to the fact that individual need for thiamine, other mitochondrial co-factors, and response to repletion, varies considerably.

There are no known toxicities to high doses, however, there can be negative reactions in the initial phases of thiamine repletion for a subset of patients. These reactions can occur at any dose. In some cases, the reaction involves the specific formulation of thiamine. In other cases, electrolyte disturbances and/or other micronutrient deficiencies unmasked by thiamine are at fault. To mitigate these reactions, thiamine should always be given with magnesium (~50% of the population consumes less than the RDA and magnesium is required to activate thiamine), a clean, lower dose multi-vitamin and a potassium rich diet. It should be noted that additional calcium may also be needed (here, here), especially when dietary calcium has been low for an extended period. Hypophosphatemia may develop as well in patients with recent or extended GI illnesses and/or have a history of low protein consumption and sodium disturbances are also common.

Consider Thiamine

Thiamine is a safe, non-toxic, essential nutrient that has become increasingly difficult to maintain in the face of modern dietary practices and chemical exposures. Thiamine sufficiency is fundamental to energy metabolism, mitochondrial capacity, and thus, health. Consider thiamine in your practice.

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

Yes, I would like to support Hormones Matter. 

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

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This article was published originally on February 14, 2022. 

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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Image: PickPic royalty free.

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

 

Everyone Needs a Little Extra Thiamine: New Podcast

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Several months ago, I had the great pleasure of speaking with Ann Louise Gittleman, an icon in women’s health and nutrition. The topic, as you might have guessed, was modern thiamine deficiency. We dive right into why so many of us are deficient in thiamine and why so few of us, physicians included, consider thiamine as a culprit to illness.

Thiamine deficiency is quite possibly the most important vitamin deficiency of modernity. It causes a long list of ailments that can be easily remedied if you know what to look for. It is so important, that we wrote about it: Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition and have hundreds of research articles and case stories on the topic published here.

Why is thiamine so important? Well, thiamine is absolutely fundamental to mitochondrial function, and if you don’t know already, mitochondrial function is absolutely fundamental to everything else. The mitochondria take components of the foods we eat and convert that into biological energy or ATP. ATP then fuels cell function – all cell function. Diminished ATP capacity or output, as one might imagine, causes all sorts of problems, many of which underly modern illness.

If thiamine is that important, why isn’t it among the first nutrients tested when illness sets in? That is a good question. Aside from the lack of economic drivers (why prescribe an inexpensive vitamin when you can prescribe an expensive pill), the only answer that makes sense is that most people think this deficiency is impossible without starvation or alcoholism. That is what the textbooks have told us for generations.

Since we live in an era of food abundance, where obesity reigns and where most foods are either fortified or enriched with some vitamins, it is difficult to imagine vitamin malnutrition. In reality though, many of the products we call food have been so adulterated that they carry with them more toxins and more calories than even the added vitamins can overcome. I have written about this on a number of occasions as well. Here is just one of those articles, but there are many more, if you search the website.

Or, you can just have a listen to this latest podcast here.

thiamine podcast

 

We Need Your Help

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

Yes, I would like to support Hormones Matter. 

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