thiamine deficiency Archives - Page 2 of 14

Thiamine and Heart Function

Published on January 15, 2025

10841 views

Since there are many posts on this website about thiamine, it is entirely possible that some readers will regard it as being an obsession of the author’s. I can well imagine a reader believing that an explanation for so many different conditions is the fruit of such an obsession. I will counter this by stating that a paper in a prestigious medical journal reported 696 separate papers in which over 250 human diseases had been treated with this vitamin as long ago as 1962. I think that the explanation for recognizing the place of thiamine in human metabolism is a professional lifetime of clinical observation, resulting in the conclusion that disease is a representation of cellular energy deficiency. To use a simple analogy, spark plugs used in older cars were necessary to ignite the gasoline. Loss of a single plug made the engine run badly and if they were all affected, the car became completely useless. I have used the analogy frequently: thiamine deficiency is like an inefficient spark plug in the engine of a car.

Heart Disease and Beriberi: Case Stories

Heart disease has been central in beriberi, the classic thiamine deficiency disease, for centuries and the painstaking efforts that uncovered thiamine deficiency as the cause is unfortunately a little-known saga of human effort. Modern physicians have been completely convinced that no vitamin deficiencies exist in America, because of vitamin enrichment by the food industry. So is there any evidence that physicians are beginning to wonder whether thiamine plays a part in modern heart disease? This post is designed to show that there is indeed an awakening that could make a big difference to the role of cardiologists in treating heart disease.

Before I go to some medical literature, I want to describe a personal experience that occurred many years ago because it illustrates the incredible psychological resistance of the medical community to a vitamin deficiency. I was a pediatrician at Cleveland Clinic at the time. In the medical hierarchy, a pediatrician is regarded as being largely ignorant concerning disease in adults. A 67 year old anesthesiologist at a Columbus hospital reported to his colleagues with the symptoms of heart failure. He was subjected to heart catheterization and found to be perfectly normal in that respect.

His son was in medical school and studying his father’s case, he came to the conclusion that he had beriberi. For some reason unknown to me, the patient was referred to cardiologists at the Cleveland Clinic. Because my colleagues knew of my particular interest in thiamine, I was asked to see the patient. The story he gave me made the son’s diagnosis virtually a guarantee. Each day, as he went to get into his car in the morning, he would get the “dry heaves” in the garage. He would drive to the hospital where he gave anesthesia to as many as 10 patients. He would then go to the pediatric ward and cut himself a large piece of chocolate cake. When he got home he was too tired to eat dinner and would go to bed. I gave my reading of the case in the patient’s record and had no further contact. He was returned to the Columbus cardiologists and although I believe that he continued to receive thiamine, he died. I never received any information concerning his further care or whether the cardiologists really believed that this was beriberi. One can only conclude that the state of his heart was precarious and the history of thiamine treatment in beriberi had already showed us that there was a “tipping point” beyond which there was no response to thiamine treatment. Whether the cardiologists were aware of this or not is unknown. It is possible that his failure to respond may well have caused them to reject the diagnosis. What really impressed me was the extraordinary resistance to this diagnosis.

I am reminded of another case in my experience. There was a lady pathologist at Cleveland Clinic who was known to be brilliant. I visited her in the Department of Pathology for a reading on one of my patients. She told me that she was so utterly fatigued that a few days previously she had turned around on her way to work and gone home. I found to my amazement that she had a chocolate box in every room in her house and would take a chocolate at random as she went around her house. Without further advice I simply suggested to her to discontinue that practice and to take a supplement of thiamine, whereupon she recovered quickly. Fatigue is a symptom arising in the brain that notifies its owner of energy deficiency and undue fatigue is a logical result in beriberi.

Recognizing Vitamin Deficiencies in Disease

The problem with thiamine deficiency is that a physician has to change his attitude radically towards the cause of disease. This is because the underlying mechanism is derived from cellular lack of energy. If this is not perceived, a physician can be puzzled by a combination of heart and nervous system disease in a single patient. In the present medical model, he believes that he is confronted with two separate conditions.

Because of this resistance, in 1982 I joined a private practice specializing in nutrient-based medicine and began seeing adults as well as children. I joined a group that came to be known as the American College for Advancement in Medicine (ACAM). This relatively small group of physicians had all come to the same conclusion: nutrient-based therapy is, or should be, the methodology of the future. Many of these physicians were practicing alongside their orthodox colleagues in their local hospitals. One of my

ACAM friends told me the following story. He had a patient in the hospital with a pneumonia caused by antibiotic resistant infection. Together with the antibiotic treatment, he had given the patient intravenous vitamin C and she recovered. A patient in the next bed was under another physician with the same pneumonia and my friend approached him, suggesting that he tried the use of the same treatment. He was told to mind his own business and the patient subsequently died. I know of no better example of resistance and rejection of a principle that has yet to reach full acceptance in American medicine. As long as the psychological resistance to vitamin deficiency remains, it is seldom considered. I am happy to say that this resistance is beginning to break down as we shall see by looking at some of the recent medical literature. Not only that, the therapeutic use of vitamins in pharmacological doses it gradually being recognized for its therapeutic value.

Recent Reports of Thiamine’s Role in Clinical Care

Hear what a physician wrote as recently as 2015. The title of the paper is “Thiamine in Clinical Practice” and the author notes that the active form of the vitamin plays a role in nerve structure and function as well as brain and heart metabolism. Unexplained heart and kidney failure, alcoholism, starvation, vomiting in pregnancy or intestinal surgery “may increase the risk for thiamine deficiency”. Understanding the role of thiamine as a potential therapeutic agent for diabetes, some inborn errors of metabolism and neurodegenerative diseases all warrant further research. Surely, this is an indictment of our present approach by merely trying to control symptoms instead of addressing the primary cause.

A group of Canadian physicians stated that “the management of heart failure represents a significant challenge for both patients as well as the health care system in industrialized countries”. The abstract of their paper notes that thiamine is required in the energy-producing reactions that fuel heart contraction. Previous studies have reported a wide range in the prevalence of thiamine deficiency in patients with heart failure and the impact of its supplementation in patients is inconclusive. Of course, Dr. Marrs and I are appalled because such treatment is not only easy, it is completely non-toxic and therefore safe. If there is clinical evidence, why not use a non-toxic agent? However, the psychological restraints of being accused of being a charlatan are very real and can expose a physician to colleague ridicule.

Another paper reported that a total of 20 articles were reviewed and summarized. Recent evidence has indicated that supplementation with thiamine in heart failure patients has the potential to improve heart contractions. These authors recommend that this simple therapy should be tested in large-scale randomized clinical trials to further determine the effects of thiamine in heart failure patients. Diuretic treatment for heart failure may lead to an increased urinary thiamine excretion and in the long-term thiamine deficiency, further compromising heart function. Nine patients with diuretic treatment for chronic heart failure were studied with thiamine supplementation, producing beneficial effects on cardiac function. The authors state that subclinical thiamine deficiency is probably an underestimated issue in heart failure patients. It has even been shown that thiamine pyrophosphate, the active form of the vitamin, prevents the toxic heart injury caused by the cancer treating agent cisplatin. Dietary thiamine that has not been activated by the body did not prevent this.

It has been known for some time that thiamine in the diet has to be absorbed into the body by means of a protein known as a transporter of which there are quite a few. These transporters are under genetic control and absence of one or more of them will make it difficult for a given person to obtain an adequate amount of thiamine from diet into the part of the body where that thiamine transporter is active. A new thiamine transporter has been discovered whose genetic variants have an effect on blood pressure.

Although this post is about heart disease, I want to end by pointing out that vitamin treatment goes well beyond the consideration of just heart disease. Several years ago I received a letter from an aging physician who had specialized in OB/GYN. This letter was so poignant that I am repeating some of this letter:

I am writing to you, because I have found another mortal being who is particularly interested in the biological activities of thiamine. I had previously thought that I was nearly the lone believer in the benevolent effects of thiamine particularly for the treatment and prophylaxis of the toxemias of pregnancy and its many associated problems. I had even written to the chief of the Cleveland Clinic OB-GYN about the “miracles” I was performing and offered to work with him in further development of the concepts.

It was enclosed in a copy of a book by John B Irwin, M.D., the author of the letter.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Image credit: Daniel Capilla, CC BY-SA 4.0, via Wikimedia Commons.

Mural que presenta un corazón en su forma anatómica sobre un fondo de rombos y triángulos blancos, negros y azules, a la altura del número 2 de la calle Alonso Benítez, barrio de Lagunillas, Málaga, España.

This article was published originally on May 30, 2018.

Rest in peace Dr. Lonsdale.

Unraveling Symptoms and Syndromes

by Derrick Lonsdale MD, FACN, CNS

Published on January 7, 2025

14023 views

What Is a Syndrome?

A syndrome is the name given to a collection of symptoms and physical signs that have been observed in the past in a single patient or in a group of similar patients. This is often named after the first person to report this set of observations. It is called a syndrome when others have made the same observations, sometimes years later. The terminology is purely descriptive, even though there may be a constellation of abnormal laboratory tests associated with the clinical facts. Unfortunately, the underlying cause is seldom, if ever, known.

Chronic Fatigue Syndrome

Chronic fatigue syndrome (CFS) is also known as myalgic encephalomyelitis (ME). In a review, it is described as a “challenge to physicians”. Its prevalence is reported as approximately 1% in the general German population. The author states that there are no convincing models that might explain the underlying cause as an independent unique disease. A variety of conditions such as chronic infectious disease, multiple sclerosis, endocrine disorders and psychosomatic disease are suggested in a differential diagnosis. There is said to be a significant overlap with major depression.

Another review describes CFS as characterized by debilitating fatigue that is not relieved with rest and is associated with physical symptoms. In order to make the diagnosis, these authors indicate that at least four of the following symptoms are required to make the diagnosis. They include feeling unwell after exertion, unrefreshing sleep, impaired memory or concentration, muscle pain, aching joints, sore throat, or new headaches. They also say that no pharmacologic or alternative medicine therapies have been proven effective.

Fibromyalgia Syndrome

According to the American College of Rheumatology, fibromyalgia syndrome (FMS) is a common health problem characterized by widespread pain and tenderness. Although chronic, there is a tendency for the pain to fluctuate in intensity and location around the body. Deficient understanding of its true cause gives rise to the false concept that it is neurotic. It is associated with chronic fatigue and patients often have sleep disorders. It is estimated that it affects 2 to 4% of the general population and is most common in women. It affects all ages and the causes are said to be unclear. FMS patients may require psychiatric therapy due to accompanying mental problems. Gonzalez and associates concluded that the combination of psychopathological negative emotionality, interpersonal isolation and low hedonic capacity that they found in a group of patients has implications for the daily living and treatment of these patients.

Regional Pain Syndrome

Complex regional pain syndrome (CRPS) is another common and disabling disorder, characterized by defective autonomic nervous system function and inflammatory features. It reportedly occurs acutely in about 7% of patients who have limb fractures, limb surgery, or other injuries, often quite minor. A small subset of patients progress to a chronic form in which autonomic features dominate. Allodynia (pain due to a stimulus that does not usually provoke pain) and hyperalgesia (increased pain from a stimulus that usually provokes pain) are features of CRPS and require a better understanding.

Sleep Apnea Syndrome

Apnea is the term used for a temporary cessation of automatic breathing that usually happens during the night. This syndrome is described as the most common organic disorder of excessive daytime somnolence. Its prevalence is highest among men age 40 to 65 years and may be as high as 8.5% or higher in this population. It is associated with cigarette smoking, use of alcohol and poor physical fitness.

Similar Cause with Different Manifestations

Complex Regional Pain Syndrome is related to microcirculation impairment associated with tissue hypoxia (lack of oxygen) in the affected limb. Without going into the complex details, hypoxia induces a genetic mechanism called hypoxia inducible factor (HIF-1 alpha) that has a causative association with CRPS. It has been found that inhibiting this factor produced an analgesic effect in a mouse model. The interesting thing about this is that thiamine deficiency does exactly the same thing because it induces biochemical effects similar to those produced by hypoxia (pseudo[false]hypoxia). A group of physicians in Italy have shown that high doses of thiamine produced an appreciable improvement in the symptoms of three female patients affected by fibromyalgia and are probably pursuing this research. Dietary interventions have been reported in seven clinical trials in which five reported improvement. There was variable improvement in associated fatigue, sleep quality, depression, anxiety and gastrointestinal symptoms.

Dr. Marrs and I have published a book that emphasizes deficient energy metabolism as a single cause of many, if not all, diseases. The symptomatic overlap in these so-called syndromes is generated by defective function of cellular metabolism in brain. Fatigue is the best symbol of energy deficiency and the English translation of the Chinese word beriberi is “I can’t, I can’t”. Fatigue is a leading symptom in beriberi. When physicians diagnose psychosomatic disease as “it’s all in your head”, they are of course, quite right. However, to imagine or conclude that the variable symptoms that accompany the leading one of fatigue are “imaginary” is practically an accusation of malingering. The brain is trying to tell its owner that it has not got the energy to perform normally and the physician should be able to recognize the problem by understanding the mechanism by which the symptoms are produced. Every thought, every emotion, every physical action, however small, requires the consumption of energy. Obviously we are considering variable degrees of deficiency from slight to moderate. The greater the deficiency the more serious is the manifestation of disease that follows. Death is a manifestation of deficiency that no longer permits life.

Our book is written primarily for physicians, but it is sufficiently lacking in technological language to encourage reading by patients. It emphasizes, by descriptions of case after case, the details of how genetic risk and failed brain energy are together unable to meet and adapt a person’s ability to meet the daily stresses of life. Stress, genetic risk and poor diet all go together. A whole chapter discusses the functions of the autonomic nervous system and how it deviates when the control mechanisms in the lower brain are defective. This system is the nervous channel that enables the brain to communicate the adaptive body actions necessary to meet living in an essentially hostile environment. We show that an excess of sugar and/or alcohol produce deficiency of vitamin B1 and the so-called psychosomatic disease that results is really early beriberi “I can’t, I can’t”. Variability in symptoms caused by this effect is because the cellular energy deficiency distribution varies from person to person and is affected by genetically determined differences.

This is illustrated by the case of a boy with eosinophilic esophagitis whose first eight years of life were marked by repeated diagnoses of psychosomatic disease. At the age of eight, upper endoscopy revealed the pathology in the esophagus. There was a family history of alcoholism and he was severely addicted to sugar. Many of his symptoms cleared with the administration of a thiamine derivative and resulted in a dramatic increase in stature. No pediatrician or other physician whose attendance was sought through those first 8 years evidently had ever questioned diet or the gross ingestion of sweets. They simply treated each condition as a confirmation that they were “psychological”.

It is worth noting that references 1 through 4 refer to both CFS and FMS syndromes being affected by psychological issues. This implies that the patient is “inventing” the poorly understood (and often bizarre) symptoms as a result of neurosis. The unfortunate complainant may easily become classified in the mind of the attendant physician as a “problem patient”. I have become aware that this can rise to such a degree of misunderstanding that the patient is denied access to the physician and even to other physicians in the same clinic. It is indeed about time that an overall revision be made to the absurd concept that the brain can “invent” a sensation that has no importance in solving the electrochemical problem. When we see the statistics of incidence of these common syndromes we have to conclude that there is an underlying cause and effect that pervades the general population. We are very conscious that our cars need the right fuel to work efficiently but rarely take it into consideration that the quality of food is our sole source of energy synthesis.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Image created using Canva AI.

This article was published originally December 2019.

Rest in peace Dr. Lonsdale. May 2024.

Thiamine Insufficiency Relative to Carbohydrate Consumption

by Chandler Marrs, PhD

Published on September 18, 2024

27540 views

Thiamine (vitamin B1) is an essential micronutrient responsible for key reactions involved in the conversion of the foods we consume into the chemical energy substrate requisite for cellular function, adenosine triphosphate (ATP). Absent sufficient ATP, all sorts of metabolic functions become disordered leading to the disease processes that dominate western medicine. Chronic inflammation, altered immune function, hormone dysregulation, cognitive and mood disorders, and dysautonomias, all can be traced back to insufficient thiamine > inefficient mitochondrial function, reduced ATP, and the compensatory reactions that ensue.

Among the most common but least well-recognized contributors to thiamine deficiency is the regular consumption of a high carbohydrate/highly processed food diet. Although most of these foods are enriched or fortified with thiamine, perhaps staving off more severe deficiencies, the density of sugars overwhelms mitochondrial capacity to process these foods, both the thiamine and any other potential nutrients are excreted, while the carbohydrates themselves are stored as fat for future use. High-calorie malnutrition is a common contributor to thiamine deficiency in obesity but also may develop in presumed healthy athletes whose diets focus heavily on high carbohydrate intake.

Thiamine, along with other B vitamins is often deficient in vegetarian and vegan diets as well. Not only do fruits, vegetables, and carbohydrates contain minimal, if any, thiamine, but some have anti-thiamine factors and are high in what are called oxalates. Anti-thiamine factors found in some fruits and vegetables interfere with the absorption or digestion of thiamine. Oxalates are mineralized crystals of sorts that tend to build up and store in places like the kidneys (kidney stones), but also may store and cause problems anywhere in the body like bones, arteries, eyes, heart, and nerves. Effective oxalate metabolism and clearance requires thiamine. Since vegetarian and vegan diets are also carbohydrate intensive, thiamine deficiency and oxalate issues may be compounded. Thus, a number of common diets not only contain reduced thiamine content but cause an increased need for thiamine by at least three mechanisms; higher carbohydrate consumption overwhelming capacity, which is then magnified by poor carbohydrate and oxalate processing.

Add daily coffee, tea, and/or alcohol consumption to any diet, and whatever thiamine that is consumed is either inactivated by enzymes before being used or is unabsorbable. Add a medication or four and thiamine availability will tank simultaneously with an increased need. Medications both block nutrient uptake and/or increase the need for nutrients by inducing mitochondrial damage. Given that 70% percent of the US population takes at least one medication regularly, while 20% take four or more, it is safe to say, that a good percentage of the population is consuming insufficient thiamine to maintain mitochondrial function and health.

Are We Really Thiamine Deficient?

As an essential nutrient, thiamine must be consumed regularly to maintain sufficient concentrations. The question is how much thiamine is sufficient to maintain health? Current RDA values for daily thiamine intake suggest a little over a milligram per day is adequate for most adults. If this is true, then the minimum value can be attained through just about any diet including those dominant in highly processed, carbohydrate-dense foods, which are commonly either enriched or fortified with thiamine. Everything from bread to cereals and even junk food like Oreos have thiamine. Per the RDA values, none of us ought to be thiamine deficient and none of us ought to require thiamine supplementation, and yet, many of us are and do. Indeed, several studies, across disparate populations show that even by this minimum standard, deficiency is a serious health problem. From our book:

76% of diabetics (type 1 and type 2)
29% of obese patients, 49% of post-bariatric surgery
40% of community-dwelling elderly, 48% of elderly patients in acute care
55% of cancer patients
20% ER patients (random sample, UK)
33% of congestive heart failure patients
38% of pregnant women, more with hyperemesis
30% of psychiatric patients

It takes approximately 18 days to completely abolish endogenous thiamine stores in a diet that is completely devoid of thiamine. Except under total starvation, medical or industrial food production mishaps, and experimentally contrived situations, thiamine consumption is never completely abolished. It waxes and wanes by dietary choices and life stressors. According to rodent studies, it takes a reduction of greater than 80% of thiamine stores before the more severe neurological symptoms are recognizable. In humans, these symptoms include those associated with Wernicke’s encephalopathy, the various forms of beriberi, and dysautonomic function. These include but are not limited to: ataxia, changes in mental status, optic neuritis, ocular nerve abnormalities, diminished visual acuity, high-output cardiac failure with or without edema, high pulse pressure, polyneuropathy (sensorimotor), enteritis, esophagitis, gastroparesis, nausea and vomiting, constipation, hyper- or hypo-stomach acidity, sympathetic/parasympathetic imbalance, postural orthostatic tachycardia syndrome (POTS), cerebral salt wasting syndrome, vasomotor dysfunction, respiratory distress, reduced vital capacity, and/or low arterial O2, high venous O2.

With a less severe thiamine deficiency, symptoms are rarely recognized as such and often attributed to psychological manifestations. A not entirely ethical study done in 1942 involving 11 women on a low thiamine diet over a period of ~3-6.5 months found striking symptoms.

During this time all subjects showed definite changes in personality.
They became irritable, depressed, quarrelsome, and uncooperative.
Two threatened suicide. All became inefficient in their work, forgetful, and lost manual dexterity.
Their hands and feet frequently felt numb.
Headaches, backaches, sleeplessness, and sensitivity to noises were noted.
The subjects fatigued easily and were not able to vigorous exertion.
Constipation was the rule, but no impairment, of gastrointestinal motility, could be demonstrated fluoroscopically.
Anorexia, nausea, vomiting, and epigastric distress were frequently observed.
Low blood pressure and vasomotor instability were present in all patients.
At rest, pulse rates were low (55 to 60 per minute) but tachycardia followed moderate exertion. Sinus arrhythmia was marked.
Macrocytic, hypochromic anemia of moderate severity (3.0 to 3.5 million red cells) developed in 5 cases.
A decrease in serum protein concentration occurred in 8 subjects.
Basal metabolic rates were lowered by 10 to 33 points.
Fasting blood sugar was often abnormally high.

The study above demonstrated a rapid and dramatic onset of symptoms relative to a diet with limited thiamine. Depending upon caloric intake, the amount of thiamine allowed was approximately 1/3 to 1/5 of the amount recommended by the RDA. Admittedly, the RDA for thiamine is low, to begin with, but even so, this was not a complete absence of thiamine. Since the study took place in the early 1940s, it is difficult to ascertain the specifics of the diet. Nevertheless, it demonstrates a clear association between general health and one’s ability to function, and thiamine insufficiency.

High Carbohydrate Diets Equal Lower Thiamine

More recently, a short and very small study (12 days and 12 participants) of active young men and women (ages 25-30) investigated the relationship between carbohydrate intake and thiamine status. Thiamine was measured in blood, plasma, urine (creatinine), and feces at four time points: at baseline, before the study began, during an adaptation phase where carbohydrate intake represented 55% of the total caloric intake, and during the two subsequent intervention phases, where carbohydrate intake was increased to 65% and 75% of the total caloric intake, respectively. Both caloric and thiamine intake was held constant throughout the study despite the increased intake of carbohydrates. Activity levels were also held constant. Across this short-term study, as carbohydrate intake increased, plasma, and urinary thiamine decreased. Excretion through feces remained unchanged. Transketolase enzyme activity was also measured but remained unchanged. Given the short-term nature of this study, the fact that transketolase remained unchanged is unexpected. In addition to the decreasing thiamine values, there were several changes in lipid profile as well. Despite the short duration of this study, however, the results show a clear relationship between carbohydrate intake and thiamine status; one that would likely be magnified over time and certainly if other life stressors and medical and environmental toxicants were added to the mix.

It is important to note current dietary guidelines suggest carbohydrate consumption should fall between 45-65% of total calories, percentages which, per this study would decrease thiamine availability significantly. From the baseline diet to the 55% adaptation phase, thiamine dropped precipitously, only to drop even further at the 65% phase. A recent study surveying macronutrient consumption showed that average carbohydrate consumption across the US population represented approximately 50% of total caloric intake. Importantly though, the study found that 42% of the carbohydrate consumption came in the form of what researchers termed ‘low-quality carbs’ e.g. sugary processed foods with no nutritional value. Thiamine is only found in pork, beef, wheat germ and whole grains, organ meats, eggs, fish, legumes, and nuts. It is not present in fats/oils, polished rice, or simple sugars, nor are dairy products or many fruits and vegetables a good source. Indeed as mentioned previously, some fruits and vegetables may contain anti-thiamine factors. A diet that is 42% empty calories, that contains limited to no nutritive value, save except what has been added post hoc via enrichment, begs for mitochondrial damage and the illnesses that ensue. And yet, that is precisely the nutritional landscape in which most of us exist.

Admittedly, both studies were very small, but the research connecting thiamine deficiency to ill-health and carbohydrate consumption to thiamine loss is clear. Given the dominance of ultra-processed carbohydrate-dense foods in the modern diet, is likely that high-calorie malnutrition underlies much of the chronic illness that plagues western medicine. To learn more about thiamine deficiency and the havoc it wreaks on health: Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition.

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.

Maternal Thiamine Deficiency and Fetal Brain Damage

by Chandler Marrs, PhD

Published on July 25, 2024

12669 views

maternal thiamine deficiency microcephaly

Over the last several months, Dr. Lonsdale and I have been working on a book about thiamine deficiency and dysautonomia. Last week I wrote about the presumed connection between the Zika virus and microcephaly where I hinted at a thiamine connection. One might say, that I have thiamine on the brain and that would be a fair assumption. The old adage, ‘if one has a hammer, everything becomes a nail‘, may apply. I may be focusing too much on thiamine and its role on mitochondrial health. Alternatively, it could be that thiamine is just that important. After all, it sits atop at least two of the four energy producing pathways that give us ATP and is deeply embedded within the remainder of the oxidation process. The consequences of impaired oxidative metabolism in the brain are vast and include a range of disease processes like Alzheimer’s disease, amyotrophic lateral sclerosis (Lou Gerhig’s disease), Parkinson’s disease, multiple sclerosis, alcoholic brain disease, and stroke. Without thiamine, the mitochondrial factories stop producing energy or ATP and without ATP, stuff slows and then dies. So yes, thiamine is critical to health.

It is not difficult to imagine what happens to energy levels when thiamine concentrations diminish even slightly in an adult. An unrelenting fatigue is one of the early symptoms of struggling mitochondria and thiamine deficiency. More fundamentally, however, all the organs tasked with maintaining life, demand energy. When energy stores diminish, those organ systems struggle. The organ systems requiring the most energy, like the brain and the heart, are hit hardest. Maintain a slight deficiency chronically and damage ensues. In Cuba, for example, trade embargo policies resulted widespread thiamine deficiency in the population, which in turn initiated an epidemic of neuropathy – nerve damage. Over 50,000 Cubans were reported to have developed optic neuropathy, deafness, myelopathy, and sensory neuropathy related to embargo imposed dietary changes. In contrast to the more insidious damage initiated by chronically low thiamine concentrations, severe and acute thiamine deficiency is life-threatening, especially in children, but also in pregnant women.

With low maternal thiamine concentrations, the effects on fetal development, especially fetal brain development that requires enormous amounts of energy, are likely to be devastating. And indeed, they are. But we don’t study that very often, even in rats. Do a search on the subject and there is not much research out there. Sure, some researchers have investigated maternal thiamine deficiency in fetal alcohol syndrome (FAS), postulating thiamine might be the mechanism by which FAS develops, but that is about it. Given how critical it is to fetal development, I expected more research.

It is not just alcoholics who are at risk of thiamine deficiency. An increasing percentage of Western populations are likely thiamine deficient. Thiamine depletion occurs with numerous medications and vaccines via multiple mechanisms, many of which are just beginning to be understood. Conventional farming practices use herbicides and pesticides that block vitamin B absorption and so even diets presumed healthy may not be as nutrient dense as in the past. Poor absorption from altered gut microbiomes may be another common mechanism for thiamine deficiency and emerging evidence finds that Type 1 and Type 2 diabetics excrete significantly more thiamine than non diabetics, making them thiamine deficient as well. Not studying this more broadly is leaving millions of folks to suffer with entirely preventable disease processes. During pregnancy, however, this lack of recognition and research is just downright negligent, especially when we consider fetal brain development.

Thiamine During Pregnancy

Thiamine is absolutely critical for both maternal health and fetal development. Women with hyperemesis gravidarum, excessive vomiting during pregnancy, are at a particularly high risk for thiamine deficiency and though there is increasing awareness of maternal Wernicke’s encephalopathy during pregnancy, a condition typically associated with thiamine deficient alcoholics, the full scope of damage associated with maternal thiamine deficiency is insufficiently understood. There is little to no appreciation of the long term effects on maternal health and even less recognition of how the deficiency impacts fetal development in either the short or long term.

Provided mom survives a thiamine deficient pregnancy, what happens to the growing fetus? In 37% of the cases of severe maternal thiamine deficiency, spontaneous fetal loss occurs. If thiamine is critical for mitochondrial energy production, and fetal development requires exorbitant amounts of mitochondrial energy, what happens if one of the key components to that energy production process is lacking? All sorts of things, it turns out, including microcephaly. Beyond a rare congenital defect in thiamine transport believed to affect only consanguineous Amish, there are very few studies that have considered the effects of epigenetic and more functional maternal or fetal thiamine deficits. We know from the Amish cases, that when the fetal thiamine transporters are impaired, microcephaly ensues. Is it so hard to imagine that we might impair those transporters epigenetically or reduce maternal thiamine concentrations functionally by dietary choices, medications or environmental toxicants that leach nutrients and/or by malabsorption? And yet, as I dig into this, I find only a few studies that have addressed maternal thiamine and fetal brain development. Here they are.

Maternal Thiamine Deficiency and Fetal Brain Damage

A 2005 study from researchers in West Africa showed that the pups from thiamine deficient dams, had significantly smaller brains by weight. Digging deeper, they found far fewer neurons in the hippocampus, the region of the brain responsible for memory consolidation and retrieval, than the pups from thiamine sufficient diets. Brain damage in the offspring could be induced by maternal thiamine deficiency either leading up to, during, or after pregnancy (while lactating) but varied in scope, severity, and pattern. The most significant damage occurred when the dams were deficient during pregnancy.

In the offspring from perinatal thiamine deficiency, hippocampal volume was reduced by almost a third due to neural cell death. The neurons that survived were smaller than normal and misshapen. The hippocampus is critical to memory. Hippocampal damage in human adults causes all manner of amnesias and aphasias (speaking and language comprehension deficits) and is found in neurodegenerative disorders like Alzheimer’s disease.

The neurons affected most by the thiamine deficiency, the CA1 neurons, are especially susceptible to oxidative damage and insult. Thiamine is integral to brain oxidation and so this makes sense. What we have to remember though, is that in a fully developed human brain, oxidative damage to the CA1 region is associated with hippocampal ischemia, limbic encephalitis, status epilepticus, and transient global amnesia – very serious conditions. To a developing brain, requiring vast amounts of energy to grow, the consequences of hippocampal deficits are largely under-recognized except again in fetal alcohol syndrome.

Another animal study looked at the effects of maternal thiamine deficiency to the cerebellum of the offspring. The cerebellum is the region of the brain responsible for balance and coordinated motor movements. Here again, the damage was severe with a significant reduction of size, loss of neuron viability, and conduction. There have been a smattering of studies across the decades (here, and here, for example) looking at thiamine deficiency and brain damage in non-pregnant rats, but that’s about it.

Not much else is out there.

From these few animal studies, the work on Amish microcephaly and the work connecting neurodegenerative disorders to thiamine deficiency, we can surmise that thiamine is essential to brain development. More specifically, in pregnancies where thiamine concentrations are low, cerebral development of the offspring will be impaired in some pretty significant ways. Namely, the number and size of neurons is reduced, and as a consequent, total brain volume is reduced. If the deficiency is severe enough, microcephaly is possible and has been identified in the two of studies mentioned above. I think this is what is happening in Brazil. That is, a combination of seemingly unrelated factors, coalesce to produce fetal thiamine deficiency which results in microcephaly and other sorts of brain damage. The questions that remain include:

By what mechanisms specifically is thiamine deficiency produced?
What are the risks for maternal thiamine deficiency in other regions?

One of the most direct routes to thiamine deficiency during pregnancy is hyperemesis gravidarum, excessive vomiting. Case studies abound where it is often not recognized until the mother is in critical condition. It is considered a rare complication, but is it? Unless and until those questions are answered more fully and physicians recognize maternal thiamine deficiency as a potential problem, women and children will continue to be at risk for what are entirely preventable complications of pregnancy.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Image credit: Centers for Disease Control and Prevention, Public domain, via Wikimedia Commons

This article was first published on June 16, 2016.

Sleep Requires Energy

by Derrick Lonsdale MD, FACN, CNS

Published on July 23, 2024

23732 views

It is widely believed that almost no calories are used during sleep. That is incorrect: while the body rests during sleep and energy consumption is not high, it is a long way from zero. A convenient way to measure energy use is known as the “metabolic equivalent” (ME). This is defined as the rate of energy used by a person sitting and awake, the “resting metabolic rate”. A person riding a bicycle may be using five MEs; a runner, nine or more. A sleeping person uses about 0.9 MEs, so we burn calories when we are asleep about 90% as fast as while sitting on the couch watching television.

Energy conservation is important in sleep, but it’s expenditure is still required. It has been proposed that sleep is a physiological adaptation to conserve energy but little research has examined this proposed function. In one study, the effects of sleep, sleep deprivation and recovery sleep on the whole-body, total daily energy expenditure was examined in seven healthy participants aged 22+/-5 years. The findings provided support for the hypothesis that sleep conserves energy and that sleep deprivation increases total daily energy expenditure. I read somewhere that an enthusiastic young astronomer decided that sleep was unnecessary and used his telescope for 13 nights without sleeping during the day. He became extremely ill, thus showing the importance of sleep in survival. The recognition that sleep is one of the foundations of athletic performance is vital.

Research in the general population has highlighted the importance of sleep on neurophysiology, cognitive function and mood. In a post on Hormones Matter, we reported several young people who had a post Gardasil vaccination crippling condition that turned out to be due to thiamine deficiency. All of them had been exceptional athletes and students before the vaccination. We concluded that the brain energy requirement for exceptional people put them at greater risk of succumbing to stress if their capacity for MEs was limited, either for genetic or nutritional reasons. We assumed that their thiamine deficiency before vaccination was marginal and either asymptomatic or producing trivial symptoms ascribed to other “medically more acceptable” causes. The stress of the vaccination required an energy dependent adaptive response that precipitated fully symptomatic thiamine deficiency. You might say that they were “weighed in the balance and found wanting” as the proverb says.

The Stages of Sleep

Sleep is a complicated process. The first sensation is known as “sleep latency” and registers the time taken from eye closure to falling asleep. The sleep cycle is then divided into five stages, each cycle lasting approximately 90-120 minutes. Stage one is known as light sleep. In stage 2 the brain is resting the parts used when awake. Stages 3 and 4 are deeply restorative. Stage V is known as rapid eye movement (REM) sleep and may be the most important part. Movement of the eyes behind closed lids is observed. The autonomic nervous system is activated for unknown reasons. It is in this stage when we dream and most sleep disorders occur.

Circadian Rhythm

The word circadian means “about 24 hours”. The circadian clock is a complex, highly specialized network in the brain that regulates its day/night metabolism and is a key for metabolic health. It is modulated by behavioral patterns, physical activity, food intake, sleep loss and sleep disorders. Disruption of this clock is associated with a variety of mental and physical illnesses and an increasing prevalence of obesity, thus illustrating that it is dependent on energy balance (production/consumption). Reduced sleep quality and duration lead to decreased glucose tolerance and insulin sensitivity, thus increasing the risk of developing type 2 diabetes. In other words there is a close link between circadian rhythm and available energy . I have seen patients who were unable to take the night shift at work because they were unable to adapt. The increase in obesity has been paralleled by a decline in sleep duration but the potential mechanisms linking energy balance and the sleep/wake cycle are not well understood. An experiment was reported in 12 healthy normal weight men. Caloric restriction significantly increased the duration of deep (stage 4) sleep, an effect that was entirely reversed upon free feeding.

Sleep Apnea

This condition is fairly common in the United States and is probably generally fairly well-known by most people. The patient stops breathing during sleep and may repeatedly awaken with a start. The disease was discovered because a woman reported that her husband kept waking up with a start because “he was affected by an evil spirit”. Fortunately, the physician took her seriously and it led to the studies that determined its cause. Many patients with, or at risk of, cardiovascular disease have sleep disordered breathing (SDB). These can be either obstructive because of intermittent collapse of the upper airway, or central because of episodic loss of respiratory drive. SDB is associated with sleep disturbance, hypoxemia, hemodynamic changes and sympathetic activation. Brainstem dysfunction combined with heart disease is the hallmark of the thiamine deficiency disease, beriberi.

What that means is that there are two types of sleep apnea. In the obstructive type, the tongue falls back into the pharynx and blocks the airway. In the one where there is loss of respiratory drive, the centers in the brain stem are compromised. It is these centers that completely take over the control of breathing when we are unconscious as in sleep. If their supervisory mechanisms fail, breathing ceases. Carbon dioxide concentration increases and stimulates the brain controls that restart breathing. Occasionally these mechanisms are so sick that breathing does not restart. Hence a form of nocturnal sudden death follows. When we are awake we can override these centers and control our breathing voluntarily. Obesity and obstructive sleep apnea have a reciprocal relationship depending on the regulation of energy balance. When I was in practice I treated several patients with sleep apnea using large doses of thiamine. Because of this I hypothesized that the association of dysautonomia with so many different diagnoses is because of loss of oxidative efficiency and subsequent disorganization of controls that are mediated through the limbic system and brainstem. I came to the conclusion that energy deficiency in the brain was the core issue.

I recently had a letter from the parents of a then five-year-old child who came under my care 35 years ago. She has a genetically determined disorder that affects energy balance and I had treated her by dietary restriction and providing non-caloric nutrients. They informed me that she was doing very well. The condition is known as Prader Willi syndrome, a terminology that indicates that nothing was known about its cause when it was initially described. Today, 10 studies have provided evidence that total energy, resting energy, sleep energy and activity energy expenditure are all lower in individuals with this syndrome. Dietary discipline and nutritional supplementation had paid off.

An Explanatory Analogy

You may think that comparing the human body with an automobile is manifestly absurd, but the principles that I will use in the analogy are simple.

Fuel

First of all, both use fuel: gasoline is the fuel for a car, but it must be calibrated to the design of the engine, giving rise to the gasoline choices at the pump. Although different forms of human food may be compared to gasoline choices, the primary fuel for our cells is glucose and this is particularly true for the brain. Glucose, a carbohydrate, can be synthesized in the body from other components in the diet and different diets are sometimes used therapeutically. Unlike the car, the human body must derive its “spark plug” from the food and is the basic reason why organic, naturally occurring, food is a necessity. The food industry cannot imitate or replace it.

Engine

The engine in a car burns gasoline to create energy. It requires spark plugs to ignite the gasoline and waste gases are eliminated through an exhaust pipe.

Every cell in the human body has an “engine”. Without going into details this is known as the Krebs cycle (named after its discoverer). Its objective is to produce energy and glucose has to be “ignited” (oxidized). The oxidation process, while releasing energy, gives rise to carbon dioxide (the “ash”) that is eliminated in the breath. Energy is stored in an eletrochemical form known as adenosine triphosphate (ATP).The nearest parallel would be a battery. It releases an electrical form of energy that is then used for function. Whether we like to recognize it or not, we are electrochemical machines and the only way that we can preserve or retrieve health is by furnishing the complex of ingredients that enable food to be converted into energy.

To continue the analogy, when you put your car in the garage and turn off the ignition the car is technically “dead”. Obviously, we are unable to do that with the human body, but let us make a simple comparison. Supposing for some reason it was desirable to keep the car “alive” when it was in the garage. The engine would continue to run and it would be consuming fuel. Because the body requires energy to remain alive, the “engines” have to continue running, even when we are asleep. This does make sense for the consumption of energy when we are asleep———it keeps us alive !

Transmission

The energy developed from burning gasoline has to be transmitted to the wheels in order to produce the normal function of the car, which is the ability to move. The transmission is a series of levers that are interconnected.

The same is true in the human body, but it is biochemical in nature. A series of energy consuming enzymes use the protein, fat and carbohydrate to build the diversity of tissues that make up the body. Throughout life, cells are destroyed and replaced, so this is a continuous process of energy consumption and repair. Every physical movement, every thought and emotion, consumes energy. Like the transmission in the car, the energy produced by the citric acid cycle engine is consumed in every movement of the body, every thought occurring in the brain and every emotion.

Chassis

The body of a car is just a container on wheels designed to carry around human beings. Its sole function is to move and until we have driverless cars a human being must be the driver.

In comparison, the body of a human being is merely a chassis that carries the brain around. It might be said that the brain can be compared with the car driver and every function of the body is under the command of the brain. Another analogy that I have used is an orchestra where the brain is the conductor and the organs are banks of instruments in which the cells come under the command of the conductor.

Putting It All Together

The 2019 Nobel prize has just been awarded to three scientists who have discovered how our body cells respond to low concentrations of oxygen (hypoxia). The reaction of medical scientists is very positive since this discovery will certainly be applied to the treatment of many diseases. Apparently scientists are already trying to find drugs that will influence this effect. For example, it has long been known that hypoxia will introduce inflammation. My forecast is that the use of nutrients will often correct the genetics by epigenetic mechanisms and this is already under way.

I found the Nobel prize extremely interesting because of a little-known phenomenon that was described by the early investigators of the vitamin B1 deficiency disease, beriberi. They had found in this disease that the arterial concentration of oxygen was low while the venous concentration was relatively high. Arterial blood carries oxygen from the lung to all the tissues of the body. It has to be unloaded into the cells that then use it to produce energy. The venous blood then returns to the lung to be loaded again with oxygen. A relatively low arterial oxygen reflects an inadequate loading at the lung tissues, while a relatively high venous oxygen indicates poor utilization by the cells to which it is delivered. This means that thiamine (vitamin B1) is an essential catalyst in the delivery of oxygen to the tissues. Its deficiency induces gene expression similar to that observed in hypoxia and has been referred to as a cause of pseudo-hypoxia (false hypoxia).

The heading of this article is that sleep requires energy, but I am making the case that being alive and well simply means that oxygen is being consumed efficiently, as long as the “blueprint” of DNA is healthy. It strongly suggests that hypoxia and/or pseudo -hypoxia are the underlying causes of disease and may explain why thiamine and its derivative are such important therapeutic agents.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Image by freestockcenter on Freepik.

This article was published originally on October 14, 2019.

With Thiamine Paradox Symptoms Patience Is Key

by Jeff Mitchell

Published on June 17, 2024

43113 views

I wanted to share my experience going through thiamine paradox so that others may find hope as they navigate the process. In November of 2019, my life was completely flipped upside down. My full story is here, but briefly, I had taken an antibiotic called Tinidazole, the less popular but almost identical sister drug to Metronidazole. Within days of taking the antibiotic I began to experience frightening symptoms like loss of mobility in my hands, heart palpitations and intense feelings of depression and doom. Less than two weeks later, I went into surgery to get my wisdom teeth removed and was put on a course of penicillin for two weeks.

Within weeks, my health was in a total spiral. I began to experience constant bouts of tachycardia and panic, low blood sugar, dizziness, blurry vision and the inability to sleep. I went from somebody who sleeps 8 hours a night to sleeping for less than an hour on various nights. When sleep did come, I was jolted awake in a panic attack. At times, I was feeling symptoms that mimicked asthma…it was like I couldn’t breathe.

I had no idea what was going on. Multiple trips to the ER did nothing. I continued to get worse. It wasn’t until I traced back what drugs I had taken that I made my way to a Facebook group called “Metronidazole Toxicity Support Group.” It was in that group that I discovered that thousands of others were dealing with the same set of symptoms caused by this horrendously neurotoxic antibiotic. I had known for years that one should avoid fluoroquinolone antibiotics, but research has shown that metronidazole and others in its class present some of the same catastrophic side effects.

Through her own research and contact with Dr. Lonsdale and Dr. Marrs, the founder of the group discovered that metronidazole and other drugs in its class block thiamine in the body. The symptoms of the toxicity mimic those of Wernicke’s encephalopathy.

The solution? Take thiamine.

I thought it was going to be an easy fix. It wasn’t.

Like many posts on Hormones Matter, the topic of paradox frequently comes up, and I am the perfect case study.

In retrospect, I had longstanding symptoms of mild beriberi for a lot of my life. I was constantly dealing with low blood pressure and strange heart symptoms that date back to my teenage years. I grew up eating a typical American diet and started drinking large amounts of coffee in my teens. I loved sugar.

With longstanding thiamine deficiency, the human body changes its chemistry to adapt and survive. When thiamine is reintroduced and things get turned back, your body goes haywire until the chemistry can normalize.

For me, it took three attempts. Every time I would start even the tiniest dose of thiamine HCL, I would erupt in panic, tachycardia, feelings of “seizures” and doom and gloom, chest tightness and head pressure. It was akin to the feeling when somebody knows that they ingested way more marijuana than they should have. Sheer terror. When I took too much one time, I almost landed in the ER because I thought for sure that I was going into cardiac arrest.

My first attempt was in January 2020. I failed miserably and stopped because of the side effects. But I wasn’t getting better and my health continued to spiral. I tried again in March 2020 and made it for 2 weeks before dropping out again. I would crumble pills to get just a little thiamine HCL in my system and I would still feel like a total wreck.

Finally, on my third attempt in May 2020, I made it.

The solution is to start LOW and SLOW. I found a company in the UK that has a liquid form of thiamine HCL that allowed me to do this. I started with 10 mg per day and gradually increased by 10-20 mg over the course of many weeks. I also spread my dose out throughout the day. Dr. Lonsdale predicted the paradox will lift within a month, but for me, it took a bit longer. Within 8 weeks I began to notice that I could safely take a 100mg thiamine HCL pill without experiencing too many symptoms. It continued to get better with time.

Now, almost a year later, I’m taking 300-400mg of thiamine HCL a day and mixing in benfotiamine and allithiamine. In the last 6 months, my health has slowly started to trend upward. I’ve added in a B complex at times and I’m also working on my B12. The heart palpitations are significantly better, I’m less prone to panic attacks than I have been in years, and my brain fog has lifted. What I’m left with is some slight dizziness (though it is significantly better), blurry vision that waxes and wanes, and my blood sugar is still presenting some issues. Still, I feel like I’m trending in the right direction and that things continue to slowly improve.

My advice for those of you encountering paradox symptoms is this: BE PATIENT. It sucks. But the rewards on the other end are so worth it. I would also advise you to dramatically increase your potassium through food. This didn’t eliminate the paradox feelings entirely but it did help reduce them.

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 Aron Visuals on Unsplash.

This article was publish originally on January 26, 2021.

Beriberi: The Great Imitator

by Derrick Lonsdale MD, FACN, CNS

Published on June 6, 2024

49210 views

Because of some unusual clinical experiences as a pediatrician, I have published a number of articles in the medical press on thiamine, also known as vitamin B1. Deficiency of this vitamin is the primary cause of the disease called beriberi. It took many years before the simple explanation for this incredibly complex disease became known. A group of scientists from Japan called the “Vitamin B research committee of Japan” wrote and published the Review of Japanese Literature on Beriberi and Thiamine, in 1965. It was translated into English subsequently to pass the information about beriberi to people in the West who were considered to be ignorant of this disease. A book published in 1965 on a medical subject that few recall may be regarded in the modern world as being out of date and of historical interest only, however, it has been said that “Those who do not learn history are doomed to repeat it”. And repeat it, we are.

Beriberi is one of the nutritional diseases that is regarded as being conquered. It is rarely considered as a cause of disease in any well-developed country, including America. In what follows, are extractions from this book that are pertinent to many of today’s chronic health issues. It appears that thiamine deficiency is making a comeback but it is rarely considered as a possibility.

The History of Beriberi and Thiamine Deficiency

Beriberi has existed in Japan from antiquity and records can be found in documents as early as 808. Between 1603 and 1867, city inhabitants began to eat white rice (polished by a mill). The act of taking the rice to a mill reflected an improved affluence since white rice looked better on the table and people were demonstrating that they could afford the mill. Now we know that thiamine and the other B vitamins are found in the cusp around the rice grain. The grain consists of starch that is metabolized as glucose and the vitamins essential to the process are in the cusp. The number of cases of beriberi in Japan reached its peak in the 1920s, after which the declining incidence was remarkable. This is when the true cause of the disease was found. Epidemics of the disease broke out in the summer months, an important point to be noted later in this article.

Early Thiamine Research

Before I go on, I want to mention an extremely important experiment that was carried out in 1936. Sir Rudolf Peters showed that there was no difference in the metabolic responses of thiamine deficient pigeon brain cells, compared with cells that were thiamine sufficient, until glucose (sugar) was added. Peters called the failure of the thiamine deficient cells to respond to the input of glucose the catatorulin effect. The reason I mention this historical experiment is because we now know that the clinical effects of thiamine deficiency can be precipitated by ingesting sugar, although these effects are insidious, usually relatively minor in character and can remain on and off for months. The symptoms, as recorded in experimental thiamine deficiency in human subjects, are often diagnosed as psychosomatic. Treated purely symptomatically and the underlying dietary cause neglected, the clinical course gives rise to much more serious symptoms that are then diagnosed as various types of chronic brain disease.

Thiamine Deficiency Related Mortality. The mortality in beriberi is extremely low. In Japan the total number of deaths decreased from 26,797 in 1923 to only 447 in 1959 after the discovery of its true cause.
Thiamine Deficiency Related Morbidity. This is another story. It describes the number of people living and suffering with the disease. In spite of the newly acquired knowledge concerning its cause, during August and September 1951, of 375 patients attending a clinic in Tokyo, 29% had at least two of the major beriberi signs. The importance of the summer months will be mentioned later.

Are the Clinical Effects Relevant Today?

The book records a thiamine deficiency experiment in four healthy male adults. Note that this was an experiment, not a natural occurrence of beriberi. The two are different in detail. Deficiency of the other B vitamins is involved in beriberi but thiamine deficiency dominates the picture. In the second week of the experiment, the subjects described general malaise, and a “heavy feeling” in the legs. In the third week of the experiment they complained of palpitations of the heart. Examination revealed either a slow or fast heart rate, a high systolic and low diastolic blood pressure, and an increase in some of the white blood cells. In the fourth week there was a decrease in appetite, nausea, vomiting and weight loss. Symptoms were rapidly abolished with restoration of thiamine. These are common symptoms that confront the modern physician. It is most probable that they would be diagnosed as a simple infection such as a virus and of course, they could be.

Subjective Symptoms of Naturally Occurring Beriberi

The early symptoms include general malaise, loss of strength in knee joints, “pins and needles” in arms and legs, palpitation of the heart, a sense of tightness in the chest and a “full” feeling in the upper abdomen. These are complaints heard by doctors today and are often referred to as psychosomatic, particularly when the laboratory tests are normal. Nausea and vomiting are invariably ascribed to other causes.

General Objective Symptoms of Beriberi

The mental state is not affected in the early stages of beriberi. The patient may look relatively well. The disease in Japan was more likely in a robust manual laborer. Some edema or swelling of the tissues is present also in the early stages but may be only slight and found only on the shin. Tenderness in the calf muscles may be elicited by gripping the calf muscle, but such a test is probably unlikely in a modern clinic.

In later stages, fluid is found in the pleural cavity, surrounding the heart in the pericardium and in the abdomen. Fluid in body cavities is usually ascribed to other “more modern” causes and beriberi is not likely to be considered. There may be low grade fever, usually giving rise to a search for an infection. We are all aware that such symptoms come from other causes, but a diet history might suggest that beriberi is a possibility in the differential diagnosis.

Beriberi and the Cardiovascular System

In the early stages of beriberi the patient will have palpitations of the heart on physical or mental exertion. In later stages, palpitations and breathlessness will occur even at rest. X-ray examination shows the heart to be enlarged and changes in the electrocardiogram are those seen with other heart diseases. Findings like this in the modern world would almost certainly be diagnosed as “viral myocardiopathy”.

Beriberi and the Nervous System

Polyneuritis and paralysis of nerves to the arms and legs occur in the early stages of beriberi and there are major changes in sensation including touch, pain and temperature perception. Loss of sensation in the index finger and thumb dominates the sensory loss and may easily be mistaken for carpal tunnel syndrome. “Pins and needles”, numbness or a burning sensation in the legs and toes may be experienced.

In the modern world, this would be studied by a test known as electromyography and probably attributed to other causes. A 39 year old woman is described in the book. She had lassitude (severe fatigue) and had difficulty in walking because of dizziness and shaking, common symptoms seen today by neurologists.

Beriberi and the Autonomic Nervous System

We have two nervous systems. One is called voluntary and is directed by the thinking brain that enables willpower. The autonomic system is controlled by the non-thinking lower part of the brain and is automatic. This part of the brain is peculiarly sensitive to thiamine deficiency, so dysautonomia (dys meaning abnormal and autonomia referring to the autonomic system) is the major presentation of beriberi in its early stages, interfering with our ability for continuous adaptation to the environment. Since it is automatic, body functions are normally carried out without our having to think about them.

There are two branches to the system: one is called sympathetic and the other one is called parasympathetic. The sympathetic branch is triggered by any form of physical or mental stress and prepares us for action to manage response to the stress. Sensing danger, this system activates the fight-or-flight reflex. The parasympathetic branch organizes the functions of the body at rest. As one branch is activated, the other is withdrawn, representing the Yin and Yang (extreme opposites) of adaptation.

Beriberi is characterized in its early stages by dysautonomia, appearing as postural orthostatic tachycardia syndrome (POTS). This well documented modern disease cannot be distinguished from beriberi except by appropriate laboratory testing for thiamine deficiency. Blood thiamine levels are usually normal in the mild to moderate deficiency state.

Examples of Dysfunction in Beriberi

The calf muscle often cramps with physical exercise. There is loss of the deep tendon reflexes in the legs. There is diminished visual acuity. Part of the eye is known as the papilla and pallor occurs in its lateral half. If this is detected by an eye doctor and the patient has neurological symptoms, a diagnosis of multiple sclerosis would certainly be entertained.

Optic neuritis is common in beriberi. Loss of sensation is greater on the front of the body, follows no specific nerve distribution and is indistinct, suggestive of “neurosis” in the modern world.

Foot and wrist drop, loss of sensation to vibration (commonly tested with a tuning fork) and stumbling on walking are all examples of symptoms that would be most likely ascribed to other causes.

Breathlessness with or without exertion would probably be ascribed to congestive heart failure of unknown cause or perhaps associated with high blood pressure, even though they might have a common cause that goes unrecognized.

The symptoms of this disease can be precipitated for the first time when some form of stress is applied to the body. This can be a simple infection such as a cold, a mild head injury, exposure to sunlight or even an inoculation, important points to consider when unexpected complications arise after a mild incident of this nature. Note the reference to sunlight and the outbreaks of beriberi in the summer months. We now know that ultraviolet light is stressful to the human body. Exposure to sunlight, even though it provides us with vitamin D as part of its beneficence, is for the fit individual. Tanning of the skin is a natural defense mechanism that exhibits the state of health.

Is Thiamine Deficiency Common in America?

My direct answer to this question is that it is indeed extremely common. There is good reason for it because sugar ingestion is so extreme and ubiquitous within the population as a whole. It is the reason that I mentioned the experiment of Rudolph Peters. Ingestion of sugar is causing widespread beriberi, masking as psychosomatic disease and dysautonomia. The symptoms and physical findings vary according to the stage of the disease. For example, a low or a high acid in the stomach can occur at different times as the effects of the disease advance. Both are associated with gastroesophageal reflux and heartburn, suggesting that the acid content is only part of the picture.
A low blood sugar can cause the symptoms of hypoglycemia, a relatively common condition. A high blood sugar can be mistaken for diabetes, both seen in varying stages of the disease.

It is extremely easy to detect thiamine deficiency by doing a test on red blood cells. Unfortunately this test is either incomplete or not performed at all by any laboratory known to me.

The lower part of the human brain that controls the autonomic nervous system is exquisitely sensitive to thiamine deficiency. It produces the same effect as a mild deprivation of oxygen. Because this is dangerous and life-threatening, the control mechanisms become much more reactive, often firing the fight-or-flight reflex that in the modern world is diagnosed as panic attacks. Oxidative stress (a deficiency or an excess of oxygen affecting cells, particularly those of the lower brain) is occurring in children and adults. It is responsible for many common conditions, including jaundice in the newborn, sudden infancy death, recurrent ear infections, tonsillitis, sinusitis, asthma, attention deficit disorder (ADD), hyperactivity, and even autism. Each of these conditions has been reported in the medical literature as related to oxidative stress. So many different diseases occurring from the same common cause is offensive to the present medical model. This model regards each of these phenomena as a separate disease entity with a specific cause for each.

Without the correct balance of glucose, oxygen and thiamine, the mitochondria (the engines of the cell) that are responsible for producing the energy of cellular function, cannot realize their potential. Because the lower brain computes our adaptation, it can be said that people with this kind of dysautonomia are maladapted to the environment. For example they cannot adjust to outside temperature, shivering and going blue when it is hot and sweating when it is cold.

So, yes, beriberi and thiamine deficiency have re-emerged. And yes, we have forgotten history and appear doomed to repeat it. When supplemental thiamine and magnesium can be so therapeutic, it is high time that the situation should be addressed more clearly by the medical profession.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Image: Print ad from 1930; Public Domain.

This article was published originally on November 4, 2015.

Dr. Derrick Lonsdale passed away on May 2, 2024. He will be missed.

A Case of Classic Beriberi in America

by Derrick Lonsdale MD, FACN, CNS

Published on May 14, 2024

20351 views

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.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Image by NoName_13 from Pixabay.

This article was published originally on August 9, 2017.

thiamine deficiency - Page 2

Heart Disease and Beriberi: Case Stories

Recognizing Vitamin Deficiencies in Disease

Recent Reports of Thiamine’s Role in Clinical Care

We Need Your Help

Related posts:

You might be interested in

What Is a Syndrome?

Chronic Fatigue Syndrome

Fibromyalgia Syndrome

Regional Pain Syndrome

Sleep Apnea Syndrome

Similar Cause with Different Manifestations

We Need Your Help

Related posts:

You might be interested in

Are We Really Thiamine Deficient?

High Carbohydrate Diets Equal Lower Thiamine

We Need Your Help

Related posts:

You might be interested in

Thiamine During Pregnancy

Maternal Thiamine Deficiency and Fetal Brain Damage

We Need Your Help

Related posts:

You might be interested in

The Stages of Sleep

Circadian Rhythm

Sleep Apnea

An Explanatory Analogy

Putting It All Together

We Need Your Help

Related posts:

You might be interested in

We Need Your Help

Related posts:

You might be interested in

The History of Beriberi and Thiamine Deficiency

Early Thiamine Research

Are the Clinical Effects Relevant Today?

Subjective Symptoms of Naturally Occurring Beriberi

General Objective Symptoms of Beriberi

Beriberi and the Cardiovascular System

Beriberi and the Nervous System

Beriberi and the Autonomic Nervous System

Examples of Dysfunction in Beriberi

Is Thiamine Deficiency Common in America?

We Need Your Help

Related posts:

You might be interested in

Beriberi Is a Form of Dysautonomia

Is There a Help From the Laboratory?

What Is the Hope of Normal Health in This Person?

We Need Your Help

Related posts:

You might be interested in