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Thiamine Insufficiency Relative to Carbohydrate Consumption

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high carbohydrate diets and thiamine

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.

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Maternal Thiamine Deficiency and Fetal Brain Damage

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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:

  1. By what mechanisms specifically is thiamine deficiency produced?
  2. 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.

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

This article was first published on June 16, 2016. 

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Beriberi: The Great Imitator

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beriberi great imitator

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.

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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. 

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A Case of Classic Beriberi in America

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thiamine deficiency beriberi in america

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

 

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

 

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

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

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

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

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

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

Beriberi Is a Form of Dysautonomia

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

Thiamine deficiency beriberi in America

Is There a Help From the Laboratory?

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

What Is the Hope of Normal Health in This Person?

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

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

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This article was published originally on August 9, 2017. 

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Treating Sensory Processing Disorder in Children

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sensory processing disorder

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?

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. 

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This article was published originally on August 24, 2016. 

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Vitamin Therapy Paradox: Getting Worse Before Getting Better

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paradoxical reactions with thiamine

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.

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Thiamine Deficiency in Modern Medical Practice

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thiamine deficiency in modern medical practice

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.

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. 

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Eosinophilic Esophagitis May Be a Sugar Sensitive Disease

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Eosinophilic Esophagitis

In 2011 a mother called me and asked whether I would be able to help her 14-year old son who had been diagnosed with eosinophilic esophagitis. Because this disease had only been recognized in the past two decades I had to confess that I had never heard of it. Because I used only nutrients in therapy, I confessed my ignorance but that I was willing to have a shot at it. Obviously, the first thing that I did was to see what had been written about this newly recognized condition.

Eosinophilic Esophagitis: Inflammation of the Esophagus

The part of the gastrointestinal tract that is most commonly affected by this inflammatory infiltration is the esophagus (esophagitis), although it has been recorded in other parts of the intestine when it is known as eosinophilic enteritis. Eosinophils are specialized white cells that have a role in inflammation. They have this particular name because they stain with a dye called eosin (the postfix phil is derived from the Latin word for love) making it easy for a pathologist to recognize their presence in tissues.

Eosinophilic esophagitis (EoE) is now by far the most common form of eosinophilically infiltrated gastrointestinal disease. It represents the most recent form of food allergy, and its control by avoiding offending foods has increasingly appeared as a therapeutic approach. It is often poorly responsive to therapy and there is no commonly accepted long-term treatment. The diagnosis has to be made by endoscopy and it is distinguished from other causes of inflammation by finding eosinophils in the inflammatory area.

A Complex Medical History Misdiagnosed As Psychosomatic

The medical history of this 14-year-old boy had begun in infancy with recurrent ear infections and asthma, entailing many doctor visits. But he also had many confusing symptoms throughout childhood other than the chest pain and swallowing difficulties that might be expected from inflammation of the esophagus. In fact, these symptoms had been thought of as psychosomatic until endoscopy was performed when he was 8 years old and the esophagitis was discovered. From that time on, he had been examined repeatedly and had received conventional treatment without success at several prestigious institutions. He came to my attention 6 years after the diagnosis had been made.

His early history of repeated ear infections and asthma were important because both of these conditions are now known to be related to inefficient oxidative metabolism. Eosinophils are associated with asthma in some cases. The symptoms that had been considered to be psychosomatic included a dramatic response to any physical pain producing stimulus (hyperalgesia), emotional instability, unusual fatigue, headaches, dizziness, panic attacks and increased sensitivity to both sound and light. For example, when I came to the physical examination he would scream when I touched his abdomen and the abdominal muscles would become rigid. Another intriguing symptom was that he coughed in his sleep (an exaggerated cough reflex) without becoming awakened and he also experienced nightmares. He had also been diagnosed by a psychologist with ADHD and OCD. But on physical examination, I also found many intriguing signs that indicated autonomic nervous system dysfunction. The medical history also indicated that he was addicted to sugar, and alcoholism was widespread on both sides of the family, both being related to thiamine metabolism. People who have read some of the posts on this website will be familiar with the association of thiamine deficiency with sugar ingestion and alcohol.

A Family History of Alcoholism and Thiamine Metabolism

Because of this family history of alcoholism, his addiction to sugar, and the known relationship of thiamine deficiency with autonomic dysfunction, I used the blood test known as erythrocyte transketolase and I was not too surprised to find that it was extremely abnormal, proving a severe degree of thiamine deficiency or abnormal thiamine metabolism. He was treated with a series of intravenous infusions of water-soluble vitamins that contained thiamine hydrochloride. Although his symptoms began to improve, the transketolase test became much more abnormal, suggesting that thiamine was not being absorbed into the cells that needed it. Thiamine tetrahydrofurfuryl disulfide (TTFD: Lipothiamine, a derivative of thiamine that is absorbed more easily because it does not require the complex mechanism that is required for the absorption of dietary thiamine) was substituted for the thiamine hydrochloride with the result that the transketolase improved greatly.

Symptoms continued to improve but the most surprising thing that happened was the tremendous growth spurt that occurred throughout a year of treatment. Body weight at the beginning of treatment was 105 pounds, placing him in the 25th percentile. After one year of treatment his weight had increased to 122 pounds (+17#), placing him in the 50th percentile (e.g. male or female members of a school class). His stature increased in the same time period from 64.5 inches to 68.5 inches (+4”), raising it from the 50th to the 75th percentile. Percentiles are used in growth charts to indicate the normal height and weight of an individual as compared with subjects of the same age. For example, the fiftieth percentile would mean that 50% of a given similar group (e.g. a school class) would be taller/heavier and 50% shorter/lighter. For normal height and weight a subject remains in the same percentile throughout growth. A “jump” of this nature is extremely rare. It is unlikely that he would have been considered growth retarded if this dramatic acceleration had not occurred. He would have just been regarded as a “shorty”.

Dysautonomia

As reported in several posts on this website, dysautonomia is used to describe changes in the functional controls of the autonomic (automatic) nervous system. There are two branches to this system known as sympathetic, the action system, and parasympathetic, the “rest and be thankful” system. The first one is activated by any form of stress that includes a mild degree of oxygen lack (hypoxia) in the lower part of the brain or its equivalent from lack of thiamine and known as pseudohypoxia. There is also a genetically determined disease known as Familial Dysautonomia (FD) in which growth retardation is a constant feature. Although FD is a genetically determined disease, it is the resulting dysautonomia that causes growth failure. This suggests that the long-standing dysautonomia in this patient, due to energy inefficiency in brain cells caused by the pseudohypoxia of thiamine deficiency, was responsible for growth failure. Restoration of thiamine concentrations caused improvement in energy metabolism that enabled the growth spurt to take place.

Conclusion: Inflammation Is a Defensive Response

Inflammation is really a defensive response made by the body to some form of attack. In the case of this disease it appears that certain foods act as the attacking agent, hence the term food allergy. The inflammatory reaction is kept under very careful control by the brain acting through a nerve that runs the entire length of the intestinal tract. If this nerve fails in its suppressive action, the inflammation gets out of control. For the normal function of this nerve thiamine is a necessity. But thiamine deficiency, because it results in pseudohypoxia, also activates the sympathetic branch of the autonomic system and was responsible for the many symptoms that had been previously described as psychosomatic. It is very likely that the huge ingestion of sugar in the United States is responsible for thiamine deficiency that results in manifestations of disease that vary in their presentation according to the particular cells affected by the deficiency. Because of the family history I strongly suspect that there was a genetic relationship that created this boy’s sensitivity to foods, particularly sugar, making thiamine deficiency much more likely. It is of course possible that this is but one cause of eosinophilic esophagitis/enteritis. It suggests however that some form of pseudohypoxia (other than thiamine deficiency) is the root cause of the disease and that the inflammatory response gets out of control because of autonomic dysfunction. This case is now “in press”.

Lonsdale D. Is Esosinophilic Esophagitis a Sugar Sensitive Disease? J Gastric Disord Ther 2016;2(1):doihttp://cbcdoi.org/10.16966/2381-8689.114.

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Photo by Myriam Zilles on Unsplash.

This article was published originally on February 8, 2016.

Related posts:

seizures, EOE, Autism, thiamineASD, Seizures, and Eosinophilic Esophagitis: Could They Be Thiamine Related? Kawasaki Disease Thiamine and sugarSugar Intake and Thiamine Charcot marie tooth disease thiamineCharcot Marie Tooth Disease and Thiamine: A New Genetic Connection

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