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A New Model for Medicine

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What is a Medical Model?

 In the Oxford English dictionary the word model is defined as “design to be followed, style of structure”. Then it follows that there must be a model to distinguish health from disease, that differentiates the two states of being. No disease can be treated without knowing exactly what caused it. Let us go back to Hippocrates, 400 BCE, who said “let food be your medicine and your medicine be your food”. What Hippocrates was saying was essentially that nutrition was the core issue in the maintenance of health. At this time and throughout the Middle Ages there was no model for the cause of disease. Consequently, treatment was extremely primitive and almost purely empirical. In the time of ancient Egypt it was believed that mental illness was caused by the presence of evil spirits in a person’s head. They bored holes in the skull to let the evil spirits out. If you think about that, perhaps it relieved the occasional headache because of increased pressure in the skull caused by a brain tumor. Hence, a few successes might have caused it to be retained as beneficial. During the Middle Ages, the only treatment that seems to have been used is bloodletting. It might have been temporarily useful in people with high blood pressure. A few successes yielded the conclusion that it was beneficial for all disease.

The First Controlled Experiment

Semmelweis was a 19 th century Hungarian physician. In those days, the incidence of puerperal disease (childbed fever) was absurdly high. Semmelweis made the observation that doctors, delivering their patients, entered the delivery room and went directly to their patients without changing their garments or washing. He came to the simple conclusion that the doctors were bringing something in with their hands that caused the problem. The obstetric ward consisted of a number of beds on each side of the room and Semmelweis directed that doctors delivering their patients on one side should wash their hands in chlorinated lime, while doctors on the other side of the room would continue in the old way. Of course, the incidence of childbed fever was so different that it did not need a statistician to document the difference. Semmelweis’s observations conflicted with the established scientific and medical opinions of the time, particularly as he was unable to explain what was on the hands of the doctors. Some doctors were even offended at the suggestion that they should wash their hands. It is truly an amazing vision of human behavior. Innovation carries with it loss of reputation for the innovator, no matter how successful the innovation. Well, of course everyone today knows that it was microorganisms on the hands of the doctors that caused the disease, but they had not yet been discovered. Poor Semmelweis wound up in a lunatic asylum and died in his 40s after a beating by attendants. Today, he is regarded as the first person to introduce antiseptic medicine.

The First Paradigm in Medicine: Microscopic Organisms

Most people are aware that the invention of the microscope, and the work of historical figures like Louis Pasteur, led to the discovery of organisms, that could only be seen with the microscope, caused what we now call infection. We are all familiar with the fact that a tremendous number of diseases are due to infection by bacteria, viruses or fungi. It was a perfectly logical conclusion that the development of treatment should be aimed at killing these organisms. This was the first paradigm in medicine, meaning that it was accepted by all. A glance at history will tell us that the search for medication that would kill these organisms was hard won. It was difficult to find something that would kill the germs without killing the patient and many patients lost their lives as a result of this search. The discovery of penicillin represented a dramatic change in perspective as it gave birth to the antibiotic age. Millions of lives have been saved. However, we are now entering an era where the development of antibiotic resistance is becoming an increasing problem. More and more potentially damaging antibiotics have been synthesized that present their own problems in therapy.

The Second Paradigm in Medicine: Immunity

It has been said that Louis Pasteur made the statement on his deathbed, “I was wrong: it is the defenses of the body that matter”. I believe that this may well become the second paradigm in medicine. So what are we talking about? Everyone recognizes that we have immunity but the average person has only the vaguest idea of what this really means. In fact, body defenses against infection are exquisitely complex and incredibly efficient when the immune system is healthy. The primary mechanism for health maintenance is exactly what Hippocrates said, not only the quantity but the quality of nutrition. By recognizing this, the concept is offered that preventive medicine, the use of nutrients based on a knowledge of the biochemical machinery that give our cells function, is the second paradigm.

Presently, we stimulate our immunity by the use of vaccines. However, each vaccine gives a protection to a specific microorganism, perhaps the best example being the flu. Most of us are aware that there are many strains of the flu virus and it may not be possible to predict the particular strain responsible for the “next epidemic”. Natural immune defense mechanisms recognize most invaders as “enemies”. Those whose adaptive/immune mechanisms cannot respond will succumb to the infection. Assisting the immunity mechanisms by making energy synthesis as efficient as possible and killing the “enemy” with maximum safety to the patient might just be the way of the future.

How the Body Responds to Environmental Stressors  

Each one of us comes with a “blueprint” derived from our parents in the form of genes that carry a code called DNA. This code is unique for each person and provides the structure that makes up a living person. The body is composed of 70 to 100 trillion cells, all of which have to cooperate to produce what we call function. I think of it being like an orchestra where all the organs are made up of cells, each one of which has a specific specialty to provide its contribution. Like instrumentalists in an orchestra, the cells within each body organ have to work together. This requires a conductor, a function that is performed by the subconscious brain. Coordination is administered through an automatic (autonomic) nervous system and a bunch of glands known as the endocrine system that produce messengers called hormones.

Consider what happens when a person is attacked by a pathogenic Streptococcus, for example. The throat becomes sore, the marker of inflammation. Controlled and executed through the brain, it increases local blood supply, bringing white blood cells into the area and is part of a defensive process. Glands in the neck become enlarged and this is also a defensive process, designed to catch and destroy the germs beginning to spread. Body temperature becomes elevated because disease producing bacteria are most virulent at normal body temperature and their efficiency is reduced at a higher body temperature. A standard procedure in medicine for many years has been to reduce the fever and it has always seemed to me to be a disadvantage, based on this explanation. We sweat when the environmental temperature is high and evaporation from the skin results in cooling. When the environmental temperature is low, we shiver and the muscular activity produces heat to maintain body temperature. These are examples of how we are able to adapt to changes in our environment that threaten our well-being. All of this is purely automatic and the only thing to complete the picture is how our food (fuel) is used to create energy. Maximum efficiency of brain metabolism is mandatory. Assist and protect the “conductor”.

How We Create Energy: Enter the Mitochondria

Because any form of burning is the union of oxygen with the fuel, in the body it is termed oxidation. The process is complex and many vitamins and minerals are involved, besides calories. It has long been known that thiamine (vitamin B1) deficiency is the cause of beriberi, the disease that had plagued humanity for thousands of years. Because this deficiency affects every cell in the body, it can degrade the efficiency of virtually any organ. But because different tissues have their own rate of metabolism and the brain and heart are the two tissues that require fast and efficient oxidation, it is the cells in those tissues that are most affected. Therefore, thiamine deficiency has its major effect in the brain and heart, but they are not exclusive.

Glucose is the main fuel, but like any other fuel used to produce energy, it has to be ignited. Thiamine, much like a spark plug in a car, processes this ignition. All simple sugars taken in the diet are broken down to glucose.  But before this happens in the body, dietary sugars have two effects. The first is a signal from the tongue to the pleasure zones of the brain. It is this sweet taste that makes sugar addictive. The second is that this excess of sugar overwhelms the capacity of thiamine to oxidize glucose to create energy. A person may have a perfectly normal thiamine level in the blood that is inadequate to meet the demand. It is the ratio of “empty carbohydrate calories” to the concentration of available thiamine that counts. I have called this “high calorie malnutrition” that seems to be an oxymoron since malnutrition is generally considered to be on the way to starvation. The patients with this form of malnutrition may be obese, remain relatively active, do not look ill and multiple symptoms are regarded by their physicians as “psychologic, or psychosomatic”. There appears to be no reason to seek laboratory evidence of malnutrition and the patient is written off as a “problem patient”. It is hardly surprising that the patient leaves the doctor’s office angry and tells friends that “the doctor told me that it was all in my head”.

The irony is that it IS in the patient’s head, but because of electro-chemical changes in brain metabolism. It has always seemed odd to me that physicians often consider that “psychological issues” are somehow “invented” by patients without thinking that every thought, every action, has a mechanism produced in a chemical “machine” called a brain. Distortions are the result of a combination of cellular energy deficiency (malnutrition), coupled with a potential genetic risk and perhaps a stress factor such as an otherwise mild infection/injury, or an inoculation. Any one of the three factors may dominate the clinical presentation, but in most cases the other two are involved.

A New Model: Genetics, Nutrition, and Stress

Throughout life each of us depends on our ability to survive in an essentially hostile environment. The first thing that it depends upon is our genetic inheritance that I have called “the blueprint”. But we also know that the “engines” of our cells, known as mitochondria, have their own genes in which the DNA is more susceptible to damage than our cellular genes. A new model must consider the fact that any stress requires energy in an adaptive response to any form of environmental attack resulting from a mental or physical problem or infection. The only way that we can protect the structural components of our bodies is by the use of the natural ingredients of nutrition, the ancient teaching of Hippocrates. The new science of epigenetics finds evidence that nutrition and lifestyle can make changes to our genes that might be beneficial or not, according to the circumstances. If a person has become sick from an excess of empty calories and refuses to change, the only way to treat that person would be by increasing the concentration of the missing nutritional ingredient in the form of a supplement. It is of paramount interest that in 1962 a paper was written in a prestigious medical journal. The author had found 696 medical journal manuscripts that reported 250 different diseases that had been treated with supplementary thiamine, with varying degrees of success. This suggests the possibility that health is produced by a combination of genetic influence, how we meet the daily impacts of stress and the quality of our nutrition. Disease results from, either genetic failure (cellular or mitochondrial), failure to meet stress because of energy deficiency, malnutrition, or combinations of the three elements.

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The Warburg Effect in Cancer

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In the 1930s Otto Warburg won a Nobel Prize for an observation that has since become known as “the Warburg effect” in oncology. He had reported that most cancer cells predominantly produce energy by a high rate of glycolysis (sugar metabolism) rather than the low rate in most normal cells. The energy in cancer cells, that typically have a glycolytic (sugar metabolism in action) rate up to 200 times higher than normal cells, is produced by fermentation. This form of energy production does not require oxygen and is known as anaerobic metabolism (without oxygen). Normal cells derive their energy from a chemical process that does require oxygen, hence the term oxidative, or aerobic (requiring oxygen), metabolism. The process of fermentation in cancer cells is much less efficient in producing energy than that in normal cells that derive energy from oxidative metabolism. Curiously, this anaerobic metabolism happens in cancer cells even when oxygen is plentiful. Although this has been much studied, its importance, either in cause or effect, remains unclear. Warburg had postulated that this change in metabolism is the fundamental cause of cancer, a claim now known as the Warburg hypothesis or Warburg effect. Today, mutations in oncogenes (genes associated with cancer) are thought to be responsible for malignant transformation and the Warburg effect is considered to be a result of these mutations rather than the cause. In other words, does the Warburg effect originate the cancer or is it an effect of the cancer? It is a typical “chicken and egg” question.

The Role of Thiamine in Cancer

The relationship between supplemental vitamins and various types of cancer has been the focus of recent investigation. Supplemental vitamins have been reported to modulate cancer rates and a significant association has been demonstrated between cancer and low levels of thiamine in the blood (1). This also gives rise to a “chicken and egg” question. Is the low level of thiamine a result of treatment using chemotherapy and radiation or does it have a causative relationship? Thiamine deficiency is increasingly recognized in medically ill patients. Its prevalence among cancer patients is unknown. However, thiamine deficiency was found in 119 (55.3%) of 217 patients with various types of cancer. Risk factors included effects of chemotherapy or undergoing active treatment (2). It is possible to induce a certain type of tumor in mice. Thiamine supplementation between 12.5 and 250 times the recommended dietary allowance (RDA for mice) stimulated the tumors. Doses 2500 times the RDA resulted in 10% inhibition of tumor growth (3). This inhibitory effect of exceedingly high doses of thiamine is unexplained and certainly merits further study.

Thiamine as a Drug

The definition of a drug is “a medicine or other substance which has a physiological effect when ingested or otherwise introduced into the body”. Therefore, if thiamine is taken as a supplement, it must be considered to be a drug. Conventional wisdom sees thiamine as a food-borne particle whose function, in a minute concentration, is to assist the enzymes to which it is attached. The daily dose is governed by the RDA and is stated as 1 to 1.5 mg/day. For this reason, if its deficiency as a cause of symptoms is recognized in a given patient, the treatment would be considered to be simply replacement value. Any increase in that dose would inevitably be considered completely unnecessary. This is in spite of the hard-won history that treating beriberi demanded as much as 100 mg of thiamine a day for months. Of course, as I have mentioned in these pages many times, conventional wisdom also denies that beriberi, or any other form of vitamin deficiency, exists in America or any other developed culture. There are now many reports in the medical literature of thiamine being used in megadoses to treat virtually any disease associated with or caused by a breakdown in energy metabolism. It is therefore worth considering the potential mechanism in the already established place of thiamine, or its derivatives, in cancer.

We used to think that our genes dominated our body functions in a fixed way throughout life. The relatively new science of epigenetics tells us that nutrition and lifestyle have a powerful influence on our genetically determined mechanisms. Research in cancer has been almost completely dominated by study of the influence of specialized genes, known as oncogenes. The question that should arise is what, if ever, is the influence of malnutrition on these genes. Could thiamine deficiency “turn on” or otherwise influence oncogenes through epigenetic mechanisms? Our book (Lonsdale D, Marrs C. Thiamine Deficiency Disease, Dysautonomia and High Calorie Malnutrition) emphasizes that widespread thiamine deficiency exists in America because of an inordinate ingestion of sugar in all its different forms. The book supplies evidence that an overload of glucose ingestion provides “empty calories” that overwhelms the capacity of thiamine metabolism in processing the glucose. In other words, the intake of thiamine in the diet might be sufficient for a normal calorie load but insufficient for the load of empty calories. This is referred to as “high calorie malnutrition”. Calibration of diet depends on a study of three meals a day. We suggest that it is the inordinate consumption of sugar associated with almost all social activities that may make the difference. We question whether there is a potential relationship with the increasing incidence of cancer. Is sugar our ultimate enemy? Is our hedonistic consumption of it a threat to our civilization? Although this sounds like a fictional idea for a novel, understanding the complex role of thiamine in glucose metabolism should make us pause to wonder whether the pleasure derived from taste is a potential cause of our undoing.

Hypoxia, Thiamine and Cancer

Hypoxia is one of the hallmarks of the tumor microenvironment (referring to the local concentration of oxygen that exists around cells that become cancerous). It is the result of insufficient blood supply to support growing tumor cells (4). This would result in lack of oxygen, but also would restrict the supply of vitamins, including thiamine. It is interesting that thiamine deficiency results in a metabolic disturbance that induces a state similar to deficiency of oxygen and is known as pseudo-hypoxia (pseudo-, meaning false)(5).

The term vitamin was derived from the finding that each one of these chemical substances found in naturally occurring food is “vital” to life. Thiamine’s role is to turn chemical food substances into energy. Therefore, it must be recognized as having the same life-giving effect in the body as oxygen. Granted that it is not the only vitamin required for this, however, it appears to have a degree of importance that makes it the dominant factor. Early studies of the relationship of thiamine deficiency as the cause of beriberi showed that, as the disease progressed, there were different metabolic patterns marking the degree of deficiency. For example, patients with a normal blood sugar responded to thiamine easily. Those with a high blood sugar were slower to respond and those with a low blood sugar often didn’t respond at all. The far-reaching consequences of the increasing effect of thiamine deficiency as the disease progressed need to be understood better.

It is known that the part of the brain that enables us to adapt to and thrive in our hostile environment, is particularly susceptible to thiamine deficiency. Therefore, its deficiency provides effects that are exactly similar to partial deprivation of oxygen. Is it possible that thiamine deficiency, resulting as it does in loss of efficient oxidative metabolism, is the underlying factor that initiates the cancer by an epigenetic mechanism? The low dose/high dose administration of thiamine in producing the opposite effects may be a mystery of thiamine metabolism requiring further research. Perhaps thiamine deficiency activates the genetic mechanisms that are known to be involved in the transition of the normal cell into a cancerous one. It may be that some cancers (and a lot of other diseases) could be prevented by a rational approach to a diet that spares us from metabolic stress induced by this highly artificial “high calorie malnutrition”.

Although this article is written for general readership, references are included to show that the statements made within the article are supported by publication in the medical literature.

References

  1. Lu’o’ng KV, Nguyen LT. The role of thiamine in cancer: possible genetic and cellular signaling mechanisms. Cancer Genomics Proteomics, 2013, 10 (4): 169-85.
  2. Isenberg-Grzeda, E., Shen, M. J., Alici, Y., Wills, J., Nelson, C., & Breitbart, W. High rate of thiamine deficiency among inpatients with cancer referred for psychiatric consultation: results of a single site prevalence study. Psychooncology 2016. May 26. doi. 10. 1002/pon. 4155. [Epub ahead of print]
  3. Comin-Anduix B, Boren J, Martinez S, et al. The effect of thiamine supplementation on tumor proliferation. A metabolic control analysis study Eur J Biochem, 2001, 268 (15): 4177-82.
  4. Kumar V, Gabrilovich DI. Hypoxia-inducible factors in regulation of immune responses in tumor microenvironment. Immunology, 2014, 143 (4): 512-9.
  5. Sweet RL, Zastre JA. HIF1-α-mediated gene expression induced by vitamin B1 deficiency. Int J Vitam Nutr Res 2013, 823 (3): 188-97.

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An Unusual Treatment for Asthma

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I had a recent email from a 38-year-old lawyer to thank me for a treatment that was given to her when she was eight years of age. I do not know what prompted her to try to contact me after 38 years, but her story has to be of general interest because it is so unusual. This eight year old child had a history of crippling asthma and bronchitis for four years. She was so allergic that any kind of mattress exacerbated her symptoms and she was forced to sleep on a plastic lawn chair. When I examined her, her chest was full of the sounds that are typical of advanced chest disease. However, there was a curious observation that turned out to be important. Her body was covered with “goosebumps” and I will try to explain the importance of this later because it made me try an extremely unusual treatment.

I prescribed an oral supplement of 150 mg a day of thiamine hydrochloride. Her symptoms rapidly cleared and all medication was successfully withdrawn. During the next five months she had only two mild attacks of asthma and her weight increased by 6.4 kg (14 pounds). I lost sight of her until the email arrived recently. She told me that over the years she had had only two mild attacks of asthma in her 20s. She had participated in athletic pursuits in college with no problems. The question then is why four years of virtual crippling had been relieved so expeditiously with such a simple treatment. She is now married and has three children all of whom have recurrent episodes of asthma. On further questioning by email, she responded that one of her children develops “goosebumps” if and when she is ill.

More Aspects to the Child’s Medical History

When a patient visits a physician, the reason for the visit described by the patient is called the medical history. An important part of that history requested by the physician is about any illnesses in the family that may be relevant. So in this case the family history revealed that this child’s grandmother had advanced lung and liver disease “of unknown cause”. This suggested to me that the grandmother had an unusual genetically determined condition known as alpha-1 antitrypsin deficiency. This disease originates in the liver because of the genetically determined failure to produce an important substance in the body knows as alpha-1 antitrypsin (A1AT). This is a protein that circulates in the patient’s blood and has an important part to play in preserving the health of the lung. Sometimes, the genetic abnormality in the liver leads to disease in that organ as well as the lung but liver disease does not always occur. However, the absence of the circulating A1AT would inevitably affect the normal function of the lung. It was therefore possible that the eight-year-old child had inherited the lung disease without the liver being affected. Also, this genetic effect can be “silent”, not causing any disease at all, making it possible for this child’s mother to have passed the gene while she herself had no chest disease.

Goosebumps and A1AT Deficiency

The technical name for this phenomenon is piloerection (pilo, a hair). At one time in our evolutionary history the human body was covered with hair like an ape. Some men still have quite a lot of body hair. All these hairs grow out of a tiny organ in the skin known as a follicle. The follicle is also equipped with a tiny muscle that makes the hair stand on end. It is the movement of the follicle by the action of the muscle, whether the follicle contains a hair or not, that creates the effect that we call “goosebumps”. It has been thought that the appearance of our ancestor, with all his body hairs raised, would make him look more aggressive and dangerous, because this action depends on activating the fight-or-flight reflex. Now, I was aware that this reflex is activated by environmental danger. However, thiamine deficiency is perceived by the brain as a source of danger and I concluded that the child’s “goosebumps” might be caused by that. There were other reasons for my suspicion but they involve much more detailed knowledge concerning A1AT deficiency.

The Possible Legacy

Asthma and asthmatic bronchitis are quite common in children today. Not all of them are as serious as a child that I have just described. However a simple test could be done to ascertain whether A1AT deficiency applies to a given child or even an adult with crippling asthma and bronchitis. The A1AT protein can be measured by a blood test and if it were found to be very low, a trial with megadose thiamine administration could do no harm and might have the dramatic effect that I have described in this child.

This case and many others are detailed in: Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition.

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What is Thiamine to Energy Metabolism?

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What is Energy?

Energy is an invisible force. The aggregate of energy in any physical system is a constant quantity, transformable in countless ways but never increased or diminished. In the human body, chemical energy is produced by the combination of oxygen with glucose. This reaction is known as oxidation. The chemical energy is transduced to electrical energy in the process of energy conservation. This might be thought of as the “engine” of the brain/body cells. We have to start thinking that it is electrical energy that drives the human body. The production of chemical energy is exactly the same in principle as the burning of any fuel but the details are quite different. The energy is captured and stored in an electronic form as a substance known as adenosine triphosphate (ATP) that acts as an energy currency. The chemical changes in food substances are induced by a series of enzymes, each of which combine together to form a chain of chemical reactions that might be thought of as preparing food for its ultimate breakdown and oxidation. Each of these enzymes requires a chemical “friend”, known as a cofactor. One of the most important enzymes, the one that actually enables the oxidation of glucose, requires thiamine and magnesium as its cofactors. Chemical energy cannot be produced without thiamine and magnesium, although it also requires other “colleagues”, since all vitamins are essential. A whole series of essential minerals are also necessary, so it is not too difficult to understand that all these ingredients must be obtained by nutrition. The body cannot make vitamins or essential minerals. There is also some evidence that thiamine may have a part to play in converting chemical energy to electrical energy. Thus, it may be the ultimate defining factor in the energy that drives function. If that is true, its deficiency would play a vital role in every disease.

Energy Consumption

Few people are aware that our lives depend on energy production and its efficient consumption. A car has to have an engine that produces the energy. This is passed through a transmission that enables the car to function. In a similar manner, we have discussed how energy is produced. It is consumed in a series of energy requiring chemical reactions, each of which requires an enzyme with its appropriate cofactor[s]. This series of reactions can be likened to a transmission, enabling the human body to function. If energy is consumed faster than it can be synthesized, or energy cannot be produced fast enough to meet demand, it is not too difficult to see that it would produce a fundamental change in function. Lack of function in body organs affects our health. The symptoms are merely warning the affected individual that something is wrong. The underlying cause has to be ascertained in order to interpret how the symptoms are generated.

Why Focus on Thiamine?

We have already pointed out that thiamine does not work on its own. It operates in what might be regarded as a ”team relationship”. But it has also been determined as the defining cause of beriberi, a disease that has affected millions for thousands of years. Any team made up of humans requires a captain and although this is not a perfect analogy, we can regard thiamine as “captain” of an energy producing team. This is mainly due to its necessity for oxidation of glucose, by far and away the most important fuel for the brain, nervous system and heart. Thus, although beriberi is regarded as a disease of those organs, it can affect every cell in the body and the distribution of deficiency within that body can affect the presentation of the symptoms.

Thiamine exists only in naturally occurring foods and it is now easy to see that its deficiency, arising from an inadequate ingestion of those foods, results in slowing of energy production. Because the brain, nervous system and heart are the most energy requiring tissues in the body, beriberi produces a huge number of problems primarily affecting those organs. These changes in function generate what we call symptoms. Lack of energy affects the “transmission”, giving rise to symptoms arising from functional changes in the organs thus subserved. However, it must be pointed out that an enzyme/cofactor abnormality in the “transmission” can also interrupt normal function.

In fact, because of inefficient energy production, the symptoms caused by thiamine deficiency occur in so many human diseases that it can be regarded as the great imitator of all human disease. We now know that nutritional inadequacy is not the only way to develop beriberi. Genetic changes in the ability of thiamine to combine with its enzyme, or changes in the enzyme itself, produce the same symptoms as nutritional inadequacy. It has greatly enlarged our perspective towards the causes of human disease. Thiamine has a role in the processing of protein, fat and carbohydrate, the essential ingredients of food.

Generation of Symptoms

Here is the diagnostic problem. The earliest effects of thiamine deficiency are felt in the hindbrain that controls the automatic brain/body signaling mechanism known as the autonomic nervous system (ANS). The ANS also signals the glands in the endocrine system, each of which is able to release a cellular messenger. A hormone may not be produced in the gland because of energy failure, thus breaking down the essential governance of the body by the brain. Hypoxia (lack of oxygen) or pseudo-hypoxia (thiamine deficiency produces cellular changes like those from hypoxia) is a potentially dangerous situation affecting the brain and a fight-or-flight reflex may be generated. This, as most people know, is a protective reflex that prepares us for either killing the enemy or fleeing and it can be initiated by any form of perceived danger. Thus, thiamine deficiency may initiate this reflex repeatedly in someone that seeks medical advice for it. Not recognizing its underlying cause, it is diagnosed as “panic attacks”. Panic attacks are usually treated by psychologists and psychiatrists with some form of tranquilizer because of the anxiety expressed by the patient. It is easy to understand how it is seen as psychological, although the sensation of anxiety is initiated in the brain as part of the fight-or-flight reflex and will disappear with thiamine restoration. It may be worse than that: because the heart is affected by the autonomic nervous system, there may be a complaint of heart palpitations in association with the panic attacks and the heart might be considered the seat of the disease, to be treated by a cardiologist. The defining signal from the ANS is ignored or not recognized. Because it is purely a functional change, the routine laboratory tests are normal and the symptoms are therefore considered to be psychological, or psychosomatic. The irony is that when the physician tells the patient “it is all in your head”, he is completely correct but not recognizing that it is a biochemical functional change and that it has nothing to do with Freudian psychology.

A Sense of Pleasure

A friend of mine has become well aware that alcohol, in any form, or sugar, will automatically give him a migraine headache. He still will take ice cream and suffer the consequences. I have had patients tell me that they have given up this and that “but I can’t give up sugar: it is the only pleasure that I ever get”. They still came back to me to treat the symptoms. We have come to understand that we have no self-responsibility for our own health. If we get sick, it is just bad luck and the wonders of modern medicine can achieve a cure. The trouble is that a mild degree of thiamine deficiency might produce symptoms that will make it more difficult to make the necessary decisions for our own well-being. Let me give some examples of symptoms that are typically related to this and are not being recognized.

  • Occasional headache
  • Occasional heartburn or abdominal pain
  • Occasional diarrhea or constipation
  • Allergies
  • Fatigue
  • Emotional lability
  • Insomnia
  • Nightmares
  • Pins and needles
  • Hair falling out
  • Heart palpitations
  • Persistent cough for no apparent reason
  • Voracious or loss of appetite

The point is that thiamine governs the energy synthesis that is essential to our total function and it can affect virtually any group of cells in the body. However, the brain, heart and nervous system, particularly the autonomic (automatic) nervous system (ANS) are the most energy requiring organs and are likely to be most affected. Since the brain sends signals to every organ in the body via the ANS, a distortion of the signaling mechanism can make it appear that the organ receiving the signal is at fault. For example, the heart may accelerate because of a signal from the brain, not because the heart itself is at fault. Hence, heart palpitations are often treated as heart disease when a mild degree of thiamine deficiency in the brain is responsible. We have known for many years that sugar in all its different forms can and will precipitate mild thiamine deficiency. It is probably the reason why sugar is considered to be a frequent cause of trouble. If thiamine deficiency is mild, any form of minor stress may precipitate a much more serious form of the deficiency.

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Connecting the Symptom Dots: Discovering My Thiamine Deficiency

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discovering thiamine deficiency

As a registered dietitian nutritionist (RDN), I was surprised to find out that I had a thiamine deficiency in December 2015. My diet wasn’t perfect, but it was close. I never imagined I’d spend so much time trying to treat my own deficiency, but it’s been over a year the first lab work showed the deficiency and I’m still struggling with it. I’ve been asked to share my symptoms and experiences, so I’ll start back around the initial diagnosis.

Let me preface my story by sharing some information about myself. I’m a 46 year old female and I’ve always considered myself fairly healthy. I’m active, and I complete a minimum of 12,000 steps/day and often much more. That includes some form of aerobic activity daily. I’ve dealt with some annoying health problems, but nothing I considered major. I’ve had issues with insomnia, depression, nerve problems, migraines, hypoglycemia and GI distress (mostly diarrhea) for years or decades. I’ve also had some discomfort on the left side of my chest, on and off, which goes unexplained. I’ve seen many different types of doctors, including cardiologists, neurologists, gastroenterologists, psychiatrists, sleep specialists, endocrinologists, allergists, etc. Also, I have very early visual symptoms of glaucoma, but my doctor said there aren’t any signs of disease in my eye. No familial history of glaucoma, and I’ve never been diagnosed with diabetes. Separately, all of these symptoms seemed minor. Only within the last few years or so, did I begin to wonder if there was some sort of connection.

In the fall of 2014, I started a post-bachelors program in dietetics. I had returned to school almost two decades after completing my bachelors, and the road to this program was a long one. My insomnia seemed to be severe the night before exams. Sleep eluded me, even with the prescription sleeping pills. Anxiety, right? It never occurred to me that it was something else. After all, I’ve had insomnia issues for at least a decade. Sometime during the semester, I had seen a neurologist for some nerve testing. I had numbness and tingling in my feet, hands and arms. It would wake me up at night. I began seeing a doctor of osteopathy for manipulations to help with the nerve problems, too. Also, I had noticed some garbled speech and numbness in my tongue, but thought I was imagining it.

During finals week in December, my insomnia became severe. My physician prescribed Xanax, but I hated the way it made me feel. I felt my anxiety actually increased.  Even after finals were over, sleep eluded me. I was piecing 3-5 hours of sleep together, if that. I had trouble eating a full meal and was losing weight. In addition, I was having discomfort on the left side of my chest, something that I had experienced in the past but was yet unexplained. All of this was attributed to anxiety. By the end of December, my physician prescribed a daily anti-anxiety medication. This medication made me nauseous and I had diarrhea. Of course, these symptoms didn’t help the weight loss. At no time did my physician do any lab work while this was happening. I was so miserable that I emailed my advisor to inquire about dropping out of the dietetics program. Fortunately, she wouldn’t entertain the idea and encouraged me to continue, noting that I could take an Incomplete if necessary.

By February of 2015, I was down to 103 pounds, (I’m 5’ 4” and 130 pounds currently). I was dragging myself to school. I had lost a lot of muscle mass, and couldn’t sit for long in class because of the lack of muscle. My face looked quite thin and my temples were hollowed out. In March 2015, I was weaned off the medications and began taking 7.5 mg Remeron, and Ambien as needed. The Remeron helped my appetite and I began regaining weight and strength. With the support of my professors, I was able to complete the semester, and even maintained a high grade point average!

Early in the fall semester, I listened to a lecture by an RDN who is an integrative and functional medicine certified practitioner (IFMCP). Based on her lecture, I knew my instincts about an underlying connection to all of my symptoms was correct. In November 2015, I had an appointment with that RDN. She recommended some blood work, which my primary care physician (PCP) reluctantly agreed to do. It was a lot of blood work, and fortunately my insurance covered it. There were many positive or problematic results, but among them was low thiamine (whole blood) at 29ug/L, a positive ANA test, TPO 693, as well as magnesium and ferritin were in the low normal range. After further autoimmune testing, it was determined that I have Hashimoto’s disease, too.

The low thiamine level could explain many of my symptoms, including, insomnia, nerve issues, migraines, precordial pain, weight loss and problems processing carbohydrate. The question is why was my thiamine level low? I had always thought my diet was relatively healthful. For years, I watched my added sugar intake because of trouble with hypoglycemia. My fiber, protein and water intake seemed adequate. I’m very careful with my fat intake because I had a cholecystectomy in 2009 and still have problems with lipid digestion. I rarely drank alcohol because of the hypoglycemia and insomnia. The only other beverage I consumed was tea, usually 1-3 cups per day. Furthermore, because of my hypoglycemia, I ate mostly whole grains and very little gluten, if any.

In January 2016, I began taking a B vitamin complex, magnesium, lipothiamine and some other supplements, including Ortho-Digestzyme to aid in lipid digestion. I made changes to my diet, including dairy free and gluten free. I began seeing some health improvements. Eventually, I added yogurt and cheese back into my diet, but remained gluten free. I was having fewer migraines and began sleeping without Ambien. That spring I was taken off the lipothiamine, but continued the B vitamin complex and magnesium. I graduated from the dietetics program in May 2016, something I feared wouldn’t happen only one year earlier.

At the end of October 2016, I had an infection (perhaps, due to an insect bite) on my outer ear which wouldn’t go away. My PCP prescribed a cephalosporin antibiotic for 10 days. Towards the end of November and into December, I was having increased nerve issues, occasional insomnia, mild apathy and anxiety, which was strange given I had nothing to be anxious about. Also, I had the same chest discomfort again. My thiamine level was tested and it was low at 32 ug/L. I was taking the B vitamin complex and magnesium all along, so my PCP was unsure what to do. I’ve since learned that some antibiotics, like the one I took, can deplete thiamine.  I saw the RDN again and began taking lipothiamine again on 12/23/2016. I was taking 50 mg, twice a do with magnesium, in addition to the B vitamin complex.

My PCP planned to retest in a month to see if it was working. However, on January 20, 2017, I had an emergency appendectomy. During the surgery, I was given a cephalosporin antibiotic, but it was only during the surgery, not afterwards. It should be noted that I only missed one day of supplements because of the surgery. By the end of the first week, I strongly suspected my thiamine level had bottomed out, because my symptoms of anxiety, insomnia, nerve pain, etc., reminded me of what happened two years earlier. During that week, I was taking 50 mg lipothiamine twice a day, 200 mg magnesium and a potent multivitamin. Personally, I think the antibiotic, surgical procedure and recovery, and resulting diarrhea contributed to the low thiamine despite supplementation. I almost went to the ER in hopes that they’d give me a thiamine injection or IV, but decided to wait until Monday to see my PCP. Her suggestion was that I continue my supplements, then we’d retest in a month. One month later, my thiamine level was low still at 32 ug/L. My PCP said she isn’t comfortable giving intramuscular thiamine injections and suggested I see a gastroenterologist. I mentioned information I found on Hormones Matter, but I don’t believe my PCP was interested in reading the material.  I feel like I’m being bounced around from one doctor to another. I’m going to see the gastroenterologist, whom I’ve seen before but I’m not hopeful that she’ll be able to help. I saw a neurologist recently, who was very kind and listened intently, but could only suggest an MRI and a DO, who “might” be able to help me, but that DO’s office is 1.5 hours away. Next week, I’ll go back to the cardiologist for a check-up because of the ongoing discomfort on the left side of my chest.

For now, I’m sleeping at least 6 hours a night, which feels like a lot to someone who’s experienced severe insomnia. My hypoglycemia is under control. I’m not sure if that’s because of the thiamine supplementation, the gluten free diet or both. The last time I had gluten, I experienced both mild insomnia and hypoglycemia, but again, my thiamine was likely low too. I feel I still have occasional memory issues, but maybe that’s age related. Also, the numbness and tingling in my extremities continues. Migraines occur much less and are less severe, usually. The mild vision problems linger, as well.

The RDN I’m seeing is uncomfortable with me taking more than 100 mg lipothiamine per day. At this time, she is recommending supplements to treat continued GI inflammation too.  Here is my current regimen: 100 mg lipothiamine/day, 200 mg magnesium/day, multivitamin 1/day (RDN wants me to take 2/day), 28 mg iron w/vitamin C, sodium butyrate 600mg 4/day, NAC 600mg 2/day, Ortho-Digestzyme 2 capsules before each meal to help with lipid absorption, and about 4000 IU vit D3.

Unfortunately, I feel I’m just one missed dose of my supplements away from problems all the time now. I’m not sure how to find a physician who can help me solve this ongoing thiamine problem and don’t know where to turn next. Again, I’m going to see a gastroenterologist and cardiologist this month, but feel it may be more of the same. My father died at 45 years old of cardiovascular disease. I know thiamine deficiency can lead to cardiovascular problems too, which is why I’m going back to the cardiologist.

Any suggestions are welcomed!

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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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Sandro K., CC BY-SA 2.0, via Wikimedia Commons.

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The Sugar – Thiamine Connection in Adverse Reactions

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sugar thiamine connection in adverse reactions

As published on this web site previously, we have scientific evidence that two girls and one boy were shown to be thiamine deficient (TD) after Gardasil vaccination. On the other hand, a girl who had similar symptoms to these three had not received the vaccine and her laboratory test proved that she also had TD.  On the face of this information, it suggests that the vaccination has nothing to do with the illness of these individuals.  In a previous post, however, I have suggested that the vaccine is a “stress factor”, given to an individual in a state of marginal, or even asymptomatic thiamine deficiency, thus exacerbating the first appearance of symptoms. In this light, medications and other vaccines may also be considered stress factors and evoke or exacerbate a previously asymptomatic thiamine deficiency. There are a number of facts that need to be seen collectively in order to understand the hypothesis that follows.  In order to make this clear I am going to present the material under subheadings.

What Does Thiamine do in the Body?

All simple sugars that we take in our diet are broken down to glucose, the primary fuel of the brain.  This oversimplified fact has long been used to suggest that taking sugar is the way to meet energy demands in the body.  It is, in fact, an extremely complex chemical process which is well beyond the scope of an article like this.  It can, however, be simplified by comparing glucose, as a fuel, to gasoline in a car.

Gasoline + Oxygen + Spark Plug = Energy  + (ash/oxides)

Glucose + Oxygen + Thiamine = Energy + (ash/oxides)

Each one of these equations represents combustion, a combination of fuel with oxygen.  Because combustion is always incomplete, waste products (oxides) are formed and must be got rid of as waste.  It is obvious that combustion of gasoline without oxygen and spark plug, or glucose without oxygen and thiamine, will not occur.  What is not quite so obvious is the fact that an excess of gasoline causes choking of the engine, black smoke from the exhaust pipe (unburned hydrocarbons) and loss of engine efficiency.  This could be referred to as “oxygen/spark plug deficiency” since each of the three components must be present in proper concentration to produce efficient combustion (oxidation).  The three component parts, glucose, oxygen and thiamine are the equivalents in the body.  An excess of glucose “chokes” the “engines” (mitochondria) that create energy in all of our cells. This particularly applies to the brain because of its high rate of metabolism (energy consumption), thus providing a potential explanation for why the vaccine seems to pick off the brightest and the best students.

The Reptilian Brain and the Limbic Nervous System

All animal brains are built on the same basic principle, a lower, more primitive part and a higher, increasingly complex part. The lower part of the human brain, the limbic system, also known as “reptilian”, computes all the reflex mechanisms by which we automatically adapt to our environment.  For example, we sweat when it is hot and shiver when it is cold, both adaptations to the ambient temperature.  It also controls our emotional reflexes, represented by body language that we recognize easily.  It uses two mechanisms, the autonomic nervous system and the endocrine system.

Autonomic and Endocrine Systems

We have two nervous systems. The one that we use to will our actions is controlled by the upper brain, here described as cognitive. The autonomic nervous system (ANS) automatically controls all the actions required by body organs to meet day- to- day adaptation.  It consists of two major branches, known as the sympathetic and parasympathetic components.  The sympathetic branch prepares us for mental and physical action while the parasympathetic switches us to a period of rest.  As one goes into action, the other one is withdrawn. The endocrine system is represented by a group of glands, each of which produces one or more hormones.  These are really messengers that induce actions in the cells to which they are aimed.  When either or both of these systems are not functioning in their ordained manner in the brain/body of an individual, we can refer to him/her as maladapted.

Explanation of Symptoms in Reference to Thiamine Deficiency

As explained in previous posts on this web site, the disease known as beriberi occurs as a result of TD.  The mother of a Gardasil affected girl had done her own research and had come to the unlikely conclusion that her daughter suffered from beriberi.  Red cell transketolase, a blood test used to depict TD, showed that she was correct in her conclusion. Her daughter did in fact have beriberi and has responded, at least partially, to thiamine supplementation.  We know, from historical data, that long term beriberi responds slowly to treatment and sometimes not at all, depending on chronicity.  Since she has had her symptoms for approximately four years, I think that it would be fair to call this chronic. When the ANS is not functioning properly, it is called dysautonomia (dys, meaning abnormal: autonomia refers to the ANS).  Beriberi in its early stages is the prototype for dysautonomia, the commonest effect being dominance of the sympathetic branch of the ANS.

Published Effects of Gardasil Vaccination

Although many symptoms have been reported related to this vaccination, two resultant conditions have been nominated: POTS (Postural Orthostatic Tachycardia Syndrome) and Cerebellar Ataxia.  POTS is one of the many conditions that are described under the heading of dysautonomia and I have already reported in a post that the first case of thiamine dependency was in a six year old boy who had intermittent episodes of cerebellar ataxia, each of which was triggered by a stress episode that included mild infection, mild head injury or inoculation.  A critical enzyme that depends on thiamine for its energy producing action was able to function until some form of physical or mental stress was imposed.  The existing mechanism was insufficient to meet the energy requirement imposed by the stress.

Sugar, the Autonomic Nervous System and the Liver

New research provides one more clue to our emerging theory of thiamine deficiency in post vaccine and medication adverse reactions.  The study: The Autonomic Nervous System Regulates Postprandial Hepatic Lipid Metabolism by Bruinstroop et al. demonstrates the influence carbohydrate intake has on autonomic control of liver lipid metabolism. Triglycerides are measured in a medical laboratory as part of what is known as the “lipid profile”, that includes the various components of cholesterol. The Bruinstroop study found that when the parasympathetic system was deactivated and carbohydrates were ingested, triglyceride levels rose significantly, inducing metabolic dysregulation. Other studies have found stress, combined with diets high in refined carbohydrates can increase blood triglyceride concentrations also inducing metabolic syndrome. Indeed, stress and the concurrent increased sympathetic system activity seem key to metabolic functioning with sugar intake triggering the ill-health.

Interpretation of Technical Language

The work by Bruinstroop and associates was done in rats.  To understand what they found, it is necessary to remind the reader that the two branches of the ANS, sympathetic and parasympathetic, work synchronously.  As one branch becomes active the other one is withdrawn. This is automatically controlled by the “reptilian” brain, thus enabling us to adapt to the physical and mental changes we encounter on a day -to-day basis.  These authors were able to show that abolishing the parasympathetic input to the liver resulted in marked elevation of triglycerides in the blood. This would induce continuation of sympathetic dominance in any “stress reaction” in the animal if it was in a free living state. The effect was modulated by sugar intake. That is, when the animals were fed more, the effects were larger.

Hypothesis: High Sugar Diets Lead to Thiamine Deficiency, A Risk Factor for Adverse Reactions

I am proposing that an excess of carbohydrates in the diet, particularly fructose, results in a mild degree of thiamine deficiency.  We know, from studies done as early as 1943 (Williams R D, et al. Arch Int Med 1943;71:38-53), that this results in what is typically called psychosomatic disease, in which a large component is reflected in emotional lability (instability), so common in the modern child and adolescent.  Physical symptoms, such as unexplained “pins and needles”, in the hands or feet, may be so slight as to be ignored.  The stress of the vaccination or a medication reaction triggers an energy crisis in the “reptilian” brain, specifically evoking autonomic dysregulation, typically with sympathetic system dominance and resulting in beriberi, POTS, or cerebellar  ataxia and potentially other syndromes.  Perhaps a rise in blood triglycerides as suggested by the Bruinstroop study, indicates the partial crippling of the parasympathetic branch of the ANS and sympathetic dominance.  High blood triglycerides might well be a  mark of the early stages of underlying autonomic dysregulation and thiamine deficiency and a potential risk factor for adverse reactions to certain vaccines or medications.

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. 

Addendum

A 5th case of post Gardasil thiamine deficiency has been identified; a young woman who developed severe idiopathic hypersomnia, a variant of narcolepsy, post vaccination. The patient is undergoing treatment with success. A full case study will be presented soon.

Image by 🌸♡💙♡🌸 Julita 🌸♡💙♡🌸 from Pixabay.

This article was published on Hormones Matter previously in January 2014.

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HPV Vaccine Reactions: A Response to Walking on the Edge of a Sword

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This post is an attempt to answer the questions raised by the extraordinary post vaccination medical history of this 16 year old girl. Of all the HPV vaccine histories that have been recorded on “Hormones Matter” this is, in my view, one of the worst. We seem to be carrying out a vicious experiment on human beings and if this is not recognized as an indictment on the HPV vaccine, I do not know what will move the powers that be. With a very detailed history like this it is easy to see the relationship of the symptoms with the HPV vaccine. There is absolutely no doubt in my mind that this represents massive mitochondrial dysfunction affecting the brain and nervous system, particular the autonomic nervous system. I will try to discuss each symptom as it appears in the history.

Clues in the Pre – HPV Vaccine History

First of all it must be recognized that this young lady had pervasive developmental disorder, asthma, pyelitis, a topic dermatitis, otitis media, Candida, hemolytic streptococcus, pneumonia, “wart”, periodic fever, agrochemical sensitivity and recurrent stomatitis before she received the HPV vaccine. We are not told whether these symptoms were related to previous vaccinations. This appears to be consistent with a persistent concept among parents that infancy vaccines sometimes do more harm than good in a minority of children. The history here suggests a genetic or nutritional risk factor in addition to the stress of the vaccination.

Post – HPV Vaccine Reaction

Her attitude towards this dreadful post HPV vaccine legacy was excellent since she attended school in spite of fever. She is described as athletic with a good nature prior to vaccination and there was a major post vaccination personality change. The slow pulse suggested parasympathetic dominance that made at least a partial post-vaccination switch to sympathetic dominance. I base this on the description of an average post vaccination increase in pulse rate. I believe that the timeline reported in the medical history is important. She had the usual three injections. After the first one she developed asthma and since this was an early affliction I assume that the injection was a stress factor that triggered it. Asthma is caused by an imbalance in the autonomic nervous system. After the second injection she developed urticaria. This was again a signal through the autonomic system that delivered a message to histamine releasing cells in the skin.

The worst situation arose after the third HPV vaccine injection. Symptoms described were arrhythmia, an increase in circulating eosinophils, fever, hypersomnia, aggressiveness, childish behavior, hyperpnea, muscle weakness, headache, parotitis, temporo-mandibular joint syndrome, dysphagia, stomatitis, abdominal pain, vomiting, diarrhea, photophobia, double vision, and “blood stagnation” in the hippocampus. The gradual worsening with each injection might be compared with the repeated blows of a hammer where a nail is driven in a little bit more with each blow.  With this detailed description, a cause and effect relationship with each injection seems to be obvious and it would be stupid to regard this as a coincidence.

Oxidative Stress and the Brain

Let me try to explain these symptoms because I can assure you that they are all related to the brain. In particular, I am referring to the limbic system of the brain, that part of the brain that computes our adaptive mechanisms through the autonomic nervous and endocrine systems. The reference to the hippocampus makes it clear that the limbic system is involved because this is an important organ within that system. We can sum up the situation by saying that this young lady is now maladapted to her physical and mental environment.

When this part of the brain suffers from reduced energy efficiency from defective oxidative metabolism in mitochondria, it becomes erratic in the way it reacts to input signals delivered through the sensory system. This continuous process of brain and body signaling is how we adapt to our environment throughout life. We have to go back to the writings of Hans Selye whose professional career was spent in studying the effect of physical stress in animal systems. He reported his work as “The General Adaptation Syndrome” and referred to the diseases of mankind as the diseases of adaptation. I would have preferred to call it the diseases of maladaptation. What Selye emphasized throughout his writings was that it was consumption of energy that was required for adapting and its failure resulted in the syndrome that he described.

Now we know that the mitochondria are responsible for producing energy required for this, the General Adaptation Syndrome makes perfect sense. When Selye was doing his work, the biochemistry of energy metabolism was in its infancy. Now we have much more information about oxidative metabolism and energy production. Until recently, any mitochondrial dysfunction was considered to be invariably genetic in origin. We are now aware that it can be acquired as a result of environmental stress that results in insufficient energy to meet the mental or physical demand.

Diminished Oxidative Metabolism and the Limbic System: HPV Vaccine and Personality

The change in personality from a gentle to an aggressive individual is absolutely characteristic of diminished oxidative metabolism in the limbic system. In particular, the autonomic nervous system becomes extremely erratic in its behavior. It winds up by misdirecting the normal signals that go to the organs of the body and the associated symptoms are chaotic, referred to as dysautonomia. For example, the reaction to a mild reprimand might be an explosive temper tantrum and dietary indiscretion might well be an important factor in the waves of juvenile violence that seem to be otherwise inexplicable.  For the past 35 years I have been seeing the personality of children change because of abnormal biochemistry in the limbic system. They have wicked temper tantrums, kick the door or the wall, are rude to parents and teachers and are generally out of control. By rescuing them from their appalling diet and giving them supplements, nearly all of them would gradually come back to being a normal child.

We are suffering from an epidemic of biochemical rather than psychological disease. Of course there is a genetic principle behind it; there always is!  The smarter the child the greater the dietary risk. This should be fairly obvious to anybody because, like our cars, the better the car the better the fuel has to be.  Because the brain, central nervous system and the heart are the most oxygen consuming tissues in the whole body, it is hardly surprising that they are the first to succumb. They are the organs most affected by vitamin B1 deficiency that causes beriberi. This vitamin, like a spark plug in a car, is a necessity to the oxidation of glucose, the primary fuel used by our cells, particularly in brain. Of course, it is not the only non caloric nutrient required, but its association with energy metabolism is clearly dominant.

We have seen from previous posts on this web site that some victims of post vaccination postural orthostatic tachycardia syndrome (POTS) were thiamine deficient and the dysfunction in the autonomic nervous system could legitimately be called beriberi.  I have suggested several times that a marginal state of brain biochemistry may exist before the vaccination is given and that it acts as a stress factor. This might be from an unknown genetic risk or from a diet that does not meet the mental and physical activity required by the individual or a variable combination of both. It would explain why this HPV vaccine appears to pick off the brightest and the best.

In my opinion this young lady can only be helped by the administration of intravenous vitamins since that is the only way in which the necessary concentrations can be built up.  It can be compared with changing the spark plugs in the engine of a car to improve its performance. Thiamine tetrahydrofurfuryl disulfide is available in Japan under the trade name of Alinamin, I have no doubt that this would be an important addition to the intravenous concentration of water soluble vitamins.

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Thiamine Deficiency and Aberrant Fat Metabolism: Clues to Adverse Reactions

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Over the last several months, the writers and researchers at Hormones Matter have posted a number of articles about mitochondrial dysfunction and thiamine deficiency.  Thiamin, or thiamine as the internet search engines prefer, is critical to mitochondrial function. We’ve learned that thiamine deficiency can emerge gradually due to dietary inadequacies or more suddenly as a result of a medication, environmental or surgical insult. Regardless of the cause, deficits in thiamine evoke devastating health issues that can be treated easily if identified. More often than not, however, thiamine deficiency is not assessed and symptoms are left to escalate, mitochondrial damage increases, and patient suffering continues. Because thiamine deficiency is rarely considered in the modern scientific era, mild symptoms are ascribed to other causes such as “an allergy” or “it’s all in the patient’s head”. If, however, the cause is not revealed, the same old dietary habits will continue and can be guaranteed to produce much more severe and difficult to treat chronic disease.

Although there are a myriad reasons why mitochondria are damaged, medication or vaccine reactions paired with latent nutritional deficiencies seem to be common. Predicting who and how the mitochondrial dysfunction might appear, however, is more complicated. Quite often, athletes and individuals considered healthy are hit harder by a stress factor such as a vaccine than those whom we might not regard as particularly healthy. There are several potential reasons for this, some of which have been outlined previously. In this post, I would like to add one more reason why highly active, high performing individuals might be hit harder and more quickly than their less active counterparts with vaccine or medication reactions that induce thiamine deficiency.

Mitochondria are the Engines of the Cell

To use an analogy, the usefulness of a car obviously depends upon its engine. Mitochondria are the “engines” of each cell within our bodies, all 70 to 100 trillion cells that make up an adult body. They are known as organelles and are so small that their structure can only be seen with an electron microscope. But we can take this analogy further by comparing each cell to a different car model. A high powered car uses more gasoline than a low powered one and there are many models of each type of car. So some cells in the body require more energy than others, depending on the special function of the cell.  The most energy consuming cells are in the brain, the nervous system and the heart, followed by the gastrointestinal system and muscles. That is why those organs and tissues are most affected in the disease known as beriberi, the thiamine deficiency disease that we have discussed previously in other posts. The function of other organs is affected by the deficiency because of the changes in the control mechanisms originating in the brain through the autonomic (automatic) nervous system.

It has been pointed out that this disease in its early stages affects the autonomic nervous system by causing POTS. Beriberi and POTS, both being examples of dysautonomia (abnormal activity of the autonomic nervous system), can only be distinguished by finding evidence of thiamine or other nutrient deficiency as a cause. Thiamine is but one factor whose deficiency causes loss of cellular energy, resulting in defective brain metabolism and dysautonomia.  Although the relationship with vaccination is conjectural, some individuals with post Gardasil POTS were found to be thiamine deficient and had some relief of symptoms by taking supplementary fat soluble thiamine, an important derivative that occurs in garlic and has been synthesized. Not all of these thiamine deficient individuals have benefited to the same degree, suggesting that other deficiencies might also be involved. This post is to provide some information about more recent knowledge concerning the action of thiamine and the incredible, far-reaching effects of its deficiency, particularly in the brain. Experimental work in animals has shown that thiamine deficiency will damage mitochondria, a devastating effect for an acquired rather than a genetic cause. Far too much research has been devoted to genetic cause without sufficient attention to the way genes are influenced by diet and lifestyle.

The Importance of Enzymes to Mitochondrial Function

Before I provide this new information, let me remind the reader that enzymes, like cogwheels in a man-made machine, enable bodily function to occur. The importance of thiamine is that it is a cofactor to many of the enzymes that preside over energy metabolism. Without its cofactor an enzyme becomes inefficient. Perhaps it might be compared with missing teeth in a cog wheel. With missing teeth the cog wheel may still function but not nearly as well as it would with all of its component parts.

In previous posts we have discussed how thiamine deficiency can be caused by an excess of sugar in the diet. I have likened this to a “choked engine” in a car where an excess of gasoline, relative to insufficient oxygen concentration in the mixture, makes ignition of the gasoline extremely inefficient. Bad diet, one that is rich in sugary, carbohydrate laden foods may be one of the more common contributors to latent thiamine deficiencies. Excessive intake of processed fats and the concomitant changes to mitochondrial function and energy metabolism may be another important contributor.

Thiamine and Fat Metabolism

All the enzymes affected by thiamine deficiency have a vital part to play in obtaining cellular energy from food by the process of oxidation. Most of them have been known for many years but in the nineties a new enzyme was discovered. It has a very fancy name that has been simplified by calling it HACL1.  Only in recent years has it been found that HACL1 is dependent on thiamine as its cofactor. Although not reported, it may mean that it is also dependent on magnesium. This is exceedingly important because it introduces the fact that thiamine is involved in fat as well as carbohydrate metabolism, something brand new, even to biochemists.

Here I must digress again to describe another type of organelle called a peroxisome that occurs in our cells.  Like mitochondria, they are infinitesimally small. Their job is to break down fatty acids and they have a double purpose. One purpose is to synthesize very important substances that construct and maintain cells and their function: they are particularly important in the brain. The other purpose is what might be called fuel preparation. As the fatty acids, consisting of long carbon chains, are broken down, the resulting smaller fragments can be used by mitochondria as fuel to produce energy.  Failure to break down these fatty acids can result in the accumulation of natural components that may be toxic in the brain and nervous system or simply result in lack of one type of fuel. That is why feeding medium chain triglycerides by administration of coconut oil has been reported useful to treat early Alzheimer disease. They can be oxidized in mitochondria.

The Important Use of Fatty Acids in Mitochondrial Health

Here, I want to use another analogy. Imagine a lake that admits water to a river through a sluice gate that has to be opened and closed by a farmer who regulates the supply of water. If the gate is open the river will supply water to the surrounding fields. If however the gate is closed, the river will begin to dry up and the crops in the fields will suffer. Perhaps the farmer half closed the gate during a rainy period and has forgotten to open it when a dry period follows. High temperatures in the dry period results in insufficient water to meet the growth needs of the crops.

In this analogy, the lake represents food, the sluice gate is the HACL1 enzyme and the farmer who controls the gate represents thiamine. The water in the river represents the flow of fatty acids to the tissues for the double purpose of cellular construction and fuel for oxidation. The half open gate represents a minor thiamine deficiency, more or less sufficient for everyday life but not enough when there is greater demand. A high temperature that increases the water needs for crops represents Gardasil and many other medications as a stress factor, placing a greater demand on essential metabolic action.  The analogy also implicates the nature of the crops, some of which require more water than others. The crops, of course, represent body tissues and organs.

If we consider high performing individuals, whether academically or athletically, like high performance cars or crops that demand more nutrients, we can see how a previously unrecognized minor deficiency might trigger clinical disease by the stressful demands of a vaccine or medication. Some pharmaceuticals can attack thiamine directly, like Gardasil and the fluoroquinolones, while others attack different pathways within the mitochondria.

No matter the pathway, high performing individuals, with high energy needs not covered by diet, may be hit harder when a medication attacks mitochondrial energy.

The Outcome of Defective Fatty Acid Metabolism

Returning back to the HACL1 enzyme, we now know that HACL1 is the first thiamine dependent enzyme to be discovered in peroxisomes. It is research news of the highest importance, affecting us all. Its action is to oxidize a diet related fatty acid called phytanic acid and fatty acids with long carbon chains that cannot be used for fuel until they are broken down. Phytanic acid is obtained through consumption of dairy products, ruminant animal fats and some fish. People who consume meat have higher plasma phytanic acid concentrations than vegans. If the action of HACL1 is impaired because of thiamine deficiency the concentration of phytanic acid will be increased. The river in the analogy actually represents a series of enzymatic reactions that may be thought of as down-stream effects, whereas thiamine deficiency, being up-stream, affects all down-stream phenomena. One of the reasons thiamine deficiency is such an important contributor to illness is because its effects are broad.

These enzymatic reactions, known technically as alpha oxidation, involve four separate stages. It has been known for some time that if another enzyme at stage two is missing because of a gene defect, the result will be damage to the neurological system known as Refsum’s disease. Symptoms include cerebellar ataxia (also reported after Gardasil vaccination), scaly skin eruptions, difficulty in hearing, cataracts and night blindness. Other genetic mutations in alpha oxidation, resulting in various biochemical effects, result in a whole variety of different diseases. This places thiamine deficiency as a potential cause for all the down-stream effects resulting from defective alpha oxidation, for it has been shown in mice that this vitally important chemistry is totally dependent on presence of thiamine. Since its complete absence would be lethal, we have to assume that it is mild to moderate deficiency, equivalent to a partial closure of the sluice gate in the analogy.

Sources of Phytanic Acid: How Diet Affects Thiamine

In ruminant animals, our source of beef, the gut fermentation of consumed plant materials liberates phytol, a constituent of chlorophyll, which is then converted to phytanic acid and stored in fat. The major source of phytol in our diet is, however, milk and dairy products.  It raises several important questions. If thiamine deficiency is capable of causing an increase in phytanic acid in blood and urine, it might be a means of depicting such a deficiency in a patient with confusing symptoms. It might also explain why some individuals who have been shown to have thiamine deficiency by means of an abnormal transketolase test have symptoms that are not traditionally accepted as those of such a deficiency, perhaps because of loss of efficiency in HACL1.

If an excess of sugar in the diet gives rise to a secondary (relative) thiamine deficiency, we are provided with an excellent view of the extraordinary danger of empty simple carbohydrate and fat calories, perhaps explaining much widespread illness in Western civilization. Interestingly, it would also suggest that something as benign as milk could give rise to abnormal brain action in the presence of thiamine deficiency, because of phytanic acid accumulation. Our problems with dairy products may go well beyond lactose intolerance and immune dysregulation.

In sum, the discovery of HCAL1 enzyme and its dependence upon thiamine suggests one more mechanism by which thiamine deficiency affects mitochondrial functioning. As emerging evidence indicates a myriad of environmental and pharmaceutical insults impair mitochondrial functioning, thiamine deficiency ought to be considered of prime importance. Deficits in thiamine evoke devastating health issues that can be treated easily if identified.  If, however, thiamine deficiency is not identified and the same old dietary habits continue, the latent thiamine deficiency can be guaranteed to produce a much more severe and difficult to treat chronic disease. Moreover, individuals with thiamine deficiency who do not respond sufficiently to thiamine replacement might also have aberrant fatty acid metabolism. This too should be investigated and dietary changes adopted.

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