thiamin Archives - Hormones Matter

What Is Scoliosis?

Published on January 18, 2022

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scoliosis and impaired oxidative metabolism

As everyone knows, the spinal column is made up of a series of bones known as vertebrae. Like bricks in a column, they collectively support the entire body in an upright position. Their anatomy is very complex because, collectively, they have to allow for the spinal column to bend in every direction without parting company with each other. Sometimes a child develops a permanent bend in the spinal column known as scoliosis. It usually develops relatively slowly and is usually watched by anxious parents as it becomes more severe. Anyone reading this who has had experience of it will know that the treatment is very advanced surgery in which the spinal column is straightened and supported with steel rods. This post is to try to explain why scoliosis happens and how it may possibly be prevented.

Brain Symmetry

Most people know that the left half of the body is controlled by the right side of the brain and vice versa. The reason for this asymmetry is unknown. However, asymmetry appears to be pretty important with many aspects of brain function. For example, I collected 17 patients, in each of whom their respective blood pressure was totally different in the two arms. The difference was so great that I imagined such an individual, when visiting a physician, would leave the office with a blood pressure pill if the pressure had been measured in the arm on the higher side, and without it if it had been taken in the arm on the low side. As most people know, the blood pressure is taken almost invariably in only one arm. The blood pressures in my 17 patients were compared with healthy controls. Although the pressures of controls varied only slightly in the two arms, the difference was extremely obvious when compared with the patients.

The asymmetry in the patients was greatly exaggerated, whereas in the controls it was minimal. This asymmetry is capable of increasing in direct relationship to loss of efficient metabolism in the control mechanisms in the brain. The loss of efficiency may be due to genetic effect or long-term malnutrition. These 17 patients had many symptoms, indicating that their autonomic nervous system was compromised because of poor oxidative metabolism. The symptoms responded to treatment with nutritional elements.

Dysautonomia

We have two nervous systems, known respectively as the voluntary and autonomic. The voluntary system enables us to use free will, whereas the autonomic is automatic and organizes brain/body functions that we cannot control voluntarily. The prefix dys means abnormal, so dysautonomia refers to abnormal function of that system. This can be due to genetic influence or from metabolic changes related to poor diet. One of the abnormalities that can occur is that the normal mild asymmetry in autonomic control can become exaggerated, giving more power to one side of the body than the other. Under normal healthy conditions, this asymmetry is much less marked. In fact, it is well known that all of us have some degree of asymmetry. One foot may be slightly bigger than the other or one eye may be a little bit more closed than the other. The autonomic nervous system is deployed to every part of the body and is the messenger system by which the brain controls all the organs that together, create body functions.

What Has This to Do with Scoliosis?

The spinal column is lined by very strong ligaments and muscles. It is these muscles that enable us to bend in every direction. However, those muscles are kept in what is called constant tone. Notice the hardness of the muscles in the low back. They feel to the touch like steel almost. This is because they are kept in tone as a permanent support. This tone is maintained through the autonomic nervous system by constant signals from the brainstem to the muscles surrounding the spinal column. The voluntary system can overcome the autonomic signals to enable us to bend as we wish. Asymmetric signaling to the muscles on either side of the spinal column occurs in health but may be only slight. If however, control mechanisms in the lower part of the brain are metabolically inefficient, asymmetric signaling evidently increases. If the tonic signals have exaggerated asymmetry, the tone of the muscles on one side of the spinal column will have stronger signals than on the other side. This explains why the scoliosis occurs gradually, but we have to realize that the real cause of the disease is because of the exaggerated asymmetry in the autonomic nervous system. In other words, scoliosis can be a disease of the autonomic nervous system as well as from genetic changes in the vertebral column.

An experimental treatment for scoliosis was reported some years ago in which electrodes were attached to the weaker muscles on the convex side of the scoliosis and tonic electrical signals attempted to straighten the spinal column. I do not know what happened to that experiment, but it seems to me that scoliosis should be treated by preventive treatment of the dysautonomia. The patients with the asymmetric blood pressures all had evidence of dysfunctional oxidative metabolism in the lower part of the brain, an effect that can be produced by thiamine deficiency. All of them were treated by nutritional therapeutic measures with variable degrees of success. Quite a few of them, but not all, had thiamine deficiency as the underlying cause. It was concluded therefore that it was oxidative dysfunction, for any cause, in the brain that was the underlying cause of the exaggerated asymmetry, whether this was genetic or nutritional in origin. They responded to a number of intravenous infusions of water-soluble vitamins, all of which contained thiamine. The control mechanisms of the autonomic nervous system in the lower part of the brain are particularly prone to develop thiamine deficiency. Therefore this is an important cause of inefficient oxidative brain metabolism.

Prevention

As far as I know, prevention of scoliosis has never been attempted and what follows is therefore a hypothesis based on some evidence. It may well be that nutrition of the mother in pregnancy can induce faulty metabolism in the fetus that may deploy its effect in many different ways. We now know that thiamine deficiency is common in pregnancy and most of its complications can be prevented by taking a modest dose of thiamine, starting even before pregnancy. Since the major effect of thiamine deficiency is dysautonomia, perhaps the exaggeration of asymmetry can be prevented. The new science of epigenetics enables some modification of genetic defects. A mouse model has shown that the combination of a genetic risk factor with short-term gestational hypoxia (oxygen deficit) significantly increases the gene penetrance and severity of vertebral defects. There is no harm in a supplement of thiamine during pregnancy. Whether it would be capable of preventing scoliosis would depend on its disappearance from the medical literature and would be a long-term goal.

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This article was published originally on August 28, 2017.

About TTFD: A Thiamine Derivative

by Derrick Lonsdale MD, FACN, CNS

Published on March 21, 2018

64710 views

I recently received notification concerning a “review” posted on HerbCustomer, a commercial website that has been active since February 26, 2010. This so-called “review” was posted on January 16, 2018 by iHerbCustomer entitled “Dangerous allithiamine derivative with no thiamine activity”. The email was posted as well. This person made a potentially libelous statement by referring to me as lying about this thiamine derivative. Its commercial name is Lipothiamine. Its chemical name is thiamine tetrahydrofurfuryl disulfide (TTFD) and this post is to refute the accusations that are made public by this individual.

History of Thiamine Research

Thiamine is the chemical name for vitamin B1 and its deficiency in the diet has long been known as the cause of beriberi. This disease has been known for thousands of years but its underlying cause was only discovered in the closing years of the 19th century. Since beriberi was commonest in the rice consuming cultures, it is not surprising that the major research came from Japan. In the middle of the last century a group of university-based scientists was convened and they wrote a book (Review of the Japanese Literature on Beriberi and Thiamine). This was translated into English, ostensibly because these scientists wished to let people in the West know and understand the pernicious nature of disease resulting from thiamine deficiency. I was fortunate enough to receive a copy of this book from one of the scientists involved. The information in this post is derived from it. Because they were scientists and were well aware of the clinical effects of beriberi, their studies were very extensive. They knew that thiamine existed in garlic and much of their experimentation focused on studies of the garlic bulb. They discovered that there was a natural mechanism in garlic that created a derivative of thiamine and called it allithiamine. Note that this is a naturally occurring substance and the term should be entirely restricted to it.

On a number of occasions I have seen thiamine derivatives being called “The alithiamines” and one commercial product is called Allithiamine with a capital a. The name was given to this naturally occurring product because garlic is a member of the allium species of plants. It can be found in other members of the allium species. Because the Japanese scientists already knew a great deal about the clinical expressions caused by thiamine deficiency, they originally thought that this new derivative might have lost its vitamin dependent activity. They went on to test it in animal studies and found that it had a much greater biologic effect than the original thiamine from which it was derived. They found that it was extremely important that allithiamine was a thiamine disulfide derivative (disulfides are important in human physiology) and they synthesized many different types of thiamine disulfide as well as many non-disulfide derivatives, carefully testing each one for their biologic activity.

What is TTFD?

Without going into the biochemical details, what we now know is that thiamine tetrahydrofurfuryl disulfide (TTFD, Lipothiamine) is, for a number of reasons, the best of the bunch of synthetically produced derivatives and has exciting possibilities in therapy. For example, it has been shown from animal studies that Benfotiamine, a non-disulfide derivative, does not get into the brain whereas TTFD enables absorption of thiamine into the brain where it stimulates energy synthesis. When we take in thiamine, occurring only in our naturally formed food, it is biologically inert. It has to be “activated” within the body that possesses genetically determined mechanisms for its absorption and activation. To cut a technically difficult explanation, let me state that TTFD bypasses this process. It enables thiamine to split away from its disulfide attachment and enter the cells where its activity is required. The concentration achieved in the target cells is much greater than that achieved by the administration of the thiamine from which it was derived.

The Japanese scientists studied the effect of cyanide in mice and found that thiamine propyl disulfide (TPD), a forerunner of TTFD, gave significant protection from the lethal effect of this poison, an incredible discovery that alone should raise eyebrows. They studied this effect and were able to show its mechanism. They also found that it would protect animals from the effect of carbon tetrachloride, a poison that affects the liver. It is using its vitamin actions in a therapeutic manner.

Being myself a consultant pediatrician in a prestigious medical institution, I was able to obtain an independent investigator license (IND) from the Federal Drug Administration, and obtained TTFD from Takeda Chemical Industries in Osaka, Japan, the makers of this product. TTFD is a prescription item in Japan, sold under the commercial name of Alinamin. I have read several publications, showing that it reverses fatigue in both animal and human studies. I was able to study the value of this incredible substance in literally hundreds, if not thousands of patients. Far from being toxic, as this person claims, I never saw a single item that suggested toxicity. Its therapeutic potential is largely untapped in America. This is because the current medical model does not recognize that defective energy metabolism, genetic errors and the nature of stress are the interrelated components whose variable effects in combination are the cause of disease. Do not mistake the use of the word stress, a word that is so commonly used inappropriately. An infection and any form of physical or mental trauma represent a form of stress. It is the ability or the inability to meet the required energy demand to resist that stress that matters in the preservation of health.

Clinical Benefits of TTFD

It is important to understand that the beneficial activity of TTFD is exactly the same as the thiamine from which it is derived. It is the mechanism of its introduction to cells, particularly those in the brain, that enable it to have such an effect on energy metabolism. Because of its strategic position in the cell, thiamine is of vast importance in oxidative metabolism in the complex mechanisms of energy production. There are at least two methods by which thiamine deficiency can be induced. The commonest one is an excess of sugar and fat that overwhelms the capacity of thiamine to conduct the mechanisms involved in energy synthesis. The discovery that thiamine has a part to play in fat metabolism is quite recent. The other one is because of genetic errors involving its biochemical action. However, we now know from a relatively new science called epigenetics that some mistakes in DNA can be overcome by the use of an appropriate nutritional substance like thiamine. The completely non-toxic use of TTFD depends merely on its ability to introduce thiamine into the cells of the body that require its magic. Under these circumstances, the big doses of thiamine are acting like a pharmaceutical by stimulating the missing action. We are not dealing with simple vitamin replacement. This should represent a new era in medicine when nutrient biochemistry takes its place in patient care.

Conclusion

The person that wrote this criticism fails to understand that TTFD and other thiamine derivatives represent a new basic principle of therapy. It recognizes that healing is a function of the body, not the activity of a so-called “healer”. All it requires is the foundation substances needed for repair and sufficient energy to use them. It demands a dramatic change in thinking about health and disease. If you understand the principles involved, it forces the conclusion that the word “cure” is a pipe dream. The only form of pharmaceutical drug that matters is one that safely kills an attacking microbe. Almost all the rest of them merely relieve symptoms and have no effect on the ultimate outcome.

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The Warburg Effect in Cancer

by Derrick Lonsdale MD, FACN, CNS

Published on September 19, 2017

3960 views

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

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.
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]
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.
Kumar V, Gabrilovich DI. Hypoxia-inducible factors in regulation of immune responses in tumor microenvironment. Immunology, 2014, 143 (4): 512-9.
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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A Case of Classic Beriberi in America

by Derrick Lonsdale MD, FACN, CNS

Published on August 9, 2017

15297 views

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

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

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

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

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

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

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

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

Beriberi is a Form of Dysautonomia

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

Thiamine deficiency beriberi in America

Is there a help from the laboratory?

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

What is the hope of normal health in this person?

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

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Connecting the Symptom Dots: Discovering My Thiamine Deficiency

by Lisa Perry, RDN

Published on March 23, 2017

21508 views

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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Diabetes and Thiamine: A Novel Treatment Opportunity

by Chandler Marrs, PhD

Published on December 3, 2015

14892 views

Underlying all diabetic conditions is poor sugar control or hyperglycemia. Hyperglycemia can be due to a lack of insulin as in Type 1 diabetes or insulin resistance as in Type 2 diabetes. In either case, the corresponding diabetic complications that evolve over time in many diabetics, the cardiovascular disease, retinopathy, peripheral nerve and vascular damage, represent the effects of sustained hyperglycemia. Until recently, the mechanisms by which diabetic vascular damage developed eluded researchers. Although multiple, seemingly discrete biomarkers had been identified, no single, unifying mechanism was understood. It turns out that diabetics, both Type 1 and Type 2, are severely deficient in thiamine or vitamin B1 and that thiamine is required for glucose control at the cell level. Why is thiamine deficient in diabetics and how does thiamine manage glucose control? The answers to those questions highlight the importance of micronutrients in basic cellular functioning, particularly mitochondrial functioning, and the role of excessive sugar in disease.

Thiamine

Thiamine (thiamin) or vitamin B1 is an essential nutrient for all living organisms. The body cannot synthesize thiamine by itself and so it must be obtained from diet. Thiamine is present in yeast, pork, fish, various nuts, peas, asparagus, squash and grains (unprocessed) and because of the severity of the illnesses that thiamine deficiency evokes, many processed foods have been fortified with thiamine. Nevertheless, thiamine deficiencies thought resolved by modern nutritional technologies, are emerging once again. Modern thiamine deficits appear to be caused by diets of highly processed, carbohydrate and fat laden foods, exposures to thiamine blocking factors such as alcohol and those found in many medications (fluoroquinolones, possibly others) and vaccines (Gardasil, possibly others), environmental toxicants and some foods. Thiamine deficiency is also common after bariatric surgery and in disease processes like AIDS and cancer. Over the course of our research, thiamine deficiency has been observed in previously healthy, young, non-alcoholic patients, post medication or vaccine, along with symptoms of dysautonomia.

Thiamine Deficiency Symptoms

Thiamine deficiency at its worst is linked to severe decrements neurological functioning, like Wernicke’s Encephalopathy that include noticeable ataxic and gait disturbances (loss of voluntary control of muscle movements, balance and walking difficulties), aphasias (language comprehension and/or production difficulties), and if it persists, Korsakoff’s Syndrome (severe memory deficits, confabulations and psychosis). Early on though and as the deficiency is evolving, thiamine deficiency presents much like the mitochondrial disease that it is – with the myriad of seemingly unrelated symptoms, that are not typically attributed to thiamine deficiency, such as fatigue and excessive sleeping, hair loss, cardiac dysregulation, GI disturbances such as gastroparesis and others, autonomic instability, demyelinating syndromes and hormone irregularities, especially thyroid, but also reproductive hormones. In diabetics, thiamine deficiency may present as ketoacidosis, lactic acidosis, hyperglycemia and persistent encephalopathy. Thiamine deficiency attacks the mitochondria. Mitochondrial dysfunction presents diversely. In fact, with mitochondrial dysfunction, symptoms are as varied as the individuals who experience them. Diabetes, may be just one more phenotype of among many.

Thiamine Deficits in Diabetes

With diabetes, thiamine deficiencies are common, though likely under-recognized. Diabetics are susceptible to thiamine deficiencies mediated by diet and exposures like most of the Western world, but also have added risk factors associated with the disease itself. In diabetics, kidney function is altered which decreases thiamine reabsorption while increasing thiamine excretion. In some people, diabetic and non-diabetic alike, thiamine deficiency can be exacerbated even further by a mutation in the thiamine transporter protein that brings thiamine into the cells.

How thiamine deficient are diabetics? One study found that in comparison to non-diabetics, individuals with Type 1 and Type 2 diabetes had 75% and 64% less thiamine, respectively. Think about this for a moment. If diabetes predisposes individuals to thiamine deficiency without any other intervening factors, imagine what happens when diabetics are nutritionally thiamine deficient, exposed to the myriad of environmentally or medically thiamine-depleting substances currently on the market, or worse yet, carry the thiamine transporter mutation. Alone, but especially in combination, thiamine deficiency diseases, many of which align with diabetes-related complications, could be magnified exponentially. The remarkable thing about this new research is that treatment is easy, it requires only dietary changes and high dose thiamine therapy alongside normal diabetes interventions. (Although one suspects with Type 2 diabetes at least, dietary changes and thiamine supplements could replace other medications entirely). Backing up a bit though, let us look at the research and mechanisms by which thiamine moderates sugar exposure at the cell level and how thiamine modifies those processes.

The Hyperglycemic Cascades

Under normal conditions, with appropriate dietary nutrients and physiological concentrations glucose, dietary sugars are converted to ATP in the mitochondria. The byproduct of that reaction is the production of free radicals also known as oxidative stress or reactive oxygen species (ROS). ROS are neither good nor bad, but too much or too little ROS wreaks havoc on cellular functioning. The cells can clear the ROS and manage oxidative stress via activating antioxidizing pathways and shuttling the excess glucose to secondary, even tertiary processing paths. However, under conditions of chronic hyperglycemia, mediated by diet or diabetes, the conversion of glucose to ATP becomes dysregulated, the production of ROS become insurmountable and a cascade of ill-effects are set in motion.

Too much ROS cause the mitochondria to produce high concentrations of an enzyme called superoxide dismutase (SOD) in the endothelial cells of both the small and large blood vessels. SOD is a powerful antioxidant, however, like everything else, too much for too long causes problems. Superoxide then upregulates the five known chemical pathways that alone and together perturb vascular homeostasis and cause the diabetic injuries that have become commonplace. Technically speaking, hyperglycemia causes:

Increased activation of the polyol pathway
Increased intracellular formation of advanced glycation end products (AGEs)
Increased AGE receptor expression and ligands
Upregulated protein kinase C (PKC)
Enhanced hexosamine pathway activity

In non-technical terms, elevated concentrations of circulating glucose increase the production of ROS and superoxide, but also, and as a compensatory survival reaction to maintain cellular health, secondary and tertiary glucose processing pathways come online. These backup pathways are not nearly as efficient and so produce additional, negative metabolic byproducts which can damage blood vessels if not cleared. The body is capable of clearing these byproducts, but only when the reactions are short term and the nutrient substrates feeding those reactions are present. If, however, the nutrients are deficient and/or the hyperglycemia is chronic, or both, those clearance mechanisms are insufficient to remove the toxins. The toxic byproducts build up and diabetic vascular diseases ensue.

High Dose Thiamine Therapy and Diabetes

Over the last decade or so, researchers have found that thiamine normalizes each of these five aberrant processes activated by sustained hyperglycemia and implicated in diabetic vascular complications. High dose thiamine (300mg/day) reduces the biochemical stress of hyperglycemia human subjects. Additionally, thiamine can prevent and/or offset incipient vascular damage in diabetic patients. Finally, in rodent models of Type 1 diabetes, thiamine transporters have been identified and emerging research shows that thiamine moderates pancreatic insulin secretion significantly. In rats fed a thiamine deficient diet, glycolysis (sugar processing and conversion to ATP by mitochondria) was inhibited by 41%, utilization of fatty acids (secondary energy processing pathway) declined by 61% in just 30 days and insulin production diminished by 14%. The connection between pancreatic downregulation of fatty acid utilization and thiamine is particularly interesting considering the recent discovery of a thiamine dependent enzyme in fatty acid regulation, the HACL1.

Diabetes and Modern Medicine

Diabetes and the destruction it causes affects every cell, tissue and organ system in the body. As such, some researchers have postulated that diabetes represents a model for the paradigm shift in modern medicine. If diabetes is the model for chronic, multi-system illness that marks modernity, then thiamine, and likely other nutrients, are the markers by which the new model of medicine must be drawn. Diabetes is, at its root a mitochondrial disorder. Whether diabetes is inherited, as in Type 1 or induced environmentally as in Type 2, diabetes exemplifies how we convert food to fuel to power cellular functions. When that food is deficient in vital nutrients, the power conversion processes adapt for survival. The compensatory actions have consequences, especially when sustained beyond their capacity to meet the needs of the body. Disease erupts, first gradually then explosively.

Consider the implications of thiamine deficiency, a single micronutrient available in food, on cellular health, and indeed, physical health. In addition its role in mitochondrial functioning, thiamine controls sugar metabolism through multiple pathways. Inefficient sugar metabolism leads to disease. Thiamine also regulates the metabolism of fatty acids and provides the necessary substrates for the neurotransmitters acetylcholine and GABA. Thiamine, much like other critical nutrients, is not only absent from the largely processed diets of modernity, but at every turn, can be depleted by medications and environmental toxicants. Against the backdrop of nutrient depleted and damaged mitochondria, accommodating medications, vaccines and environmental toxicants that also damage mitochondria, increase oxidative stress and further deplete critical nutrients, it is no wonder we are living sicker and dying younger than ever before. The depletion of critical nutrients is causing disease; diseases no medication can treat.

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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 previously on Hormones Matter in August 2014.

Thresholds and Tipping Points in Thiamine Deficiency Syndromes

by Chandler Marrs, PhD

Published on May 29, 2014

13972 views

I recently stumbled upon on a research paper published in 1968. It was not that long ago in the overall course of modern medicine, perhaps even its heyday, when all things were still possible and before the complete fealty to pharmaceuticals arrived. To the youngsters and to those coming of age in the last 20 years, however, anything published pre 1990 is ancient history. What could such old paper tell me about medicine that is new and useful? It turns out an awful lot.

Back in the day, research was a little simpler and more focused, not on finding out which drug could be fit to which symptoms, but on how things worked. Good experimental design, answered mechanical questions, like if we apply X to Y or if we remove X from Y what happens?

In this paper, Encephalopathy of Thiamine Deficiency: Studies of Intracerebral Mechanisms, the researchers identified a very important component about Vitamin B1/thiamine deficiency – the time course of the disease process. That is, with a diet deficient in thiamine, how long does it take before symptoms emerge, what is the corresponding level of deficiency in the brain, and at what point, after supplementation, does recovery begin; important questions clinically.

Vitamin B1 – Thiamine Deficiency

Remember, vitamin B1 or thiamine deficiency at its worst is linked to severe decrements neurological functioning, like Wernicke’s Encephalopathy that include noticeable ataxic and gait disturbances (loss of voluntary control of muscle movements, balance and walking difficulties), aphasias (language comprehension and/or production difficulties), and if it persists, Korsakoff’s Syndrome (severe memory deficits, confabulations and psychosis). Thiamine deficiency was originally observed in only chronic and severe alcoholics or with severe nutritional deficits as seen in famine. Fortification of food stuffs was thought to relieve much of the nutritional risks for deficit, especially in impoverished regions. More recent research, however, indicates that thiamine deficiency has reared its ugly head once again and this time in modern, non-impoverished, regions where the food supply is ample. How can that be?

Non-Alcoholic Wernicke’s Encephalopathies

Thiamine deficits can be mediated by a number of factors, including by less obvious nutritional deficits where food supply is abundant but nutrition is lacking (a diet of highly processed, carbohydrate and fat laden foods), with thiamine blocking factors found in medications/vaccines, environmental toxicants and some foods, after bariatric surgery and in disease processes like AIDS. Over the course of our research, thiamine deficiency has been observed in previously healthy, young, non-alcoholic patients, post medication or vaccine, along with symptoms of dysautonomia.

What has always struck me about the thiamine deficits we observe is the differential expression and time course of the symptoms. In some people, the reaction leading to thiamine deficit appears linear, progressive and rapid. In others, the symptoms appear to wax and wane and to evolve more slowly. How is that possible? Certainly, individual predispositions come into play. Some individuals may be somewhat thiamine deficient prior to the trigger that initiates the full expression of symptoms, while others have higher baseline stores. Additionally, anti-thiamine environmental exposures and other medical conditions/medications may also come into play. In the literature, however, the progression of symptoms from bad to worse is almost always direct and rapid, perhaps mistakenly so. Indeed, Wernicke’s Encephalopathy is a medical emergency necessitating immediate IV thiamine. How is it then, that we see more chronic, remit and relapse patterns of thiamine deficiency, even in some cases where thiamine concentrations are being managed medically?

Cerebral Thiamine Deficiency: Crossing the Black Line

It turns out, there is black line with regard to thiamine deficiency, that when crossed overt symptoms emerge, and a similar black line, that demarks recovery. It is possible then that barring a continuous blockade of thiamine, one can move above and below those lines and the corresponding symptoms may wax and wane. The paper from 1968, cited above, found those black lines, in rodents, but we can extrapolate to humans.

The research. The investigators took three groups of female rodents, a paired group of thiamine deprived and thiamine supplemented, along with a group fed ad lib (as desired) and assessed the time course and concentrations of cerebral thiamine deficiency relative to the initiation and progression of the observable neurological symptoms associated with Wernicke’s encephalopathy in rodents (ataxia, loss of righting, opisthotonos –rigid body arching). The experiment lasted about 6 weeks.

Neither the control group (thiamine supplemented) nor the ad lib group demonstrated neurological deficits at any time during the study. The thiamine deprived group, on the other hand, demonstrated symptoms that began with weight loss, progressive anorexia, hair loss (recall our observations about hair loss) and drowsiness at about 2.5 weeks into the experiment. Interestingly, no neurological signs of thiamine deficiency were seen at that time.

The results. At 4.5 weeks in, the researchers noted a rapid progression of symptoms and decline of health over the course of the next 5 days (the black line). These symptoms included: incoordination with walking, impairment of the righting reflex, reluctance to walk, walking backwards in circles, imbalance, rigid posturing and eventually a total loss of righting activity and severe drowsiness.

One can imagine, if a similar deprivation of thiamine were observed in humans, the corresponding symptoms might also include the initial hair loose and weight loss, perhaps noticeable, perhaps not depending upon the time frame and severity of the thiamine deficiency. It would also include incoordination and difficulty with walking, balance and voluntary movement, perhaps tremors, excessive fatigue or sleepiness and the myriad of neuro-cognitive disturbances noted in Wernicke’s syndrome.

In the cited experiment, one injection of thiamine reversed these symptoms to a nearly normal, or apparently normal neurological state within 24 hours.

Brain Thiamine Thresholds

Animals from each of the groups were sacrificed and examined at each of the stages of the experiment. Brain thiamine and other markers of thiamine metabolism were assayed to determine the cutoff levels of thiamine that demark symptoms and recovery. This is really interesting and the beauty of this entire study. Neurological symptoms become apparent when cerebral thiamine concentrations reach 20% of normal. Recovery begins when those concentrations climb to 26% of normal. At least in rodents, one has to deplete 80% of the brain thiamine stores before overt neurological symptoms become apparent; 80% – that is a huge deficit. Similarly, it doesn’t appear to take much to right that deficit, only a 6% increase in thiamine concentration set the course for improvement.

If we extrapolate to humans, where life span, genetic and environmental factors likely moderate the degree of thiamine stores and consumption, we still contemplate a rather large thiamine deficit needed before overt symptoms of Wernicke’s emerge. Similarly though, it is also evident that a rather small change in thiamine can have enormous effects on neurological functioning. In the case of the rodents, a mere 6% point change reversed the symptoms. One might suspect equivalent deficit/recovery thiamine parameters in humans.

Waxing and Waning Symptoms: A Case for Persistent Thiamine Deficiency

If we consider the possible course of non-alcoholic thiamine deficiency, where no extraneous variables like bariatric surgery or thiamine deficient parenteral feeding are present and where dietary thiamine varies daily and is not held constant as it is during experimental conditions or during famine, we can begin to see how thiamine related neurological symptoms may wax and wane. Different exposures and triggers may decrease thiamine periodically, even to the point where overt neurological symptoms present. When those exposures are removed and barring deficiencies in metabolism and diet, symptoms may abate, at least temporarily, and until the next trigger or until the black line is crossed anew and thiamine deficiency becomes the medical emergency observed in overt Wernicke’s.

In contrast, the more persistent or chronic thiamine deficits that do not cross the 80% depletion cutoff (or the human equivalent), may also wax and wane and show all the core neurological symptoms expected in overt Wernicke’s though to a much lesser degree. Additionally, as we have speculated, persistent thiamine deficiency might disable mitochondrial functioning in such a way that the patient presents with a myriad of seemingly unrelated symptoms, that are not typically attributed to thiamine deficiency, such as cardiac dysregulation, gastroparesis, autonomic instability, demyelinating syndromes and hormone irregularities, especially thyroid, but also reproductive hormones. These too may be related to thiamine deficiencies. Although, we cannot and should not rule out other causes as well, sub-optimal thiamine may be involved with a host of complex disease states and medication adverse reactions where neurological symptoms are present. Thiamine deficiency should be tested for and ruled out before more invasive therapeutic options are contemplated.

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Poor Nutrition Stress: The Enemy of Health

by Derrick Lonsdale MD, FACN, CNS

Published on May 6, 2014

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In previous posts, I have indicated that stress can initiate or exacerbate disease and medication or vaccine adverse reactions. Read that statement, you might think I am attributing the onset of serious disease and adverse reactions to a psychosocial cause. That is not the case. Stress comes in a myriad of forms, some external, some internal, and although much of what we call stress relates to psychosocial responses to perceived threats, I think stress encapsulates so much more. At its most fundamental level, stress represents a physical state where the body is performing less than optimally. Let me explain.

What is Stress?

I define the word “stress” as a physical or mental force that is acting upon you. An example of mental or psychosocial stress might be an insult from a person, meaning that the stress comes from a source outside the body. On the other hand, it might be the realization that a deadline has to be met, a mental source from within. Any form of injury is an obvious source of physical stress. Physical action such as shoveling snow is another form of stress, demanding energy consumption imposed by the individual who wishes to get rid of the snow. Being infected with a virus or by bacteria is a form of stress that demands a defensive reaction. In each of these instances, the body reacts to the inflicting stressor. Sometimes, when the resources are available, it reacts efficiently. Other times, when the resources are not available or when additional factors intercede, the body’s response to the stress is ill-adapted.

Your Body is Your Fortress, Your Immune System the Soldiers

Perhaps an analogy might help to provide an explanation for the remarks that follow. I imagine the body as being like an old fashioned fortress. The people living within it go into action when the fortress is attacked by an enemy from outside. It would be of little use if the defense soldiers went to the eastern battlements if the attack came from the west and so there had to be a central figure that would coordinate the defensive reaction. The nature of the attack would be spotted by a guard on duty and the central figure informed by messenger.

The body represents the fortress and the lower part of the brain represents the central figure that coordinates the defense. The cells in the blood known as white cells can be thought of as soldiers, armed with the necessary weapons to meet the nature of the enemy. Suppose, for example, a person’s finger is stuck by a splinter carrying a disease bearing germ. The pain, felt in the brain, recognizes its source and interprets it as a signal that an attack has occurred. White cells in the area can be regarded as the “militia under local command” and a “beachhead” is formed to wall off the attack. The white cells sacrifice themselves and as they die, they form what we call pus. If the beachhead is broken and the germs manage to get into the bloodstream, it is then called septicemia and the brain/body goes into a full defensive reaction where high fever is the most obvious result. Such an illness is an attack/defense battle.

The symptoms that develop from such an infection represent the evidence for this defense, feeling ill, pain and developing a fever are excellent examples. Micro-organisms are most efficient at 37° C, the normal body temperature. The rise in body temperature, initiated by the brain, makes the microorganisms less efficient and may kill some of them. One therefore has to question the time honored method of reducing the fever, during illness, as being an example of good treatment. While reducing fever improves the symptoms caused by the infection, it also reduces the efficiency of the immune battle raging within.

The outcome against the stressor is death or recovery; although it is possible sometimes to end up in a kind of stalemate, represented by prolonged symptoms of ill health. Chronic illness may be viewed as the immune system’s inability to eradicate fully the stressor.

Poor Nutrition and Stress

As I have emphasized in previous posts, the autonomic (automatic) nervous and endocrine systems are used to carry the messages between the body and the brain that enable the defense to be coordinated. This demands a colossal amount of cellular energy, no matter the nature of the stress. That energy to fight stress comes from oxidation of the fuel that is provided from nutrition. Of course, the greater the stress the greater the energy demand, but in the end the equation is quite simple. If the energy required to meet the stress is greater than the energy that is supplied, there must be a variable degree of collapse within the defensive system. That collapse presents as intractable symptoms, where the body is unable provide the energy needed to sustain health. This is the secret of the autonomic dysfunction in the vitamin B1 deficiency disease, beriberi. It is also the secret behind the initiation of POTS because both conditions are examples of defective oxidation. You can read more details regarding thiamine deficiency, beriberi, POTS and other health issues from previous posts on this website

High Energy Demands Equal High Nutritional Demands

Nutrient density of diet might appear to be perfectly adequate for a given individual, but inadequate to meet the self-initiated energy demands of a superior brain/body combination in a highly active individual such as an actively engaged student or athlete. Our genetic characteristics, the quality of nutrition and the nature of life stresses each represent a factor that all combine together to give us a profile for understanding health and its potential breakdown.

Epigenetics and Mitochondria: The Stress of Our Parents

Epigenetics, the science of how our genes are influenced by diet and lifestyle, is relatively new. Epigenetics considers the possibility that genes can be activated and deactivated by nutrition and lifestyle. Stress can come in many forms, from psychosocial trauma, poor nutrition, environmental and medical toxin exposures, to infections. Stress impacts how our genes behave. Even though one may inherit a hard-coded genetic mutation from a parent, that mutation may not be activated unless exposed to a particular type of stress. Similarly, an individual who may have no obvious illness-causing genetic abnormalities but stress, in the form of nutritional depletion, exposures or trauma, can turn on or turn off a set of genes that induce illness. What is remarkable about epigenetics is the transgenerational nature of the stressors. The memories of stressors affecting our parents and even our grandparents can affect our health by activating or deactivating gene programs.

We also have to consider the state of our mitochondria, the “engines” in each of our cells that produce the energy for cellular function (to learn more about mitochondria and health, see previous posts on this website). Mitochondria have their own genes that are inherited only from the mother. Damage to the DNA that makes up these genes sometimes explains the similarity of symptoms that affect a given mother and any or all of her children. For example, although this damage may be inherited, we also have scientific evidence that thiamine deficiency, known to be the result of poor diet, can damage mitochondria. A bad gene might be the solitary cause of a given disease, but even where this is known as the cause, the symptoms of the disease are sometimes delayed for many years, suggesting that other variables must play a part. A minor change in cellular genetic DNA might be alright to meet the demands of normal living, but impose a risk factor that could be impacted by prolonged stress or poor nutrition, and disease emerges.

Nutrition is the Only Factor that We can Control

The imposition of stress on any given individual is variable, most of which is accidental and out of our control. Therefore, if we represent these three factors, genetics, stress and nutrition as three interlocking circles, all of which overlap at the center of such a figure, there is actually only one circle over which we have control and that is nutrition. We now know from the science of epigenetics that nutritional inadequacy can affect our genes. By examining the mechanism by which we defend ourselves against stress, we can also see the effect of poor nutrition.

Poor Nutrition Equals a Poor Stress Response

Using these three variables, perhaps we can begin to understand several unanswered questions. Why does a vaccination negatively affect a relatively small percentage of the total population vaccinated? Or why do some medications negatively impact only some individuals? It might be because of a genetic risk factor or because of a collapse of the coordinated stress response related to quality of nutrition or a combination of both. Why does a vaccination tend to “pick off” the higher quality students and athletes? Again, the same kind of answer; high quality machinery demands high quality fuel. Since the limbic system of the brain has a high energy demand and represents the computer that coordinates a stress response we can understand the appearance of beriberi or POTS and cerebellar ataxia, all examples of a deviant response to stress. Nutrition, therefore, should not be looked at as supplement to good health, but as the foundation of health. When disease or medication and vaccine reactions emerge, efforts to identify and then restore nutritional deficiencies must be the first line of immune system health. Without critical nutrients, the body simply cannot mount a successful stress response and the battlefield will expand and eventually fall.

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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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