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Allergies, Autonomic Response, and Thiamine

Published on September 25, 2018

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allergies, hypersensitivity, intolerance

Allergic diseases are a number of conditions caused by hypersensitivity of the immune system to typically harmless substances in the environment. They include hay fever, food allergy, asthma and anaphylaxis. Symptoms may include red eyes, an itchy rash, sneezing, runny nose, shortness of breath, or swelling. In many cases, allergy is little more than a nuisance but can be severe and even life-threatening.

Hypersensitivity, Intolerance, and the Vagus Nerve

Also called hypersensitivity reaction or intolerance, this represents a set of undesirable effects produced by a normal immune system. They include allergy and autoimmunity, effects that may be just uncomfortable or damaging, but occasionally fatal. An entirely new perspective has been introduced by the discovery that the vagus nerve, an important part of the autonomic (automatic) nervous system, modulates the immune response. The importance of this cannot be overemphasized, because it is forcing us to think differently about the whole subject of disease in general and how antiquated the present medical model is. I turned to the medical literature to see what has been published concerning the activity of the vagus nerve.

A publication, noting that the innate immune system is a defense mechanism of vital importance for our survival, goes on to note that excessive or unwanted activation of the system is as bad as too little. It illustrates the important philosophical concept “everything in moderation”. This important nerve has its beginnings in the brain and exhibits its anti-inflammatory effects through what is called the “cholinergic anti-inflammatory pathway”. This means that this nervous mechanism suppresses inflammation and absence of its activity allows it to continue. The word cholinergic refers to the chemical substance known as acetylcholine, the neurotransmitter that the vagus nerve uses. I mention this because it becomes important later in this article.

The vagus nerve has its origins in the brain and extends to the spleen, the organ that has a major effect on immune responses. It also extends to the alimentary tract, carrying messages from and to the brain and obviously having a major effect on the mechanical and biochemical control of the digestive tract. The objective of a review on the subject was to explore the supporting evidence for the importance of the vagus nerve in its anti-inflammatory characteristics and surprisingly, the evidence for its importance in epilepsy and depression, both “mental” conditions. The authors suggested that stimulation of the vagus nerve could be harnessed therapeutically in human inflammatory disorders such as inflammatory bowel disease, irritable bowel syndrome, post-operative ileus (bowel paralysis) and even rheumatoid arthritis. Since the discovery of the role of the vagus nerve in this reflex mechanism, numerous animal studies have shown beneficial effects of stimulation of this pathway in models of inflammatory diseases either through electrical or pharmacological stimulation of the nerve.

Eosinophilic Esophagitis (EoE) and Asthma

EoE, described only relatively recently, is a chronic allergic, immune-mediated disease associated with increased risk of comorbid atopic conditions (a form of allergy in which a hypersensitivity reaction such as dermatitis or asthma may occur in part of the body not in contact with the offending substance). A study reported 950 patients with EoE. Comorbid atopy including pollen, food and drug allergy, anaphylaxis and psychiatric conditions were more common in the EoE group than recorded in the general population. Attention deficit, hyperactivity disorder, allergic rhinitis, autistic disorder, autoimmune disease and diabetes mellitus, were also associated with EoE . Eosinophils are a group of white blood cells that act as mediators of allergic inflammation and are implicated in the pathogenesis of numerous conditions, including some cases of asthma.

Comorbidity in EoE

Comorbidity refers to a disease condition that exists at the same time as the primary condition being considered. Therefore, I would like to emphasize the many symptoms that occurred in a 14-year-old boy with EoE. Apart from the painful act of swallowing and chest pain that were due to the inflammation in the esophagus, he experienced other symptoms related to brain function. These symptoms included hyperalgesia (an exaggerated response to painful stimulus), emotional instability, headaches, fatigue, dizziness, panic attacks, ADD/ADHD/OCD, and coughing during sleep without being awakened. All of these symptoms are the result of chronic lack of efficient brain cell oxidation. The physicians that had been taking care of him for the first eight years of life considered his symptoms to be due to psychosomatic disease, in spite of the fact that he had experienced many episodes of ear infection. Even ear infections are now known to be due to inefficient oxidation in the ear mechanisms. The diagnosis of esophagitis was made at the age of eight years and for the next six years there was no response to any of the orthodox treatments that were attempted. He came to my attention at the age of 14 years. My contention was that he suffered only one basic condition and that was lack of cellular energy with its major effect in the brain. When blood tests proved that he had thiamine deficiency disease, my contention proved to be an appropriate conclusion that needs some explanation.

Inefficient Brain Oxidation, Dysautonomia, and Thiamine

One of the earliest signs of thiamine deficiency is abnormal activity of the autonomic nervous system, referred to as dysautonomia. Panic attacks are emphasized above because they are merely fragmented examples of the well known fight-or-flight reflex, mediated by stimulus of the autonomic system related to inefficient oxidation in brain cells. He was addicted to sugar, long known to be able to precipitate thiamine deficiency in the brain, like alcohol. It became apparent that the vagus nerve, as noted above as part of the autonomic system, was defective. Thus the inflammation caused by food allergy, perhaps with a particular emphasis on sugar, was continuing without the benefit of suppression by the vagus nerve. If this is understood by the reader, it should be noted that the esophagitis was secondary to the biochemical change produced by thiamine deficiency. This had resulted in failure to produce acetyl choline, the chemical used as a neurotransmitter by the vagus nerve. This neurotransmitter is used by many parts of the brain, perhaps explaining the symptoms that were referred to as “psychosomatic”. True, this was but one case and does not prove that it is the only cause of this disease. However, since thiamine is a key member of the complex chemistry, but not the only chemical that gives rise to energy synthesis, it emphasizes a principle that the true cause of this inflammatory disease was related back to energy metabolism. When this boy was treated with thiamine, his symptoms improved and his stature accelerated over a year of treatment. However, perhaps because he persisted in taking sugar, some of the symptoms related to esophagitis had continued.

There is a genetically determined disease called Familial Dysautonomia and one of the important effects of this disease is growth failure. My contention was that dysautonomia was the major underlying defect in this boy, possibly from birth. Since the dysautonomia was the result of thiamine deficiency, we can conclude that his growth failure was energy-related and correction of the deficiency accelerated his growth, aside from its benefit to the autonomic system. It also suggests that Familial Dysautonomia, a genetically determined disease, might have a relationship with energy metabolism responsible for the associated growth failure. Although thiamine deficiency was proved, it did not tell us why it had developed, but it had caused a persistent defect in autonomic function, giving rise to many symptoms interpreted as psychosomatic. There was a strong paternal family history of alcoholism, suggesting an underlying genetic relationship since alcohol and sugar both precipitate thiamine deficiency.

The Dysautonomia of Asthma

Many years ago I was faced with an eight-year-old girl who had suffered recurrent life-long asthma. She was so intensely allergic that virtually any mattress she had attempted to lie on had induced asthma. She had to use a plastic lawn chair as a bed because of this. Without going into the scientific details, I had concluded that she was suffering from dysautonomia affecting the bronchial tubes and treated her with megadoses of thiamine hydrohydrohchloride. She had immediate relief and when I saw her three months later the mother reported that she had only had two mild attacks of asthma. She is now grown up and has remained free of a scourge that had been virtually crippling. Again, I must point out that this is but one case. However, asthma is so common in children, a clinical trial would seem to be worth attempting. It was noted above that eosinophilia is often associated with asthma and it may be that a similar mechanism applies to this as it does in esophagitis.

Thiamine Derivatives

Many years ago, I was working at a multiple specialty clinic as a pediatrician. I had published what proved to be the first case of a six-year-old child who had vitamin B-1 dependency. Dependency is the term used when megadoses of the vitamin are necessary in order to produce prevention of the clinical effects of the specific vitamin deficiency. This child had an intermittent brain disease that was completely prevented with enormous doses of the vitamin. It was so intriguing and so exciting that I embarked on clinical studies on the therapeutic use of vitamin B1 (thiamine). As a result of these studies, involving much library work and clinical experimentation, I received a gift copy of a book from a Japanese scientist. This book, entitled “Review of Japanese Literature on Beriberi and Thiamine” was written by a group of university-based medical researchers known as the “Vitamin B Research Committee of Japan”. Written in 1965 and published in Tokyo, this was an English translation. It had been translated deliberately to try to inform Western physicians about the thiamine deficiency disease known as beriberi. Because this disease was so common in Eastern cultures, these scientists considered correctly that Western physicians were completely ignorant of the far-reaching effects of this disease. They had in fact given me the responsibility of trying to spread information about its devastating manifestations.

A whole chapter was devoted to a discussion of a group of compounds known as thiamine derivatives. They had discovered that there was a form of thiamine in garlic (allium sativum) that had powerful therapeutic properties and they had called it “allithiamine”. The prefix “alli” refers to the group of plants known as the allium species, of which garlic is perhaps the most important. This derivative is sometimes referred to as “fat soluble thiamine”, an unfortunate choice of words because the “fat soluble” refers to its remarkable capacity to deliver thiamine into body cells. In cell membranes there is a layer of fat known as the “lipid barrier”, so fat solubility refers to the fact that it can pass thiamine through this fat layer in the cell membrane. The Japanese scientists had synthesized a whole set of derivatives of thiamine and I began to study the one which is known today by its trade name, Lipothiamine. Its chemical name is thiamine tetrahydrofurfuryl disulfide (TTFD). Contrary to its term as “fat-soluble”, it is water-soluble and can be given intravenously. Allithiamine, with a capital A, is a trade name for TTFD.

TTFD and Epilepsy

Children with epilepsy are often extremely resistant to the various drugs that have been invented. A common method of trying to find the right drug is to admit the child to hospital and remove one drug while substituting another, on clinical trial. When a given drug for epilepsy is abruptly stopped, a dangerous state known as “status epilepticus” can occur. The epileptic seizure continues indefinitely and is difficult to interrupt. It may even be lethal. While I was working at the multidiscipline clinic, a 12-year-old child was being investigated by a neurologist and for reasons that had extenuating circumstances, the current drug that he was receiving had been stopped. He went into the dreaded clinical expression of status epilepticus. The responsible neurologist was unavailable and I was called to treat the emergency. For some basic reasons that are beyond the scope of this article, I gave him an intravenous injection of TTFD that promptly stopped the protracted seizuring. On the following day he remained seizure free and was walking around the pediatric ward talking to other patients. What truly amazed me was that when the neurologist became available, he remained completely disinterested in the benefit that had accrued from the intravenous use of TTFD and resumed the drug trial. Nor did he question me as to my reasoning for its use. This was back in the 70s and vitamin therapy was considered to be virtually a form of charlatanism, so this successful treatment only appeared to blacken my reputation.

A New Approach to Medicine

The idea of helping the body to heal itself is far from being new. It was voiced in 400 BCE by Hippocrates, who is somewhat casually known as the “father of modern medicine”. This article introduces factual evidence that multiple diseases, each known by its name, have a common underlying cause, namely the failed requirement of cellular energy. Even diabetes, noted above in the text, is now known to have thiamine deficiency as an important part of its underlying mechanisms. It has been shown here that three different conditions had been successfully treated with a single agent. This is not simple vitamin replacement. It is the skillful use of body chemistry and emphasizes that nutrients are really the only essential components necessary for the body to heal itself. For example, acetylcholine is an essential component of energy production and its deficiency would affect the inflammatory suppressive action of the vagus nerve as described above.

Of course thiamine is not the only non-caloric nutrient required, but it holds a vitally important place in energy synthesis and I have likened it to a leader in an orchestra, where the brain is the conductor. Many mysterious and complex illnesses are prevalent today. Beriberi is the great imitator because its many different facets are produced by the individual distribution of defective energy metabolism from person-to-person. Thus, the symptoms and physical expression vary and are often interpreted erroneously as a specific disease of unknown cause. Because energy deficit has not yet entered the collective psyche of doctors of medicine as a common cause of disease, many patients are suffering prolonged illnesses. Their polysymptomatic presentation and lack of current laboratory studies is confusing, often considered to be somehow caused by the sick psychology of the patient (psychosomatic). This is ironic since the symptoms are indeed from distorted electrochemical mechanisms “all in the head”.

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Migraine, Diet, and Thiamine

by Derrick Lonsdale MD, FACN, CNS

Published on August 15, 2018

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In US population studies, the prevalence of migraine is approximately 18% in women and 6% in men. About 90% of sufferers have moderate or severe pain and 75% have a reduced ability to function during the headache attacks. One third require bed rest during an attack. A study at the Mayo Clinic showed the incidence in women increased 56% during the 1980s and 34% during the same period in men. Although the term “migraine” is often used to describe any severe headache, a migraine headache is the result of specific physiologic changes that occur within the brain leading to the characteristic pain and associated symptoms. They are usually accompanied by sensitivity to sound, light and odors and there may be nausea or vomiting. Typically, the headache involves only one side of the head but in some cases it may be bilateral. The pain is often described as throbbing, pounding and maybe made worse with physical exertion. Silent migraine is a variant where the patient may experience aura, nausea, vomiting and other nervous symptoms without headache.

Migraine headache is estimated to affect up to 28% of adolescents, most of whom are female. It has been associated with reduced quality of life and academic disruption due to missed school days. In 2014 the US Food and Drug Administration approved an existing medication called topiramate for prophylaxis in adolescents between the ages of 12 and 17 years. There are several possible adverse effects from this drug, some potentially serious. Prophylactic drugs are unpromising and unpredictable. A mild degree of prevention could be obtained from the use of acupuncture.

Migraine Precipitants

Of 171 patients who fully completed a survey, 49.7% reported alcohol as a precipitating factor of headache other than migraine. Only 8.2% reported aspartame and 2.3% reported carbohydrate. Patients with migraine were significantly more likely to report alcohol as a trigger. They also reported aspartame as a precipitant three times more often than those having other types of headache. Non-nutritive sweeteners, including aspartame, saccharin, sucralose, neotame, acesulfame-K and stevia have all been questioned as to their safety. Pregnant and lactating women, children, diabetics, migraine and epilepsy patients, represent the susceptible population. Although sucralose is not considered to be a migraine trigger, a patient was reported with attacks of migraine consistently triggered by this sweetener.

Hypoxia, Pseudo-hypoxia, and Migraine

Migraine with aura is prevalent in high-altitude populations, suggesting that hypoxia has a part to play in etiology. Of 15 patients with migraine headaches, artificially induced hypoxia triggered migraine attacks in eight patients.

Thiamine deficiency produces abnormal gene expression in brain exactly like that induced by true hypoxia. Migraine is a risk factor for thiamine deficiency and Wernicke encephalopathy (WE), the classic thiamine deficiency disease that affects the brain. Two female patients have been reported with chronic migraine. They also had clinical signs and laboratory support for WE. Both patients received intravenous thiamine supplementation, leading to improvement of both WE and the associated headache. The authors suggested that nausea and vomiting, occurring with migraine, may lead to the thiamine deficiency. However, headache, nausea, vomiting and loss of appetite are symptoms that occur in the early stages of WE, thus simulating migrainous features and the association is by no means clear. The authors suggest that thiamine supplementation might be a promising therapy in a subset of patients with chronic migraine.

Also, the range of pathologies associated with magnesium deficiency is staggering, including migraine, multiple sclerosis, glaucoma and many other disorders. It is important to emphasize once more that magnesium and thiamine work together in the cellular machinery that produces energy and deficiency of either is critical. Chronic recurrent nausea in childhood is a poorly described symptom and in a study of 45 affected children, 62% had migraine headaches. They also suffered from dizziness, anxiety, fatigue and sleep problems. The exact incidence of dizziness and vertigo during adolescence is not known. For those few adolescents who seek outpatient evaluation, the majority are diagnosed with migraine headaches and many suffer from postural orthostatic tachycardia syndrome (POTS), a condition that has been reportedly due to thiamine deficiency in some cases.

Autonomic Asymmetry

Normally there is a balance between the autonomic tone of the right and left half of the body. However, under stress or with hypothalamic instability this balance may be disrupted and result in the marked autonomic asymmetry seen in migraine. Abnormal regulation of the large cranial arteries appears to play a significant role in the mechanisms of migraine pain, also reflecting abnormal autonomic function.

Migraine and Diet

Attack frequency of migraine in children was associated with higher intake of high fat or sugar. The processing of both is dependent on thiamine. With these strong associations in the medical literature, it is impossible not to contemplate that the sweet sensory input from the tongue to the brain is an important trigger for migraine. There has been a steady increase in sugar consumption in America over the past few decades, suggesting the possibility that it represents the published increased incidence of migraine in the 1980s as mentioned above. It also suggests the possible implication of artificial sweeteners as migraine triggers.

The association of migraine with alcohol ingestion might be an important observation, since alcohol has long been known to be a cause of thiamine deficiency in the part of the brain that controls the autonomic nervous system. It has also long been known that beriberi, the classical thiamine deficiency disease, causes autonomic dysfunction in its early stages. One of the most important observations that I observed in practice was that a mild degree of this deficiency makes the brain extremely sensitive to many different input stimuli. It results in a high degree of sympathetic nervous system activity, hence so-called panic attacks that are really distorted fight-or-flight reflexes. Patients complain of constant anxiety, heart palpitations, unusual sweating, nausea, vomiting, dizziness and brief fainting attacks known as syncope. This collection of symptoms, thought by many physicians to be psychological in nature, is also referred to as postural orthostatic (positional) tachycardia (rapid heart) syndrome (POTS).

In a person who is in a marginal state of malnutrition, any mild stress such as a vaccination, a mild infection or some form of trauma may initiate POTS. A reader might conclude that this diversity of symptoms, that include the incidence of migraine, cannot be caused by a deficiency of a single nutritional element. In order to understand, it is necessary to be aware that a deficiency of energy in the brain resulting from a common form of malnutrition creates a multiplicity of cellular dysfunction according to the distribution of the deficiency. If this is the truth, it makes a mockery of the present medical model in which each described disease is thought to have a specific underlying cause. Hence, money is collected to find the cause of Alzheimer’s disease and is probably a pipe dream. It is well known a published association with thiamine metabolism strongly suggests that we should be looking for prevention rather than spending millions in trying to find a curative drug.

Conclusion

The clues that alcohol, sugar and artificial sweeteners are major triggers for producing migraine headaches are so strong, their avoidance would appear to be mandatory. However, it is almost certainly true that many sufferers know this, but make no attempt at avoidance, marking the taste of sweeteners as addictive. I became aware that there were millions of people in America suffering from symptoms that are constantly being unrecognized in medical clinics. Even if they are recognized as nutritional in nature, the doctor and patient are likely to ignore the appropriate prevention by adopting the consumption of an appropriate diet. Since most of the population is ingesting pills of one sort or another, perhaps advising the use of vitamin supplements as part of the dietary discretion might at least partially serve in the reversal of these common symptoms.

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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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Thiamine Deficiency Amid a Constellation of Mitochondrial and Metabolic Disorders

by Susan N

Published on August 8, 2018

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This is a bit of a long story because I can’t tell if I have a genetic problem that only shows up under stress or just plain deficits due to extreme stress. I am a 58 year old woman having some pretty severe health problems that I have recently begun to think might be due to thiamine deficiency, malnutrition and/or possibly some sort of genetic problem.

Medical History

I was hospitalized with pneumonia three times before I was 5 years old, once again in isolation ward at age 7. I also had several childhood illnesses including Rubella, chicken pox, and mumps. At age 5, I was diagnosed with exercise induced asthma and prescribed Quibron. Once I hit puberty, my respiratory problems seemed to resolve themselves as long as I avoided aerobic exercise.

At age 9, I was diagnosed with progressive sensorineural hearing loss (an indicator of mitochondrial disease that I only recently learned about). I had a curved loss with 60% gone in the higher frequencies down to about 40% loss in the low ones. My mother was also diagnosed with hearing loss that had gone unrecognized. My daughter also has a mild hearing loss that was diagnosed as an adult.

Major Life Stressors and Emerging Problems with Nutrient Absorption

From 2000 to 2012, had several major life stressors including the death of my second husband to colon cancer, a dog snapped at me and severed my lower lip, my third husband lost his job and attempted suicide, early retirement, bankruptcy, foreclosure on my home and then moving to a new state. I was diagnosed with post-traumatic stress disorder (PTSD) and received weekly trauma therapy for a year.

During the aftermath of the PTSD trigger event, I began having problems with nutrition. I would eat a meal and get no energy from it. After taking an early retirement from my job and losing my house to foreclosure, we packed up and moved out of state.

I never recovered from the exhaustion and stress of the move. We were nearly homeless one night after our car broke down and I had no more money because we had just paid the deposit to rent a house. I managed to leave all our keys in the car at the repair shop. My first husband wired us money for a hotel for the night.

The problems with digestion continued and my health seemed to go downhill. I was tired all the time and my brain was not functioning well. I tried going for walks but would come home exhausted. To make matters worse, we were scraping by on one third of the income I had before I retired and I had no health insurance. I didn’t know how to go about finding help in those conditions. I’ve always been in the system.

Catatonia-like Episodes upon Eating

Starting in 2013, I started having episodes that I call zonking. I would eat something and almost immediately get very sleepy and usually would just fall into a sort of zombie-sleep-like state for 10-30 minutes. Sometimes it seemed sort of catatonic and others is was more like a strong urge to sleep. It wasn’t normal sleep in that there was no dreaming. Sometimes I was in a kind of frozen pose instead of laying my head sideways or getting comfortable. At first it seemed like they were correlated with high-availability carbs, but over time they became an almost daily occurrence with any type of food I ate. These episodes would sometimes disappear for a few weeks and then reoccur. There was no pattern I could discern nor tie to hormonal cycles.

I have been keeping daily logs from 2013-2016. I reported the zonking episodes to my NP and she prescribed Lactulose which just made the diarrhea worse. She ordered an ultrasound on my gallbladder and liver and no major problems were found.

The zonking episodes were really disabling. I would be feeling fine until I ate something and within a 1/2 hour I would zonk out and feel very groggy afterwards. It didn’t feel safe to drive so my husband had to take me shopping or do the shopping himself when I was too tired. I didn’t drive from 2013 to 2016. At times, I didn’t want to eat at all so I could keep myself functional long enough to do something. I found out the limits of fasting pretty quickly.

Left Temple Headaches, Migraines with Visual Aura, and Cognitive Deficits

I also had left temple headaches starting in 2013 and a few migraines also involving left temple pain but mostly just visual aura. I never had migraines previously. After I fell going up the concrete steps to our front door, I became very cautious about moving when I was in one of these states. I noticed that I became very clumsy with tasks that you normally don’t think about like opening a can or a pill bottle.

I also noticed a significant decline in my ability to comprehend speech when I was in one of these states. This was first mentioned in my logs in 2013. I have always had a problem due to my hearing loss but there seemed to be a magic something taking place in my brain that took care of turning sounds into words. Somehow that process was failing when I was in the dizzy and ditzy state.

My condition was deteriorating in 2016 and I was experiencing more severe brain problems that are what I now call dizzy and ditzy. Dizzy and ditzy feels like being very drunk. I was spending more and more time in bed which was making my diabetes worse. When my brain was functional I was researching and trying to figure out what might be causing my condition.

In August 2016, I came across a description of gluten ataxia. The symptoms seemed similar to what I was experiencing so I tried eating a gluten free diet for a few weeks and started feeling better. After two weeks, I decided I was imagining the improvement and tried eating something with gluten in it. After about two hours I began to experience the dizzy state and the left temple headache. From that time I have remained gluten free.

It was my intent to get tested for Celiac at my next appointment, but my husband was hospitalized in October 2016 for sepsis due to undiagnosed type-1 diabetes. This was the worst kind of trauma for me because my second husband died of colon cancer. Knowing that, I applied the techniques I learned during trauma therapy to keep my stress level down. As a result I was able to return to the hospital for his follow-up visits with no increase in blood pressure or other signs of HPA activation. I think it helped me overcome my doctor phobia and I have been increasingly more able to deal with medical situations. My health and energy levels were also improving due to the gluten free diet. I tried various diets and found that I had the best energy levels on a gluten free vegan diet.

Since I did not get in to see my primary until six months had passed gluten free my celiac tests were inconclusive. I found a really good allergist and in January 2017 was diagnosed with 44 food allergies including wheat, barley, oats, eggs, milk, and assorted nuts, fruits, and vegetables and yeast which is everywhere. Six months later, I was diagnosed with multiple environmental allergies. My condition began improving dramatically as I stopped eating the foods that I was allergic to. However I found that I was still unable to eat solid food and get energy from it. Meanwhile my NP added 10 mg glipizide which caused hypoglycemia when I was feeling well and active.

I didn’t experience any more dizzy and ditzy episodes from October 2016 through March 2018.

Diet and Malnutrition

I did have, and still have, episodes where I become very sleepy and nauseous after eating something. This leads to a feeling of being ill and not enough energy for normal activity. My condition improves if I semi-fast for the remainder of the day and then reduce my intake of protein and fat for a few days. As a result, I became more depleted nutritionally as time went by.

I don’t think I’ve managed to convey to anyone just how my diet has shifted from normal and especially what they seem to expect of diabetics. Many days I was unable to even manage 50 mg of protein and if I didn’t eat enough carbohydrates I had difficulty sleeping. I was on homemade liquid meals from 2017-2018 and only recently was able to transition onto whole foods after stopping Metformin.

I still struggle to explain why I suspect nutritional deficits in the face of a body that is down 10lbs but still 220. I think my body compensates by doing things like lowering my body temperature. It was 96-97 on a regular basis over the past 6 years, yet my thyroid panels are normal except for high TSH which may be due to my Biotin supplementation. In May 2018, I had more thyroid testing done.

TSH: 7.5
fT3: 3.1
fT4: 1.34
rT3: 22.2
TPO: 12
Antibody <1.

Sometimes my body heats up immediately after eating. I’ve also had iron deficiency anemia where my hands and feet got painfully cold. Sometimes I get chilled and find my body temperature is 95.8 – even in July.

Other Weird Symptoms

Visual Disturbances

I haven’t been able to match up these phenomenon with technical names so I am just describing them as best I can. There is some overlap as I am not sure what is part of which phenomenon.

Problem: After-images occurring too easily
Duration: 3-4 years
Frequency: Intermittently – seems to be worse when I am having diarrhea episodes
Details: Can’t find exactly what these are called. In normal vision if you stare at something for a long time then look at a blank surface you can see a phantom image of inverted colors. What has been happening intermittently with me is that I will see these images instantly and they take longer to fade than normal. This is especially bad in the mornings. I made up a test for myself to track how bad my vision was on any day by looking at the GOOGLE logo. On bad days it bounces around in afterglow very strongly; other days not at all or not as strong. Sometimes if we are out on a sunny day a glance at a bright reflection off metal will create a strong after image that persist for 20-30 seconds or more. I have to be very careful not to let my eyes linger on anything shiny.

Along with the above problem I also experience a kind of sparkle sometimes where if I look out the window, even on a gray day and then back inside there is a brief field of sparkle in my vision.

Problem: Seeing my pulse in my eyes
Duration: 6 years
Frequency: Not as much these days, but was especially bad when my blood pressure was uncontrolled.
Details: I would see a grayed pattern around the lower outer edge of my vision that would flash in intensity seemingly in conjunction with my heart rate.

Finally, my left eye seems to flutter and roll.

Problem: Left eye flutter and involuntary eye roll and moving illusions in vertical images.
Duration: 9 months in 2015, confirmed by eye doctor.
Frequency: Started very infrequently but has progressed to almost daily.
Details: Irritating flutterly feeling in my left eye. When I looked in the mirror I noticed the left eye was rolling left or attempting to roll left involuntarily. This may be related to another problem I have been having for several years where my vision wobbles. It comes and goes in severity, but if I look at any image that has strong vertical contrast it appears so move. For example a picture of a coliseum or tiger will appear to be moving like the way optical illusions move. The moving illusion also occurs more frequently when I am having bouts of diarrhea.

Migraines With Aura

Problem: Migraines with Aura
Duration: 2 years
Frequency: 3-4 times a year – sometimes in clusters
Details: I get migraines where I see an aura. It starts with a blind spot in the center of my vision, in less severe ones it is more of a sparkle overlay and not as blind. The circle then becomes a semi-circle of the outer edge of each eye that becomes bigger until it moves out of the eye. Then pain comes or not. I can sometimes reduce severity by immediately going into a dark room and lying down. Sometimes I get the headache and sometimes just the visual aura. I mention these here because I have wondered if some of my visual problems are migraine auras that haven’t fully developed.

Allergy Shots and More Symptoms: Ophthalmoplegia, Dizziness, Speech Impairment

In January 2018, I started desensitization shot therapy with my allergist. In February 2018, I had another episode of dizzy and ditzy that was complicated by additional symptoms of hypoglycemia. After consulting with my allergist, he set my shots back a few weeks and set up a standing lab order to see if he could tease out the problem. In March, I had the worst episode of dizzy and ditzy I have experienced to date. It included ophthalmoplegia, dizzy, very sleepy, altered consciousness, and personality changes. I was walking with a sort of limp as if my left leg were injured. I laid down on a bench outside the allergist office until the sleepiness passed. When the people at the allergy clinic got back from lunch they checked my blood pressure which was normal and did a blood draw for labs.

I also had the worst episode of speech impairment ever. I remember thinking it was funny because it sounded like they were speaking so much gobbledy gook. I used mindfulness to notice and try to quantify what it was like. I noticed that my intellect was intact, which distinguishes the condition from brain fog where it’s hard to think at all. But things like trying to speak or find words was hard and I got confused easily. Oddly, I had no problems reading and comprehending research papers and I could write, except I made more typing errors. I had a quarter sized mark on one of my arms from the previous day’s shots, but my allergist did not consider my brain symptoms to be due to the allergies. My movements and general condition was very much like being very, very drunk.

Up until that point I had associated dizzy and ditzy with gluten exposure. Once I was sure there was no gluten in the shots, I was a lot more worried about my condition. I regretted not going to the ER since that might have helped me get a diagnosis. As it was, the allergy doctor only checked my tryptase levels and blood sugar which was 119. That level of blood sugar is hypoglycemia for me. I start getting symptoms under 130. This second episode was much harder to recover from than the first and I had lingering symptoms for months afterwards.

Medication Reactions

The glipizide combined with 1000 mg Metformin ER for the type 2 diabetes was causing me severe problems, even as my energy levels and inflammation was improving. The repeated episodes where I had to lower my protein and fat intake was really difficult with the medications I was on.

One day I had a different sort of drunk feeling with sweating and distorted vision while out shopping. It got better when I ate something. I got home in one piece and spent the entire afternoon eating every hour until things improved. That was the last time I took glipizide. I started looking for a new primary who understood nutrition.

I found a new primary two hours away who seemed like a good fit but this story is already too long to describe what went wrong. Sometimes a bad thing has to happen before good ones. I found myself without a primary and experiencing more dizzy and ditzy symptoms. The problems started at the request of my new primary PA, I changed my metformin dose from 2 500 mg tablets in the evening to 500 mg morning and 500 mg evening. After a few days I woke up with a 206 fasting glucose. So I doubled down and started taking 1000 mg 2 times a day. That made modest improvement of fasting glucose but also caused steatorrhea and diarrhea to return.

Thiamine Pyrophosphate Order Delayed

I began taking 13 mgs of thiamine pyrophostate (TPP) in 2014. Recently, I ran out of the TPP sublingual I normally take due to a shipping delay, so I switched to oral 500 mg Thiamine HCL capsule. Over the next two days, I had cramps in my calves, congestion and coughing after my normal light exercise and a body temp of 95.8 in the evening. Then another episode of dizzy and ditzy with mild ophthalmoplegia and dehydration. I was drinking salt water and still couldn’t retain water. I always drink my water with electrolytes and I went through a whole gallon in a day. My blood glucose was 289 in the evening.

I’ve been having problems with burning feet and neuropathy since March 2018, it comes and goes and makes it hard to get to sleep. I first reported mild symptoms of neuropathy in my logs in 2013. TPP and B2 and sometimes calcium supplements help.

Once TPP arrived I started taking it 3 at a time (3x13mg) as well as extra magnesium glycinate and other B vitamins, but my symptoms weren’t improving as much as I expected so I started looking for other causes.

While researching various genes, I came across a paper on thiamine transporters and metformin. I have at least one mutation in one of those transporters but it doesn’t have any established meaning that I can find. I had not considered thiamine deficiency as a possible cause for dizzy and ditzy even though the symptoms seemed similar because I was taking 13 mg of TPP sublingual daily.

I started easing off metformin and my energy and burning feet symptoms improved. A side effect was the metabolism issues that had kept me on a liquid diet improved and I can eat and metabolize solid food again.

Going off metformin caused a slight rise in my fasting glucose so I had a lab test run myself that shows I still have normal insulin production. My glucose response varies quite a bit but I sometimes get good response when I do daily treadmill with glucose in the 110 range two hours after a meal

One night I had a lot of congestion and couldn’t sleep so I took a dose of 3x TPP and the congestion went away and I was able to sleep. I have had ongoing issues with lung congestion since 2010. I think this may be a return of the lung problems I had as a child. I believe my body compensated with hormones and is now decompensating due to menopause. The fact that the congestion got better after thiamine intake is worrying. But I have a strong placebo response so I have to be careful about creating correlations. The lungs issue has been observed by both my primary and my allergist. I frequently get very thick mucus that may be due to inadequate fat digestion.

Ran out of Thiamine AGAIN!

I had a dizzy and ditzy episode with temple headache 7/11/2018. I went through three bottles of 60 Sublingual TPP in a few weeks and was unable to order more due to factory back order. I researched other versions of thiamine. Benfotiamine was having no effect that I could detect. Sulbutiamine helped with some of the brain problems like short term memory. I had concerns that I wouldn’t be able to absorb some of the other forms due to my fat malabsorption. Fortunately, I came across the blog where Dr. Lonsdale explained what “fat soluble” really means regarding lipothiamine and allithiamine, so I ordered both of those as well as liquid TPP from the UK.

Neither of those had arrived by July 14, when I took my last TPP. I had a return of symptoms over the next few days. I started using a B-complex that had TPP in it, but even with that I had another dizzy and ditzy episode that lasted several days. During that time, I got sleepy every time I ate a meal. My meals are small to start with because of the GERD: one cup lentils with tofu or a tofu taco with avocado. Both of those meals that were normally well tolerated gave me symptoms of sleepiness and fatigue.

I found a comment somewhere about the need for manganese, so I got manganese glycinate supplements and that helped ease the neuropathy until the Lipothiamine and TPP liquid arrived. The first Lipothiamine was like magic, my eyes cleared up in about 15 minutes. They do that sometimes after I eat. The neuropathy symptoms were down by the time I went to bed in the evening. In the morning, my feet were hypersensitive and I had leg cramps due to low magnesium. I still have to take extra magnesium during the day and at night as well as other B-vitamins. I have some mild brain symptoms too but they may be due to the stress of starting with a new primary.

The big difference is in my energy levels, which are sufficient to make it through the day and no burning feet at bedtime. I still have limited ability to metabolize food, I tried to add 1/2 cup brown rice to my daily lunch and it sent me into borderline dizzy and ditzy. A typical day’s intake for me is 1 slice tofu, 1/2 cup lentils, and tofu taco with avocado, some vegetables, and a big leafy green salad with avocado, beans and nuts. Sometimes I can have a snack of fruit but more than that I start having problems. I suspect I have other deficits that may be slowing my recovery. I am waking up at 1 am and having to eat something to get back to sleep.

I had another episode this past week. I was preparing my allergy records for a trip to ER and was very dizzy and clumsy and a band of pressure in my forehead. I had been taking 2 50 mg enteric tablets 3 times a day of Lipothiamine but was experiencing symptoms of illness after eating and tiredness. I was only rescued from ER by modifying Lipothiamine dose so that it would be absorbed in my stomach instead of my intestines. I’ve had symptoms of intestinal malabsorption which haven’t yet been evaluated by a GI. I have checked several nearby GI practices without finding one who takes a self pay patient.

Genetic Testing

Genetic testing has helped me discover other problems I have involving metabolism. I haven’t cataloged all my mutations but I have a diabetes related set of 3 homozygous SNPs called TCF7L2. The way I understand it is that people with this phenotype have increased signaling mechanisms such that when they have excess fat, the pancreas responds by lowering insulin response to food and the liver increases morning glucose. Losing the weight, reduces the expression and returns things to normal. I have other genetic mutations which may be impacting me such as MTHFR(++), MTRR(++), and a rare BCHE mutation that impacts my choline levels. It also makes me vulnerable to pesticide exposure. I have to take Trimethylglycine (TMG) and various B vitamins to keep homocysteine in check. If I don’t take enough TMG and CDP choline, I get depressed.

I am seeing a new primary who is a doctor of Internal medicine. The new doctor’s choices for medications are spot on for my genetic type, they both work on the GLP-1 pathway, but they also increase insulin response. I don’t see how that doesn’t cause hypoglycemia, since I have normal insulin production. I have more research to do before making a decision on new medications.

While I can see that the deficiency symptoms I have been experiencing may be a result of poor diet and digestion, the fact that Thiamine HCL did not work and my condition improved so much after stopping metformin leads me to believe I may have a genetic condition. I really need to find a university that is researching metabolic and genetic conditions so I can get a diagnosis.

Medications and Supplements

Most of these supplements were added in 2017 after I started homemade liquid meals. Prior to this I was taking a sublingual B-complex & Magnesium glycinate.

Current Medications

Singular 10 mg x 1
CoReg 12.5 x 1
Lisinopril 10 mg x 1
Cetirizine HCL 10 mg x 1
Omeprazole DR 40 mg x 1

Most of these were added when I started liquid diet

B-6 Pyridoxal-5-phosphate sublingual 15mg x 1 (more if homocysteine symptoms)
B-1 Thiamine pyrophosphate (TPP) sublingual 13 mg x 1 (the one that is backordered)
*TPP liquid 3 x a day or as needed with malabsorption due to intestinal swelling
*Lipothiamine tetrahydrofuryl disulfate 100 mg 3 times a day with extra Mg.
*Liquid CoQ10 100 mg x 3 times a day
B-2 Flavin mononucleotide sublingual 18 mg x 1
B-3 27 mg as Inositol Hexanicotinate, 25 mg as NAD sublingual 25 mg x 1
Liquid B5 + Carnetine
MethylCobalmin, sublingual 1 mg x 1
MethlyFolate (S6)-5-MethylTetraHydroFolate glucosamine salt sublingual 800 mcg x1
Biotin 5000 mcg sublingual 1 x
Chelated Zinc, zinc glycinate 22 mg x 1
Selenium as L-Selenomethionine, capsule 200 mcg x 1
Kelp 325 mcg Iodine, 325 mcg x 1
TriChromium Chromium Picolinate, Chelavate, & polynicotinate, 500 mcg x 1
Magnesium Glycinate (capsule at home) ~ 800 mg per capsule 50% Mg x 2
Liquid chelated Iron biglycinate 10 mg, Yellow dock 10 mg x 1 (not long term)
D-3 5000 iu with K2 1 sublingual 125 mcg D3+ 90 mcd K2
Ultra K with K2 softgel, K1-1000 mcg + K2 1400 mcg x 1
Algae DHA 200 mg x 1
Phosphatidylcholine softgel 1300 mg x 1
Source Naturals Vitamin A as palmitate 1 x 10,000 iu
Buffered C-1000 complex Calcium Ascorbate 1 g x 2
Southwest Botanicals Mucuna Powder (self capsule) ~ 810 mg x 1
Citicholine (self capsule) ~820 mg, 1-2 as needed
Nootropics Sulbutiamine 200 mg (thiamine derivative) 1 capsule, 200 mg x 4
TrimethylGlycine (Betaine) 1 g x 2 with each meal containing methionine
*Taurine 1000 mg
Liquid Calcium, Magnesium, D3, Phosphorus as needed for sleep

*Recent additions

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Thiamine Deficiency, Dysautonomia, and High Calorie Malnutrition

by Derrick Lonsdale MD, FACN, CNS

Published on June 14, 2018

8525 views

This book by Lonsdale D, and Marrs C, is available on Amazon books. It is published by Elsevier. Written particularly for physicians who are practicing in the field of Integrative Medicine, it would be of interest to the educated public, particularly those affected by chronic disease.

Beriberi, the classical thiamine deficiency disease, long known to have been caused by consumption of white rice, is thought to have been abolished in developed cultures. It is actually widespread in America due to the colossal ingestion of sugar and is usually diagnosed as psychosomatic disease. Because the standard laboratory studies are negative or nonspecific, it is assumed that no organic disease is responsible.

Beginning with a review of the many symptoms of beriberi, it is described as the “great imitator” of a large number of disease conditions, each of which is thought to have its own etiology. It is relevant in all mitochondrial disease, because thiamine sits astride the vital initiation of energy synthesis. Thiamine deficiency interferes with carbohydrate, fat and protein metabolism, but is particularly important in the etiology of diabetes, types I and II and metabolic syndrome. It also has a place in the etiology of Alzheimer disease and may have an important part to play in cancer.

Evidence is provided to show that the relatively new science of epigenetics is crucial to the understanding of the part played by nutrition and lifestyle in genetic function. If the early symptoms of nutritional deficiency are treated symptomatically and high calorie malnutrition continues, the result is an array of chronic brain diseases. When thiamine deficiency was discovered as the cause of beriberi, the early investigators recognized that therapeutic doses of the vitamin involved the administration of 100-300 mg a day for months. The book reviewed here should be in the library of any Integrative Medicine physician.

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Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition

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Thiamine and Heart Function

by Derrick Lonsdale MD, FACN, CNS

Published on May 30, 2018

7662 views

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

Heart Disease and Beriberi: Case Stories

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

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

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

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

Recognizing Vitamin Deficiencies in Disease

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

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

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

Recent Reports of Thiamine’s Role in Clinical Care

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

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

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

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

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

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

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

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

Solving the Medically Unsolvable: Gene, Nutrient, and Diet Interactions with Dysautonomia

by Tanya Dawson

Published on May 14, 2018

11312 views

Years of Pain, Fatigue, and Weird Symptoms

I have had chronic fatigue syndrome, excessive Non-REM (NREM) dreaming, mood issues and muscle pain 24/7 for as long as I can remember. I have been to more than 100 health practitioners of various flavors, from the conventional doctors and specialists, to herbalists, energy medicine doctors, hypnotists and acupuncturists as well as taking pretty much every test available. Most tests were frustratingly normal. I had deficiencies in iron and B12 at various times but that came right after being diagnosed with Celiac Disease and starting a strictly gluten free diet.

Still, the fatigue and 24/7 pain persisted, and with the start of menopause, new symptoms emerged. I experienced periods of vertigo, brain fog, unexplained cold sensations in my chest, and after taking bioidentical progesterone for a few days I experienced daily dizziness and eventually got diagnosed with postural hypotension when the cardiologist measured a drop in systolic blood pressure of more than 30 upon standing. This daily dizziness continued for more than three years.

I tried all of the usual dietary interventions as well as the low oxalate diet, the anti-candida diet, the Failsafe diet and other elimination diets. All failed to make a dent in symptoms. The only time I noticed an improvement was when, after several bouts of gastroenteritis, I was forced to subsist on dry gluten free bread, a whey protein based meal substitute drink and skinless chicken. People commented that my skin looked good and I had improved energy, however, over time I returned to my normal diet and the benefits gradually disappeared.

Resolving the Dizziness, Brain Fog, Dysautonomia / POTS with B Vitamins and Diet

For more than three years, I have had daily dizziness pretty much all day as a symptom of dysautonomia/postural hypotension. An OAT test showed low thiamine and I had high hopes that thiamine would be the magic ticket that would get me out of dizzy brain fog hell. Thiamine and a reduced sugar diet did help a lot with energy, mood and general well-being, but unfortunately the reductions in postural hypotension were minor.

I experimented with supplements and lifestyle changes. I increased my meditation time, and did gratitude journaling and worked on taking in the good and rewiring my brain. This helped me better manage the stress of chronic illness and reduced some of my symptoms of depression and agitation.

I also found improvements in taking thiamine and riboflavin (B2) 3-4x a day along with high doses of the other B vitamins once a day. But, again the daily dizziness and brain fog persisted.

My big breakthrough came when I discovered that I had been taking the wrong form of niacin. I had been taking niacin and inositol hexanicotinate for the last three years, but it wasn’t until I returned to taking niacinamide that the symptoms dysautonomia dialed down. I started with a 50mg dose and by the end of the day I noticed that I had been less dizzy. I gradually increased the dose to the full 500mg and the symptoms kept reducing. I also got my brain back! No longer was I feeling constantly brain fogged, sluggish and mentally confused. Now that the niacinamide had my blood circulating properly and fueled my biochemistry things started working. My thyroid numbers had always been on the cusp of hyperthyroidism, yet I had a sluggish metabolism. Within a week, I noticed that with no other dietary changes my post-menopausal muffin top had reduced, my energy increased, and my skin was looking better.

The Missing Pieces: HACL1 and Phytanic Acid

I had high hopes that I would be able to completely eliminate the symptoms of dysautonomia, however, there is still some lingering dizziness. Over the last few weeks, I have been experimenting and have noticed two interesting associations.

The first, is sugar intake. Additional fruit or anything high in sugar increases my symptoms of postural hypotension. This could be linked to thiamine or niacin.

The second, is a reaction to foods high in phytanic acid. I first learned about the HACL1 gene from the Hormones Matter blog and I quickly realized that this made sense of the fact that I reacted to both A1 and A2 cheeses and yogurts as well as butter, but am fine on whey protein. I also react to oily fish and red meats but I am fine with pork and chicken. I live in New Zealand where all of our lamb and beef are grass fed, so all of our dairy products and red meat are higher in phytanic acid than the same products from grain fed animals.

In the past, I had noticed that any of these foods that are high in phytanic acid trigger feelings of rage and anger. There seems to be a threshold, so I can do an elimination diet and reintroduce butter and be fine, but over time, I believe that they phytanic acid accumulates and then the symptoms appear. Once I reach the threshold, I “hulk out” within minutes of eating beef, lamb, fat containing dairy products and oily fish. I have also had similar reactions in the past when I ate sugar or drank alcohol. I had in the past noticed that my dysautonomia was worse with all of these things. It would appear that thiamine is required to process all of these things, either directly in the case of sugar and alcohol or through the HACL1 gene for the other foods. This suggests that my body struggles to maintain thiamine levels and get the thiamine to where it is needed.

HACL1 rs17485390 (C)	TT
HACL1 rs6784844 (T)	CT
HACL1 rs6797119 (T)	CT
HACL1 rs7648958 (A)	AG

Feeling confident after increasing my niacinamide to 1,000mg spaced throughout the day, I reintroduced foods high in phytanic acid and the dizziness increased fairly quickly. I am now sticking to a low phytanic acid with only occasional red meat, fish or butter. (Yogurt and cheese are gone for good and maybe the other foods will need to be completely eliminated too.)

I found an old test that showed that my urinary l-lysine was low. After more research, I discovered that lysine helps maintain tryptophan activity and reduces the draw on niacin in the body. My tryptophan levels were normal on both urinary and blood tests but perhaps a lysine deficiency was indirectly affecting my niacin levels. After an initial dose of lysine I felt almost euphoric. This effect quickly leveled off. I am wondering if, after decades of fatigue, my body likes homeostasis and is counteracting the effects of nutrients that I clearly need. This has happened in the past with medications. After a few doses, they are basically rendered useless. This applies to antihistamines, psychotropics, painkillers, and so on.

Possible Secondary Pellagra

Is it possible that I have secondary pellagra? I initially dismissed the idea of pellagra as the symptoms seemed more severe than mine. My dermatitis was minor compared to the pictures online, I had an explanation for the dizziness (diagnosis of dysautonomia), the diarrhea has been an issue on and off, so it didn’t seem significant, and my mental confusion didn’t seem enough to qualify as dementia and yet I can now see that I did have the 3 Ds of pellagra despite adequate niacin intake. I don’t eat corn and rarely eat grains and have a diet high in niacin but I had many of the symptoms of pellagra including sensitivity to light, dermatitis, diarrhea, dizziness, feeling cold all the time, brain fog and mental confusion, difficulty falling asleep and weakness.

Interestingly, some of these symptoms overlap with thiamine deficiency symptoms and I feel very sure that I have had severe thiamine deficiency because I have also had tingling sensations and muscle pain, as well as a history of high intake of sugar, carbs and alcohol and a very positive response to thiamine and benfotiamine.

Going Forward: More Questions

My plan is to continue with my supplements and a low sugar diet and low phytanic acid foods. I am hopeful that this will completely eliminate the dysautonomia and leave me free to work on my other symptoms. My brain function is good when the dizziness is kept at bay and I feel more optimistic and happy and have a small but noticeable uptick in energy and strength.

Although I have made huge strides in my health, I am left with some lingering questions:

I have been on high doses of many B vitamins for years and yet it seems that my body still craves them. Could years of undiagnosed Celiac Disease have affected the enzymes that take vitamins and converts them to the active form and transports them into organs and tissues? Is it realistic for this to still be happening after eight years of being gluten free?
The literature glosses over the conversion from niacin to niacinamide as something that the body can easily do, however, I have taken high doses of niacin and inositol hexanicotinate without benefit and eat a diet rich in niacin foods without getting the benefits that I got from small doses of niacinamide. Is it possible that some people have challenges converting niacin to niacinamide? I have yet to find any research to support this other than a study suggesting that niacinamide is twice as effective as niacin. However, I was taking triple the dose of niacin with no benefits. I believe that my body is inefficient at converting niacin to niacinamide. If anyone knows of a specific illness that may cause this I would be interested in learning more.
Is my reaction to phytanic acid foods due to a deficiency in thiamine (despite taking very large doses for years) or is there another reason that my body appears not to tolerate phytanic acid foods?
Are there still more vitamin or amino deficiencies that I am yet to discover? In the future I will probably do another OAT or Nutreval to see whether my levels have improved but for now I want to let my body get used to the lower phytanic acid levels and see if things settle.
My body seems to like homeostasis. For the first couple of days that I took niacinamide I noticed that I felt very warm, but I have returned to feeling cold all of the time. The dizziness has improved and it had almost disappeared but then crept back in. Could this be due to more vitamin or amino deficiencies that I am yet to discover, problems with my enzymes or is there some sort of ANS wiring issue that is better addressed by neural retraining?
Sleep is another big issue for me and until I consistently sleep well without excessive NREM dreaming it is possible that these other issues will not fully resolve, but progress is exciting and I am hopeful that the last puzzle pieces will fall into place.

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Thiamine, Epigenetics, and the Tale of the Traveling Enzymes

by Chandler Marrs, PhD

Published on April 17, 2018

6194 views

For some time now, we have been covering all the ways in which thiamine deficiency influences disease. The primary mechanisms are through the down regulation of mitochondrial enzymes critical for ATP production. The lack of thiamine impairs mitochondrial functioning significantly leading to complex, debilitating, chronic, and sometimes, deadly illnesses. With mitochondrial energy a requisite for cell functioning and survival it is easy to see how the diminishment of mitochondrial functioning would negatively impact health and how high-energy physiological systems like the nervous and cardiovascular systems might be particularly hard hit. More than just just derailing cell function, as if that wasn’t problematic enough, when mitochondrial energy production slows, the adaptive cascades that ensue include epigenetic modification, not only at the level of mitochondrial DNA (mtDNA), but also, at the level of gene expression from the cell nucleus or nDNA. This is a huge discovery with broad implications about health and disease. It means that all sorts of things considered innocuous, are directly influencing gene activation and deactivation by way of the mitochondria.

Epigenetics: How the Cells Adapt to the Environment

Epigenetic modification refers to the activation or deactivation of chromosomal gene expression absent mutation. These changes can be heritable and often are. Strictly speaking, epigenetics involves changes in methylation, histone modification and/or alterations in non-coding RNA that affect transcription. Epigenetics is the way our genome adapts to environmental circumstances and prepares our offspring to do the same. The majority of epigenetic work focuses on genomic changes. That is, those variables that affect gene expression from the cell nucleus or nDNA. There is a growing body of evidence, however, that mitochondrial DNA (mtDNA) are affected by epigenetic factors in much the same way as nDNA. In fact, given the mitochondria’s role in cell survival, one might suspect that mitochondria are more susceptible to environmental epigenetics, perhaps even the first responders and/or the initiators of chromosomal genetic changes.

Considering that nDNA accounts for over 90% of the proteins involved in mitochondrial functioning, how could damaged mitochondria, even functionally inefficient mitochondria, not affect gene expression in the cell’s nucleus? Though we tend to think of mitochondria as self-contained and discrete entities, black boxes of sorts, where stuff goes in and ATP magically comes out, this is not only not the case, it seems biologically illogical to think that way. So much of mitochondrial functioning is related to its environmental milieu. In fact, increasingly researchers are finding that the mitochondria are the center of the organismal universe, sensing and signaling danger, and effectively, regulating all adaptive responses, including epigenetic modification of the proteins encoded by the cell nucleus.

Beyond the strict definition of epigenetics, it seems to me that any factor that altered mitochondrial function, would eventually alter gene expression by any number of mechanisms, not just the direct ones. That is, because the mitochondria produce the energy required for cell survival, anything that derails their capacity to produce ATP, pharmaceutical and environmental chemicals, for example, should be considered, ipso facto, epigenetic modulators. Energy is a fundamental requirement for life. How could energy depletion not affect gene expression? It does, and now we know how.

Starve the Mitochondria, Alter the Genome

It turns out, when the mitochondria are starving and/or damaged the key enzyme complex that sits atop the entire energy production pathway and is critical for the production of the substrates involved directly (yes, I said directly) with gene expression, migrates from the mitochondria across the cell and into the cell’s nucleus where it then sets up shop and begins its work there. Sit with that for a minute. The entire enzyme complex decides that things are not working where it is, so it hitches a ride with some transporter proteins, several of them along the way, to find a more suitable home. The enzyme complex ‘knows’ that its functions are critical for survival and so it must move or die. What an incredible bit of adaptive capacity. A symbiosis, if you will.

To make matters even more interesting, the traveling enzyme complex just so happens to be the pyruvate dehydrogenase complex (PDC) and you guessed it, the PDC is highly, and I mean highly, thiamine dependent. But wait, there’s more. Several other enzymes involved in mitochondrial bioenergetics are also thiamine dependent. These include: alpha-ketoglutarate dehydrogenase (α- KGDH) in the tricarboxylic acid (TCA) or citric acid cycle, transketolase (TKT) within the pentose phosphate pathway (PPP), the branched chain alpha-keto acid dehydrogenase complex (BCKDC) involved in amino acid catabolism and, more recently, thiamine has be identified as a co-factor in fatty acid metabolism via an enzyme called 2-hydroxyacyl-CoA lyase (HACL1) in the peroxisomes (organelles that break down fatty acids before transporting them to the mitochondria). So thiamine deficiency is problematic. It not only causes dysfunction in the mitochondria, reducing bioenergetic capacity, but if severe enough and/or chronic, it alters the genome. And those changes are likely heritable. That is, your thiamine deficiency likely will affect your children’s ability to process thiamine.

Thiamine Deficiency and Gene Expression

Without sufficient thiamine, the PDC enzyme complex does not function well and because of its geographic position at the entry point into the citric acid cycle, when it is not working at capacity, everything below it eventually grinds to a halt resulting in severe neurological and neuromuscular deficits. Absent congenital PDC disorders, however, when it simply is inefficient or starved for its cofactors, metabolic disorders ensue because we cannot convert carbohydrates into ATP and the sugars that normally would be converted into energy, remain unmetabolized, floating around outside the cells and causing the whole cascade of effects that mark type 2 diabetes. When the PDC is inefficient, ATP levels wane and fatigue ensues. Systems that are highly energy dependent are hit the hardest. Think brain, heart, muscles, GI tract. When mitochondria are inefficient or damaged, reactive oxygen species (ROS) increase. Anti-oxidant capacity decreases and further damage to the PDC ensues. Inflammation increases, immune function decreases. Cell level hypoxia grows. Alternative energy pathways are activated, those that are endemic of cancer. Yes, cancer can be considered a metabolic disorder.

When the PDC is inefficient, mtDNA heteroplasmy, the balance between mutated mtDNA and healthy mtDNA grows with each mitogenic cycle. This, of course, further derails mitochondrial capacity (and increases the need for thiamine). Absent available resources, mitochondrial death cascades are initiated. And now, we know at some point in this disease and death spiral, when ATP diminishes and the litany of adaptive measures fail to maintain sufficient energy availability, the PDC up and leaves its mitochondrion and sets up shop in the cell nucleus, in what is presumably a last ditch effort to save its cell and the organism as a whole. What a remarkable bit of adaptive capacity.

The researchers, who discovered this, ruled out the possibility that the PDC enzyme complex was already in the cell nucleus. It wasn’t. It traveled by way of several transporter proteins. They also found that once in the nucleus, it began producing acetyl-coenzyme A (CoA). Acetyl-CoA is requisite for the acetylation and deacetylation of histones, post translational changes in DNA, but also lysine acetylation, which further affects metabolism – mitochondrial energy homeostasis. With insufficient acetyl-CoA and insufficient acetylation, DNA replication is aberrant. Moreover, without sufficient acetyl-CoA, acetylcholine synthesis, an incredibly important transmitter for nervous system functioning, diminishes.

A Constitutively Active Enzyme: What Could Possibly Go Wrong?

Even more interesting, the PDC in the cell nucleus appears to be constitutively active. Unlike in healthy mitochondria where checks and balances prevail, when the PDC travels to the nucleus it has no feedback control to temper its activity. The enzymes that normally shut down PDC production (pyruvate dehyrodgenase kinase) in the mitochondria, were not present in the cell nucleus, and thus, once the PDC was turned on, it stayed on. That means when the PDC translocates to the cell nucleus it operates independently much like a Warburg effect in cancer metabolism; one that fully supplants healthier metabolic pathways. Can you say tumorogenesis?

This research has enormous implications for everything from cancer to Alzheimer’s disease and everything in between that involves metabolic disturbances like diabetes and heart disease. Metabolism begins and ends with the mitochondria, at the PDC, and the PDC is highly dependent on thiamine. Every pharmaceutical and environmental chemical damages the mitochondria in some manner or another and that damage inevitably reduces ATP capacity. Some chemicals also deplete thiamine directly, thus downregulating the activity of the PDC and the other thiamine dependent enzymes. Even when these chemicals don’t deplete thiamine directly, the western diet is more often than not thiamine deficient, sometimes only marginally, others time quite significantly so with symptoms already expressed, but very rarely recognized. We have known that thiamine was critical for health and survival for some time. Now we have one more reason to tread carefully with lifestyles and exposures that deplete thiamine.

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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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David Goodsell, CC BY 3.0, via Wikimedia Commons

This article was first published on April 25, 2017.

About TTFD: A Thiamine Derivative

by Derrick Lonsdale MD, FACN, CNS

Published on March 21, 2018

64707 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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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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Image by Alexa from Pixabay.

thiamine deficiency - Page 10

Hypersensitivity, Intolerance, and the Vagus Nerve

Eosinophilic Esophagitis (EoE) and Asthma

Comorbidity in EoE

Inefficient Brain Oxidation, Dysautonomia, and Thiamine

The Dysautonomia of Asthma

Thiamine Derivatives

TTFD and Epilepsy

A New Approach to Medicine

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Migraine Precipitants

Hypoxia, Pseudo-hypoxia, and Migraine

Autonomic Asymmetry

Migraine and Diet

Conclusion

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Medical History

Major Life Stressors and Emerging Problems with Nutrient Absorption

More Digestive Problems

Catatonia-like Episodes upon Eating

Left Temple Headaches, Migraines with Visual Aura, and Cognitive Deficits

Diet and Malnutrition

Other Weird Symptoms

Visual Disturbances

Migraines With Aura

Allergy Shots and More Symptoms: Ophthalmoplegia, Dizziness, Speech Impairment

Medication Reactions

Thiamine Pyrophosphate Order Delayed

Ran out of Thiamine AGAIN!

Genetic Testing

Medications and Supplements

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Publisher Discount

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Heart Disease and Beriberi: Case Stories

Recognizing Vitamin Deficiencies in Disease

Recent Reports of Thiamine’s Role in Clinical Care

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Years of Pain, Fatigue, and Weird Symptoms

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The Missing Pieces: HACL1 and Phytanic Acid

Possible Secondary Pellagra

Going Forward: More Questions

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Epigenetics: How the Cells Adapt to the Environment

Starve the Mitochondria, Alter the Genome

Thiamine Deficiency and Gene Expression

A Constitutively Active Enzyme: What Could Possibly Go Wrong?

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History of Thiamine Research

What is TTFD?

Clinical Benefits of TTFD

Conclusion

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