thiamine deficiency

Diet and Medication Induced Thiamine Deficiency – Dry Beriberi

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I am 41 years old and experiencing weird, scary, and upsetting symptoms that began a year and half ago. I have numbness in my feet that has moved up into my calf and super tight calves, ankles and feet. I have peripheral neuropathy, carpal tunnel symptoms, circulation issues without swelling and some sciatica like symptoms with achiness in my legs. I am exhausted all of the time, have no energy and symptoms of depression, but I am not depressed other than these health issues. I am overly irritable and always cold. My hair is falling out and I become dizzy when I standup from a sitting position.

In the past, I believe at some point I had insulin resistance but was never diagnosed. I did, however, have issues with my blood sugar. I was put on Metformin for 6 years, during which time I had a lot of stomach issues, nausea, and diarrhea. I was never a big drinker at all, nor did I use tobacco. I was under a ton of stress for many years though. Despite the stress, I was always healthy and worked out, ran on a treadmill, and was active. I worked as a nanny 55 hours a week.

My diet before metformin was not the greatest with lots of carbs and processed foods. I may have had a thiamine deficiency back then and but did not know about it. No one ever tested me for thiamine until recently. A lot of my symptoms started at a time where I was dealing with some heavy things, so I believe stress was definitely involved. For the past three years, I have not been on medication. Currently, I eat a low carb/keto diet and my A1c is 5.2 and insulin is 3.

Discovering Thiamine Deficiency

I started to experience these symptoms about a year and a half ago. I have tried many things to feel better and help with my symptoms and nothing has worked. Of the nutrient testing that I have had, my thiamine was low. It was 66nmol/L. The reference range was 78-185nmol/L. My vitamin D was barely above the deficiency range at 30ng/mL, my methylmalonic acid was on the low end of the range at 107nmol/L (range 87-318), and my vitamin B6 was high at 29.5ng/mL (range 2.1-21.7). Nothing was discussed regarding the other low vitamins and high B6. I was, however, told by my neurologist to take 100mg a day of vitamin B1/thiamine. She never indicated that this was the reason for my symptoms though.

I began doing my own research and found that I had all of the classic symptoms of dry beriberi – thiamine deficiency that affects the nerves. In other words, my symptoms were related to thiamine deficiency. I began supplementing with Benfotiamine 600mg a day am taking magnesium (Optimum health) at 150×2= 300 at night. My FM doctor said my magnesium was at 4.5 and they like to see it at 5.3. I also take vitamin D3/K2. My vitamin d was on the low side.

When I began supplementing with thiamine at 100mg per day and the Benfotiamine, I notice I was not as tired or fatigued. I was feeling pretty weak there, and I feel better, but the nerve issues have not changed.

Six weeks after finding out I had a thiamine deficiency, I got bloodwork from my FM doctor and my thiamine was now too high, almost as if I wasn’t absorbing it. I should mention that the second test was a plasma test while the first test was done from the serum. From what I have learned, plasma thiamine measures are less accurate. Even so, should I be worried?

My FM doctor wants to test again for Lyme disease. Beyond that, I just don’t know what else to do to resolve the nerve issues. Thank you!

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

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This story was published originally on October 5, 2023.

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Post Lupron Mitochondrial Collapse: A Case Story

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Dr. Marrs and I became aware of the symptoms and some of the laboratory results in a 38 year old woman. We wish to describe the case because it represents what should be an entirely new approach to medicine in general.

Before Lupron

The patient had been an active 38-year-old woman caring for her home and two children, ages 7 and 9 that were her focus, prior to Lupron. She had walked her dog daily, worked out at the gym twice a week and she had renovated her home in the summer of 2017. She had had her gallbladder removed in 2016, said to be because of a polyp. She had received allergy shots once a month for a couple of years. She took birth-control pills. Her history revealed that she had had a severe reaction to penicillin as a child, resulting in a rash and joint swelling causing inability to walk for a short time. She also had a history of frequent sinus infections and antibiotic treatment. In 2017, she began experiencing heavy menstrual bleeding and hysterectomy was recommended. She refused this and a second doctor recommended Lupron in an attempt to change her hormonal balance before hysterectomy.

After Lupron

She had received an injection of Lupron into her left hip and side effects, beginning within a few days, included:

  • Fatigue
  • Skin redness
  • Severe weakness in the legs, and tingling in the left side of the head and right leg.
  • A few days later she developed severe headaches and vomiting.

An initial estradiol patch caused no improvement, so another one at double the dose was prescribed with some improvement (presumably in menses).  By November 2017 the patches were discontinued. She began to experience

  • Joint pain
  • Pain throughout her body
  • Nervousness
  • Shaking
  • Panic attacks
  • Changes in personality.
  • In December she experienced cyclic vomiting and weight loss.

The estrogen patches were prescribed again. She saw an endocrinologist and some laboratory tests were abnormal, including what was described as a borderline high blood glucose.

These symptoms continued and in February 2018, three drugs were prescribed (Celexa, Neurontin, Ambien). They were discontinued two weeks later because there was no relief of symptoms.

In March, she experienced severe fatigue and had episodes of difficulty in walking which were intermittent and described as “almost like being paralyzed”.

In April, she saw a geneticist and some lab tests were performed that I will comment on shortly. A diagnosis of fibromyalgia and possible chronic fatigue syndrome were each entertained. The endocrinologist said that test results indicated that she was not producing estrogen or progesterone.

Based upon conversations with us, she began supplements of thiamine, fish oil, alpha lipoic acid, B complex, folinic acid, ferrous sulfate and methyl B12. Estradiol patches were resumed. We suggested the use of intravenous water-soluble vitamins, since Dr. Marrs and I agreed that giving the nutrients by mouth probably could not reach the necessary concentration of vitamin therapy needed. This was not followed through on by her current physician.

Discussion of Symptoms and Side Effects

The patient’s medical history indicated that she had experienced many different symptoms throughout her life. These included a severe reaction from penicillin and multiple sinus infections. The side effects from Lupron were fatigue, leg weakness, headaches, general body pain, panic attacks and cyclic vomiting. In other words, she had been a classic “problem patient” to her physicians. Since the symptoms could not be defined by usual and customary laboratory evidence the general conclusion was repeatedly that this was evidence of psychosomatic disease. Curiously, this common diagnosis in modern medical circles appears to be that the patient is thought of as inventing her symptoms neurotically without ever considering an underlying mechanism. Even worse, polysymptomatic disease of this nature is usually experienced by the brightest and the best. This is because high intelligence is developed within a brain which is more energy consuming than that of a less intelligent person. Such individuals are much more prone to unforeseen stress events, making them more susceptible to side effects from medication and inoculations. A car engine uses more energy to climb a hill. Stresses that we meet in life are like “hills to be climbed” and involve a commensurate supply of energy.

Laboratory Results: Low Amino Acids, Vitamin Deficiency and Defective Energy Metabolism

Many tests were performed on this patient. Two amino acid tests were performed, one measuring the amino acids found in blood plasma, the other measuring those excreted in urine. A word of explanation is necessary. Amino acids are the building blocks of proteins in the body and finding a given amino acid in very low or unusually high concentration can be used to define important aspects of body chemistry. Of 34 amino acids recorded in the plasma of this patient, aspartic acid, serine, ethanolamine, and tyrosine were severely decreased, while glutamine, histidine, alanine, ethanolamine and tyrosine were severely decreased in urine. All the others were in their expected normal concentration.

Amino acids are used in the body to create proteins, and this is an energy consuming mechanism. One of the deficient amino acids was aspartic acid whose metabolism is important in a mechanism known as transamination. The enzyme that carries out this function requires vitamin B6.

Two of them, ethanolamine and serine, play an important part in transmethylation, a mechanism that is dependent on folate and B12.

The fourth one was tyrosine and it is involved in the synthesis of thyroid hormone.

These low levels suggested that their respective vitamin dependent mechanisms were at fault. Since all the vitamins involved are water-soluble, it invited their administration by intravenous infusion. However, because they were energy dependent reactions, it is likely to construe the possibility that the underlying common fault was energy synthesis.

Was there any evidence from these laboratory results for defective energy metabolism? Yes.

Isocitric and citric acids were reported to be low in the urine and they are vital metabolites in the citric acid cycle, the “engine” of the cell. Also, there was a deficiency of pyruvic acid and this is the fuel that enables the citric acid cycle to function. This constituted strong evidence for energy deficiency with its major effect on the brain and nervous system.

Mitochondrial Energy Synthesis

Our bodies consist of 70 to 100 trillion cells that are being broken down and reconstructed throughout life. Relatively simple molecules are acted on by enzymes in a series of chemical reactions known by biochemists as “pathways”. Each enzyme requires a vitamin and/or essential mineral that assists the action of the enzyme and are known as cofactors to the enzyme. Several pathways reflect the synthesis of energy that is stored in the cell as ATP (adenosine triphosphate). ATP is a little like a battery that is being continuously charged and discharged and most of this occurs in the mitochondria. All the other pathways consume energy, either in enabling function or rebuilding cells. They might be compared loosely to the transmission in an automobile. In other words, the healthy body functions because energy synthesis meets energy demand. The abnormally low amino acids each could be used to suggest a defect in the energy consuming pathways and possibly a reflection of missing cofactors, making the “transmission” defective.

Vitamin Cofactors, Energy Deficiency, and Symptomology

The symptoms expressed by this unfortunate patient pointed strongly to cofactor deficiencies derived from diet that could easily be tested by their administration and clinical effect. The net effect is produced by a gap between energy synthesis and its utilization to meet the stresses of life in general. The administration of cofactors does not necessarily answer the underlying question because of the possibility of unknown genetically determined factors. However, it is safe, non-toxic, may have an epigenetic effect and is relatively cheap. It therefore should be the first approach. The greater the urgency or the severity of symptoms, the stronger the indication for intravenous administration of all the water-soluble vitamins. I have successfully treated many polysymptomatic patients this way, suggesting that mitochondrial function is as much an acquired disease as well as being genetically determined.

A Note About Oxidants and Antioxidants

Think of the body as a machine that consumes fuel by uniting it with oxygen to produce energy. This combination is called oxidation. Like a fire or any form of burning, it can be slow or fast and cellular oxidation seeks an intermediate level. If the oxidation is too slow, energy production is imperiled. If it is too fast or too vigorous, oxygen atoms are “thrown out” of the oxidation process like sparks are thrown out of a vigorously burning fire. These are referred to as “free oxygen radicals”. Like sparks from a fire, they can do damage. Some vitamins act to assist or accelerate oxidation, an example being B complex. They are known as oxidants. Others quench the free oxygen radicals (sparks) and are known as antioxidants. Vitamins C and E are examples.

Without going into the highly technical details, thiamine acts as an oxidant and an antioxidant, thus increasing its importance in metabolism. From this it is easy to see the essential importance of these substances that are obtained from naturally occurring foods and why their deficiency causes disease. Of course, we have known this for a long time, but current medical belief is fixed in the concept that “vitamin deficiency disease has been conquered and the resultant diseases are only of historical interest”. For example, this patient had “borderline high glucose”, something that would occur in the thiamine deficiency disease beriberi. She also had frequent “infections”, now known to be related to free oxygen radical production, indicating that her regulation of metabolism was extremely inefficient. The  amino acids that were extremely low in the plasma and urine could be used to interpret the possibility of missing cofactors, reflecting a chaotic state of metabolism. I must end this by saying that the use of vitamins and minerals in this manner is not (repeat not) simple vitamin replacement. We believe that the vitamin/mineral combination used in high-doses is resuscitating the activity of the corresponding enzyme and it is therefore acting as a drug. Identifying the underlying biochemical lesion is the essential nature of future diagnosis.

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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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Share Your Story

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Image Credit: Image by Steve Buissinne from Pixabay

This article was published originally on July 25, 2018. 

Rest in peace Derrick Lonsdale, May 2024.

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From Mother to Daughter: The Legacy of Undiagnosed Vitamin Deficiencies

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This is a story of a mother with undiagnosed vitamin B deficiencies who gave birth to a daughter who was also born with undiagnosed vitamin B deficiencies. In the eyes of conventional doctors and labs, there was not much wrong with us, but we knew that life was harder than it should be. We lived managing debilitating dizziness, daily migraines, fibromyalgia pain, chronic fatigue, allergies, hormonal changes, anxiety, and depression. Until we discovered that we were both hypermobile with histamine issues, hypoglycemic, and had many vitamin B deficiencies. The biggest challenge was for my daughter to start taking thiamine (vitamin B1). Her heart rate was all over the place and she had such a bad paradoxical reaction to thiamine that we believe she had been living with undiagnosed beriberi along with POTS.

Mom’s Health Marked by Asthma, Anxiety, Migraines, and a Difficult Pregnancy

All I remember as a child is being afraid to talk in school even if I knew the answer to a question. I had allergies and could not exercise due to asthma. During college, I had to read over and over the same thing because I could not concentrate. I worked extremely hard because the fear of failure was too much to bear. I started to have hormonal imbalances and missing periods. I successfully finished college and moved away to another state. That is when migraines started. Later, I became pregnant with my first child and started having blood clots. Anxiety and depression would come and go with hormonal changes.

When I was pregnant with my second child, my daughter, I was sick every morning with nausea.  After 6 months of pregnancy, I had gained only 6 pounds. Ultrasounds showed that the baby was growing normally, but I was losing weight. At that point, I also could see blood clots on my leg. I was placed on bed rest. By the 8th month, my water broke and my daughter was born. She was jaundiced and placed under UV light for a week. I also stayed in the hospital for a week dehydrated, with blood clots, and with the “baby blues”. We left the hospital after a week, and she had a “normal” development. However, you could see that she was a baby that would not go with anyone, not even the people close to us, indicating some anxiety.

Daughter’s Early Health Issues: Selective Mutism, Asthma, Concentration Issues

When my daughter turned four years old, we moved out of state and that is when she stopped talking outside the house. I later found out that it is called selective mutism, a form of severe social anxiety. She started seeing a school counselor to try to help with her anxiety and self-esteem issues. I brought a girl scout group to my house so that she could start having friends and talk to others in her area of comfort. She also developed asthma and needed nebulizer/albuterol treatments frequently and daily QVAR for prevention. She was given Singulair, but it made her very depressed. Her grades in all classes were all over, from A to D.  She would spend the whole time after school trying to complete homework, but she couldn’t. Her teacher told me that she really did not have that much homework. I would ask her to watch the dog eating and to take her outside as soon as the dog finished but she would be wandering around the kitchen and could not pay attention to the dog. Her neurologist gave her Strattera and that helped a little. Her EGG also showed some abnormal activity. The doctor recommended anti-seizure medicine and said that she was probably having mal-petit seizures. I refused medication based on how she reacted to Singulair and because the doctors were using words like “probably” and “just in case”. I kept an eye on her and noticed when she ate ice cream and got asthma. I had her stop sugars and dairy.  Soon after that, a teacher called me, excited to tell me that my daughter was talking at school. She also was able to stop all asthma medication except for 2 weeks every year when seasonal allergies would hit. At this point, it had been already four years since she stopped talking outside our house. She started excelling in all classes and we were able to stop Strattera. However, the continuous anxiety remained.

The Teenage Years: Continuous Migraine, More Medications, and No Answers

At 16 years old, she got a cold that turned into asthma with a continuous headache that just would not go away. She started waking up every day with a migraine, depressed with no energy. We had to wait three months to see a pediatric neurologist. Meanwhile, I would take her to my chiropractor early in the morning, give her an Excedrin, and she would go to school whenever she felt better. She began drinking at least 2 cups of coffee every day to help with the pain. Sometimes she would go to school at 11am, sometimes at 1pm. Even if there was just one class left, she would go to school. At this point, she felt that she wouldn’t have a future.

When we finally went to the neurologist, he recommended amitriptyline. I had been on amitriptyline and woke up one day not knowing which year or season was, but I was told that the issue was the high dose given to me (125mg), after decades of it increasing it every year. I agreed as long as it was a low dose.  Amitriptyline lessened the continuous headache, but it was not really gone, and she still needed some Excedrin. She started daily aspirin as well. She was just getting by day to day trying to manage her pain and mood and trying to have a normal teenage life.

Increasing Weakness When Outdoors: Untangling Root Causes

She became very weak whenever we would go to the beach or to a park. We would have to drag her indoors and give her water. On some occasions, she would say that she could not see. Somehow, she successfully managed to graduate from high school. We started seeing functional doctors. We found that she had some variants related to mitochondria dysfunction, but we really didn’t know how to address this. We also found out that she had Hashimoto’s and antibodies against intrinsic factors, which was indicative of pernicious anemia. We knew right there, that she had issues that conventional doctors had missed.

We also did a Dutch test and found that all of her hormones were high. The functional doctors suggested sublingual B12, folinic acid, and a B complex. She said the vitamins made her feel awake for the first time. However, chronic fatigue was still a major struggle for her. Eventually, she had to stop folinic acid because it made her depressed and unmotivated. Meanwhile, she managed her anxiety with herbs, but it was a real struggle.  She also continued to have asthma requiring albuterol every fall season. She chose a very challenging career in cell biology with biochemistry. She went through college with many cups of coffee just to control migraines, have energy, and be alert.

Discovering Her POTS Symptoms

The summer of 2019, before her senior year of college, the nurse checked her vitals as part of her new summer internship. The nurse thought the pulse monitor was broken because her heart rate was 120 sitting down. After a few minutes, it went down to 99, so the nurse dismissed it. When she told me that, I started paying attention to her heart rate. We went to her physician and neurologist and in both instances, her heart rate was 100, just sitting down waiting for the doctor. I asked if it was normal, and they said that it was in the upper range but not a concern. I was still concerned and made an appointment with a cardiologist but also bought her an iwatch. She noticed right away how her standing heart rate would be over 100, and by only taking a few steps, her heart rate would go even higher and she would become fatigued and even dizzy. From the heart rate monitor on her iwatch, we could see how quickly her heart rate would climb upon standing and then slow a bit when sitting.

That is when I remember that I have read about POTS and hypermobile people. I remember that when she was a child, the neurologist had said that she was hypermobile, but never said that it could be a problem for her. It just seemed like a fun thing to have. I started asking in health groups and someone mentioned that her medications could also cause high heart rate. I searched and amitriptyline did have that side effect.  That is when my daughter showed me that her resting heart rate was in the 90s and it would fluctuate from 29 to 205 without exercising. When we went to the cardiologist and explained all of this, he said that he did not even know how to diagnose POTS because it is rare. He did testing and said that the heart was fine but there was some inefficiency due to some valve leaking but that it usually does not cause symptoms. I asked about amitriptyline and he confirmed that it could raise heart rate.  At that point, she stopped amitriptyline and her maximum heart rate was 180 instead of 205.

She went back to her last year of college when Covid hit. She came back home and we could see the lack of energy and how much doing any little thing or stress would crash her for days. Since I needed glutathione for chemical sensitivities, I decided to see if it would help her. Glutathione with co-factors helped her recover, instead of crashing for days, she would recover the next day. That is when she told me that every time she walked to school, she felt that she would pass out. When she gets up in the morning, she ends up lying on the floor because of dizziness. Despite her dizziness, daily muscle pain, daily migraines, and chronic fatigue, she had big dreams. She just kept pushing through day by day, with coffee, herbs, and whatever it took, but she knew that something had to change. She successfully graduated in May, Magna Cum Laude, and she had a couple of months to deal with her health before she would leave to start her graduate studies and research job. That is when I found people that knew about Dr. Marrs’ work and thiamine, and her life finally changed.

Introducing Thiamine and Other Micronutrients: Navigating the Paradox

A functional doctor recommended magnesium and niacin for her migraines and they significantly helped. This gave the functional doctor the idea to try tocotrienols. High doses of tocotrienols worked better for reducing her migraine pain than amitriptyline and aspirin combined. Then she started taking high doses of B6. This helped her muscle pain and improved her mobility. Despite being hypermobile, easy stretches gave her intense muscle cramps prior to starting B6. Guided by very knowledgeable researchers belonging to Dr. Marrs’ Facebook group, Understanding Mitochondrial Nutrients, we started Allithiamine. The first thing she said was “wait, the sun does not hurt?”.  I asked her what she meant.  She explained that all her life, being in the sun gave her pain in her eyes and forehead and that she couldn’t understand why people wanted to be outside. No wonder she never wanted to go outside. She also said her migraines were gone. We have waited 4 years to hear that!

After just a couple of days, she started having a lot of nausea and lower-intensity migraines returned.  The researchers knew right away that she needed more potassium. She started to eat apricots, coconut water, or orange juice every time she had nausea and it helped. However, it was happening every hour so we decided to try a different Thiamine. We tried half Lipothiamine and Benfotiamine but she didn’t feel as much benefit and still gave her issues. We went back to 1/10 of Allithiamine. Chatting with the researchers, one asked if she also experienced blinding episodes. Yes! Finally, someone that knew about that! They recommended B2 and we started it. That’s when we discovered that her pain in the sun and dizziness were caused by a B2 deficiency. She continued waking up with crashes needing potassium every hour. She did not sleep that week. The researchers suggested taking cofactors including the rest of the B vitamins, phosphate salts, phospholipids, and beef organs. Beef organs and phospholipids helped with energy and bloating, phosphate salts helped with nausea and irritability.

Then researchers suggested that she needed to stabilize sugars and have more meat. That is when we realized that she had some type of hypoglycemia. We had noticed that she would get very tired and got shaky hands if she didn’t eat. Functional doctors had mentioned that she may have reactive hypoglycemia since she had a fasting glucose of 70. She started having more meat to stabilize her sugars and removed all packaged foods, sugars, grains, and starches. She started having just fresh meat, veggies, rice, beans, nuts, and berries. She felt that she was so much better with beef that she started using it for potassium between meals and bedtime.

She was able to increase allithiamine little by little. She would mix a little bit with orange juice since it tasted so awful. Little by little, she started having fewer crashes and feeling better. It took a month for her to be able to tolerate one capsule of Allithiamine. She was sleeping more but not the whole night. That is when our functional doctor suggested supporting adrenals. That really helped but then she began having stomach pain and nausea after eating beef and developed frequent diarrhea. Chicken always increased her hunger and reduced her energy compared to beef and but now she was afraid of having beef. She stopped all sources of beef and phospholipids.

We consulted a very good functional doctor. She did Nutraeval and confirmed that all her B vitamins were low or deficient and recommended TUDCA and Calcium D Glucarate along with trying lamb and bison first. Both helped in reducing bloating/nausea and she was able to start eating lamb and bison along with reintroducing a minimal amount of carbs. Soon after, she was eating beef again with no pain.  After starting TUDCA, her bilirubin levels were normal for the first time in her life. We continued to work with the functional doctor to fix other deficiencies.

Recovery from Multiple Nutrient Deficiencies and the Prospect of a Normal Life

After Allithiamine and vitamin B2, we worked with our functional doctor to balance the remaining B vitamins. She is now able to go out in the sun without bothering her eyes and without passing out. She gained weight after starting the B vitamins and began looking healthier, compared to how skinny and underdeveloped she looked before. She also learned how to manage electrolytes. She sometimes needs more sodium, but other times needs more potassium. She feels sick when electrolytes get out of balance. Although she still had some continuous pressure in her head, she no longer needs any amitriptyline, aspirin, or Excedrin for pain. One thing that remained problematic was folate deficiency. She still became depressed with folinic acid, so she tried methylfolate instead. She felt so unmotivated that preferred not to have it, but she realized that it was key to something that she struggled with all her life: anxiety. She figured that she could have methylfolate every other day, so that she could have less anxiety.

Now, for the first time, she began to have a normal life. She can now exercise daily without dizziness and her heart rate skyrocketing.  Her heart rate in general is more normal, doesn’t go down to 29 or up to 205. She had not had any asthma requiring albuterol.  She started driving without having to deal with anxiety and panic attacks.  She was able to walk to her office without fainting.  She now can now live alone dealing with the stress of having a full-time job, graduate classes, cooking her food, and exercise every day! She is not cured completely but for a person that once thought she couldn’t have a future, she is doing pretty darned good!

We Need Your Help

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

Yes, I would like to support Hormones Matter.

This article was published originally on July 22, 2021. 

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Thiamine Testing in Clinical Practice

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In Thiamine Deficiency in Modern Medical Practice and Threats to Thiamine Sufficiency in the 21st Century, I introduced the concept that thiamine deficiency underlies many common conditions plaguing modern healthcare and identified exposures and mechanisms threatening thiamine stability. In Hyperglycemia and Low Thiamine: Gateways to Modern Disease, I summarized the pattern of metabolic changes associated with modern dietary practices that lead to thiamine insufficiency, hyperglycemia, diabetes, cardiovascular and Alzheimer’s disease. In this document, I will tackle thiamine testing.

Background

As discussed in the previous articles and elsewhere on this website, thiamine is a critical and rate-limiting nutrient for several of the cytosolic and mitochondrial enzymes responsible for the conversion of food into cellular energy or ATP. As such, decrements in thiamine ingestion imperil cell function systemically, leading to the onset, maintenance, and/or exacerbation of a host of illnesses.

Thiamine has a short half-life, 1-12 hours, and absent sufficient and/or regular consumption, thiamine reserves will be depleted entirely within 2-3 weeks. The risk of acute deficiency is common after an extended illness where consumption or absorption is reduced, while excretion or metabolism is increased. This includes any illness where nausea, vomiting, and/or diarrhea are present; where intestinal absorption is compromised, such as with Crohn’s, Celiac, constipation, dysbiosis, or gastric bypass; where excretion is increased such as with diabetes and kidney disease; where fever or the severity of the illness increases the demands of metabolism e.g. hypermetabolic states such as sepsis, burn patients, and in critical care cases more broadly where the metabolic demands of the illness itself and the anti-thiamine qualities of many medications overwhelm thiamine availability. Pregnancy, especially when hyperemesis is involved, should also be considered a hypermetabolic state where thiamine deficiency develops more frequently than recognized and is associated with common complications.

Of the studies that have investigated thiamine deficiency in critical care, the incidence range for deficiency varies by study criteria from 10% to 90% upon admission and increases steadily with each day in the ICU. This suggests that even if the patient is not thiamine deficient upon admission, he/she may become so as time progresses.

The progression to severe thiamine deficiency in the face of critical illness will be expedited if the patient’s premorbid health was challenged by chronic illness that included the use of thiamine-depleting medications, and/or where poor diet and chronic alcohol, drug, or tobacco use were present. Subclinical thiamine deficiency or insufficiency may characterize a majority of patients dealing with chronic illness. It is not well defined, but given the chemistry of thiamine against the backdrop of modern diets and medicines, it is logical to presume that many patients dealing with chronic illness consume insufficient thiamine relative to the demands of their metabolism and are but one crisis away from frank deficiency (see Threats and Hyperglycemia documents for details).

Ideally, the recognition and treatment of thiamine insufficiency would be considered before frank deficiency manifests. Unfortunately, current laboratory testing provides neither guidance on subclinical thiamine deficiency or insufficiency nor consistent definitions of what values constitute frank deficiency. As such, a patient tested at one lab may be considered deficient, while at another, may fall within the normative ranges, even if each lab uses the same methods. Similarly, depending upon the testing equipment and methods, the patient’s thiamine status may be more or less sensitive to recent thiamine intake or other confounding variables that skew the results towards sufficiency when in fact the patient is deficient.

Conventional Methods of Measurement

For clinical purposes, the most important thiamine analyte is thiamine pyrophosphate (TPP), also called thiamine diphosphate (ThDP/TDP). Additional phosphates can be added or subtracted to form thiamine triphosphate (TTP/ThTP) and thiamine monophosphate (TMP/ThMP), which are detectable by different laboratory measures, but as of yet, their utility in the clinic has not been fully extrapolated. It should be noted that the phosphorylation of free thiamine into TPP, requires magnesium and ATP, and so, among the factors that will affect TPP values is magnesium deficiency.

Thiamine may be tested from whole blood, erythrocytes, serum, plasma, and urine. From whole blood, all three derivatives of free thiamine can be obtained. Thiamine pyrophosphate accounts for almost 90% of circulating thiamine, 80% of which, is found in erythrocytes. Free thiamine, TMP, and TTP are found primarily in serum, plasma, and urine.

Whole Blood TPP

Whole blood measures of TPP utilize liquid chromatography-tandem mass spectrometry (LC/MS/MS) or high-performance liquid chromatography (HPLC). In the US, the reference ranges TPP from two major labs, Quest Diagnostics, and LabCorp, are 78-185 nmol/L and 66.5−200.0 nmol/L, respectively. Both use LC/MS/MS. Published reference intervals for whole-blood TPP vary widely across labs, however, from a lower limit of 63–105 nmol/L to an upper limit of 171–229 nmol/L. There is no consensus regarding what value constitutes deficiency and little recognition of what may constitute borderline or insufficient thiamine. Under some conditions, TMP, TTP, and total thiamine values will be reported. There are no consistent reference ranges for these analytes either.

Erythrocyte Tests

Erythrocyte tests derived from whole blood samples may measure TPP directly from isolated erythrocytes, such as with HPLC, or indirectly, such as in the case of the erythrocyte transketolase activation test (ETKA). TPP measured erythrocytes using HPLC requires additional laboratory steps, mostly done for research purposes. Reports suggest that HPLC whole blood TPP and HPLC erythrocyte TPP correlate. Similarly, the research suggests that HPLC whole blood TPP and ETKA tests correspond, but there is much debate regarding which one is more accurate.

Unlike the direct assessment of circulating TPP, the ETKA test measures both basal and thiamine-stimulated activity of the thiamine-dependent enzyme transketolase. Test values are reported as a ratio or percentage of enzyme activation. When thiamine concentrations are sufficient, the addition of thiamine will not activate the transketolase enzyme. When thiamine is insufficient or deficient, transketolase activity will increase proportionately to the deficiency. Higher values correspond with the severity of deficiency.

Although there is no consensus regarding what constitutes deficiency for this test either, the continuum of values supports a gradation of need, which may be more useful clinically, particularly with borderline cases and when clinical symptoms correspond. Accordingly, greater than 17% enzyme activation is indicative of thiamine deficiency clinically whereas experimentally, particularly when comparing the sensitivity of different laboratory tools, >25% activation is considered deficient. It should be noted that the ETKA may correlate better with clinical conditions in thiamine-replete patients but may be problematic in patients with magnesium deficiency or when transketolase protein levels are diminished due to liver disease or diabetes.

The EKTA test was considered the gold standard for 50 years, but it is a time and manpower-intensive test, with a high risk for inter-batch variability. As such, and despite its favorable clinical utility, it has fallen out of favor. Currently, the EKTA test is performed only by research institutions and in a few private labs.

Plasma, Serum, and Urinary Tests

Plasma/serum contains only a small fraction of circulating thiamine relative to the erythrocytes and is sensitive to recent intake. As such, tests using plasma or serum are considered less accurate diagnostically but some labs still offer these tests. The reference range for Quest is 8-30 nmol/L.  More commonly, plasma measures of thiamine are used for research purposes. Similarly, urinary measures of free thiamine, TMP, and other thiamine metabolites are used in research protocols involving excretion rates relative to medication, deficiency states, and/or dietary intake.

Challenge Tests of Old

In the late 1960s, a pyruvic acid challenge test was devised to assess thiamine sufficiency in healthy pregnant and pre-eclamptic women. Much like the testing for gestational diabetes where blood glucose is measured before and after consuming glucose, with the pyruvic acid challenge test, blood pyruvic acid concentrations were measured before and after dextrose ingestion. Pyruvic acid is inversely correlated with thiamine status such that when thiamine is low, pyruvic acid increases.

While healthy women exhibited within range values of pyruvic acid concentrations for both fasted and the dextrose challenged portions of the test, pre-eclamptic women, depending upon the severity of the disease process, showed markedly elevated pyruvic concentrations post challenge. The most severely ill women, those hospitalized, had elevated pyruvic acid both pre and post dextrose challenge. Although, to my knowledge this test has not been used in other populations or for anything other research purposes, it illustrates clearly how thiamine deficiency is a sugar sensitive disease.  Should this type of testing be developed more fully, it could identify pending thiamine deficiency before it becomes testable via other methods.

To Test or Not To Test

Thiamine testing is a complicated topic. On the one hand, laboratory confirmation of thiamine deficiency aids in treatment decisions, but on the other, current testing, such as it is, carries the potential for a high false negative rate and may fail to detect anything but the most severe deficiencies. Since there is no consensus on what constitutes deficiency, much less insufficiency relative to diet, illness, or other metabolic variables that contribute to and precede frank deficiency, thiamine testing in some populations may prove unenlightening. In light of these issues, it is tempting to forego testing altogether and proceed directly to treatment based on clinical symptoms. Insofar as thiamine is a safe and essential, water-soluble nutrient, clinical suspicion may suffice and should suffice in acute cases where time is critical. To the extent that medicine strives to be data-driven, however, regular testing, before and during treatment, in conjunction with symptom tracking, may afford much needed insight on the relative value of thiamine in health and disease and may aid in the expansion and refinement of clinical reference ranges.

Postscript: Since this article was published originally, a new version of the transketolase test has been developed: the Erythrocyte Transketolase Activity Coefficient (ETKAC). It is being offered by the Clinical Immunology Laboratory, in North Chicago, IL.

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This article was published originally on May 9, 2024. 

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A Life of Low Thiamine Leading to Wernicke’s Encephalopathy

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severe thiamine deficiency Wernicke's Encephalopathy

I am a 40 year old male with recently diagnosed, but chronic, severe thiamine deficiency (plasma thiamine <6 nmol/L September 2025) – Wernicke’s Encephalitis. I have all of the classic symptoms like nystagmus, ataxia, and cognitive issues, along with a long list of other symptoms that have accrued over time. I have had a horrible diet since childhood, consisting mainly of fast food, and in my twenties, I drank a fair amount of alcohol. I have also had several bouts of food poisoning, including a c diff infection in August 2025. Antibiotics have been a mainstay since childhood. Once thiamine deficiency was recognized, I was given IM injections and told to supplement orally. I feel worse. Something is missing and I need help. Below is my case story. If there is anyone out there that can help, please comment.

Childhood Marked By Poor Diet, Infections, and Failure to Gain Weight

My youth was filled with many upper respiratory and ear infections that I was giving antibiotics for. I had a “fast metabolism” and could never manage to gain weight, no matter how much I ate. I never wanted to eat the healthy food that my mother would cook and always wanted candy and junk food. I would eat things like lucky charms, brown sugar and apple cinnamon instant oatmeal. By the time I reached high school, I was consuming fast food quite often, and then when I got into sports and weight lifting, I was consuming sugar-filled meal replacements, and protein supplements, and microwave meals.

At 16, I developed a rash on my hands every winter. It would crack and bleed and my joints became stiff. I later learned that this was eczema or psoriasis. I was given a corticosteroid cream. After high school, the rash continued to get worse, and never healed. When I was about 21 years old my hands were so stiff that I couldn’t bend my fingers. They were completely cracked and bleeding all over.

Along with this, my ears, and all of the cartilage in my body, turned solid. I wasn’t even able to flex my ears or ear lobe and every time breathed in it felt like I was being stabbed in my left lung. The doctor diagnosed me with relapsing polychondritis, pleurisy, and psoriasis. High dose corticosteroids and corticosteroid creams were prescribed.

The Poor Diet Continues: Heart Symptoms Emerge

In my twenties, I lived off of cheesesteak sandwiches, pizza pockets, French fries, and soft drinks. I only at couple meals a day and usually skipped breakfast. I worked, partied and fluctuated being not enough eating too much. I lost a bunch of weight and began losing my hair.

In my late twenties, I got a much better job with a lot more responsibility and a lot of stress but my diet was still horrible. I would skip breakfast and then gorge of double orders of fast food meals for lunch. I began gaining weight but I was going to the gym so I’d managed to build an unhealthy muscular physique.

At some point, I began having episodes where I would have my heart racing, chest pain, and other symptoms that felt like I was having a heart attack. Hospital visits concluded that these episodes were panic attacks, however, they did note that my cholesterol, and triglycerides were high.

A Healthier Diet But More Alcohol and More Unexplained Symptoms

In my thirties, I made some changes to my diet. I began eating a healthy breakfast but was still eating out for lunch and having large portions. I added in raw vegetable powders and multiple organ capsules to diet. I also began drinking more alcohol.

My psoriasis flared. I developed random internal vibration episodes and very subtle full body tremors, as well as being jolted awake in the middle of the night. I decided at this point it was time for a change. I tried to eliminate dairy, grains and gluten, chocolate, sugar with the hope that this would resolve my inflammatory issues. Unfortunately, it made matters worse, likely at least partially due to the alcohol consumption.

Magnesium Oxide, a Benzodiazepine and an SSRI

Within about a year, I had lost a significant amount of weight, ended up with significant sleep issues, increased anxiety, and had the worst brain fog of my life. I could not function properly at work and was losing my hair in significant amounts. I visited my doctor who was very well meaning and spent quite a bit of time trying to help. He found that my magnesium was low (1.6), so he gave me magnesium oxide as a prescription. This caused severe loose bowels and just made things worse.

He also told me that I had a genetic predisposition for high adrenaline, and proceeded to give me propranolol to calm that down, as well as a benzodiazepine and SSRI that would “help with my insomnia”. I was not depressed. I just couldn’t sleep and felt like I was in high gear all the time. Instead of doing research and because I trusted this doctor, I took the medication as he advised.

The SSRI made me want to crawl out of my skin, but the benzo allowed me to sleep 6-7 hours, stopped the tremors and being jolted awake. We went through three different SSRI’s until settling on Lexapro. I was on these for about a year until I actually did some research and learned how they were harming my body. I then decided to ween myself off. That process was brutal, with the feeling of brain zaps, worse tremors than before, and intense insomnia.

Brain Fog and Dizziness Worsen

Around this time, a friend and I started a snow removal company. The job was extremely physically demanding. I was out for 24+ hours at a time in freezing temperatures, not only in the truck, but also out shoveling and carrying around a 50lb buckets of salt to spread. I didn’t eat much while out, and lived off coffee, milk and orange juice. We also started going out on the road for weeks at a time, staying in hotels and working 12-16 hour days in food factories, repairing their equipment, and starving myself.  During this time, I experienced some of the worst brain fog I had ever felt. I couldn’t make sense of anything.

In 2016, I discovered the Ray Peat way of living. I eliminated a number of foods from my diet and began consuming a lot of coconut oil, ice cream, milk, orange juice, but at a significant calorie deficit. The diet made me weaker and I wasn’t able to keep up with the business. In 2017, I got a part time job at a grocery store, thinking it would be easier physically but beginning work at 4 am became problematic. The brain fog continued to worsen.

First Bout of Food Poisoning: Cipro and Flagyl Prescribed

Sometime between 2018-2019 I got campylobacter food poisoning from an undercooked burger. I was given Cipro and Flagyl. The Cipro caused joint inflammation and so they advised to discontinue it and finish the Flagyl. After these meds, I had a horrible time concentrating and completing department order at work. I was spaced out while driving, which even led to a couple auto accidents, more frequent tremors that even my girlfriend noticed, and I would randomly wake up with full on shaking, followed by nausea and vomiting. My magnesium still continued at the very bottom of the range, so I started using ReMag in an attempt to move the needle, which mostly just put me in the bathroom. I also started taking taurine, niacinamide, and thiamine HCl. My cholesterol and triglycerides were still elevated.

In 2020, I worked through COVID, as we were essential workers. Luckily, I did not get COVID at this point. I continued taking vitamins, taurine, magnesium, and began desiccated thyroid. I also ate bags of dried organic apricots and mangoes daily. They seemed to help with energy levels.

First COVID Infection and New Onset Food Allergies

In 2021, I began a new job and got COVID for the first time. At that time, I consuming a daily smoothie with full packs of frozen 365 organic strawberries, mangoes, dark sweet cherries, peaches, a cup of orange juice, and Mt. Capra casein protein. The casein protein exacerbated the brain fog. When I eliminated it, the brain fog wasn’t as bad. Odd because I was able to drink milk in the past, just not consume whey protein.

COVID hit hard and took me out for almost a month. I had fever, low O2, and high heart rate. I took aspirin every 4 hours and this seemed to lessen the symptoms pretty quickly. I spent most of my days in bed, eating scrambled eggs, butternut squash soup, chicken soup, and mozzarella cheese. Toward the end of the COVID infection, I developed excruciating pain in my left thigh. I thought it was a blood clot from lying in bed for too long, but an ultrasound ruled that out. The pain and COVID-related shortness of breath remained for about a month. After that everything was back to normal, except now I had food allergies. I could no longer eat the butternut squash soup nor could I eat mozzarella, or the sweet potatoes or French onion soup I would eat prior to getting sick.

Few Good Years with Thiamax Despite Another COVID Infection

Late 2021, I began taking Thiamax to replace the thiamine HCl I had been taking. When I began, I had a little extra brain fog, but I attributed it to the COVID. I also added methylene blue to the mason jar of orange juice I would take with me to work to sip on, along with great lakes collagen. Things started looking up. The brain fog started subsiding and I was able to function at work.

I continued to have the startle awake reactions and tremors. These mostly would happen if I tried to take a nap during the day. Any time I would start to fall asleep, I would be immediately jolted awake and then experience a full body vibrations sensation. This happened every time I started to nod off. I was thinking maybe it was due to the thyroid, but I was still at the very bottom of the level for magnesium when tested.

2022 Was fairly uneventful year, although I did catch COVID again. This time it was very mild and I was only out of work for less than a week. I had all sorts of allergies to food, but the brain fog seemed much improved. The startle awake and vibrations remained and my magnesium was still low.

In 2023, I was in ER early in the year with odd abdominal and back pain, nausea. I thought it could be food poisoning from daily Uber eats lunch orders. Some blood was found in urine. They said it was gastritis and to take Pepcid. The rest of the year was uneventful. I was still taking Thiamax and desiccated thyroid daily. My energy levels were better. I had less brain fog and my body temperature improved. Magnesium was still borderline low but calcium on many blood tests above 10.

Food Poisoning Again and More Antibiotics

Towards the end of October 2024, I got food poisoning again. This time it was salmonella. I had non-stop vomiting and loose bowels for over a week. I was prescribed Flagyl, but did not take it, and Cipro, which I took for 7 days, with gradually worsening joint pain and inflammation. Cipro was discontinued and replaced with Cefixime. A stool test one month later revealed that salmonella had colonized, and they would not give any additional antibiotics to help clear it up. From this point on into 2025, I never felt the same. I had also stopped the Thiamax and was only taking forefront health b-complex and forefront health desiccated thyroid. I was still borderline low magnesium.

The Downward Spiral

By early 2025, I had much worse brain fog, frequently lost train of thoughts, couldn’t concentrate at work, started getting odd reactions to ice cream, mashed potatoes and other foods. They would cause a full body itching, and internal vibrations when I would eat them. Constipation was the norm, and my doctor told me to take two magnesium oxide tablets a day to help, my gastroenterologist told me to take biscodyl daily to help. I started to have a constant feeling like my throat was inflamed.

In May, I was diagnosed with eosinophilic esophagitis. For the endoscopy, I was given propofol and fentanyl for anesthesia. It took over an hour to wake up from and the entire week following, I felt like I had just woke up from the anesthesia. A few weeks later, I was given high dose Omeprazole to correct the eosinophils. I was also advised to eliminate eggs, dairy, wheat, soy, fish, nuts, and corn from my diet.

In June, I received the results for the buccal swap Mitome profile. It showed 404% citrate synthase, normal Complex I, low-normal Complex II, low-normal Complex II-III, and low (24%) Complex IV.

I tried to start implementing the proposed protocol but it seemed to be causing more symptoms. I started tracking glucose, ketones and lactate daily per Chris Masterjohn’s recommendation. I was going out for daily walks and hitting around 8k steps.

A Tick Bite, More Antibiotics, and a C. Diff Infection

In July, I had a bullseye tick bite and the doctor prescribed doxycycline. The doxycycline causing worsening tremors and severe tinnitus, I stopped taking it, after which both began to subside. I was walking daily.

In early August of 2025, I went to the ER with nausea and vomiting. They sent me on my way after doing a CT with contrast and seeing inflammation of the stomach and intestines. They said it was the stomach flu and to stay hydrated. This persisted and worsened for a week and so I was admitted to the hospital. A stool test it was found that I had an active c.diff infection and was colonized with salmonella from the prior food poisoning. I was given ceftriaxone IV, and vancomycin oral.

In addition to the antibiotics, I was given IV’s with sodium chloride and lactated ringers and initially and I felt better. Then they switched over to D5NS, a saline solution that contains 5% dextrose and I felt worse again. Dextrose depletes thiamine and I was already malnourished and thiamine deficient. Nevertheless, within three days of my hospital admission, I was able to consume food by mouth again, around 2,100 calories per day consisting of burrito bowls for breakfast, lunch and dinner, that contained carnitas, rice, pinto beans. I walked the halls doing lunges and calf raises to stay as active as possible.

The morning I was to be discharged I was advised that my magnesium and potassium were both low and given two pills to correct those levels. Vitamin B1/thiamine was not checked. I was also given a 10 day dose of azithromycin.

Severe Thiamine Deficiency Lurking

At discharge, I felt very weak, had tingling and weakness in the legs and severe brain fog. That night at 6pm I took my dose of vancomycin, and my first dose of azithromycin. The next day, I awoke with severe digestive distress continuous diarrhea throughout the day. I returned to the emergency room feeling like I was dehydrated, but they stated that all of my levels were normal and I was discharged.

The following morning, I awoke again with severe digestive distress, and upon standing my heart rate spiked to over 160 beats per minute. I rushed to the kitchen and grabbed some Pedialyte, thinking it was just dehydration, but this made my heart rate beat faster and caused blurred vision. I thought I would faint and I felt an impending doom sensation like I was going to die.

I called 911, and medics arrived and proceeded to perform an EKG, which merely showed sinus tachycardia. They were unable to get my heart rate down in the ambulance, and upon arriving back to the emergency room, I was left to wait for 6 hours before I was able to get any fluids. When they attempted to draw my blood, my veins were flat and they weren’t able to get blood to flow into the vial. This would later become a trend, with blood vessels in the arms and hands constantly appearing shriveled and misshapen, and my mouth felt dry like sandpaper despite trying to drink water.

Oddly, my electrolytes all came back in normal range. My heart rate stayed around 110 to 120 beats per minute the entire wait even while seated in a wheelchair. When I was finally brought into the ER, I was given one large bag of sodium chloride administered rapidly. This initiated a weird sensation in my chest and uncontrollable coughing.

They took me for a CT scan with contrast, and then for a chest x-ray to check for fluid in my lungs, but found none. I was then given a bag of lactated ringers and my pulse began to normalize. During an orthostatic test, my pulse spiked over 100bpm upon standing. They gave me another bag of sodium chloride, performed another orthostatic test and my pulse remained under 100bpm. I was advised to discontinue the azithromycin, and my diagnosis was listed as severe dehydration.

After discharge, my legs were very weak and I had an odd internal vibration, buzzing sensation. My whole nervous system felt very irritated, worse than I ever experienced before. The nerves in my spine and lower back felt raw and like they were being poked. This and tremors, prevented sleeping. I also developed muffled hearing. I was switched from vancomycin to dificid 3 days later.

From that point on, I had worsening neurological symptoms, odd episodes of confusion while driving. I didn’t know where I was even though I was near home. If I looked in the mirror it felt like the room spun. I finished my round of dificid on September 1st.

Increased Need for Sodium and the Continued Downward Spiral

Since my hospital stay, I the only way to keep my heart rate somewhat normalized was to drink several electrolyte beverages or consume large amounts of salt throughout the day. On September 2nd, I developed severe neurological symptoms and diarrhea after consuming a large fruit smoothie.

I noticed that when I ate pulled pork, I would I had more energy and was in a better mood but developed reactions to the garlic and spices used in it. As a result, I switched to a more bland diet consisting mostly of a plain ground chuck, plain chicken with salt, and applesauce.

In mid-September, I added plain white rice to my bland diet with hope of adding more calories. I had lost over 40lbs at this point. The rice probably made matters worse. I developed episodes fuzzy vison. I saw floaters in my eyes, as if I was staring into a bright light. My hearing would go out and I would just have a loud ringing or buzzing in my ears. My pulse would spike to 150 or higher. I became dizzy and felt completely intoxicated, despite not drinking alcohol. Every muscle in my body twitches including my face muscles, and I’ve been told that my eyes will twitch when trying to look straight forward. This is triggered when exposed to heat, bright light, exercise, strong smells or any sort of stimulating experience.

Polyuria and More Thiamine Deficiency Symptoms

In late September, I was excreting around 2L of urine in a few hours despite normal consumption. I went to the ER for IV fluids and then again two days later after having that feeling of impending again. I had white rice for dinner.

I had an EKG, blood work, and was given a potassium in IV, as my potassium was low. They tried to discharge me, but I argued for admission. Nephrology and endocrinology performed a variety of tests. A 24 hour urine test measured 8 liters of urine despite consuming only 2 liters. After urine began to concentrate again, I was discharged. Upon discharge, when I attempted to stand my legs were so weak they almost collapsed beneath me. I felt numb from the waist down.

We Finally Tested Thiamine: Undetectable

That night, I went to a university hospital emergency room and during my 13 hour wait to get in, I desperately searched for answers. I chanced upon hormonesmatter.com and ordered the kindle version of Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition and began to read. Once a bed was finally ready in the ER, I told them my story and they started running a number of labs.

I was seen by several doctors, neurologists, and a pulmonologist. They ran orthostatic vitals, several blood labs, and upon my doctor’s recommendation they admitted me for observation (he was leaving his practice that day). They did an MRI of my spine, took me for an EMG and nerve conduction tests. In the MRI they noted some slight degeneration in the spine, and red marrow reconversion throughout. EMG and nerve conduction tests were mostly normal, however, they noticed some diminished sensation in my left lower extremities and toes and a mild gait disturbance.

I requested a vitamin B1 plasma test, along with copper, iron, zinc, and others. I was kept for observation for a few days and given IV fluids, which kept pulse fairly normal. The thiamine test had not returned by the time of discharge.

A week later when the result came back, it was <6 nmol/L, which is basically undetectable.

I was extremely excited, finally getting some answers as to why all of these things were happening. The doctor prescribed intramuscular thiamine 500mg in total, to be given daily for a week, followed by 400mg thiamine HCl orally and IM shots every three days for the next two weeks. The first shots were that very night.

Thiamine Repletion Has Been Brutal

After my first dose, I slept well for the first time in months but the next morning when I attempted to stand, my pulse spiked up but my blood pressure tanked to 89/62. I could no longer walk for more than a short distance. I tried to continue my regular 8-10k steps daily, but after a couple hundred steps, my body would completely shut down. My vision became fuzzy, I saw floaters or like flashing lights and my pulse would skyrocket even though it was already high. The Holter monitor recorded sinus tachycardia and some SVT’s. My legs were so weak, they tremor and felt like they were going to give out beneath me and I felt like I could not get enough air in.

This entire time I was getting the thiamine shots, I struggled to consume enough calories on a daily basis.  Surely, eating only 900-1000 calories didn’t help my situation, I just couldn’t eat any more. When the shots were stopped in November, my health declined further. At this point that, I began significantly increasing my dose orally and adding other forms of thiamine. This made everything significantly worse.

By mid-November, at this time I was getting around 300mg of magnesium malate per day, taking a daily multivitamin (Seeking Health One Chewable), as well as Forefront health thyroid B-complex), and only able to eat boiled chicken and applesauce. Anything else made my GI symptoms unbearable and caused worsening tremors and internal vibrations. Per my records, here is the dosing I followed.

  • Week 1 (first 5 days): 500mg IM thiamine HCl shots, once per day.
  • Days 6 & 7 picking up with 200mg of thiamine HCl by mouth twice per day for 400mg.
  • Week 2: 200mg thiamine HCl by mouth twice per day for 400mg, with one 400mg IM shot on Thursday.
  • Week 3: 300mg thiamine HCl, plus 150mg benfotiamine by mouth twice per day, with one 400mg intramuscular thiamine HCl shot on Monday and 400mg IM thiamine HCl shot on Thursday.
  • Week 4: 300mg thiamine HCl plus 300mg benfotiamine by mouth twice per day, with one 400mg IM thiamine shot on Thursday.
  • Week 5: 300mg thiamine HCl, plus 300mg benfotiamine by mouth twice per day, no intramuscular shots.
  • Week 6: 300mg thiamine HCl, plus 300mg benfotiamine by mouth twice per day, no IM shots. Wednesday and Thursday attempted to add morning and afternoon dose of Thiamega and cut benfotiamine back to 150mg and thiamine HCl back to 100mg. This led to extreme anxiety, significant increase in pulse and panic attacks.
  • Week 7: same as above but have begun having random panic attacks, adrenaline surges, pulse spiking to 160bpm randomly. I can’t sleep at all (last week and the weeks before I was getting 7 to 8 hours per night typically). Now I wake up at 2am and feel air hunger and have random surges in pulse, spasms and closing of my esophagus. I went to the ER yesterday and they found nothing wrong. All electrolytes were on the lower end of normal. I have tremors, dysautonomia and POTS symptoms again and I am losing weight again.”

The Hell Continues: Confusion and Food Intolerances

Thinking I was taking too much thiamine, I reduced intake to just 150mg benfotiamine and 350mg thiamine HCl for a couple days. This was right before Thanksgiving. My neurological symptoms were getting worse, and now I was experiencing dizziness, cognitive decline and new vision problems, but the shortness of breath had begun to subside.

I had an appointment to see a nutritionist. I showed up at the appointment and had this new surge of confusion, as well as a significant increase in pulse while walking in, my body felt ice cold even inside the building.

After going over all of the foods that I was having issues with and what my allergist told me to avoid, we were left with almost nothing. She said, at this point you’re going to just have to try to start eating anything you possibly can to add more calories, because you’re lucky if you’re getting 600 calories per day.

As I walked out of the building from this appointment, I experienced the worst brain fog that I had experienced to date. I walked around the entire parking lot but I could not remember where I parked my car. My pulse extremely high and I was dizzy. I felt like I was in a dream and I could not make sense of anything that was going on around me. I eventually found my car about 20 minutes later.

Since I was struggling to come up with ideas of what I could eat and unable to tolerate most of the things that I tried at home, I decided to go back to trying Chipotle. It turns out, I can tolerate Chipotle carnitas. So now, I eat two chipotle bowls with double meat, double brown rice and light beans. It’s nowhere near an ideal healthy meal but at least I can eat – sort of. I now get migraines a few hours after eating and internal vibrations and tremors.

I started taking Zyrtec daily, because I tested positive for a rice allergy on both blood and skin tests. I continue to eat Chipotle and use Zyrtec to manage the allergic reactions. I also take quercetin, a mast cell stabilizing supplement, and butyrate supplement.

Another Medical Procedure With Anesthesia

Mid December, I had a recommended colonoscopy and endoscopy. Given my problems with anesthesia, I was worried. The prep process was very rough on my body and caused even more palpitations and higher heart rate. I don’t think the thiamine I was taking was absorbed and not eating made things worse. Surprisingly, coming out anesthesia was okay, but the first time I tried to drive, I had a major energy crash. I felt like everything was moving in slow motion and my brain was running out of energy would shut down. My vision was fuzzy, my hearing went out and I just had a loud ringing as my pulse spiked up. I felt like I was completely intoxicated. Every muscle in my body started twitching, tremoring and then lost strength. I messaged my neurologist and they responded that it sounds like a panic attack, and I should take some Tylenol for my intense migraine headaches. I was not a panic attack.

I have been unable to drive since. Every time I am in the car with someone going to an appointment, all of the visual stimulation from trying to process cars and what’s going on the road and around me, causes what feels like a mental shutdown. I also feel like I’m intoxicated constantly, especially when in the car, or looking into a mirror. It has gotten to the point where it is hard for me to focus on things mentally, or make sense of things I read or watch. I’m not sure if this is all due to the B1 deficiency or if it’s partially due to the c diff infection and all of the antibiotics.

My Health Is Failing and I Don’t Know What to Do

I am struggling daily to maintain a proper electrolyte balance. If I sip a 33oz coconut water throughout the day and add a little salt here and there, in addition to the sodium I’m getting from food, I end up feeling dizzier, like my blood pressure is too low. If I take 450 mg of sucrosomial magnesium, I still have full body tremors, muscle twitching and a migraine. If I increase the magnesium the twitching subsides, but dizziness increases and I feel faint. I’ve even tried using 350mg sucrosomial magnesium with 144mg of magnesium l-threonate (hoping this would help with brain symptoms.

I’ve tried to introduce healthier foods, such as the farm eggs that I used to eat every morning, ground lamb, fresh-squeezed orange juice, but my body just seems to reject these. So I am left with the Chipotle, with double carnitas, double brown rice, and light pinto beans. I realize these meals are not the healthiest options and probably not doing me any favors with the brain fog, migraines and other symptoms but I don’t know what else to do. Are my continuing symptoms all related to the thiamine deficiency, my diet or something else?

Adding More Supplements

On December 19th, I began taking Lipothiamine. I began with 12.5 mg once at breakfast, along with 150mg benfotiamine, and 250mg thiamine HCl.  For lunch, 150mg benfotiamine and 100mg thiamine HCl. That day I had much more severe dizziness, my head felt like it was in a vice, and I was experiencing lapses in time. I went to the ER thinking maybe it was an electrolyte issue. They said electrolytes looked fine. Potassium and sodium were at the very low end of normal, but they were not concerned. They did a CT of my brain (again) and did not find any irregularities. I was offered a migraine cocktail consisting of antihistamines and morphine or something like that, and they offered to keep me for 24 hour observation. Since there was nothing else they could do for me, so I declined. I was given a bag of sodium chloride and discharged.

On the 20th, I increased to 12.5 mg with breakfast (plus 150mg before/250mg HCl), and then 12.5 mg with lunch (plus 150mg benfo/100mg HCL. I held that dose until December 23rd, when I was able to resume the intramuscular shots.

After the intramuscular shots, I felt like I had more energy, I was much more social, and felt like symptoms had improved slightly. The next day, I increased my Lipothiamine dose to 25mg with breakfast, keeping the same benfo and HCl doses as the prior days. All of the symptoms got much worse. I felt a significant increase in the dizziness, heart rate picked up, it felt like I was walking through a dream.

On December 25th I added another 25mg of Lipothiamine with lunch and kept the bento and thiamine HCl the same (so 25mg lipothiamine with breakfast and 25mg with lunch). Symptoms continued to worsen. I also began taking CoQ10 ubiquinol (50mg with breakfast and 50mg with lunch), mitosynergy copper (split .5mg with breakfast and .5mg with lunch), black seed oil/curcumin (one capsule with breakfast, one with lunch). Lactoferrin (one capsule with breakfast, one with lunch), Jarrow reduced glutathione (one capsule before breakfast, one before bed), liposomal vitamin C (twice a day), creatine (4 split doses 3g total per day),

Elite IgG ImmunoLin blend for gut healing (one scoop before breakfast), ProButyrate (2 capsules before breakfast, two before dinner), and Hesperidin capsules (one capsule with breakfast to help with neuroinflammation).

From December 25th on I have been following the same protocol, with everything listed above, with the exception of adding Thiavite to my morning doses which adds all cofactors and increases TTFD by 15mg in the morning dose.

Reasoning Behind the Recent Supplements

I added the lactoferrin and black seed oil/curcumin as part of my Mitome protocol. When I did the Mitome test back in May 2025, it showed complex IV was at 24% and noted that I should be supplementing with heme iron, or if my ferritin levels were high that I should utilize whey protein/lactoferrin, with black seed oil and curcumin to lower inflammation so that trapped iron was released from ferritin.  It also noted that I should be using copper to support complex IV cytochrome C oxidase enzyme.  For the low complex II and II-III it noted coq10.  I’ve added all of these in, and hope that if what I’m also dealing with an addition to a thiamine deficiency, is also mitochondrial dysfunction, that this will help to support my mitochondria and correct all of the issues that I’m having. In recent lab tests my copper was on the low end of normal, but so was ceruloplasmin, with a free copper over 15.  In my iron labs, my iron was at the low end of normal, with transferrin below the normal range, and ferritin at the top of the normal range, with saturation at around 30%.

On December 31st, I did another 400mg of thiamine HCl intramuscular shots, and again the first day I felt more social and talkative, but since the 3rd I’ve been feeling very off. Migraines are back even worse, a sensation of extreme nervous system irritation and randomly losing hearing in my right ear. I feel like I still cannot get my electrolytes managed properly, and I’m left feeling like I’m never going to get back to my old self. My pulse was somewhat normalized in the morning before eating breakfast and at night, now it’s elevated again.

Where I Am Now

The last few days I’ve also had a lot of digestive upset. I’m getting more hives like reactions to all foods. Overall, I am very fatigued and feel like I’m walking through a dream. I don’t know how to continue supporting my body without causing more inflammation. I don’t know if this is all related to the B1 deficiency or if this is a much larger issue that I need to be working on.

I’m trying to walk around as much as possible so that my body will stimulate more mitochondrial biogenesis. I would to get to the point where I can drive again but my legs feel weak and I have very low energy levels. My doctors are pushing for me to do a stress test in one week, and if all goes well, they would like me to start physical therapy and occupational therapy. At this point, I feel like that is just going to make things worse, because every time I try to do anything physically or mentally taxing, I crash and then the next few days are miserable.

My time is also running out for being able to return to work. If I’m not able to return in the next 4 weeks, my position will be opened up. I’ve even tried to spend time with family, and simply holding a conversation causes the over stimulation reaction where I start to feel faint, my pulse rises, and my vision gets fuzzy, etc.

Please help me get my life back. I want nothing more than to return to work, spend time with family, and friends and help others who are in similar situations.

Post Script: I just learned that the IM thiamine shots I was prescribed contain 400 mcg/mL of aluminum each. I have been injected with a neurotoxin for months now. I have not been able to find a clean IM. If anyone knows of an IM thiamine without aluminum, please let me know.

We Need Your Help

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

Yes, I would like to support Hormones Matter. 

 

Photo by Marco Bianchetti on Unsplash.

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Narcolepsy, Basal Ganglia, Mitochondrial Fitness, and Kickboxing

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Several years ago, when I just beginning to understand the role of nutrient co-factors in mitochondrial health, I was working with a young woman who had been injured by Gardasil. She was my first ‘case’, contacting me online after a post I wrote about the thyroid damage done by this vaccine. Thyroid damage is among the more common disease processes initiated by many drugs and vaccines. It is one of the easiest problems to rule in or out, but more often than not, it is missed by most practitioners. Inasmuch as thyroid and mitochondrial function are reciprocally connected, where there is damage in one, there is damage in the other, and inasmuch as thiamine is requisite for healthy mitochondria, correcting thiamine deficiency can, in many cases, improve thyroid function. When I first met this woman, I did not yet fully appreciate that connection. Eventually, I would be introduced to Dr. Lonsdale and his work on thiamine deficiency, and so began my education. Together, we wrote a book about the role of thiamine deficiency in mitochondrial illness: Thiamine Deficiency Disease, Dysautonomia and High Calorie Malnutrition.

Exercise and Mitochondrial Healing

Her case is unique for a number of reasons, but mainly because, in addition to the thiamine and other nutrients required to heal, she used, and continues to use, exercise to manage her health. That is what I would like to talk about today: the role of exercise in mitochondrial health. Before we do that, below is a synopsis of her case, as reported in our book on pages 286-87. Her full story was provided on our website here.

In 2008, 26-year-old G.C., a previously healthy, athletic young woman, finishing a Master’s program in finance, received the three injections of the Gardasil vaccine. It bears mentioning that 2 years prior  she received several travel-related vaccines including diphtheria, typhoid, yellow fever, hepatitis A and B, the flu vaccine, and a tetanus boost and suffered no apparent ill effects.

After the second injection of Gardasil she experienced a flu-like episode with high fever lasting over a week. Full-blown hypersomnia manifested shortly thereafter and worsened to the point where she was able to sustain wakefulness for only 45 min to a maximum of 3 h per day. She experienced fatigue, muscle weakness, and dizziness. Over the next several months she developed tachycardia, intense salt cravings, with concurrent dizziness and thirst. The salt cravings led to blackouts and as she described “waves of extreme somnolence” that included slurred speech, lack of coordination, and imbalance. She learned to keep salt with her at all times. Both physical (e.g., walking, standing up, cooking) and mental exertion were profoundly draining. She reported that if she became angry or experienced any emotional event, she would immediately fall asleep. Multiple doctors had been seen and tests completed. By 2010, only low levels of vitamin D had been recognized.

Narcolepsy, Hypersomnia and Exercise

In late 2010, the fifth physician seen, it was diagnosed as narcolepsy without cataplexy–hypersomnia. She was prescribed 300 mg per day of Modiodal (Modafinil, Australia; Provigil, United States). Wakefulness increased, but she was still dizzy and required multiple hour naps after any exertion. She returned to working out. By the end of 2010 she began a PhD program and was determined to “power through.” She found that exercise, though difficult, allowed her to avoid blackouts. Of note, cardio-type workouts provided respite from the dizziness for 4–6 h, whereas weightlifting netted 24 h without dizziness. Similarly, she observed that if she ate simple sugars or carbohydrates the dizziness and blackouts would return.

Six months after beginning Modiodal her health continued to decline despite experiencing greater wakefulness. She developed severe noise and light sensitivity, continued to experience dizziness, and required excessive amounts of sleep, sea salt, and water. She developed a thick, dry, painful scale on her scalp. Another series of doctors could offer nothing and suggested the illness was in her head, inferring that she “needed to pull herself together.” Despite her health issues she defended her PhD in July 2013.

By October 2013 she had seen 10 physicians as her health continued to decline. She read our work on post-Gardasil thyroid dysfunction and other adverse reactions and requested additional testing. Hashimoto’s, hypogammaglobulinemia, vitamin B deficiencies, and low potassium levels were identified. On several occasions she attempted to get transketolase testing but was unsuccessful. In Nov. 2013 she decided to treat empirically beginning with 100 mg thiamine tetrahydrofurfuryl disulfide (TTFD). She subsequently developed the paradoxical reactions discussed in Chapter 4, with her symptoms worsening.

The Paradox or Refeeding Syndrome

With the dizziness and increased heart rate she reduced her dose to 50 mg of TTFD. Over the course of the next 5 weeks, the tachycardia landed her in hospital on four occasions. By December 2013 her body adjusted to the dosage of TTFD and the tachycardia and dizziness subsided. This is important to note. Long-term dysfunction of this nature requires new knowledge from the physician. Though not damaging to the patient it is regarded as “side effects” and either the patient or the physician stops the treatment. This effect was known to the ancient Chinese and regarded as examples of yin and yang by acupuncturists.

Over the course of the 5 years of progressively declining health she saw a total of 24 doctors. None of whom was able to identify or treat what was ultimately a metabolic disturbance brought on by thiamine deficiency that was likely triggered by the vaccine. Her final diagnoses included cerebral salt wasting, POTS, beriberi, hypersomnia, and Hashimoto’s. Arguably, the thiamine deficiency and the mitochondrial damage that ensued were at the root of each of these diagnoses.

Maintaining Health Post Gardasil

Since 2013 she has continued to maintain her health with thiamine, magnesium, and a cocktail of other mitochondrial supplements (which included very high doses of coenzyme Q10), along with thyroxine for Hashimoto’s and Modiodal to treat the somnolence. As of this writing she is doing well, training in various Asian forms of kickboxing daily and working full time. Without the balance of heavy training, the cocktail of supplements, the Modiodal, and thyroxine, her symptoms reappear.

Her case is remarkable for a number of reasons. First, that she recovered at all is impressive. Many women injured by Gardasil do not recover. She did and continues to thrive all of these years later. Her recovery was not linear though and her continued health requires aggressive attention. I think this process throws many people. We have been trained to expect that recovery from illness proceeds in a logical, linear, and expeditious manner. It does not. There were many setbacks, including several hospitalizations when she first began supplementing with thiamine. Had she not persisted through these setbacks, she might not have recovered her health. Moreover, had she not recognized the fragility of this recovery and continued to actively manage her health all of these years later, she could have easily become seriously ill again. kickboxing, basal ganglia, narcolepsyIndeed, there have been many relapses over the years, where her health declines significantly and requires extended periods of recovery. Nevertheless, she is able to recover and that is remarkable.

Secondly, and what I think is particularly unique about her case, is the role that exercise has played in her ability to recover and maintain her health. It is not something that conventional or even functional medicine gives much credence too. Sure, we all recognize the role of exercise in health generally, but mostly, we ignore it. I think this is a mistake. In her case, exercise was and remains critical to maintaining her mitochondrial health and as I have come to understand recently, the type of exercise that she gravitated towards naturally, kickboxing, may be exactly what her brain needs to function.

The Role of Exercise in Recovery

From the beginning of her illness, she forced herself to exercise, even though it was an immense struggle. On her own, she learned that certain types of exercise would prevent her dizziness and blackouts. Specifically, if she did cardio-type exercise, she could prevent a blackout for 6 hours or so, but if she added some weightlifting, the effects would last for up to 24 hours. I attributed this to exercise-induced mitochondrial biogenesis. That is, exercise was forcing the birth of new mitochondria, and somehow, shifting her balance of unhealthy to healthy mitochondria more favorably. It was also likely improving the respiratory capacity of her existing mitochondria. Although it is still not clear to me why one modality yielded better results than another, as the research in this area seems to suggest that the opposite is true, that cardio yields more mitochondrial benefits than weightlifting, the research is clear that exercise induces both mitochondrial biogenesis while improving their functionality.

Her seemingly innate realization of this was and remains one of the more noteworthy aspects of her case. Remember, for several years after Gardasil vaccine, she was seriously ill. When she first contacted me, she weighed less than 100 lbs, was severely fatigued, and could not maintain wakefulness for more than a few hours at a time without blacking out; and yet, somehow, she managed to drag herself to a gym to exercise (and maintain her graduate work in finance). Not only that, she observed a pattern of response to exercise (and salt and other dietary components) and used what she learned to help herself function better. Indeed, throughout her recovery, she would actively observe the patterns and optimize those that appeared beneficial and eliminate those that did not; something that we all should be doing as a matter of course, and yet, very few of us do.

To exercise throughout an illness where intractable fatigue, excessive somnolence and blackouts dominate is very difficult to do, and more often than not, would be discouraged. When I first wrote about her using exercise to heal, the backlash was immediate and intense. For her though, the exercise became an integral component of maintaining her health just as surely as the nutrient elements. Even now, 12 years from initial vaccine-induced illness and with 7 years of recovery under her belt, she indicates that when she misses training because of work or travel, her health declines rapidly and does so in a fairly specific manner. She becomes dizzy, loses balance, and her cognitive capacity diminishes significantly. Her ability to maintain wakefulness declines while fatigue increases. Additionally, when the stress of normal everyday illnesses come into play, a viral infection for example, and her exercise program naturally takes a hit, in order to fully recover she has to double-down on the training for a period of time once the illness passes.

Is this need to exercise unique to her case specifically or could we learn something about how we approach recovery from illness? I would argue that given the mitochondrial fitness attributable to exercise and the noted mitochondrial decline in its absence, some form of movement or exercise should be approached with any recovery plan. If this is the case, the questions become, at what point in the illness or recovery should exercise be considered, how much, and in what form? While the answers to these questions are far too individual to explore fully here, what we learn from her case is that exercise, when implemented early, improves recovery. That brings us to a more complicated question; why kickboxing, boxing, or other dynamically challenging programs might be useful for narcolepsy specifically. From what I have learned, it may be related to activating and training neural connections in a region of the brain called the basal ganglia. And of course, the mitochondria are still involved.

Enter Kickboxing and the Basal Ganglia

I believe there is damage to the basal ganglia for her and other Gardasil injured women. To this point, among the more common symptoms associated with Gardasil injury are tremors, ataxia, and gait issues. While those symptoms can easily be attributed to cerebellar and thyroid damage as well, and both of which are affected by the vaccine and thiamine deficiency, it is not without warrant that we look at the basal ganglia for these symptoms, as well as for the sleep and wakefulness issues. Neural tracts between the cerebellum and basal ganglia suggest that if one is damaged, messaging and functioning to the other would be impaired. Indeed, research shows both efferent and afferent disynaptic (from and too, two neuron) connections between the cerebellum and the basal ganglia. Additionally, personal communications with other women affected by Gardasil regarding imaging results confirm damage to the basal ganglia in some women. This is in addition to potential cerebellar damage.

Symptomatically, many post-Gardasil women display an ataxic, drunken sailor like gait, which is indicative of cerebellar involvement while their tremors occur at rest, along with muscle rigidity and dystonia, indicating basal ganglia involvement. All of them suffer from what could be termed hypersomnia and excessive fatigue, but none that I have met thus far were diagnosed with narcolepsy, like this patient. Of course, that does not exclude the possibility that it does not exist. The post vaccination symptoms are diverse as one might expect with mitochondrial damage and autonomic system dysfunction.

Why the Basal Ganglia?

The basal ganglia are set of nuclei buried deep in the brain that are responsible for controlling movement, motor learning, executive function (via connections with the frontal cortex) and emotional regulation and motivation (via connection to the limbic system). See figure 1.

brainstem basal ganglia
Figure 1. Tracts of the basal ganglia.

The basal ganglia act as a breaking system to complex movement patterns and activities.

The most well known disorders of these nuclei include Parkinson’s and Huntington’s diseases. These are dis-inhibition syndromes, where the normal inhibitory control that the basal ganglia hold over motor movements is lost resulting in tremors and chorea respectively. There are also problems with initiating movement. This occurs via connections to the limbic system, particularly a set of nuclei located in what is called the ventral tegmental area (VTA). These nuclei are central to motivating behavior, addictive behavior in many cases, but also, behavior in general. The dopamine released by the VTA neurons provide reward and reward, as we all know, encourages habit and learning. That hit of dopamine gives us the drive to act. As Parkinson’s disease progresses, patients lose these connections and with them that internal, unconscious motivation that initiates behavior. They become stuck and so absent an external cue, patients will become unable initiate a movement internally on their own. This stuckness might sometimes also manifests as a sort of depression; one where there is no motivation to act at all.

One of the latest alternative treatment modalities for Parkinson’s disease, aside from thiamine, involves boxing. Yes, boxing. Boxing, because of the balance requirements, the bilateral, stop/go and cognitively active nature of the exercise seems to activate tracts in the basal ganglia that increase inhibitory control, reduce tremors, and allow for a smoother initiation of movement patterns. It also improves gait speed and balance, conditioning, cognitive ability, and overall quality of life.

What does all of this have to do with the ability to maintain wakefulness, and as our patient indicated, cognitive clarity? This, as far as I can tell, has not been studied, but I suspect it has to do with enhancing motivation. Not motivation in the psychobabble sense, but motivation as a fundamentally physiological, survival-based behavior; motivation that is controlled by the basal ganglia via connections to the limbic system and the frontal cortex, respectively. That hit of dopamine that engenders motivation is key for not only movement but arousal. When there is damage to that system, wakefulness is near impossible. Rodent studies have born this out. Without ‘motivation’ we cannot remain awake and we cannot sustain the arousal necessary for mental acuity.

Consider for a moment, the key aspect among all of the behaviors controlled by basal ganglia is that they necessitate wakefulness. Given that, it makes sense from a purely logical perspective that the basal ganglia might be involved in maintaining the arousal necessary to perform these activities. Similarly, it makes sense that damage to certain tracts within these nuclei could impair not only one’s ability to maintain wakefulness, but also, one’s ability to manage motor movement with altered sleep/wakefulness patterns. Finally, absent sustained and vigilant wakefulness, mental acuity is impossible. The cognitive fogginess, so often reported by these patients, may very well be linked to disruptions in basal ganglia functioning.

But Wait, There is More: The Orexin System and the Basal Ganglia

When narcolepsy and other sleep/wake disorders are researched, the basal ganglia have only recently come into view. This is despite the fact that the most well-known disorders of the basal ganglia, like Parkinson’s, demonstrate clear sleep/wake disturbances. Instead, another set of neurons located in the hypothalamus, called the orexin/hypocretin neurons (same neurons, different name), dominate the research landscape. Damage to these neurons is clearly linked to narcolepsy, cataplexy and other sleep/wake disturbances, and for our purposes, directly attributable vaccine reactions, especially the flu vaccine. The basal ganglia, not so much. How do we reconcile the known connections between orexin system, narcolepsy, and vaccine damage, the paucity of research on the basal ganglia. Well, like everything in the brain and body, we look for communication patterns. And it just so happens, the orexin neurons clearly interact with the basal ganglia to manage arousal, both directly via orexin receptors in various regions of the basal ganglia and indirectly, via vast projections throughout the limbic system, which then project to the basal ganglia.

Backing up just a bit, the release of orexin induces wakefulness. I have written about this system here, here, here, and here. When orexin neurons are turned on and firing appropriately, arousal is maintained. When orexin neurons are turned off, diminished or dysfunctional, melatonin, the sleep promoting hormone, is turned on. The two work in concert to manage wakefulness and sleep. Orexin receptors are located throughout the central nervous system and in the body. For our purposes, the orexin receptors in the amygdala and throughout the limbic system directly activate the release of dopamine from the VTA. Recall, dopamine projections from the VTA to the basal ganglia are critical for motivating and sustaining wakefulness in Parkinson’s patients. Additionally, orexin receptors have been found in different regions of the basal ganglia themselves, suggesting direct regulation of arousal. Perhaps even more importantly, the orexin neurons have been found to be instrumental in integrating motor movement patterns.

“…numerous neuroanatomical and immunohistochemical studies reveal that essential subcortical motor structures, such as the basal ganglia, cerebellum, and vestibular nucleus, receive direct innervation from orexin neurons. Moreover, during movements, orexinergic neurons are particularly active and orexin release increases. The evidence suggests that the orexinergic system directly participates in central motor control.”

So what we have is an integrated system of arousal, movement control, and cognitive behaviors that relies heavily on the health and functioning of the basal ganglia and its connections through out the brain, including with orexin system in the hypothalamus. And the orexin system itself relies heavily on functioning mitochondria, as does everything, but the orexin neurons are particularly sensitive to diminished mitochondrial function as these neurons require as much as 5-6X the amount of intracellular ATP to maintain firing compared to other neurons. The orexin neurons cease firing when ATP stores become low, inducing sleep to allow the reallocation energy towards more basic survival functions like heart rate and respiration. That means that excessive sleep is to be expected with mitochondrial damage.

Putting It All Together

With direct stress to the mitochondria via vaccines and medications we can expect  a variety of negative symptoms. In this case, our patient developed thyroid damage, autonomic dysfunction (cerebellar and brainstem involvement), and likely also, some degree of basal ganglia injury. The hypersomnia, so commonly experienced during illness or adverse medication/vaccine reactions, represents diminished orexin activity likely initiated by diminished mitochondrial capacity. Narcolepsy suggests a specific injury to oxexin system. With the diminished orexin capacity, we can anticipate that basal ganglia function would be impacted, and with it, the ability to maintain the requisite ‘motivation’ for arousal and wakefulness and to coordinate movement and maintain cognitive acuity. Nutrients and exercise improve the respiratory capacity of mitochondria, which in turn, provides the requisite energy to manage autonomic function from the brainstem and cerebellum and to sustain wakefulness by maintaining orexin firing in general and to the basal ganglia more specifically. Additionally, exercise that demands dynamic, bilateral, complex movement patterns, such as kickboxing, may serve to retrain or maintain the strength of synaptic connections to, through, and from the basal ganglia, which ultimately, may offset any damage done by the initial insult.

We Need Your Help

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

Yes, I would like to support Hormones Matter. 

This article was published originally on March 12, 2020. 

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Western Medicine: A House Built on Sand

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Let Food Be Medicine

At the risk of repeating myself too much as in former pages of this website, I want to return to discussing in some depth the fallacies incorporated in our present approach to health and disease. You may or may not remember that I have stated a number of times that Hippocrates (400 BCE) uttered the formula “Let food be thy medicine and medicine thy food”. Having been construed as the “father of modern medicine”, it has seemed to me for a long time that he has been ignored as a “parent”.

For centuries, there was no idea about disease. The early Egyptians bored holes in people’s heads “to let out the evil spirits”. Throughout medieval history the only treatment seems to have been “bloodletting”. In our modern world, horns from the rhinoceros are regarded so highly for their medical properties, that this wonderful animal is reaching the point of annihilation. Pharmaceutical drugs, with the exception of antibiotics, only treat symptoms. I ask you, does this make any sense at all in the light of what Hippocrates suggested?

Because humanity tends to follow a collective pattern and only rarely listens to an idea derived from rational deduction, I view medicine as like a traveler on a road without a known destination. In my imagination, he comes to a fork in the road, but the signpost records information on only one fork. It reads “kill the enemy”, reminding me of the story of Semmelweiss, a lone thinker in his time and who “gave thought to the message on the signpost”. Most physicians are familiar with this story but it is worth repeating.

Semmelweiss was a physician who lived at a time before microorganisms had been discovered. He presided over an obstetric ward where there were 10 beds on one side and 10 beds on the other. The physicians would deliver their patients without changing their clothes or washing their hands. As we would expect today, the death rate from infection was extremely high. Semmelweiss said to himself, “they must be bringing [the enemy] in on their hands” and he devised the first known clinical experiment. He made it a rule for the physicians on one side of the ward to wash their hands in chlorinated lime before they delivered their patient. The physicians on the other side of the ward continued to deliver their patients in the same old way. As we would easily recognize today, it did not require a statistician to see the difference between the incidences of infections on the two sides of the ward. Irrespective of the fact that this was a dramatic discovery that later had obvious meaning, Semmelweiss was accused by the medical authorities of the day of being non-scientific because he could not explain what it was that was supposed to be on the hands of the physicians. Of course the medical establishment had no idea that their model for disease was catastrophically wrong, although collectively certain that their philosophy bore all the hallmarks of scientific truth. Semmelweiss had offended the medical establishment and they threw him out of the hospital. He died a pauper in a mental hospital.

The First Medical Paradigm: Kill the Enemy

When microorganisms were discovered to be responsible for infections, it fulfilled the message on the signpost and it became the first paradigm in medicine. Kill the bacteria: kill the virus: kill the cancer cell, but try not to kill the patient. If we look at the history of this time, we find that a lot of patients were killed in the concerted attempts to find ways and means of killing the enemy. We all remember the discovery of penicillin and how it led to the antibiotic era, still the major therapeutic methodology, even though we know that it is running into bacterial resistance and has never been a good idea for viruses or cancer cells.

Although the germ theory had been around for a long time, Louis Pasteur, Ferdinand Cohn and Robert Koch were able to prove it and are regarded as the founders of microbiology. However, Pasteur was said to have uttered the words on his deathbed “I was wrong: the microbe (germ) is nothing. The terrain (the interior of the human body) is everything”. Perhaps he had unknowingly voiced the principles of the next paradigm in medicine.

The Second Medical Paradigm: Genetic Determinism

The monk, Mendel, by his work on the segregation of peas, formulated what came to be known as the genetic mechanisms of Mendelian inheritance and the discovery of DNA modeled the next stage in our collective development. The fact that each of us is built from a complex code that dictates who we are was a remarkable advance. The fact that the construction of the code sometimes contained mistakes (mutations) led us to explaining many diseases and for a long time we believed that the genes were fixed entities, dictating their inexorable commands throughout life. However, the newest science of epigenetics has shown us that the DNA that makes up our genes can sometimes be manipulated by nutrition and lifestyle, as well as by artificial means in the laboratory.

Health: The Ability to Respond Effectively to a Hostile Environment

We are surrounded by germs that exist everywhere, many of which cause disease as we are all too well aware. Nevertheless, whatever evolutionary mystery guides our development, we are all equipped with an extraordinarily complex, genetically determined, defense system. We now know that this is organized and directed by the brain. Assuming that the genetic determinations of the terrain are completely intact, we can be reasonably assured that we can defend ourselves from any germ that Mother Nature can throw at us. Built in mechanisms in the brain require a huge amount of energy when it goes into action directing the traffic of the immune system. It is a crisis and can be likened to a war between the body and the attacking organisms. Thus, if Pasteur may have stated the next paradigm in medicine, what does it mean?

As an example, a typical microbial attack causes a common disease that goes by the name of febrile lymphadenopathy (strep throat). The throat becomes inflamed, perhaps because the increased blood supply brings in white blood cells, acting in defense. An increase in circulating white cells also occurs, bringing a brigade of defensive soldiers. The glands in the neck become swollen because they catch the germs that get into the lymph system.  Lastly, the increased temperature of the body is also part of the defense. Germs are programmed to have their most intense virulence at 37°C, the normal body temperature. If this temperature is increased, the attacking germ does not have its maximum efficiency. In other words, what we are looking at as the illness is really the act of brain/body defensive interaction. Besides attempting to kill the attacking germ as safely as possible, should we not be assisting the defense? The answer calls into question the relationship between genetic intactness and the required energy to drive the complex defensive action. Perhaps a genetic mistake (mutation) can sometimes be manipulated by an epigenetic approach through nutrients, just as advised by Hippocrates.

Disease: The Inability to Adapt to the Environment

If we look at health as the ability to respond effectively and adapt to environmental, mental and physical stressors, it is possible to re-conceptualize illness by the manner in which that response is carried out. A healthy individual will respond to stressors without problem, because of an efficiently effective mobilization of energy dependent mechanisms. In contrast, individuals who are not healthy will respond in one of two ways. Either the defense mechanisms will be incomplete or absent or over-reactive and inconsistent. Listed below are examples of both. Note that this is in line with the ancient philosophy of Yin and Yang or, in modern terms “everything in moderation”. Too much of anything is as bad as too little.

Exhausted Defense Systems

When I was a resident in my English teaching hospital, before the antibiotic era, I admitted a patient with pneumonia who was known to have chronic tuberculosis. He was seen to be “unconsciously picking at thin air with his fingers” and the physician for whom I was resident pointed out that it was a classic example of “a sick brain” and that he would die. He never had any fever, elevation of white blood cells or any other marker of an infection but at autopsy, his body was riddled with small staphylococcal abscesses. He had lived in the east end of London, notorious for poverty and malnutrition at that time. In fact, as an organism, he never showed the slightest sign of a defense. His “sick brain” was completely disabled in any attempt to organize his defense.

Excessive or Aberrant Defense Mechanisms

Many years ago I was confronted with two six-year-old unrelated boys who for several years had each experienced repeated episodes of febrile lymphadenopathy. Both boys had been treated elsewhere as episodes of infection. In each case the swollen glands in the neck were enormous. One of the boys had been admitted to a hospital for a gland to be removed surgically for study. It had been found that the gland was just enlarged but had a perfectly normal anatomy, only contributing to the mystery. One of the curious parts of the history was that each of these boys had been indulged with sweets. Because I was well aware that sweet indulgence could induce vitamin B1 (thiamine) deficiency, I tested them and found that both were indeed deficient in this vitamin. Treatment with large doses of thiamine completely prevented any further attacks. The mothers of the boys were advised to prohibit their sweet indulgence. I needed some evidence and asked one of the mothers to stop giving thiamine to her son. Three weeks later he experienced a nightmare, sleep walking and another episode of lymphadenopathy that quickly resolved with thiamine.  A nightmare and sleep walking supported the contention that the brain was involved in the action. In addition, his recurrent illnesses had been associated with increased concentrations of two B vitamins, folate and B12, both of which decreased into the acceptably normal range with thiamine treatment. Of course, this added complexity to an explanation.

What I had already learned about thiamine deficiency is that it makes the part of the brain that controls automatic mechanisms much more sensitive. One or more reflexes are activated unnecessarily. No reflex activation is as bad as too much. Thus, the “trigger-happy” defense mechanisms were being activated falsely. Thiamine is perhaps the most important chemical compound derived from diet that presides over the intricacies of energy metabolism. All that was required was an improved energy input to the brain. Folate and B12 are vitamins that work in energy consuming mechanisms and I hypothesized that their respective functions were stalled for lack of energy, causing their accumulation in the blood. Whatever the explanation, the facts were as described. It is interesting that the high levels of folate and B12 had been found at the hospital where a lymph node had been removed. The mother had been accused of giving too many vitamins to her child. She had told me that she did not understand this explanation because she had not given any vitamins to him. I had measured them solely to verify this finding.

The Treatment of Disease Should Begin with Host Defenses

We exist in a hostile environment. Each day throughout life we live in anticipation of potential attack. A physical attack may be an injury, an infection or an ingested toxin. A mental attack, divorce, grieving, loneliness, generally referred to as “stress” may be virtually anything that causes the brain to go into increased action. In facing both physical and mental forces, it is the brain that organizes the defense and it demands an increase in energy output that depends solely on the ability to burn fuel. The fuel burning process is governed by a combination of genetically determined ability and the nature of the fuel. Thus, the treatment of all disease is dependent on this combination being effective. It can be seen as obvious that killing the enemy is insufficient. As our culture exists at the present time, trying to get people to understand the necessity of perfect nutrition is a pipe dream. This particularly applies to youth and the artificiality of the food industry. However, our culture is also virtually brainwashed to accept tablets as a means of treating anything.

In our recently published book “Thiamine Deficiency, Dysautonomia and High Calorie Malnutrition“, Dr. Marrs and I have shown that thiamine deficiency is extraordinarily common and that supplementary thiamine and magnesium together balance the ratio of empty calories to the required concentration of cofactors necessary for their oxidation. The question remains, would vitamin supplementation, just as artificial, be a more successful sell as a preventive measure? We have shown that the symptoms derived from prolonged high calorie malnutrition can last for years as an unrecognized polysymptomatic illness that haunts many physicians’ offices. Early recognition represents an easy cure. There is a good deal of evidence that ignoring the symptoms and the persistence of high calorie malnutrition creates a gradual deterioration that then turns up as chronic disease. Some drugs, metronidazole being an example, will precipitate thiamine deficiency, so we have to recognize the precarious nature of the present medical approach in the use of drugs whose action in treating disease is often unknown. Although recognition of the artificiality of thiamine supplementation is implicit in this proposal, it is better than allowing a common example of continued morbidity to exist.

We Need Your Help

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

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Photo by Phil Hearing on Unsplash.

This article was published originally on July 19, 2018. 

Rest in peace Derrick Lonsdale, May 2024.

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Elimination Dieting and Progressive Thiamine Deficiency

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Elimination diet

My issues began after the birth of my second child 21 years ago. I would get extreme indigestion for a couple days each month and my skin broke out. This continued for years until I ended up having several rounds of antibiotics. Months later, I developed severe and never ending acid reflux. After struggling for a year, my local health food store owner mentioned the blood type diet and recommended I avoid dairy. The result was magic. Unfortunately, this started a cascade of elimination diets that would set the tone for the next fifteen years.

After eliminating dairy and seeing a resolution of symptoms, at least temporarily, I decided to eliminate gluten too. As with the dairy, the indigestion disappeared temporarily when I eliminated gluten, but other symptoms eventually crept in, including hypothyroidism and bile reflux. I read about a vegetarian diet and decided to give it a try. Again amazing results from removing meat. The bile reflux disappeared.  I thought things were going pretty well, but in these years I started to have other issues: ataxia, fatigue, heat intolerance, numbness and tingling, gait and bladder issues. In addition, I was always starving. I ate a tremendous amount of food each day, but at the same time I was losing weight.

My naturopath had mentioned possible problems with my gallbladder, but I didn’t think too much about it until I had constant pain. It was eventually discovered that I had a non-functioning gallbladder and I reluctantly had it removed, hoping it would solve my problems. I had tried changing my diet to the autoimmune paleo several times, but would always crash after a couple weeks. After surgery, I could eat meat without major issues, but nothing seemed to digest well. I felt like I never really recovered and other issues started to creep in.

My calf muscles would spasm upon standing and I was so weak I was having difficulty walking a block. A year after surgery, I was diagnosed with primary progressive multiple sclerosis, as it matched my symptoms and lesions were seen on my cerebellum and down my spine. The hallmark of PPMS is neurodegeneration without inflammation. The next three and a half years were a quick decline. I quickly became unable to walk unaided, mainly because I was too fatigued and my muscles too weak. PPMS used to be called creeping paralysis and that is exactly what was happening; I was unable to move my arms or legs, my equilibrium was so off that I couldn’t stand without tipping over and I couldn’t look down to even zip up my jacket.

I had really bad edema in my lower legs and feet and they were a nice shade of purple. My brain was easily overwhelmed and not committing things to memory, which left me going in circles. I lost my appetite, but blamed it on my ever changing diet and my fear of eating the wrong food. I would alternate between diets, cutting various food groups with very limited success.

I visited multiple naturopaths, a functional medical doctor, a NUCCA chiropractor and a MS specialist. I have researched endlessly and have a cupboard full of supplements. I had tried B vitamins before but had not noticed a difference. I joined a Facebook group called Understanding Mitochondrial Nutrients and did not think much about the vitamin I needed most, thiamine, until a post by a desperate husband came up in my feed. I began to research thiamine and found I was able to piece together a timeline of my life based on a progressing thiamine deficiency. I am only three weeks into dosing with thiamine (I take 200mg thiamine HCL and 240mg benfotiamine) and a B complex, but it has made such a difference in my balance, fatigue, edema and mental energy. My appetite is back and I can zip up my coat! I am cautiously optimistic, only because I have suffered so much disappointment in the past. I am hopeful that I can make a recovery.

We Need Your Help

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

Yes, I would like to support Hormones Matter. 

Photo by Thought Catalog on Unsplash.

This story was published originally on March 7, 2023.

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