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Migraine Energy Metabolism: Connecting Some Dots

Published on October 10, 2023

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I have been reading some of the fascinating posts by Angela Stanton PhD concerning her research in migraine headaches. I regard the substance of her discussions as somewhat like dots on a chart that need to be connected. I learned a great deal about the chemistry involved in migraine. One of her comments that involves ion homeostasis in brain metabolism is fascinating. She noted that “serotonin is created by a normally functioning brain. Why it decreases or increases in the brains of migraineurs has always puzzled me. Should we not try to find out why?” That simple three letter word is the heart and soul of research and I believe that I may be able to add some information that might provide an answer.

Ehlers Danlos and Migraine

In one of Angela’s posts she discusses a subject which has been of interest to me for many years, the overlap of symptoms in disease. She noted that 60% of migraineurs have one type of Ehlers Danlos syndrome (EDS) and 43% of EDS have minor changes in DNA (SNPs) found in migraineurs. She concludes that they must be related. Over 70% of migraineurs have Raynaud’s disease and there is an overlap with EDS and Raynaud’s. Therefore, she concludes that these three diseases are variants. In fact, there is an association between EDS, Postural Othostatic Tachycardia Syndrome (POTS) and a group of conditions known as mast cell disorders. EDS-HT, (one of the manifestations of this disease), is considered to be a multisystemic disorder, involving cardiovascular, autonomic nervous system, gastrointestinal, hematologic, ocular, gynecologic, neurologic and psychiatric manifestations, including joint hypermobility. Many non-musculoskeletal complaints in EDS-HT appear to be related to dysautonomia, consisting of cardiovascular and sudomotor dysfunction. Many of the clinical features of patients with mitral valve prolapse can logically be attributed to abnormal autonomic function. Myxomatous degeneration of valve leaflets with varying degree of severity is reported in the common condition of mitral valve prolapse.

A woman, with what was described as a “new” type of EDS, died after rupture of a thoracic aortic aneurysm. Autopsy revealed myxomatous degeneration and elongation of the mitral and tricuspid valves. Patients with POTS, a relatively common autonomic disorder, may have EDS, mitral valve prolapse, or chronic fatigue syndrome and are sensitive to various forms of stress, as depicted in the clinical treatment of a dental patient affected by the syndrome. Dysautonomia has been described in the pathogenesis of migraine, featured by nausea, vomiting, diarrhea, polyuria, eyelid edema, conjunctival injection, lacrimation, nasal congestion and ptosis. In general, there is an imbalance between sympathetic and parasympathetic tone.

Energy Metabolism and Migraine

Technological studies have confirmed the presence of deficient energy production together with an increment of energy consumption in migraine patients. An energy demand over a certain threshold creates metabolic and biochemical preconditions for the onset of the migraine attack. Common migraine triggers are capable of generating oxidative stress and its association with thiamine homeostasis suggests that thiamine may act as a site-directed antioxidant. It strongly suggests that migraine is a reflection of an inefficient use of brain oxygen. An intermediate consumption of oxygen between deficiency and excess appears to be a necessity at all times. In fact,” moderation in all things” is an important proverb

Backing up energy deficiency, two cases of chronic migraine responded clinically to intravenous administration of thiamine. However, the authors are in error when they state in the abstract that “nausea, vomiting and anorexia of migraine may lead to mild to moderate thiamine deficiency”. An otherwise healthy 30-year-old male acquired gastrointestinal beriberi after one session of heavy drinking. Nausea, vomiting and anorexia relentlessly progressed. He had undergone 11 emergency room visits, 3 hospital admissions and laparoscopy within 2 months but the gastrointestinal symptoms continued to progress, unrecognized for what these symptoms represented. When he eventually developed external ophthalmoplegia (eye divergence), he received an intravenous injection of thiamine which reversed both the neurologic and gastrointestinal symptoms within hours.

In other words it is important to be aware that nausea, vomiting and anorexia are primary symptoms of beriberi due to pseudohypoxia in the brainstem where the vomiting center is located. Chronic migraine has a well documented association with insulin resistance and metabolic syndrome. The hypothalamus may play a role. One of Angela’s comments concerns ion homeostasis in migraines. Thiamine triphosphate (TTP) can be found in most tissues at very low levels. However, organs and muscles that generate electrical impulses are particularly rich in this compound. Furthermore, TTP increases chloride (ion) uptake in membrane vesicles prepared from rat brain, suggesting that it could play an important role in the regulation of chloride permeability. Although this research was published in 1991, the exact role of TTP is still unknown. It has been hypothesized that thiamine and magnesium deficiency are keys to disease.

Angela wondered why serotonin might be increased or decreased in migraineurs. I strongly suspect that it is due to brain thiamine deficiency as the ultimate underlying cause of the migraine. In a review of thiamine metabolism, it was pointed out that metabolites could be high or low according to the degree of the deficiency. Victims of beriberi were found to have either a low or a high potassium according to the stage of the disease. If they were found to have a low acid content in the stomach, treatment with thiamine resulted in a high acid content before it became normal. If the stomach acid was high it would become low before it became normal. Since low and/or high potassium levels may be found in the blood of critically ill patients, thiamine deficiency should be a serious consideration in the emergency room or ICU Thiamine deficiency may be the answer for the fluctuations of serotonin observed in migraine.

Redefining Disease Models

According to the present medical model, each disease is described as a constellation of symptoms, physical signs and laboratory studies, each with a separate etiology. The overlap discussed by Angela suggests that the various conditions nominated have a common cause and that they are indeed nothing more than variations. If energy metabolism is the culprit, it would make sense of the infinite variations according to the degree and distribution of cellular energy deficiency. EDS-HT, described above is reported as a multi-system disease, exhibiting cardiovascular, autonomic gastrointestinal, hematologic, ocular, gynecological and psychiatric symptoms as well as the joint mobility. It seems to be impossible to explain this multiplicity without invoking energy deficiency as the cause. People with prolapsed mitral valve and a patient with a “new” form of EDS, reportedly have myxomatous degeneration as part of their pathology and it is tempting to suggest that such an important loss of structure might well be because of energy deficit.

The controls of the autonomic nervous system are located in the lower part of the brain that is particularly sensitive to thiamine deficiency and beriberi is a prototype for thiamine deficiency in its early stages. Dysautonomia is frequently reported as part of many different diseases, offering energy deficiency as the etiology in common. Yes, it is true that thiamine is not the only substance that enables the production of ATP. Nevertheless, it seems to dominate the overall picture of energy metabolism. It has long been considered the essential focus in the cause of beriberi, even though all the B complex vitamins are found in the rice polishings. Milling and the consumption of white rice was the prime etiology of the disease when it was common in rice consuming cultures.

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This article was published originally on June 22, 2020.

Diet and Medication Induced Thiamine Deficiency – Dry Beriberi

by Lyn Williams

Published on October 5, 2023

3196 views

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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Poor Diet, COVID, and Thiamine Deficiency: A Perfect Storm

by HR

Published on October 3, 2023

2948 views

A bit of information about me: I am 24 year old man. I have always been fit, always exercised at least 5 times a week, and have had physical jobs. I never really cared about what I ate and my diet consisted of a load of protein (mainly protein shakes and chicken) with massively high carb/sugar consumption. I went out drinking with friends on most weekends. About two years ago, I had COVID and since then my health seemed to decline massively. I did not see a doctor initially, because I was not aware of how bad my health would become.

About a year after having COVID, my anxiety levels were through the roof. It was so bad, I couldn’t even leave the house without worrying something was going to happen. The symptoms I developed included: a change in personality, hand a feet neuropathy, shocking circulation to hands and feet, severe bowl issues, really low body temperature, extreme fatigue to the point where I was unable to get off the sofa after work most days, memory problems and an inability to think.

A year into this, I realized that I had to do something about my health. I was literally at breaking point. I did not know what was going on with my body or mind. At first, I thought I was diabetic because I matched so many symptoms but blood test showed normal sugar levels. I went back to the doctors numerous times. They basically told me that I was mad. They told my family all my symptoms and that I was really struggling, but no one believed that I was ill. They said it was all in my head and led me to believe that I was actually going mad.

Heart Problems, Breathlessness, and Thiamine Deficiency

Then the heart problems started. I have always played football, since I was 10 years old, and I have always been extremely fit, but I began having trouble breathing when playing. It gradually got worse and I became unable to walk the stairs without becoming breathless. As the breathing problems worsened, I had to stop all exercise. The exertion seemed to make me worse.

At this point, I was positive my symptoms were not imagined and so I did endless research online and found a video by Dr. Berg about thiamine/vitamin B1. I ordered some Benfotiamine and it definitely seemed to help. The anxiety vanished almost instantly and most of my symptoms went away except neurological ones. So I took about 4 tablets, 250mg each, per day for about 9 months. After this time, I felt I was not progressing any further. I thought I would never get circulation back in my hands and feet. My brain was still confused all the time and my breathing became slightly better but it was still nowhere near where I wanted to be.

I returned to internet for research and found Elliot Overton’s YouTube channel and ordered some TTFD, b-complex, magnesium, potassium. Thiamega, the product from Objective Nutrients, has 100mg thiamine HCL, 200mg Benfotiamine, 50mg Sulbutiamine and 50mg TTFD. At first, the paradox reaction, getting worse before getting better, was absolutely shocking. I remember being on the sofa each weekend and just sleeping most of the day. The brain fog was the worst it had been for months but after maybe a month that seemed to clear up and my brain problems seemed to have massively improved.

I forgot to mention earlier that prior to beginning supplementation with Benfotiamine and then TTFD, I had a private MRI scan on my brain. It showed high T2W right signal – a sign of lesions and demyelination and confirmation that I had thiamine deficiency. So, I went for another MRI with contrast recently to see if I have improved any. I am still waiting for the results on that one.

Improved But Still Missing Something

I am at the point now, where I feel I am back to normal health with most of my symptoms improved. All that remains to be resolved are the circulation and breathing problems. The rest do seem nearly resolved.

I have recently tried the carnivore/keto diet, but I usually get to day 3 or 4 and have to stop because it seems to make my symptoms worse especially the breathing and circulation. My current diet is mostly whole foods, with high protein, high fat and lower carbs. I try and eat a lot of red meat and that seems to help.

I was wondering if there was anything I can do to repair this issue, or is it for life now? Sugar and alcohol definitely seem to make me worse, but then so does keto and so I am unsure what to do. Maybe if I manage to push past the first week on keto I would feel better and my nerves would start to repair? All I know is that I must have had a serious case of beriberi disease, which has caused all this damage to my body. Obviously, I know it is my fault for not taking care of my diet, but I also feel the doctors are partly to blame as they seem to know absolutely nothing about thiamine deficiency. All they want to hear about is anxiety and depression. Any help at all would be massively appreciated. Thanks.

Photo by Paul Zoetemeijer on Unsplash.

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How Can Something As Simple as Thiamine Cause So Many Problems?

by Derrick Lonsdale MD, FACN, CNS

Published on September 19, 2023

131004 views

I have read a criticism that thiamine deficiency is “too simple” to explain the devastating nature of the post Gardasil illnesses or the systemic adverse reactions to some medications. Sometimes, it is the simple and overlooked elements that are the most problematic.

Understanding Thiamine’s Role in Complex Adverse Reactions – The Limbic System

The lower part of the brain, called the brainstem, is a like computer, controlling the most basic aspects of survival, from breathing and heart rate, hunger and satiety, to fight or flight and reproduction. This computer-like function within the brainstem is called the autonomic system (ANS). The ANS together with the limbic system act in concert to regulate our most basic survival functions and behaviors. Both require thiamine to function.

Postural Orthostatic Tachycardia Syndrome or POTS , a type of dysautonomia (dysregulation of the autonomic system) seems to be the among the commonest manifestations of the Gardasil effect. Many cases have been diagnosed already, while others present all of the symptoms but have yet to receive a diagnosis. Dysautonomia and POTS have also been observed with adverse reactions to other medications, as well. Dysautonomia and POTS, at the most basic level, represent a chaotic state of the limbic-autonomic system. Let me explain.

Fragmented Fight or Flight

The brainstem autonomic system together with the limbic system enable us to adapt to our environment, presiding over a number of reflexes that allow us to survive. For example, fight-or-flight is a survival reflex, triggered by perception of a dangerous incident that helps us to kill the enemy or escape. This kind of “stress event” in our ancestors was different from that we experience today. Wild animal predators have been replaced by taxes/business deadlines/rush hour traffic etc. These are the sources of modern stress. The beneficial effect is that the entire brain/body is geared to physical and mental response. However, it is designed for short term action and consumes energy rapidly. Prolonged action is literally exhausting and results in the sensation of fatigue. In the world of today where dietary mayhem is widespread, this is commonly represented as Panic Attacks, usually treated as psychological. They are really fragmented fight-or-flight reflexes that are triggered too easily because of abnormal brain chemistry.

Thiamine and Oxidative Metabolism: The Missing Spark Plug

Our brain computers rely completely on oxidative metabolism represented simply thus:

Fuel + Oxygen + Catalyst = Energy

Each of our one hundred trillion body/brain cells is kept alive and functioning because of this reaction. It all takes place in micro “fireplaces” known as mitochondria. Oxygen combines with fuel (food) to cause burning or the combustion – think fuel combustion engine. We need fuel, or gasoline, to burn and spark plugs to ignite in order for the engines to run.

In our body/brain cells it is called oxidation. The catalysts are the naturally occurring chemicals we call vitamins (vital to life). Like a spark plug, they “ignite” the food (fuel). Absence of ANY of the three components spells death.

Antioxidants like vitamin C protect us from the predictable “sparks” (as a normal effect of combustion) known as “oxidative stress”. Vitamin B1, is the spark plug, the catalyst for these reactions. As vitamin B1, thiamine, or any other vitamin deficiency continues, more and more damage occurs in the limbic system because that is where oxygen consumption has the heaviest demand in the entire body. This part of the brain is extremely sensitive to thiamine deficiency.

Why Might Gardasil Lead to Thiamine Deficiency?

We do not know for sure how Gardasil or other vaccines or medications have elicited thiamine deficiency, but they have. We have two girls and one boy, tested and confirmed so far. More testing is underway. Thiamine deficiency in these cases may not be pure dietary deficiency. It is more likely to be damage to the utilization of thiamine from as yet an unknown mechanism, affecting the balance of the autonomic (automatic) nervous system. It is certainly able to explain POTS (one of the many conditions that produce abnormal ANS function) in two Gardasil affected girls. Beriberi, the classic B1 deficiency disease, is the prototype for ANS disease. Administration of thiamine will not necessarily bring about a cure, depending on time since onset of symptoms, but it may help.

Thiamine Deficiency Appetite and Eating Disorders

Using beriberi as a model, let us take appetite as an example of one of its many symptoms. When we put food into the stomach, it automatically sends a signal to a “satiety center” in the computer. As we fill the stomach, the signals crescendo and the satiety center ultimately tells us that we have eaten enough. Thiamine deficiency affects the satiety center, wrecking its normal action. Paradoxically it can cause anorexia (loss of appetite) or the very opposite, a voracious appetite that is never satisfied and may even go on to vomiting. It can also shift from anorexia to being voracious at different times within a given patient. That is why Anorexia Nervosa and Bulimia represent one disease, not two.

Thiamine Deficiency, Heart Rate and Breathing

The autonomic nervous system, responsible for fight or flight, regulates heart activity, accelerating or decelerating according to need. So heart palpitations are common in thiamine deficiency. Its most vital action is in control of automatic breathing and thiamine deficiency has long been known to cause infancy sudden death from failure of this center in brainstem.

Thiamine Deficiency and Sympathetic – Parasympathetic Regulation

The hypothalamus is in the center of the brain computer and it presides over the ANS, as well as the endocrine (hormone) system. The ANS has two channels of communication known as sympathetic (governs action) and parasympathetic (governs the body mechanisms that can be performed when we are in a safe environment: e.g. bowel activity, sleep, etc.). When the ANS system is damaged, sometimes by genetic influence, but more commonly by poor diet (fuel), our adaptive ability is impaired. A marginal energy situation might become full blown by a stress factor. In this light, we can view vaccines and medications as stress factors. From false signal interpretation, we may feel cold in a warm environment, exhibiting “goose bumps on the skin”, or we may feel hot in a cold environment and experience profuse sweating. The overriding fatigue is an exhibition of cellular energy failure in brain perception.

Sometimes, it really is the simple, overlooked, elements that cause the most devastating consequences to human health. Thiamine deficiency is one of those elements.

To learn more about thiamine testing: Thiamine Deficiency Testing: Understanding the Labs.

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

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This article was published originally in October 2013.

Childhood Seizures Precipitated by Thiamine Deficiency

by Sonja

Published on September 11, 2023

2003 views

The seizures started for the first time with a frightened expression in my then 4 year old precious daughter’s eyes, and I thought she had seen a ghost. She held her chest, looked wide eyed, ran over to me and buried her head into my stomach where I felt her heart beating hard and fast. It lasted a few seconds and then I reassured her and on went on. She said it was like strong butterflies in her belly. It also was the morning after her lovely grandparents left after a 3-month visit back to Ireland and we were all very sad.

For approximately one year prior to this, she had been complaining of stomach aches, top and bottom, occasionally under her ribs. She had reduced appetite and a very worrying paleness. She also was very car-sick so we had to prepare for longer journeys. I had been to the ER after Christmas lunch when she had terrible stomach pain. She was checked to be ‘fine’ but I was advised to see a pediatrician to follow up.

Panic Attacks or Seizures?

Basic blood tests confirmed she was in ‘great health’, with the only thing they found in a stool test being h-pylori. So it was their opinion that she wasn’t having seizures but instead must be anxiety/panic attacks as she is a sensitive child. I was always skeptical, but in absence of any other data, we waited a long time for the referred psychologist. After 3 sessions, I realized they had no intel and were chasing the wrong dragon. I kept saying she looked somewhat unwell. The seizures were happening quite infrequently then, perhaps one episode a month, or every 2-3 weeks, but then when she started kindergarten they ramped up a little more frequently. She would stop, look to be catching her breath, hand twisting for a few seconds and then it was over. I thought it was a reaction to the food they fed her there that we didn’t have at home, or a recent childhood vaccination or that she hated being away from me there. I also noticed she reacted with bad behavior and potential episodes after certain foods- e.g. ice cream especially and any food dyes/flavors. So our already healthy diet went up a notch to exclude these. I also did gluten and dairy free on advice from naturopaths. It was strict and sad.

Then these episodes changed to resemble a seizure more directly, not a panic attack. I got rid of the useless pediatrician who was actively gaslighting me to try to minimize the symptoms or their own incompetence and I demanded to see a neurologist. It was again a very long waiting game. When the day came, we were very nervous but were looking forward to some potential answers. He was a neurologist at a prominent Children’s Hospital, so I had high expectations. I still had many questions and areas to workshop but after he ran through my extensive notes and a video I took, he said ”let me stop you, She has epilepsy and ‘NOTHING YOU DO WILL EVER MAKE A DIFFERENCE. She will need medication for life and if that fails an operation”. This was also via video link, as it was during a Covid lockdown. No physical examination and a script sent in the mail. I accepted these, as I know you don’t refuse unless you want trouble, but my intention was to never band-aid or experiment, especially not with a young child and my family’s history of sensitivity to medication. Thank god he lied so blatantly when he said ”there’s no side effects from the anti-seizure meds” to know we weren’t dealing with the truth or someone who could be trusted.

We did another two MRIs, but they were clear. They wanted a third with dye contrast but I refused that and as I learned more about her case, know why I felt so strongly about that.

A Parade of Doctors

We embarked on the alternative/functional medicine pathway, as that is something I am familiar with. I didn’t realize how challenging it was going to be. We went from one to the other. I was constantly seeking experts who possibly knew more than the last. I needed help to decode this horror. I know a healthy child doesn’t get a whisper of issues that then progress to a scream over years for no reason.

With each new practitioner, we did another test. This included blood tests, stool test, hair tests, OAT test, Pyrrole and extensive Genetic testing. She was found to have higher copper ceruloplasmin to be treated simply with zinc, which was always met with a seizure so we stopped that. She had high vitamin D and B12, but another test found that potentially wasn’t a true representation. It can be in the blood reading but not necessarily in her cell. This is where you really throw your hands-up and say what chance do we have if some test results can also be falsely represented!!!!!

The genetic testing provided the best clue that we weren’t dealing with an easy case- she had heterozygous compound MTHFR, and many other compromising genes that are not ideal on many pathways, especially detox. This also got me remembering how I haven’t felt optimal for years. I put it down to extreme stress with my daughter. A huge thing I always wanted to understand was why I was so incredibly sick with Hyperemesis Gravidarum the entire pregnancy with her. I have always believed this had to have impacted her somewhere but could never nail down a connection.

After 5 naturopaths and numerous consults from other medical professionals, listening to one bogus diet restriction after the next, many different versions of expensive supplements that basically all triggered her. Nothing was working. She was having seizures weekly or more particularly is she was sick or overly stressed. The closest theory I could deduce of was a type of MCAS or histamine intolerance and the symptoms were:

Crying out prior
Frequently occurring in sleep waking her bolt upright
Hyperventilation/can’t get air
Big scared eyes
Drooling, disorientated
Body shaking, head was twisting hard to the side like dystonia, arms curled, torso completely contorted.

This would last for about 30 sec-1 min. The horror of witnessing this is imprinted on my soul forever. She began to lose balance so we would have to grab and hold her and I would blow hard in her face to try to get it to finish. It started to become dangerous if we weren’t around to catch her.

I also simultaneously worked back one item at a time to try to fix every variable I could, including environmental. There was a mold spot in our house in the room she slept in the bathroom. It took a long time to get repaired, I pondered about that exposure and if the builder actually fixed the leak properly. Our awful neighbor had smoky barbeques numerous times a week on the fence-line using building offcut wood. The smoke permeated our house. We sold our house to see if that made a difference and moved to the country with my parents’ house in the green clean air.

Thiamine and Riboflavin Deficiencies With Genetic Underpinnings

I finally found a practitioner trained in epigenetics with a naturopath background as I wanted someone like Ben Lynch. His YouTube videos were the only things that made sense to break down a complex health issue. She was a blessing and truly eclipsed the level of detail of knowledge (and empathy) by all others. She looked at the OAT test (shown to 5 people previously) and saw immediately she had very high lactic acid and some other markers indicating thiamine deficiency, critically followed by a riboflavin (B2) deficiency. She advised to not give a B complex and work through one at a time.

When we tried to treat this with thiamine and a B2 capsule. I am sure she had a paradoxical reaction as she had 8 seizures in the night. It was horrifying. I wanted to abort this plan like so many other failed attempts, as I never prolong anything that’s not showing positive traction, but something told me to break it down and do one step at a time. I went back into her genetics myself and looked at the thiamine related genes. She had homozygous defects in a key thiamine transporter (SLC19A2) and an enzyme (thiamine pyrophosphokinase – TPK1) that turns free thiamine into its bioactive form thiamine pyrophosphate. She also had SNPs in several other key thiamine genes, in addition to SNPs in several other mitochondrial genes.

I also came across and watched Elliot Overton’s Thiamine videos on YouTube and how to correctly dose-up. I also read many insightful articles on the Hormones Matter website. I tried again with low dose of b1 (about 5mg), some magnesium and potassium-coconut water. The seizures, in the midst of a horrible flare, stopped immediately and didn’t return for over 2 months. I dosed twice a day and worked up to 50mg of thiamine in total, which is where she is currently. She also got much better color in her face. It truly felt like a miracle!

What Else Are We Missing?

The miracle, however, ended and the seizures have been creeping back in and I’m not sure why. They seem not quite as severe in presentation, however they still occur about once a week to every 2 weeks. I need to understand why and how to help her as my intuition screams at me to find the answer, and quick! She is now 8 years old and I am struggling to comprehend any more of her childhood being stolen.

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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, and like it, please help support it. Contribute now.

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Blood Brain Barrier Integrity and Early Thiamine Deficiency

by Chandler Marrs, PhD

Published on September 7, 2023

2453 views

In my quest to understand oxythiamine (oxythiamine is an anti-thiamine molecule that appears to be synthesized in individuals with kidney disease), I stumbled upon a study from the mid-nineties where researchers examined blood brain barrier (BBB) integrity in early and late thiamine deficiency. They found that BBB breakdown not only preceded the pathogenesis of the more commonly considered white matter lesions associated with severe and chronic thiamine deficiency, but that BBB disintegration drives the deficiency-induced brain damage. This makes sense, of course, given thiamine’s role in energy metabolism and the fact that barrier function is energy intensive. If metabolic energy declines, then the barrier’s ability to prevent noxious molecules from reaching the brain will decline, as will its ability to filter out endogenously created waste products and other toxins. The entire exchange process will be weakened and across time, brain damage will accumulate.

Insofar as the gut barrier and the brain barrier are intimately connected, might we surmise that if BBB disintegration precedes and drives much of the brain damage evoked by thiamine deficiency, then would not ‘leaky gut’ and the symptoms therewith come before the leaky brain? I believe so. This was not part of this experiment and in no way indicated directly, but there were some hints that point me in this direction and certainly research published over the last decade or so supports this.

In this particular study, the investigators were looking at the patterns of dysfunction that arose when thiamine deficiency was induced by different mechanisms. To explore these differences, they used four groups of mice:

Group 1: Mice fed a thiamine-free diet and given pyrithiamine, a thiamine antagonist that readily crosses the BBB.
Group 2: Mice fed a thiamine-free diet and given oxythiamine, a competitive thiamine antagonist that blocks the transketolase enzyme, but does not appear to cross the BBB.
Group 3: Mice fed a thiamine-free diet and given pyrithiamine for 10 days, and then fed a normal diet and given thiamine (20mg/kg) injections. This was to determine whether recovery was possible.
Group 4: The control group fed a normal diet.

Groups 1, 2, and 4 were sacrificed on days 8, 9, and 10, while group 3 was sacrificed on day 14.

I should note that estimates equating mouse lifespan with human lifespan propose that 9 days in the life of a mouse is equivalent to about one human year. In contrast, for rats, researchers estimate that 13.2 days equal one human year. Keep these numbers in mind when considering animal research. Other differences apply, of course, but lifespan differences are huge.

With that in mind, in this particular study where thiamine was completely abolished from diet and blocked using anti-thiamine molecules, neurological symptoms appeared after 10 days of thiamine deprivation in mice and if thiamine was not repleted, the animals died within 48 hours thereafter. In contrast, rodents can live up to 4-5 weeks before succumbing to the effects of thiamine deficiency.

This would seem to suggest that we, as humans, might survive the complete absence of thiamine from diet, plus anti-thiamine blockade via pyrithiamine, for up to a year. This is unlikely. However, experiments using extremely low doses of thiamine (.15-.45mg p/day) have shown survival, with severe neurological deficits and damage, but survival nevertheless, for up to 6 months. We also have reports of patients with significant, lab tested deficiency who, though quite ill, live for years.

In contrast to the experimental conditions though, with human thiamine deficiency, especially as it develops later in life (genetic defects that appear at birth are a different story), there is rarely a complete blockade of thiamine or absence of thiamine from diet. Dietary consumption and anti-thiamine factors vary considerably from day to day and year to year and so the trajectory from deficiency to illness in humans will be prolonged and non-linear. That being said, there are some things we can learn from experimental protocols such as this one. Namely, that the mechanism of deficiency matters as it will affect which body compartments are affect most prominently in the early stages.

The Compartmentalization of Thiamine Deficiency

In this study, we saw the effects of long term thiamine deficiency in different tissues generated by the different anti-thiamine molecules. Pyrithiamine affected the brain and nervous system, while the effects of oxythiamine were most prominent in the periphery, likely the GI system and in the heart, although these were not tested.

We also see the time course of symptomology, where early on symptoms are not as noticeable until a certain threshold of damage is met. For example, neither histological lesions nor symptoms were obvious prior to day 8 of thiamine deprivation in the pyrithiamine group. This is roughly equivalent to almost a year in human life span. The animals showed an initial weight gain followed by a sharp decline on day 9 and the onset severe neurological symptoms at day 10. According to the researchers:

The initial neurological signs of thiamine deficiency appeared acutely and precisely on day 10, consisting of loss of activity, hyperactivity on acoustic or tactile stimulation, and ataxia.

Commiserate with the neurological symptoms in the pyrithiamine group, disturbed BBB function, necrosis, and numerous brain lesions were observed. If thiamine was withheld, the animals died within 48 hours. If thiamine was repleted (this was done only with the pyrithiamine group), most, but not all, of the animals survived and neurological symptoms abated. This is promising, but suggests there are still unrecognized variables that influence recovery.

In contrast, there were no lesions within this timeframe for the oxythiamine group. With oxythiamine, the only observable symptoms were weight loss and decreased activity. In fact, the oxythiamine animals maintained normal weight and activity until day 6 and then on day 8, there was observable weight loss, anorexia and decreased activity. There were no behavioral signs of neurological damage. It is not clear at what point the oxythiamine animals would have died naturally or by what means, as they were sacrificed at day 10 regardless of state.

The Heart of the Matter

Another study using rodents, points to oxythiamine affecting the heart more prominently than pyrithiamine. Here, oxythiamine treated rats showed a similar pattern of weight loss beginning after the 7^th day, but also developed bradycardia and cardiac hypertrophy, which progressively worsened over the next few weeks. In contrast, the animals treated with pyrithiamine did not show heart-related changes until after developing the neurological symptoms. Moreover, the heart-related changes were not as prominent as those in the oxythiamine group. I will discuss this study more fully in a subsequent post, but it seems to suggest different mechanisms for what we call wet and dry beriberi. That is, oxythiamine results in peripheral metabolic symptoms perhaps related first to the GI system (weight loss and anorexia) and then to the heart, while blockade of thiamine via pyrithiamine results in brain and nervous system symptoms and damage. In both cases, I suspect there is disruption to gut barrier function. With pyrithiamine though barrier dysfunction seems to begin in the brain and nervous system and progress to the periphery, whereas with oxythiamine preferentially targets tissues in the periphery and only later reaches the BBB and the nervous system. Again though, this is not clear. As most of the studies I have read seem to investigate only one or the other.

Obviously, the mechanisms by which these two molecules deplete thiamine differs significantly, which then explains many of the differences observed in the animals, but what intrigues me is how closely the ‘symptoms’ align with human cases of thiamine deficiency where neither compound is administered. This begs many questions, not the least of which is whether and how we might produce these molecules endogenously or be exposed to them in everyday life. How could these patterns observed experimentally so closely align with the human experience (wet beriberi – oxythiamine, dry beriberi – pyrithiamine), where neither compound is provided. I do not know the answer. Yet. In the meantime, here is some more information on the mechanisms of oxythiamine and pyrithiamine and how we might be synthesizing them endogenously: Can We Synthesize Oxythiamine and Pyrithiamine Endogenously?

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It All Comes Down to Energy

by Derrick Lonsdale MD, FACN, CNS

Published on August 10, 2023

14656 views

The Threat Around Us

Animals, including Homo Sapiens, survive in an essentially toxic environment, surrounded by microorganisms, potential poisons, the risk of trauma, and adverse weather conditions. Evolutionary development has equipped us with complex machinery that provides defensive mechanisms when any one of these factors has to be faced. Before the discovery of microorganisms, medical treatment had no rhyme or reason, but killing the microorganisms became the methodology. The research concentrated on ways and means of “killing the enemy”, the bacteria, the virus, the cancer cell. The discovery of penicillin reinforced this approach. We are now facing a period of potential impotence because of bacterial resistance, failure of attempts to kill viruses, and the resistance to chemotherapeutic agents in cancer. Louis Pasteur is purported to have said on his deathbed, “I was wrong, it is the terrain that matters”, meaning body defenses.

Hans Selye, whose research into how animals defend themselves when attacked by any form of stress, led to his description of the General Adaptation Syndrome (GAS). He recognized the necessity of energy in initiating the GAS and its failure in an animal that succumbed to stress. He labeled human disease as “the diseases of adaptation”. In Selye’s time, there was little information about energy metabolism but today, its details are fairly well-known. The suggestion of a new approach depends on the fact that our defenses are metabolic in character and require an increase in energy production over and above that required for homeostasis. If the GAS applies to human physiology and that we are facing the “diseases of adaptation”, it is hypothesized that research should be applied to methods by which energy metabolism can be stimulated and mobilized to meet the stress.

Energy Deficiency, Defective Immunity, and COVID-19

There is evidence that energy deficiency applies to each of the diseases described here. It may be the unrecognized cause of defective immunity in Covid-19 disease. Although in coronavirus disease the clinical manifestations are mainly respiratory, major cardiac complications are being reported involving hypoxia, hypotension, enhanced inflammatory status, and arrhythmic events that are not uncommon. Past pandemics have demonstrated that diverse types of neuropsychiatric symptoms, such as encephalopathy, mood changes, psychosis, neuromuscular dysfunction, or demyelinating processes may accompany acute viral infections or may follow infection by weeks, months, or longer in viral recovered patients. Electrocardiographic changes have been reported in Covid-19 patients. The authors suggest that it may be attributed to hypoxia as one possibility. Because the total body stores of thiamine are low, acute metabolic stress can initiate deficiency. Thiamine deficiency has a clinical expression similar to that observed in hypoxic stress and the authors referred to it as pseudo-hypoxia. It is therefore not surprising that defective energy metabolism can express itself clinically in many different ways.

The present medical model regards each disease as having a separate cause, but the large variety of symptoms induced by thiamine deficiency suggest the ubiquitous nature of energy deficiency as a cause in common. Obesity, a reflection of high calorie malnutrition, has been published as a risk factor for patients admitted to intensive care with Covid-19. Thiamine deficiency was reported in 15.5-29% of obese patients seeking bariatric surgery. Hannah Ferenchick M.D. an emergency room physician commented online that many of her patients with Covid-19 had what she called “silent hypoxemia”. These patients had an arterial oxygen saturation of only 85% but “looked comfortable” and their chest x-rays “looked more like edema” It has long been known that patients with beriberi had low arterial oxygen and a high venous oxygen saturation. All that would be needed to support the hypothesis of thiamine deficiency in some Covid victims would be finding a high venous oxygen saturation at the same time as a low arterial saturation. Also, edema is a very important sign of beriberi, and thiamine deficiency has been noted in critical illness.

Disrupted Autonomic Function

There have been many articles in medical journals describing dysautonomia, mysteriously in association with a named disease, but with no suggestion that the dysautonomia is part of that disease. More recently, there is increasing evidence that dysautonomia is a feature of chronic fatigue syndrome (CFS), manifested primarily as disordered regulation of cardiovascular responses to stress. Manipulating the autonomic nervous system (ANS) may be effective in the treatment of CFS. Dysautonomia is also a characteristic of thiamine deficiency. Patients with Parkinson’s disease begin to lose weight several years before diagnosis and a study was undertaken to investigate this association with the ANS. Costantini and associates have shown that high dose thiamine treatment improves the symptoms of Parkinson’s disease, although the plasma thiamine concentration was normal. They have also shown that high dose thiamine treatment decreases fatigue in inflammatory bowel disease, Hashimoto’s disease, after stroke, and multiple sclerosis. As already noted, it is also an important consideration in critically ill patients.

Multiple System Atrophy is a devastating and fatal neurodegenerative disorder. The clinical presentation is highly variable and autonomic failure is one of its most common problems. Dysautonomia was found to be a clinical entity in Ehlers-Danlos syndrome, a musculoskeletal disease, and this syndrome frequently coexists with Postural Orthostatic Tachycardia Syndrome (POTS), a disease that is included in the group of diseases under the heading of dysautonomia. Some cases of POTS have been reported to be thiamine deficient. This common condition often involves chronic unexplained symptoms such as inappropriate fast heart rate, chronic fatigue, dizziness, or unexplained “spells” in otherwise healthy young individuals. Many of these patients have gastrointestinal or bladder disorders, chronic headaches, fibromyalgia, and sleep disturbances. Anxiety and depression are relatively common. Not surprisingly the many symptoms are often unrecognized for what they represent and the patient may have a diagnosis of psychosomatic disease.

Immune-Mediated Inflammatory Diseases (IMIDs) is a descriptive term coined for a group of conditions that share common inflammatory pathways and for which there is no definite etiology. These diseases affect the elderly most severely with many of the patients having two or more IMIDs. They include type I diabetes, obesity, hypertension, chronic pulmonary disease, coronary heart disease, inflammatory bowel disease, rheumatoid arthritis, Sjogren’s syndrome, systemic lupus, psoriasis, psoriatic arthritis, and multiple sclerosis. The recent recognition of small fiber neuropathy in a large subgroup of fibromyalgia patients reinforces the dysautonomia-neuropathic hypothesis and validates fibromyalgia pain. These new findings support the disease as a primary neurological entity.

Energy Deficiency During Pregnancy: The Cause of Many Complications

Irwin emphasized the energy requirements of pregnancy in which the maternal diet and genetics have to be capable of producing energy for both mother and fetus. He found that preventive megadose thiamine, started in the third trimester, completely prevented all the common complications of pregnancy. Hyperemesis gravidarum is the most common cause of hospitalization during the first half of pregnancy and is second only to preterm labor for hospitalization in pregnancy overall. This disease has been associated with Wernicke’s encephalopathy, well known to be due to brain thiamine deficiency. The traditional explanation is that vomiting is the cause, but since vomiting is a symptom of thiamine deficiency, it could just as easily be the cause rather than the effect. In spite of the fact that migraines are one of the major problems seen by primary care physicians, many patients do not obtain appropriate diagnoses or treatment. Migraine occurs in about 18% of women and is often aggravated by hormonal shifts. A complex neurological disorder involving multiple brain areas that regulate autonomic, affective, cognitive, and sensory functions, it occurs also in pregnancy. Features of the migraine attack that are indicative of altered autonomic function include nausea, vomiting, diarrhea, polyuria, eyelid edema, conjunctival injection, lacrimation, nasal congestion, and ptosis.

The Proteopathies: Disorders Involving Critical Enzymes

The earliest and perhaps best example of an interaction between nutrition and dementia is related to thiamine. Multiple similarities exist between classical thiamine deficiency and Alzheimer’s disease (AD), in that both are associated with cognitive deficits and reductions in brain glucose metabolism. Thiamine-dependent enzymes are critical components of glucose metabolism that are reduced in the brains of AD patients. Senile plaques and neurofibrillary tangles are the principal histopathological marks of AD and other proteopathies. The essential constituents of these lesions are structurally abnormal variants of normally generated proteins (enzymes). The crucial event in the development of transmissible spongiform encephalopathies is the conformational change of a host-encoded membrane protein into a disease associated, fibril forming isoform. A huge number of proteins that occur in the body have to be folded into a specific shape in order to become functional. When this folding process is inhibited, the respective protein is referred to as being mis-folded, nonfunctional, and causatively related to a disease process. These diseases are termed proteopathies and there are at least 50 different conditions in which the mechanism is importantly related to a mis-folded protein. Energy is required for this folding process. Because of their reported relationship with thiamine, it has been hypothesized that mis-folding might be related to its deficiency on an energy deficiency basis.

It All Comes Down to Energy

A hypothesis has been presented that the overlap of symptoms in different disease conditions represents cellular energy failure, particularly in the brain. If this should prove to be true, the present medical model would become outdated. An attack by bacteria, viruses or an oncogene might be referred to as “the enemy”. The defensive action, organized and controlled by the brain, may be thought of as “a declaration of war” and the illness that follows the evidence that “a war is being fought”. This concept is completely compatible with the research reported by Selye. It underlines his concept that human diseases are “the diseases of adaptation”, dependent on energy for a successful outcome in a “war” between an attacking agent and the complex defensive actions of the body. Killing the enemy is a valid approach to treatment if it can be done safely. Unfortunately, the side effects of most medications sometimes makes things worse and that is offensive to the Hippocratic Oath. We badly need to create an approach to research that explores ways and means of supporting and stimulating the normal mechanisms of defense.

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

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This article was published originally on May 11, 2020.

Health Shattered By Poor Diet and Conventional Medicine

by Tawnya Bareis

Published on August 8, 2023

8901 views

My health has declined over the last few decades, to the point that I am totally disabled and haven’t driven in 10 years. I have severe POTS with high blood pressure while sitting and laying down. Previously, it was low. I am not able to stand up as my heart rate goes too high and I feel as though I’ll pass out. I have coat hanger pain, jaw tension, and headaches daily. I am very irritable and impatient. Emotional outbursts crying spells, depression. I feel like I am a completely different person. I am in survival mode. My body cannot shift out of sympathetic dominance. All of this has developed over the last 20 years; a progressive decline until everything hit the fan.

I thought I had a relatively healthy childhood and into my early 20s. I did have mono in 7th grade. Looking back though, I ate poorly growing up and did a lot of crazy starvation diets. I also consumed a lot of alcohol in my later teens through my early 20s. I stopped drinking in 1994. However in 2006, I started drinking on and off again and the night I had the severe vertigo attack, I had been drinking. Since then I haven’t touched alcohol.

My mom passed away when I was 22 and I had my first child at 23, which was a C-section. At 26, I developed rosacea. This was really my first health problem. At 27, I was divorced (1993). I remarried a year later and had another child at 30 years old. Three months later, I had my gallbladder removed. With all of this, I was still active and healthy with only rosacea that would come and go, but it would get really bad on occasions and was very distressing. This was until 2007, when life stressors, poor diet and illness caught up with me.

Unending Vertigo and the Protracted Decline of Health

I started working again in 2000 after we relocated to Arizona. I was a preschool teacher, a wife, and was raising my two sons. I had a very full schedule. I was always a high achiever. In 2004, I opened my own school with another teacher. Things got even more stressful. In January 2007, I had a very emotional falling out with my father and a couple weeks after that I was diagnosed with viral pharyngitis. Within a couple weeks of this diagnosis, I was thrown out of bed with the worst vertigo you can ever imagine. This went on for three days and I was unable to walk for over two weeks. As things were improving, the dizziness never did go away. I sought out multiple practitioners, including neurologists and audiologists, but none were able to help.

I went back to work but I was never the same, having to deal with constant dizziness and feeling of being off-balance. In October of 2007, I wound up in the ER with a resting heart rate of 160. This had come on out of nowhere over the day and by the evening I was very frightened. They gave me lorazepam and sent me on my way. I continued with the constant dizziness and then the anxiety and panic attacks started. My GP gave me a script for benzodiazepine and offered an anti-depressant. I tried the antidepressant and I had a bad reaction. I felt completely numb. I couldn’t laugh smile or have any sort of reaction. That was after just try half a tablet. I never tried that again.

In 2009, I had an ankle injury and was wearing a boot for most of that year. In October, of that year I ended up having a surgery on it. What was interesting is that I was not experiencing much of the dizziness for most of that year. It wasn’t until a couple months later when I had a sudden onset of the dizziness during my physical therapy session. So the dizziness had come back and the anxiety and panic attacks were getting worse. In September 2010, I basically collapsed at work. It was about four or five days later at home, I experienced a severe shift of my energy. I was severely fatigued and now was experiencing POTS.

Is it Lyme? Maybe. Maybe Not.

November 2010, I was diagnosed with Lyme, however, my test was not conclusive. The Lyme literate doctor said my immune system was so weak that it was hard to get a positive result. He diagnosed me clinically. This set me off on a seven year journey of protocols that included benzodiazepines, two IV chest ports, supplements, herbs, homeopathics, bio-hormones, coffee enemas, detoxification therapies, chelation, IV and oral antibiotics, Flagyl, anti-fungal drugs, and every diet imaginable. You name it I did it. We had spent our life savings and I was still disabled and incredibly ill.

I became addicted to the benzodiazepines that he prescribed. He never told me about how addictive they were. I was on them for three years and they made me so much worse! I tried to come off of them several times. They turned me into a 3 year old. I was so fearful I couldn’t leave my bedroom even to cross the hall into bathroom. Finally, in 2014 I was able to kick the addiction. It took me six months of liquid titration.

As If Things Weren’t Bad Enough: Cancer Too.

Also in 2014, I had a huge fibroid and had a procedure called UFE ( uterine fibroid embolization ) to cut off blood supply so it would shrink. I know now I had severe estrogen dominance.

In 2017, I hit menopause and stopped menstruating. I was using sublingual progesterone at the time. The doctor also had me on hydrocortisone for adrenals and a time-release thyroid supplement. These supplements never helped and only made me worse. I was in such bad shape. I wasn’t sleeping for 3 to 4 days at a time and then when I would sleep it was only couple hours. This sleep regime went on all year.

In May of that year, I woke up one morning and left breast had shrunk significantly overnight!! The doctor I was seeing, had me come in. He physically examined me and felt that it was not anything to worry about. He said that I needed to detoxify my breast because it was probably blocked lymph. He told me to do skin brushing on it. I was in such bad shape that I wanted to believe him but I was so frightened. In October, I saw a different doctor and she said I had to get a biopsy. It was cancer. I did not see an oncologist. I did not have any lymph nodes removed or chemo radiation. I just had a surgeon remove it. I left the rest up to God. At this point, I could not endure anything else mentally or physically. The pathology report indicated the cancer was 98% estrogen driven.

A Dysautonomia Specialist Prescribed More Antibiotics

In 2018, I tried one more doctor. He was an autonomic dysfunction doctor and his protocol was quite simple. It was focused on lowering inflammation in the brain and body and balancing gut bacteria. At this point, I had suffered from chronic constipation for at least 10 years, on top of POTS and all of the other health issues. I was put on fish oil, olive oil, Rifaxamin and Flagyl for the possible SIBO and a vagus nerve stimulator. He told me not to use any other supplements of any kind. He claimed that most all supplements were fraudulent and using them would interfere with progress. I could not finish the Flagyl. I was feeling severely agitated and I thought it was due to the drug. I took most of it though. He assured me that the Rifaxamin was very safe and that they actually have renamed this antibiotic as a eubiotic. I did see my rosacea clear up. I had read some research and trials were they used Rifaxamin for rosacea and had a very positive outcome. So over the last 2 1/2 years I’ve been faithful on this protocol. It seemed like I had periods of time where I was able to stand up longer and do more around my house but I always relapsed. I was using the Rifaxamin on and off as per his direction for 10 days at a time. This year he put me on it indefinitely to use daily. I’ve been on it now for 8 months straight, but in July I started to go downhill very fast. I was having a decent spell able and had been able walk around for a a bit, do some limited chores and even able to be out in the pool, but one night my heart just went crazy and began to race. The vertigo came back too. I have been bedridden again since.

Discovering Thiamine Deficiency

After going back to doing some research, I came upon Dr. Lonsdale and Dr. Marrs’ book Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition. I am thinking thiamine deficiency could be a piece of my puzzle. After reading one of Dr. Lonsdale’s articles on high B12 correlating with thiamine deficiency, I remembered two of my B12 tests. One in 2014, where it was 2000 and one in 2017 was 1600. The max upper range is 946.

Although my ill health was progressive at first, over time, everything has just become unbearable. I have been bedridden now for 10 years. The POTS symptoms are severe and I think I have the hyperadrenergic POTS. My blood pressure is very high when both sitting and laying and when I stand up, both my blood pressure and heart rate climb. I feel as though I’ll pass out. As I mentioned previously, I also have coat hanger pain, jaw tension, and headaches daily. I am very irritable and impatient. Emotional outbursts crying spells, depression. I feel like I am a completely different person. I am in survival mode. My body cannot shift out of sympathetic dominance. I am hoping to get some direction and advice on using thiamine to possibly help my condition.

Supplements, Medications, and Diet

Upon learning about thiamine and mitochondria, I stopped taking the Rifaxamin about two weeks ago. Below is a list of supplements I currently take and some information about my diet.

Magnesium hydroxide, Magnesium glycinate, 100mg, magnesium citrate, 100mg and some magnesium oxide in an electrolyte drink, in some variation for the past 3 years
3000mg daily (6caps) DHA 500 by Now Foods for past 3 years
Liver capsules 4 daily past 3 months
Camu Camu powder, a natural Vitamin C, 100-300 mg just started about two weeks ago
Rice bran 1 tsp before bed started two weeks ago
Bee pollen 1/2 tsp daily, started 3 months ago
I follow gluten free diet. I eat beef, chicken, raw liver, raw dairy, raw kefir, cheese, bone broth, some fruit, oatmeal and some vegetables like tomatoes, green beans, onions.

Since learning about thiamine, I have begun using Thiamax but am having a rough time of it. I took my first half dose (50mg) of Thiamax on December 26, 2020 and continued that dose through December 31st. It seemed to increase my fatigue more than my normal, which is already pretty debilitating so I switched to 50mg thiamine HCL on January 1st. By January 3^rd, I had a big crash. Hoping to minimize these reactions, on January 4th I took 25 mg thiamine HCL with 12 mg Thiamax in two divided doses. The next evening, however, I rolled over at 2 AM and my heart rate went crazy. I was shaking and went into a panic attack. It took hours to settle down. I haven’t had anything like this in quite a few years and I can’t imagine this would be from the tiny doses of thiamine I’ve been taking. I also took 600mcg of biotin that night at around 6pm. This was for a longstanding fungal infection. The biotin may have contributed to my reaction, but I do not know. I skipped the thiamine and biotin the next day and was able to sleep. I have resumed the thiamine once again and so far, I am tolerating it. I understand that people with chronic health conditions have difficulty adjusting to thiamine and I am trying my best make it through to the other side, but these reactions are difficult to manage. Any input from others who have been through this would be appreciated. I desperately want to recover my health.

We Need Your Help

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

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Image by (El Caminante) from Pixabay.

This story was published originally on January 11, 2021.

thiamine deficiency - Page 3

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