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Lessons Learned About Recovering From Thiamine Deficiency

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It has been a year since I started taking high dose vitamin B1 (thiamine) for a variety of chronic symptoms including: Lyme disease, CFS/ME, endometriosis, histamine intolerance and other food intolerances, SIBO, chronic complicated migraine with aura, chronic insomnia, chronic severe light and exercise intolerance, to name a few. By traditional medicine, each of these conditions was considered unique and thus treated individually. I have learned that they are not separate conditions, but simply different manifestations of disturbed mitochondrial metabolism. In my case, all of this was related to deficiencies in thiamine and other vitamins and minerals. My recovery has been difficult and I have made many mistakes along the way, but hopefully, I learned from them. I am publishing my story here so that you may also learn from my experience. You can read my original story here.

Lesson 1: Magnesium Formulation Is Important

Magnesium is required to change thiamine from its free form to the active form called thiamine pyrophosphate (TPP). Without sufficient magnesium, supplemental or consumed thiamine remains inactive and basically useless. This means that magnesium deficiency can cause a functional thiamine deficiency. I understood this, but what I did not understand, was that there are many different formulations of magnesium supplement, each with pros and cons relative to the individual’s specific needs. I thought they were all interchangeable.

For me, and for individuals with heart related symptoms, magnesium taurate is preferred. One of my first mistakes I made was to ignore Dr. Lonsdale’s comments in which he talked about the importance of taking magnesium taurate. I understood it as meaning that magnesium was important and did not understand that it was a special form of magnesium with cardio protective effects due to the taurine content.

When I initially took magnesium taurate, I noticed an increase in my wellbeing, especially in the fatigue and headache that I would develop after walking around the house or being intellectually active, but I didn’t know that it was the taurine component that was responsible for that change. For a while, I stopped taking magnesium taurate and returned to using other forms of magnesium (magnesium citrate or malate). They did not help as much as the taurate. During this time, I also realized that I do not tolerate magnesium glycinate or bisglycinate. If I take that form, I have a terrible headache on the right side of my head. The glycine activates glutamate via NMDA receptors in the brain causing some excitatory activity. This may be why I could not tolerate it. Others do not have a problem with magnesium glycinate.

Over the last two weeks, I was that taking magnesium malate and taurine separately.  I wanted to avoid spending a lot of money on magnesium taurate, so I tried to buy a cheap form of magnesium – magnesium malate – and combine it with taurine which is inexpensive when purchased in bulk. This did not provide the same benefits as magnesium taurate. I experienced chest pressure and pain and my resting pulse went back to being higher than 65-70 BPM. Once I began taking magnesium taurate again, my heart rate and chest pain/pressure disappeared.

So the lesson here, is that different formulations of magnesium work for different people. It is important to research which form may work better for you and your set of symptoms and not to assume they are interchangeable.

Lessons 2-3: TTFD Degrades with Heat and Light and Interruptions to Thiamine Repletion Cause Setbacks

One other important thing I realized was that thiamine is destroyed by UV light. This meant that in August, when I put my TTFD powder (a form of synthetic thiamine that crosses cell barriers more easily) in a transparent container on the kitchen table, and left it there all day long while sunlight shone directly on it through the big windows in my kitchen, it was being destroyed every day. I experienced a big crash during that month, especially since I was taking all the other vitamins and minerals that were serving as co-factors. I could not explain it and was thinking that even this therapy was losing its effect, that my recovery was over, and that I could no longer hope for a better quality of life.

However, in September, I received my new order of TTFD powder. The very day I received it, I took my regular dosage from this new batch. The difference was incredible in terms of my symptoms. It was night and day. The effects were truly remarkable and unmistakable. I’m very careful now with my TTFD powder and make sure it stays in an opaque container.

Lesson 4: Treating My Carnitine Deficiency. Once Again Formulation Matters.

Another thing that I had not been able to fix was my carnitine deficiency. This was discovered by the neurologist who suspected that I was dealing with a FAOD (fatty acid oxidation disorder) or a mitochondrial disease back in February. Free carnitine levels in blood are supposed to be between 17 and 49, while mine was 6. I tried taking various forms of carnitine (L-carnitine, acetyl-L-carnitine, l-carnitine tartrate, Optimized Carnitine, propionyl-L-carnitine) but they all had a laxative effect which was aggravating my symptoms. I asked my neurologist if there were injections with carnitine that could replace the pills, but was left to figure it out for myself. And I did.

Through much research, I found a form that worked for me. It is called Propionyl-L-Carnitine. This form of carnitine is a known agent that protects against ischemia  – quote from the linked study:

Free CoA and propionyl-CoA cannot enter or leave mitochondria, but propionyl groups are transferred between separate CoA pools by prior conversion to propionyl-L-carnitine. This reaction requires carnitine and carnitine acetyl transferase, an enzyme abundant in heart tissue. Propionyl-L-carnitine traverses both mitochondrial and cell membranes. Within the cell, this mobility helps to maintain the mitochondrial acyl-CoA/CoA ratio. When this ratio is increased, as in carnitine deficiency states, deleterious consequences ensue, which include deficient metabolism of fatty acids and urea synthesis.

This form of carnitine has made a huge difference in my health, especially with one particular symptom – the wet cough that had accompanied my walking around the house since April 2021.

More Energy and Exercise Tolerance with the Correct Supplements

In October, I began taking magnesium taurate and I also added higher doses of potassium to my regimen, just to see if I tolerated them. I had taken rather lower doses of potassium on and off since starting high dose TTFD. One of the things higher potassium solved, was the aftertaste (or after smell) that I used to get with 300 mg TTFD. I know most people dislike it, since it’s a sulphur smell, although I never disliked it.

After about two weeks on magnesium taurate and higher potassium intake with every dose of TTFD, I began propionyl-L-Carnitine HCL and Optimized Carnitine again. I noticed that they no longer had a laxative effect and I doubled my dose of propionyl-L-carnitine HCL so that I was taking about 600 mg three times a day, combined with one capsule of Optimized Carnitine.

After about a week, I noticed that I had more energy. I no longer needed to eat every three or four hours, I no longer had dyspnea or wet cough during the day when I was walking around the house. All those symptoms speak of cardiomyopathy and were resolving with the supplements. I still need to avoid sleeping on my left side and instead sleep on an incline on my back to be able to sleep through the night, but it my sleep is so much better now. My headache, something that has tortured me since I attempted intermittent fasting in 2018, is now gone. This makes me think that the right-sided headache is one of the symptoms of my heart not being able to do its job properly.

One of the things that helps the most with mitochondrial biogenesis is exercise and it is highly recommended for people with mitochondrial disease. However, in many studies it is noted that if cardiomyopathy is present, then this therapeutic cannot really be used. This is important because many people recovered and improved their exercise intolerance, but still develop symptoms after too much physical effort and wonder what they could further do to improve their symptoms.

After finding the right supplements to correct my deficiencies, I’m able to walk around the house without it aggravating or triggering my symptoms. Prior to this, I was largely bedridden and would have flares every time I attempted to do anything. I have a device that measures how many steps I take and it shows that I walk at least 1000 steps per day when I do nothing and spend 95% of the day in bed.
Now I’m able to go out and walk around my apartment building, which is about 150 meters and do not suffer any consequence. I tried walking more than that and if I do, my main symptoms come back (insomnia, heart symptoms and headache). It is progress, but I still have a long way to go.

I am also capable of learning a little bit of German every day. While my memory is still very poor, at least what I learn “stays” in my brain and the knowledge/understanding of the language accumulates slowly day by day. Intellectual activity no longer triggers the terrible, hours-long headache it once did.

Improved Sleep: Correcting the “Histamine Bucket”, Insomnia, and Heart Symptoms

Since becoming ill, I have had insomnia, likely due to my heart struggling to maintain a constant rate and rhythm. One of the very first things I heard that could explain my constant awakenings especially around 2-3am in the morning is the theory of the “histamine bucket”. This theory argues that around 2-3 am, there is some shift in our body’s physiology and histamine is released. Thus, if you already have a lot of histamines in your body, due to mast cell activation or low DAO, your histamine bucket is full and it will make you wake up. While this is plausible, I do not believe it is sufficient to cause these early morning awakenings. It is not a cause in and of itself, but one of the many things that get dysregulated downstream after nutritional deficiencies are ignored for a period of time.

My chronic early morning insomnia began in 2015, when my thiamine levels dropped and the aggravated mitochondrial disease began to unfold. I remember waking up and I would feel my heart beating more strongly (though not pounding), sometimes I would hear a pulsatile “whoosh” sound in my ear. I would also feel weird sensations in my chest, though not pressure. During those months, I would experience on and off dyspnea while walking to my office. I didn’t think anything of it because I approach my health in the exact opposite manner people with real hypochondria do. I just thought it was a subjective “feeling”, thus not worthy of an inquiry into a possible objective cause for it.

The experience I had in the last few weeks with the supplements mentioned above makes me doubt that mast cell activation or histamine “bucket” overflow are the main causes of waking up constantly at 2 or 3 a.m. I believe it’s most likely connected with the impact histamines have on the heart – they are a known factor in developing heart failure and using antihistamines does help in preventing/postponing the onset of heart failure. This also explains why of all medications, antihistamines were the only ones that helped with a lot of my symptoms in 2016/2017.

When I started taking magnesium taurate, potassium in high enough doses and propionyl-L-carnitine, my heart symptoms improved and my sleep improved. Recently, I woke up at 3 a.m. and I immediately took a low dose of magnesium taurate and a little bit of potassium citrate. I fell asleep again in 15 minutes and in the morning I felt ok. In the past, when I would take something like L-theanine. It would force my body to go back to sleep immediately after 2 a.m., but I would feel much worse in the morning, more than if I just had insomnia.

Restoring Normal Heart Rate

One of the most important things has been reducing my resting pulse from 75-80 BPM to my normal, prior to 2016 resting pulse which used to be 60-65 BPM. I remember I used to complain about it and doctors or nurses just brushed me off. They would say that if it is under 90 BPM, then it is not a medical symptom of anything. I knew they were wrong, but how could I argue? Somehow these people in white coats think that heart failure or other cardiac diseases start out of the blue, when in fact these diseases represent years and years of ignored symptoms before the onset of the full-blown disease with typical manifestations is recognized.

Lessons Learned

Everything that helps my heart function better and recover faster improves all of my symptoms, no matter how much they may seem unrelated. This is what I observed about my own body and I encourage everyone to listen to their body and understand that all symptoms are related.

If one version of one supplement does not work, try another form and combine it with different forms and dosages of other supplements. By supplement, I understand all substances that are naturally found in food or produced by the body.

When I saw that simple forms of L-carnitine don’t have an observable effect, I simply started searching for better forms of carnitine and found propionyl-L-carnitine, which is the physiologically active form of carnitine. Why I looked for other forms of carnitine? Because I learned from experience that high dose vitamin B1, as thiamine HCL didn’t help, but that high dose Allithiamine (a formulation with TTFD) helped and still helps my body working again as it should.

I found taurine (again) by searching for supplements that improve heart failure symptoms. When I first heard about it while reading one of Dr. Lonsdale’s comments, I didn’t understand why it was important.

No one should ever quit trying to figure out their own matrix of symptoms. Begin with the vitamins and minerals, while at the same time addressing infections, limiting damaging diets, limiting exposure to toxic substances and so on. I firmly believe that all diseases with chronic fatigue involve some degree of mitochondrial dysfunction – inherited or acquired. The prototype documented, unquestionable illness that causes hundreds of symptoms, i.e. a multi-systemic illness, is inherited mitochondrial disease.

I know personally of two other people who were completely bedridden, suffering from constant light intolerance, having to live in my bed for two years with a sleeping mask all day and all night, unresponsive to any treatment or approach promoted by the online integrative medicine doctors and communities. I did not think I would ever be able to become house bound, not able to tolerate light, to think or cook for myself. The ability to no longer be bedridden and forced to live in total isolation in darkness and to be house bound is nothing short of a miracle. I owe that to thiamine.

Usually people who end up in that state for so long never recover because all known alternative treatments are exhausted and high dose thiamine for chronic illness is virtually unheard of. I will make sure to do everything in my power to change this, no matter the costs, because there’s just too much unnecessary suffering out there.

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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This article was published originally on December 9, 2021. 

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The Red Thread and Thiamine

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There is a saying in China about a Red Thread connecting people who are destined to meet and/or help one another in a profound way no matter how far apart they may be. Our adopted daughter Abby is that red thread. Abby was abandoned and found on the day our oldest daughter, Kayla, turned thirteen. It was at this time Kayla’s health issues were becoming worse. Although we didn’t know exactly what was amiss, we knew that something was wrong. In our efforts to help Abby, our family’s health issues were brought into stark relief. It seems that all of us have suffered from longstanding thiamine insufficiency. Even though my two daughters were born worlds apart, that red thread connects us. We published Abby’s story last week in the hopes that it might help someone else. Here is Kayla’s story.

Unhealthy Beginnings for My Beautiful Daughter: IVF and Induction

Common sayings like ‘you are what you eat’ can be haunting, leading to guilt when we see our children suffer the consequences of our own ill health, especially during pregnancy. My gut was messed up and had been for a very long time before becoming pregnant. I was likely deficient in thiamine and other nutrients and perhaps that is why I struggled to get pregnant in the first place. Sometimes gut dysfunction is obvious, as with constipation or diarrhea, but more often it manifests itself in other ways. That was me. I had/have Ehlers Danlos Syndrome (EDS) and most likely also, Mast Cell Activation Syndrome (MCAS) and Postural Orthostatic Tachycardia syndrome (POTS). I did not know any of this though before pregnancy and have only recently, after hours upon hours of research, come to learn how my health impacted my daughter’s health.

Kayla was our first hard-fought-for child. We were married 10 years and had undergone numerous fertility treatments before we finally achieved a successful IVF. Looking back, I realize that I was not healthy prior to or during my pregnancy, even so it was mostly an uneventful pregnancy with little to no typical unpleasantries. I had low progesterone early on that required progesterone injections and suppositories, but after 13 weeks everything stabilized. I had a high blood pressure reading at only one routine visit in my 39th week. The doctor decided to induce. We didn’t question it at the time, but later did. At the hospital, he administered Pitocin, a synthetic oxytocin, without any nurses in the room and left.  The nurses later commented that they were surprised, since my blood pressure was back in the normal range upon admission. Pitocin is just one of my regrets. Why was my body not triggering labor? Gut dysbiosis? Maybe/possibly/probably or maybe she just wasn’t ready to come out.

A Truly Gifted Child

Kayla was an extremely bright child. She wanted to learn chess at four years old. By age 9, I stopped playing with her because she always won. She gave her math brilliant-grandfather a run for his money.  She was homeschooled through 9th grade followed by private and then public school. She was a straight ‘A’ student, participated in various athletics (swim, track, dance, horse riding, etc.) and mastered two musical instruments by the end of high school. Kayla ranked in the top 5th percentile nationally and did well in first semester of college, but little did we know how precarious her health had become. Perhaps because of her intelligence and achievements, many of her health issues and difficulties were disregarded by physicians. On the surface, she looks well. She is very high functioning, but she has been plagued with an assortment of complicated and largely unrecognized health and neurological issues since birth. During her first semester of college, a series of stressors brought her health crashing down and she is only now beginning to recover. Part of her recovery has been diet, part involves thiamine, but we are still missing some pieces, which is why we are publishing her story.

Early Childhood Symptoms and Triggers

Her early childhood was marked by early bouts of bronchitis necessitating antibiotics. She suffered croup through age 7 years and seasonal allergies through her teens for which she used Claritin regularly. Nighttime enuresis was a problem until we removed gluten from her diet when she was 12 years old. Similarly, her speech was often and seemingly randomly slurred. She received speech therapy through the school to no avail. In 2018, we removed dairy from her diet and the slurring disappeared. It appears that just as a gluten reaction triggered her nighttime enuresis, the ingestion of dairy was some sort of trigger for her slurred speech. I should note, before learning this, we experimented with probiotics, fish oils, digestive and pancreatic enzymes, and a variety of other supplements off and on for years with no noticeable or lasting changes. Her younger years were marked also by body temperature dysregulation, i.e., hot in the winter, cold in the summer. Finally, most things, not all, came easy to her. She had extreme strengths and weaknesses with her strengths often masking her weaknesses. Noticed by many of her extracurricular teachers hard things seemed easy, and easy things hard. Her brain craved complexity.

Vaccinations, Cyclic Fevers, and Green Drinks

In her preteen years, she received numerous vaccinations (required and strongly recommended) prior to our trip to China to adopt her sister. Shortly after, she began to develop worsening mood swings, anxiety, depression, brain fog and has experienced dizzy spells off and on since then.

When her menses began, she bled heavy for three straight weeks. Her doctor put her on birth control pills to stop it; again, a symptomatic treatment. She was borderline to severely anemic and often had PMS and painful periods.

During her teen years, she had repeat and unexplained fevers. She was sick with high fever/flu-like symptoms for three days every four weeks for three years. She’d get sick like clockwork! She would become weak, sleep a LOT, as if she were in a coma. Her doctor was stumped. I had been reading a lot about the use of systemic enzymes used by German doctors. The book by Karen DeFelice mentioned viruses often have a cyclical pattern. So we used high doses of ViraStop2x according to her protocol for a 3-week “holding spell” and it was gone. No more cyclical episodes.

In trying to get healthier, she began “green drinks” (spinach/fruit) 5-6x week. Six months later she was very sick: anemic again, double ear infection, abnormal EEG with heart palpitations, chest pain, and shortness of breath. The cardiologist had put her on a heart monitor for three days, but the results were normal. Perhaps oxalates? I began learning more about oxalates and we began eating less of these foods overall. I’m grasping at straws…

The Red Thread and Thiamine

In 2018, we learned about TTFD/thiamine and began taking Sulbutiamine. My younger daughter, Abby, has improved immensely. In fact, my entire family now uses thiamine and we all feel much better. Before taking thiamine, we all used to be so tired after spending a day at the beach and everyone would need to nap. Now, after supplementing with thiamine for a while, everyone still has high energy levels after these trips. Except for Kayla. Her results with thiamine have been mixed. There seems to be more at play. Perhaps she requires a higher dosage of thiamine or maybe additional nutrients are needed.

Her recent labs for CBC/CMP, thyroid, A1C, vitamin D are all normal. Manganese is low and prostaglandin F2 is elevated. There is some indication of malabsorption based on her bloodwork.  Recently, an Organic Acids Test indicated normal oxalates, low dopamine and serotonin, and extremely high ketones/fatty acids. She has had high folate levels in the past, but at present are normal. Her B12 levels at present are elevated.

In 2019, she began having occasional extremely painful periods where she would be on-the-bathroom floor curled in the fetal position until Ibuprofen kicks in. Her skin is often very pale. Her doctor is not concerned about the increasingly painful menses or the ketones/fatty acid elevations.

My frustration as a parent is that because most of my child’s bloodwork is normal, the doctors write-off her symptoms as stress-related and recommend things like yoga, meditation or saunas or some fluff. Not that these things are bad, but there is something more at work here and no one seems interested in figuring it out. I am bothered that when they do see markers of inflammation or malabsorption they ignore them or really don’t know what to make of it.

Environmental Causes Of Ill-health and Longstanding Thiamine Insufficiency

Over the course of these last years, I have come to realize how important diet and environment are to health. When the pond is poisoned, sadly the tadpoles are hit first, are hit the hardest and display the affects most noticeably. Our youngest child was hit hard. Her circumstances prior to adoption were not conducive to health and she has had many struggles to overcome those early stressors and nutrient deficiencies. Likewise, owing to my ill-health prior to and during my pregnancy and the subsequent western medical treatments, Kayla struggles too. The pond was poisoned for both of them. All lifeforms that drink from a poisoned pond will manifest problems at some point, in some way. Perhaps if we had known about thiamine when they were younger, their problems wouldn’t have manifested the way they did.

Fortunately, Kayla has always eaten healthy, and has been active and athletic throughout her life. As an adult, she experiments with the removal of foods for periods of time to see if things improve, such as grains or cow’s milk and she is cooking creatively. She has been sugar-free for over a year. She takes vitamins and minerals and Sulbutiamine. She recently switched to Lipothiamine and Allithiamine and is now slowly increasing it to see if her dizziness will abate at some point.

I would trade all of her past accolades to have her in better health. We don’t know where her road will lead. Healing is multi-dimensional and someday we hope to look back at today with those oft used words “remember when…”.

Michelangelo was nearing 90 when he said “I am still learning.”  I hope to be too.

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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This story was published first on August 31, 2020. 

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Treating Intractable Insomnia and Cerebellar Ataxia With Thiamine

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Treating insomnia with thiamine

Twenty years ago, I attempted suicide after years of alcohol and drug abuse. I almost succeeded, but by some miracle I survived. I suffered a cerebellar stroke and as result was left with severe cerebellar damage. The doctors said that I had lost almost 75% of my cerebellum. I couldn’t walk or talk, I could not swallow and was barely functioning, if you could call it that. At some point, I decided I would live and forced myself to improve. I worked the physical therapy and eventually began lifting weights. I wrote about my journey here. Despite my gains in strength and balance though, since the stroke I had suffered from severe and intractable insomnia. Although I was under the care of multiple doctors, none could offer any help beyond increasing this or that medication, none of which worked. Insomnia is common in individuals with cerebellar injury. Then I learned about thiamine.

Persistent Insomnia Treated with Thiamine

Around the time my initial article was published, I began supplementing my diet with thiamine. This vitamin may have been mentioned in passing by some of my physicians, but it was never prescribed or even really emphasized to any great degree. Neither was it ever touted by the medical community during my initial stroke recovery in 2003. I am fairly sure much of the reluctance to use thiamine could be attributed to the pervasive fear of it not benefitting my health.

Being entrenched in the world of mental health and alcoholism for about 25 years (sober 9), I am well aware of Wernicke-Korsakoff’s syndrome. I had heard about massive doses of thiamine being administered to others in medical detoxification facilities. I also have loved ones grappling with Parkinson’s Diseases. I quickly began to see how many of our neurological symptoms were similar, and that thiamine was slyly mentioned to help all of us.

In early 2021, it was strongly suggested that I gradually increase to a large dose of thiamine (not by doctors, mind you, but by others from this website). At the time, I was lucky if I slept 3 hours per night, which of course, exacerbated my ataxia symptoms. I was on so many medications that it raised red flags, but I was never warned about the negative neurological effects. And worse yet, nothing was working.

Once my initial dose of thiamine was entrenched in my system (50 mg of Thiamax), I began sleeping with greater ease. At first, this was approximately an hour, but I discovered that I also slept more soundly and had acquired greater rest during the night. As time progressed, my sleep patterns became increasingly regular.

Better Functioning With Improved Sleep

For several years, I have been making progress in all areas of my life. By August of 2022, thanks to the thiamine, I was off of all prescription medications. I was sleeping through the entire night, soundly. I was also able to complete difficult feats at the gym without falling asleep on a mat in the stretching area (usually resulting in me being taken home, so I didn’t sleep at the gym.) This is one of the reasons that I didn’t train publicly until recently. With my sleep problems, I wasn’t sure if I’d be overcome with an insatiable need to sleep mid-workout.

In addition to the improvements in sleep and the elimination of medication after thiamine came on board, I was able to lift a barbell by myself, while standing. This is no small feat for someone with ataxia. Remember, I was told I would not walk again, or function in any semblance perceived as normal. They said that all my neurological systems had crossed the threshold believed salvageable. In September of 2022, I competed in my first powerlifting meet, where I deadlifted 182 pounds and bench pressed 78 pounds. I am currently deadlifting 225 pounds (January 2023). While I am still ataxic and I still have struggles relative to my injury, I have improved so much since beginning the thiamine.

thiamine for insomnia and cerebellar ataxia
Me lifting 225lbs at the gym.

As I write this, right before the New Year of 2023, I am overcome with the amount of remarkable progress that has been made in my life since August. To deny that would fact would be denial of any amount of truth or reality in existence. I fail to see how anyone can deny the differences in my life since using regular thiamine.

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. 

Photo by Jake Charles on Unsplash.

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Podcast Alert!

Yes, I have been talking about thiamine again. This time with Dr. Kurt Woeller, as part of his series: Functional

Oxalate Degrading Microbes: Reconsidering Pathogenesis

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oxalate degrading bacteria - lactobacillus

An exciting new paper was published recently which should turn the oxalate world upside down. The authors hunted public databases and compiled a list of microbes that possess variations of a gene called oxalyl CoA decarboxylase. That gene makes a protein that degrades oxalate.

Oxalate is an ion used by microbes for communication between fungus and bacteria, but it is found at varying levels in plant food. Our bodies also manufacture oxalate during a stress response. Everybody makes some amount of oxalate in their bodies and eats sometimes huge amounts of oxalate in foods like spinach, beets, nuts and seeds, and also (alas!) chocolate. When oxalate in our bodies gets too high, it causes dysbiosis and becomes dangerous, tangling with mineral metabolism, and delivering harsh changes to mitochondrial function, adding in distressing levels of oxidative stress.

Humans lack any oxalate-degrading gene in our own genome. That means we cannot degrade oxalate using our own talents. Instead, we are reliant upon our microbes in the gut to degrade oxalate. From studying isolated human beings who have never seen an antibiotic, scientists have realized that like them, our ancestors had plenty of oxalate degrading microbes in the gut (termed oxalotrophic microbes). The job of these microbes was to keep oxalate from food from getting into the inside of their bodies. That system worked well even when the diet was high in oxalate, but things changed when our microbiome began to be damaged by antibiotics and antifungals, and other hits.

In this discussion, I would like to examine findings from this recently published study from China:  Abundance, Functional, and Evolutionary Analysis of Oxalyl-Coenzyme A Decarboxylase in Human Microbiota where they identified the microbial species that possess one of the two genes that we know are used to degrade oxalate in our intestines. We will also examine some other issues that this new knowledge unwraps.

Oxalate Degradation Is Dependent upon Thiamine and Is Impaired by Antibiotics

The protein oxalyl coenzyme A decarboxylase is dependent upon thiamine. It requires thiamine that is in other forms to be converted into thiamine diphosphate (TPP). Scientists have told us that this is the primary form of thiamine that microbes will make and use.

Some of us have inborn errors in our thiamine chemistry. Those errors might limit our delivery of thiamine to the inside of our gut so that our oxalate degrading microbes can use it. Another issue is that some antibiotics kill bacteria by attacking those microbes with a direct hit to their thiamine chemistry.

I had my own tangle with these issues very many years ago. Back in 1967, I was given two rounds of chloramphenicol, an antibiotic that attacks the thiamine chemistry in bacteria. In March of the following year, four months after I stopped taking the antibiotic, I developed bone marrow failure and almost died. The same blood disease, called aplastic anemia, has been found on occasion in primary hyperoxaluria, which is a genetic disease where the body makes fatal levels of oxalate coming mostly from producing oxalate in the liver.

Chloramphenicol was taken off the market in the US in 1968 because so many people died from blood problems that came on slowly like mine. Another antibiotic that attacks thiamine chemistry is Alinia and it is used broadly by functional medicine doctors. There may be even more antibiotics that would also cause this problem, but no one has done a systematic review of vitamin deficiencies caused by antibiotics. If someone would do this type of analysis of all licensed antibiotics, then doctors would have a list of antibiotics to avoid if their patients had a genetic weakness or a deficiency in thiamine or other vitamins. Also, some viral infections may purposefully impair thiamine chemistry to weaken the host. Polio is an example. That is why after certain infections, someone may actually develop a new oxalate problem.

Oxalate Degrading Species May Not Be Pathogenic

In the paper mentioned above, the researchers found 1739 Oxalate degrading species in humans. All of the different species they identified were equipped with oxalyl-Coenzyme A decarboxylase that allows microbes like oxalobacter formigenes to degrade oxalate. You may be surprised to learn that you have probably never heard of most of these species. Because I was curious about their identity, I looked for how many oxalate degrading bacteria show up on the GI Microbial Assay Plus (GI-MAP) test from Diagnostic Solutions Laboratory, or were found on the comprehensive-digestive-stool-analysis-(CDSA) from Genova Diagnostics. These are tests frequently ordered by functional medicine doctors or naturopaths. I have noticed how often these tests are ordered when a patient has some sort of GI distress because I routinely review that sort of lab work during consults and find out from the patient what his doctor prescribed after seeing the results of the test. Most often, the patient was given antibiotics. Of course, which antibiotic the doctor chose varied significantly.

Included in the list of bacteria that degrade oxalates, were many species that are believed to be pathogens because they were elevated on tests that were ordered at a time of increased symptoms. It is natural to assume these microbes were the primary cause of the symptoms, however, I cannot help but wonder if the relationship between these bacteria is what we thought it was. If oxalate is a communication method between microbes, how many of those symptoms could have been caused by the elevated oxalate or the effect of that oxalate on intestinal microbes? If oxalate is a favored food for these types of microbes, might they expand their population whenever oxalate is increased? This might be similar to how ants or flies may show up in numbers when you uncover food at a picnic. Flagging the increased count of these species on lab tests might have persuaded the doctors to treat with antibiotics, and there was no other game plan. Would reducing oxalate have helped solve the problem without antibiotics?

Oxalobacter Formigenes: An Oxalate Obligate

Within the oxalate field, a great deal of attention has been given to the microbe oxalobacter formigenes.  The man who discovered this microbe, Dr. Milt Allison, had a lot to do with inspiring me to start looking more carefully at oxalate in autism and other conditions, and that grew to include pain conditions, autoimmunity, and gastrointestinal distress.

The uniqueness of oxalobacter formigenes, as far as we know, has been that it is the only microbe that requires oxalate to survive. Its dependency on oxalate is why scientists call it an oxalate obligate. This trait is why this microbe has received the most attention from scientists and became the launching point of this Chinese paper.

In a different study that I have reviewed before in the TLO Research Corner on the Trying Low Oxalates Facebook group, scientists looked at the differences in the diversity of microbes that survive in a very high oxalate condition (which in this case was chronic kidney stones) and compared that to normal controls. These scientists found out that oxalobacter doesn’t tolerate a high oxalate environment very well. Please note that their title implies that oxalate causes dysbiosis and not the reverse.

In the last two decades, a company called Oxthera and its predecessor have spent millions of dollars trying to develop oxalobacter as a drug for primary hyperoxaluria.  Sadly, they still have no product on the market. Oxalobacter formigenes may have been the wrong microbe to pursue because the paper on dysbiosis found that this microbe really doesn’t like extremely elevated oxalate.  This may be like humans having a hard time eating a hundred hamburgers in one sitting. This Chinese paper shows that scientists now have many more choices of oxalate-degrading microbes to study for research.

What Might Cystic Fibrosis Teach Us About Oxalates?

I have talked to our TLO group about this before, but cystic fibrosis is a genetic condition very important for oxalate research. This condition involves a broken intracellular regulator which governs the secretion of oxalate and sulfate among its other duties. This is why people with cystic fibrosis are elevated in oxalate. If someone has this gene defect, the mucus becomes very thick in the lungs and it is prone to infection. People with CF often live from cradle to grave with antibiotics. Pseudomonas aeruginosa often becomes their most common infection, and yes, this microbe showed up on the Chinese list of microbes that degrade oxalate. Might pseudomonas aeruginosa be growing too high levels and turning pathogenic just because it is responding to oxalate as its favorite food?

We are used to watching with distress as flies and ants discover our food at a picnic. Does oxalate become a picnic for certain microbes?

Have we made other mistakes assuming the worst about microbes when they were actually providing a benefit to us? I recently reviewed a paper in the TLO Research Corner that showed that intestinal infections with candida protected mice from systemic infections, including systemic infections with candida.  Using antifungals destroyed that protection. Have we been confused about what was going on in microbial communities, putting black hats on microbes that might be trying to protect us from something worse?

Counting Microbial Species In Cystic Fibrosis

I used PubMed to discover that many of the oxalate degrading microbes identified in the Chinese paper have been commonly reported as infections in cystic fibrosis. This is what I found:

  • Pseudomonas – 7838
  • Burkholderia – 1624
  • Mycobacteria – 708
  • Achromobacter –  206
  • Klebsiella – 118
  • Pandoraae – 59

Is there a chance that excess oxalate in cystic fibrosis patients (which is known to occur) could be attracting and feeding these microbes in the lungs? Might the antibiotics used to kill these microbes be accomplishing something equivalent to killing the policeman or fireman who is trying to get rid of the flames to save your house? Could we have been making similar kinds of mistakes by not knowing which issues (like oxalate) were encouraging particular microbes to prosper?

Because of this Chinese paper, scientists may now have a very new direction to pursue.  Unfortunately, this direction may be politically risky for them because antibiotics have been the main thrust of treatment for decades and are considered to be lifesaving in cystic fibrosis.

Is it too late in this game for a shift of focus to happen?

Pathogenic Bacteria in Stool Tests: Maybe Not

I went through the list from this Chinese paper and identified microbes that showed up on the standard stool-sample-based test that a lot of doctors are now ordering rather routinely. Here is the count of bacterial species that are covered on these tests but which the Chinese paper identified as being microbes capable of degrading oxalate. The number of species is coming from the oxalate paper and not from the lab tests.

  • Escherichia – 252
  • Mycobacterium – 221
  • Lactobacillus – 70
  • Shigella – 46
  • Bifidobacterium – 38
  • Proteobacteria – 6
  • Salmonella – 6
  • Klebsiella – 4
  • Enterobacter – 3
  • Pseudomonas – 3
  • Yersinia – 2
  • Bacillus – 1
  • Bacteroides – 1
  • Citrobacter – 1
  • Clostridium – 1
  • Prevotella – 1

I discovered that this list of microbes from stool tests covered 48% of the species that the Chinese study identified. Other species they found that degrade oxalate will be less familiar to everyone.

Probiotics and Oxalate Degradation

The Chinese study found that 78 species of lactobacillus and 38 of bifidobacteria possess the oxalyl-coA carboxylase that degrades oxalate. These two types of bacteria are included in most probiotics, and now we know why this sort of probiotic has been so helpful maybe for centuries. Of course, our ancestors who began to use yogurts and kefirs certainly had no idea that a chief mode of their action was degrading oxalate. Were people with this habit the people who routinely ate potatoes or beets or Swiss chard? The following article on kefir also helped to identify the bacteria from kefir that the Chinese article found could degrade oxalate: acetobacter and pseudomonas as well as lactobacillus and bifobacteria.

Rethinking Our Relationship with Bacterial Oxalate Degraders

What do we know about other species they mentioned and when those species might show up? Did this list of species expand in the intestines in people after those people became high in oxalate? Might the bacteria also have increased when oxalate was leaving tissues where it had been stored during a phenomenon that our oxalate project calls dumping? This involves a sudden increase of blood and urine oxalate when previously stored oxalate comes out of tissues in a kind of rush.  Scientists have described this happening but never named it.

Could a mobilization of stored oxalate also have happened when someone was fasting while getting ready for surgery, or maybe fasting for their health? How do these bacterial populations shift when someone goes carnivore, and do we know if and when and how such a change may induce dumping?

Many previously unnoticed populations of microbes could have expanded because someone recently took an antibiotic that either killed the competitors of these microbes, or perhaps killed other oxalate-degrading microbes. Do we have any idea how these microbes would share an oxalate burden? Do we know under which circumstances one of them, versus another, would increase their population to meet that challenge?  Scientists suddenly have so many questions they need to answer.

The most glaring question is whether the symptoms that prompted a doctor to order a lab test, instead of being a response to “overgrowth”, were instead caused by the disturbances made by the way elevated oxalate affected both our microbes and our intestinal cells. Could the symptoms have arisen due to the conversations taking place between our microbes and our intestinal cells about a distressing level of raised oxalate?

Urinary Tract Infections: E. Coli

It didn’t take long for me to recognize that the genus the Chinese paper reported as the most largely represented among the oxalate degraders was E. coli, with a record number of 252 species identified. Did you know that E. coli is the most frequent microbe identified in urinary tract infections? Of course, the urinary system is where oxalate can reach a critical concentration that may provoke kidney stones. Is the E. coli showing up there in order to protect us from the oxalate in urine?

Many doctors routinely do urine tests to identify bacteria in urine during well woman visits. If they find bacteria present like E. coli, they may prescribe an antibiotic. Most frequently, this will be Cipro, a fluoroquinolone that may especially target oxalate-degraders, but it also likes to damage tendons. Previously, I have reported in the TLO Research Corner that scientists found that when doctors prescribe antibiotics for non-symptomatic urinary tract infections, it actually leads to a worsened patient outcome. That becomes glaringly obvious after a future symptomatic infection takes place after the microbes that were targeted by the antibiotic became antibiotic resistant. There is much here to think about.

Oxalate and Dysbiosis

I am listing next the species that were found to be present at higher levels in those with kidney stones versus controls in a paper I reviewed. That paper boldly stated that oxalate causes dysbiosis, rather than the reverse. Recently I looked again in their supplementary materials and found their list of species that were much more prevalent in those with kidney stones than in their control population. Those kidney stone patients had greatly elevated oxalate compared to controls. I looked for which of the microbes from that list had been identified in the Chinese paper as oxalate degraders, and these microbes made the cut:

  • Bacteroidales
  • Bacteroides
  • Bifidobacterium
  • Burkholderiales
  • Clostridia
  • Enterobacteriaceae
  • Gammaproteobacteria
  • Prevotella

Please note that many of these oxalate-degrading microbes are also on the tests for microbial overgrowth.

Are you, like me, gnawed by the question of whether these microbial populations increase merely because they found excesses of oxalate to degrade? When your doctor or practitioner orders a stool test, if these species seem to be in overgrowth compared to their reference population, will your doctor think about first suggesting that you try a low oxalate diet or identify other sources of oxalate in you BEFORE he considers the use of antibiotics?  Might addressing oxalate first be safer for your long-term intestinal health? We have learned that antibiotics might make your situation worse by perpetuating your issues with a longer term dysbiosis. Unfortunately, no one knows how to restore the anaerobic bacteria you lose with antibiotics. Probiotics won’t help you there since probiotics are cultured where air is present.

Rethinking the Role of Thiamine

We have all been in the habit of thinking that vitamins were in our diet just for our own benefit. It is a bit odd to think of vitamins also being there to nourish and equip our microbes. A new paper recently made it more certain that microbes in our colon actually make vitamins that can nourish our own colon cells and I am talking about the cells called colonocytes.

Other scientists have identified yet another thiamine requiring gene in a type of bacteria that generates acetic acid, which is a substance most of us know better as vinegar. This other protein is called oxalate oxidoreductase. They explain that the protein called oxalate oxidoreductase (OOR) metabolizes oxalate using thiamine pyrophosphate (TPP). The reaction generates two molecules of CO2 and two low-potential electrons. The gene is there to help the bacteria make acetic acid from oxalate.

This simple but elegant mechanism explains how oxalate, a molecule that humans and most animals cannot break down, can be used for growth by acetogenic bacteria.

So oxalate is good for those particular microbes, but only because they have this special gene that is only found in this type of bacteria.

A Giant Rethink Is In Order

If we have misunderstood the purpose of so many microbes, perhaps it is time that we change our thinking!

In much of the world this last year some of us learned that there were prejudices we were taught that gave us different points of view about many groups that we thought we understood. We learned that many of us needed to listen to people from other groups to find a different perspective. Groups we had belonged to had taught us to define ourselves by membership within their ranks, but those groups also perpetuated our having a narrow point of view.

Similar human influences have shaped what scientists and the public and even doctors were able to notice within scientific findings. Instead of realizing that microbes were a beneficial part of our bodies, we instead assumed they were dangerous. Why? We didn’t understand what exactly the microbes were doing with their superset of genes that outnumbered our genes by at least 140 to one. We had no tools to recognize ways that they were doing good things for us.

Now we are learning how they degrade oxalate and we are learning that their job of ridding us of oxalate is apparently a lot more important to human life than anyone ever knew before. We also learned that their task was accomplished by a much more diversified team of players than we thought. Scientists are diligently working to understand relationships that were unknown to us before.  These relationships are being revealed as we rid ourselves of some major assumptions.

So much of what we learned through these scientists deserves a giant rethink…like so many things that have happened to us this past year.

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 CDC on Unsplash.

This article was published originally on June 7, 2021. 

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Is Thiamine the Answer?

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Is thiamine the answer

Since we have shown that many people with complex disease patterns respond to megadose thiamine and magnesium, irrespective or their symptoms, we have concluded that disease is due to a breakdown of health from energy deficiency. We have proposed that 3 interlocking circles (as in Boolean algebra), labelled Genetics, Stress, and Energy (or Fuel) must be considered singly or collectively as the cause of any disease. Energy is the force that enables any form of mental or physical body function. Its deficiency affects one or more of the three circles.

Genetics is not often a sole cause of disease. It usually requires other factors and genetically determined disease can often be treated by epigenetic energy stimulation. Symptoms of Type 1 diabetes often appear in middle age, often after a mild stress event such as a common cold. Surely it would appear at birth if genetics was the sole cause.

Any form of stress (infection, trauma, prolonged mental stress) demands cellular energy to meet it. The hind brain controls the complex response and is automatic. This part of the brain is highly sensitive to cellular energy deficiency and thus, energy stimulation is the essential factor required to treat any disease.

Beyond Deficiency

It has been shown by Antonio Costantini’s group that mega-dose thiamine treats Parkinson’s disease, presently deemed to be incurable. They have reported similar clinical benefits in Friedreich’s ataxia (another neurodegenerative disease), Multiple Sclerosis and Fibromyalgia, suggesting that each of these diseases, rather than having separate causes, are all energy dependent manifestations of disease. Just last year, a group of researchers linked a damaged thiamine/biotin transporter gene to Huntington’s Disease. Just this month another group has found that thiamine/biotin treatment compensates for the genetic dysregulation, restores function, and rescues neuronal pathology associated with Huntington’s Disease in mice.

A publication decades ago in a prestigious medical journal reported that 252 different diseases had been treated with mega-dose thiamine, with varying degrees of success.

This information, published in peer-reviewed medical literature is startling, because thiamine, in minute doses, is thought to have its sole responsibility as a vitamin. To use it as a completely non-toxic drug offends the present model used to explain disease. Also, it demonstrates that our knowledge of vitamins is incomplete.

Children’s Health and Thiamine

While I was working at Cleveland Clinic in the seventies as a pediatrician, many emotionally disturbed children were referred to me by pediatricians in private practice in the Cleveland area. I found that the diet of these children was full of empty calories due to their indulgence with candy, soft drinks and a variety of substances usually known as “junk foods”. They had been treated with a variety of pharmacological drugs that either had no effect or even made the clinical situation worse. I treated them with large doses of thiamine and their symptoms disappeared. The explanation by my colleagues was the traditional one, “spontaneous remission”, usually used to explain a mystery cure. My explanation was that deficiency of brain energy was responsible for their symptoms. Thiamine was stimulating its cellular synthesis.

The RDA for Thiamine and High Caloric Intake

I looked up the history of the establishment of the Recommended Dietary Allowances (RDA) for these essential substances occurring in natural foods. I found that the original recommendations had been made by a committee of “experts” and there was surprisingly little science involved. There was no attempt to tie the RDA of the vitamin to the calorie concentration.

The dietary supplementation of vitamins to selected foods by the food industry was thought to have completely removed vitamin deficiency disease from America. Consequently, doctors in practice are commonly seeing patients with many symptoms and failing to recognize the ancient disease known for centuries as Beriberi. Because the laboratory tests, used to confirm the nature of the disease, are normal, the many symptoms described by the patient gives rise to a diagnosis of psychosomatic disease by the doctor. Even worse, the patient is told that “it is all in your head” and he or she is advised to “pull him (her)self together”.

Deficiency of thiamine and magnesium, both essential to cellular energy production in the body, need to be in a concentration that is sufficient to oxidize the calorie concentration. That explains why the concentration of blood thiamine is usually normal in this common polysymptomatic disease, because the doctor fails to recognize the overload of “empty calories”. The concentration of thiamine would be normal for a healthy calorie load, as would exist in an organic natural diet.

We have reported high calorie malnutrition as a common cause of this widespread disease. Dysautonomia is responsible for the symptoms because the hind brain, where the control mechanisms of the autonomic nervous system exist, is highly sensitive to cellular energy deficiency. It matters little whether it is called Beriberi or high calorie malnutrition as long as the biochemical cause is understood.

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. 

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Problems With the Medical Model of Disease

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medical model of disease

The use of the word model is supposed to describe the nature of disease as it differs from that of health. Hippocrates was the first person to offer a solution to the preservation of health by saying “Let food be your medicine and let medicine be your food”. Throughout most of history there was no model and treatment was based on largely futile ideas. The present age of medical thinking was ushered in by the discovery of disease producing microorganisms. The model became “kill the microorganism, the bacterium, the virus, the cancer cell”. If no microorganism or cancer cells could be found, the remaining diseases were long considered to be a mystery.

Recent research has advanced the model by discovering that the brain controls inflammation through the vagus nerve by the use of metabolites called cytokines. However, the present medical model still dictates that the various symptoms that signify loss of health are put together in collections. Each is considered to represent a particular disease that has to be named for diagnostic purposes and that a cure for each is to be found from detailed research. So we now have literally thousands of different diseases, often being called after the person who first observed a particular symptom/sign collection, such as Parkinson or Alzheimer. Each of the named diseases is supposedly recognized by a collection of laboratory tests that are “diagnostic”. What is even worse, is that this collection is often called a syndrome and the first observer has his/her name appended. From that time on, this particular collection is known as “Joe Soap’s syndrome”. Fortunately, there is change on the horizon as we gradually realize that the human body is a “machine” whose function is metabolic in nature.

The Stress of Life

When I was in active practice, I discovered that thiamine could be used as a “drug” for many of the situations that I encountered, seemingly irrelevant to the diagnostic category with which I was supposedly dealing. I was thought of by my colleagues as a medical heretic. Since it had long been known that thiamine deficiency was responsible for the disease called beriberi, I studied the history of the early attempts to find its cause. Beriberi had existed for thousands of years and was still largely a mystery at the end of the 19th century. I found how easy it was for the investigators to be misled. In Eastern cultures rice had been a staple for centuries. At that time, factories had been built in China in which buildings had been separated by a corridor. In the summer months the workers would congregate in them to take their lunch. As the sun moved around, it would shine on the congregated workers and several of them would come down simultaneously with the first symptoms of beriberi. The obvious conclusion for the investigators was that this was some kind of infection since several of them had succumbed at the same time. When it was found that thiamine deficiency was responsible, an explanation was required for this simultaneous incidence of the disease.

We now know that ultraviolet light is a source of stress. It can be concluded that the affected workers had been marginally deficient in thiamine. They were either asymptomatic or had mild symptoms attributed to other causes. The stress caused by sunlight had provoked symptoms of the disease simply because the required energy was unavailable to achieve homeostasis. This intriguing discovery caused me to seek the work of Hans Selye, whom I visited in Canada. As I have written in several posts on this website, he had determined from the study of rats that each form of stress had to be resisted and required energy. He called it the General Adaptation Syndrome (GAS) and offered the idea that human disease was a lack of sufficient energy required for adapting to the more severe environmental influences encountered on a daily basis. This included severe trauma and infections. The energy deficiency conclusion of Selye was later backed up by one of his students who was able to produce the GAS experimentally in a thiamine deficient rat without using any form of experimental stress.

It seemed to me to be obvious that I had to study the way energy is produced in the human body if I were to understand the reality of health and disease. In Selye’s time energy metabolism was poorly understood and it was a mark of his genius that enabled him to suggest that it was energy deficiency that caused the collapse of the GAS. The reason that all animals, including humans, are living is because they construct energy from food and this creates a chemical called adenosine triphosphate (ATP). From there, electrical energy has to be created and that is the energy that we use for functional activity. The transition from chemical to electrical energy is not precisely known but there is some evidence that thiamine in the form of thiamine triphosphate (note the parallel with ATP) plays an important part. This triphosphate form is exceptionally high in the electric organ of the electric eel, capable of producing a paralyzing shot of electrostatic electricity to zap its prey. The electric organ is an adaptation of a nerve ending just like ours. It is obviously important to understand that this is an evolutional adaptation and does not mean that we can produce a high energy output from our nerve endings. Indeed, the evidence is strongly in favor of the energy being in microvolts. We are identifying the electrical potential when we perform an electroencephalogram or an electrocardiogram and a recent test has been devised using the electrical potential of a person with Chronic Fatigue Syndrome (Open Medicine Foundation April 2, 2021).

Many of the people reading the information on this website are themselves patients seeking help for their misunderstood disease. The history recorded in their posts is repetitive and in each case their reported symptoms are usually thought to be bizarre by the physicians that have been consulted. In the present medical model a “real” disease is called organic and is marked by a series of abnormal laboratory tests. When these tests are reported to be normal, the conclusion is nearly always the same. The symptoms are considered to be imaginary in a person who is thought to be psychologically abnormal. They are referred to as psychosomatic and the patient is told that “it is all in your head”. It is always surprising to me that the physician seems to have the belief that the bizarre nature of the symptoms is generated in the patient’s brain without consumption of energy, that thought processes or imagination are not the result of energy consumption by brain cells.

Distorted Truth

The real trouble is that the disease model represents a distortion of the truth. To make a diagnosis, it is inherently necessary that some of the presently used laboratory tests must be abnormal. No thought is given to the possibility that energy deficiency in the brain might be the cause of the symptoms. Therefore no effort is made to obtain the right laboratory tests. It demands a totally different way of thinking about health and disease. People affected by this kind of brain energy deficiency disease are often working and living ostensibly normal lives but suffering greatly. They are in fact experiencing early beriberi, a disease that has a long morbidity and a low mortality. They can go on experiencing these symptoms for years, but if they are completely ignored as psychological misfits, one can easily imagine that permanent damage will develop. Perhaps Alzheimer’s and Parkinson’s disease are really reflections of this permanent damage and that there will never be a “cure” for them. Attention to relatively simple symptoms, usually diagnosed and treated as variable named conditions such as “allergy” may be the only way in which these named diseases can be prevented.

To give an example of this kind of thinking, I was confronted by a 12-year-old African-American girl with extremely severe asthma occurring in individual attacks. Physical examination revealed that her body was covered with “goose bumps”. Because of this I came to the conclusion that her autonomic nervous system was dysfunctional and the cause of her asthma. I had already come to the conclusion that thiamine deficiency caused the energy failure that resulted in dysautonomia and that sympathetic/parasympathetic imbalance could affect the bronchial tubes. Without further testing, I gave her thiamine in pharmacological doses. It resulted in a complete disappearance of the asthma. This patient, at the age of 30 years, contacted me to let me know that she had only experienced two mild attacks of asthma in her 20s.

Health Requires Energy

What is important to remember is that any situation involving physical or prolonged mental stress requires energy in the brain, used to organize the complex defenses of the body. The recent discovery by Dr. Marrs and myself that thiamine deficiency in America is common, suggests that brain energy is insufficient in many people. If and when they are attacked by a microorganism such as Covid-19 it is possible their symptoms and their continuation reflect brain energy deficiency. Consequently perhaps they are unable to adapt and overcome the stress of the viral attack. It also suggests that symptoms expressed by so called Longhaulers might be helped by the administration of pharmacological doses of thiamine.

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 April 7, 2021.

Image by Joshua Nicholas Vanhaltren from Pixabay.

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Energy Loss as a Cause of Disease

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medical revolution

I graduated from London University in 1948 and retired at the age of 88 years in 2012, so I have seen some remarkable changes in the practice of medicine. I have entered many reports on this website, detailing what should be a medical revolution. One of the best professional associations that I have ever made has been with Dr. Chandler Marrs, the editor of Hormones Matter. Both of us have tried hard for years now to explain the details of our experience, hoping to reach those many individuals who are being misdiagnosed and treated extremely badly. My recent experience has come from retiring in an excellent retirement home.

I am surrounded by people of my age, many of whom are taking numerous medications to treat their symptoms. The most recent example was in a gentleman who has been in and out of hospital several times with a set of symptoms whose origins are clearly due to cellular energy deficiency. When approaching him as a friend and asking him how he is faring, he told me that his list of symptoms remains as a medical mystery. In addition, two women, with whom I had become acquainted, had symptoms that were similar to his. One of them passed away without a diagnosis and the other one is presently being treated symptomatically. The reader might well ask the obvious question as to what happens if I should state an opinion. The answer is very simple; the offered explanation would fall on deaf ears. Unfortunately, this is eminently predictable and is the major reason why innovation that contradicts the medical standards of the day is regarded as heresy throughout history. Of course, “new” concepts must be backed by evidence to become accepted. We are trying to provide the evidence on this website for defective cellular energy as a major cause of disease.

Heresy in Medicine

I am pretty sure that I may have recorded the story of Dr. Semmelweiss on this website but it is a story so poignant that it is well worth repeating. It is a story that illustrates the difficulty of introducing innovation in medicine, or indeed anything new. Semmelweiss was a German Hungarian physician who lived before the discovery of microorganisms. He presided over an obstetrics ward in which there were perhaps 10 beds on one side of the room and 10 beds on the other. The physicians of the day would come in and deliver their patients without washing their hands or changing their clothes. It is difficult for some people to comprehend the total lack of any form of hygiene that doctors practiced before microorganisms were discovered. Semmelweiss observed that the physicians would often come into the ward directly from the morgue and concluded that they must be bringing something in on their hands that caused the patient to die from child-bed fever, as it was then called. From this observation, he organized the first controlled experiment in medicine. He directed the physicians on one side of the ward to wash their hands in chlorinated lime before they delivered the patient. The physicians operating on the other side of the ward carried on in the same old way.

The results were dramatic as we would expect today. Child-bed fever was reduced by 85% when the physicians washed their hands. The medical profession, including his colleagues, said that “because Semmelweiss could not explain what was on the hands of the physicians, his explanation was unscientific”.  It is important to note that they simply ignored the obvious benefit. He was discharged from his job and excluded from the hospital. He died as a pauper in a mental hospital.

The major point is that the concepts of the medical profession of the day were completely wrong,  He had clashed with the current medical model that was then accepted by mainstream medicine as “the truth”.  If we apply this lesson to today’s model of medicine, it is impossible not to wonder if the outstanding principle of the use of pharmaceutical drugs in medical practice is fundamentally wrong. Is treating symptoms without addressing their underlying cause scientifically justified? A glance at the Physicians’ Desk Reference that supplies information on the many prescription drugs available might put off the reader’s use of a prescription. For each drug there is a short description of its use, often with an admission that its action is only partly understood. Then follows a page or two describing its side effects. Does this not suggest that the use of pharmaceuticals to treat symptoms causes more problems than it solves? Are we approaching another Semmelweiss moment in medical history?

Envisioning an Alternative Approach

I envision the profession of medicine as like a traveler, hoping that the road leads to the best solution in the treatment of disease. For my analogy the traveler comes upon a fork in the road with a signpost. One sign says “Kill the Enemy“, (referring to the discovery of infecting microorganisms) and our traveler takes that road because the sign for the other fork is blank. “Kill the enemy” became the first paradigm (a model accepted by all) in medicine. We had to find means of killing bacteria, viruses, cancer cells or any other attacking agent and many years were spent in trying to find ways and means of doing this without killing the patient. The information was hard won and a lot of patients suffered untold hardship and even death until the discovery of penicillin. This in itself “proved that the correct fork in the road had been chosen”. As we know, this discovery led to the antibiotic era, but even these drugs are running into new problems.

To continue the analogy, our traveler goes back to the fork in the road and finds that the other sign has now been filled in. It reads “Assist the Defenses” and I believe that it should represent a new paradigm. Louis Pasteur and his colleagues discovered the disease producing microorganisms, but on his deathbed he is purported to have said “I was wrong, it is the terrain that matters”.  He meant that the terrain represented the defensive functions of the body that should be assisted.  Perhaps he formulated what I believe must be the second paradigm in medicine.

The Second Paradigm

How should we approach the introduction of this concept? It seems to me that the problem is that few people are aware of the basic principles of body function so I must provide another analogy that I have used before in Hormones Matter. The human body can be compared with a symphony orchestra in which part of the brain represents the conductor. The organs represent the banks of instrumentalists that make up the orchestra. Like the instrumentalists who, although they are experts in their own right, still have to obey the conductor, the cooperative function of all our cells must obey the automated signals from the brain to play the symphony of health. Each of us comes with a “blueprint” that is our inheritance and although we are all the same in principle, we are all uniquely different because of accidental or inherited variations in the “blueprint”. The autonomic (automatic) nervous system, controlled by the lower part of the brain, coordinates the function of organs in the body, behaving like a computer. It receives sensory information, enabling it to receive from and send signals to those organs, thus collectively playing the symphony. The endocrine system consists of a group of glands that produce hormones. Their function, also under the command of the brain, is to release the hormones that travel in the bloodstream to the organs and are thus signaling agents.

The voluntary nervous system, controlled by the upper part of the brain, gives us what we call willpower. The voluntary and autonomic systems are completely separate but have many connections, so some of the reflex activity conducted by the autonomic system can be influenced and overridden by an act of will. Perhaps the best example is the fight-or-flight reflex that is activated by a sense of danger but can be modified voluntarily. For example, the reflex response to an insult might result in violence if it is not modified by the voluntary system. Assuming that the blueprint provides all the machinery of survival, all it requires is energy.

The Production and Consumption of Energy

We cannot survive without food and water. There is, however, an overall tendency to ignore the appropriate nature of the food, in spite of the fact that it provides the fuel that gives us energy. Taste is the dominating influence, driving sales for the food industry without an appropriate consideration of calorie/micronutrient balance. It is clear that “vitamin enrichment” has hoodwinked us. Chemical energy is liberated from oxidation of fuel (food), but it must be transduced in the body to an electrical form of energy that enables us to function. The electrocardiogram and the electroencephalogram are both tools that identify the electrical nature of this function. The human body is well equipped with an enormously complex system of defense but its complexity requires energy that has to be increased when a person is under any form of physical (trauma, infection, severe weather etc) or mental (divorce, grief, business deadlines etc) stress. It is very important to think of stress as a “force” to which we have to adapt. The lower part of the brain, acting like a computer must automatically organize the complex defense machinery, including the immune system, so its energy requirement exceeds that required by the rest of the body and must be automatically increased to meet the required response to stress. What we call the “illness” (fever, swollen glands, inflammation, etc.) is evidence that the brain has gone into action to generate a defense. In fact, war is declared and the result is recovery, death, or prolonged chronicity where the attacker has not been completely defeated. A nutritionally deprived individual cannot muster the energy to initiate defensive action and may explain why stalemate or the stress of vaccination can be evidence of failure to adapt.

Of all the aspects of health maintenance, exercise, appropriate rest, socialization and fulfilling job assignment, perhaps nothing is more important than the nature of the food. Genetics, stress and nutrition are visualized as the “three circles of health“. I want to illustrate this relationship by retelling an incident that we reported in “Hormones Matter” a few years ago. The mother of an 18-year-old girl reported by email that her daughter had received the HPV vaccination (to increase immunity against the virus associated with cancer of the cervix) four years previously. Throughout the four years she had been more or less crippled by a condition known as postural orthostatic tachycardia syndrome (POTS). She had been seen by many physicians without any success. Her mother did her own research work and had come to the conclusion that her daughter had the vitamin B1 deficiency disease known as beriberi and she wished to prove it. A blood test clearly showed that she was correct. Because of this, several young people who had also suffered from POTS following the HPV vaccination were also found to be thiamine deficient. One young woman who had not received the vaccination also had POTS and was found to be thiamine deficient. One of the observations that had puzzled the parents of these young people was that, without exception, each of them had been recognized as an exceptionally good athlete and student before they had received the vaccine. We deduced from this that a superior brain was more likely to consume  more energy than someone less well endowed, thus increasing the risk of poor  nutrition and the ability to adapt to a potentially powerful stressor.

Although proof is not possible, we have accumulated a lot of evidence that has enabled us to hypothesize that the vaccination acted as a nonspecific form of stress in people who were marginally thiamine deficient, but asymptomatic before receiving the vaccine. For the youngster who had not received the vaccine, but who had succumbed to POTS, poor nutrition alone, with or without genetic risk, had to be blamed. Genetics, stress and nutrition are visualized as the “three circles of health“.

The Medical Revolution

We are proposing that energy loss is the major cause of disease and that it results commonly from a less than ideal diet or dysfunctional mitochondria. Failing in the balanced need of the caloric content and the  necessary non-caloric vitamins and minerals for efficient oxidation, the result of poor diet is energy deficiency. There is considerable evidence that thiamine plays a vital part in both the production of chemical energy (ATP) and its conversion to electrical energy for bodily function. We have concluded, also from evidence, that genes may or may not usually cause disease on their own. Either nutrition or overwhelming stress may be variable factors that create genetic risk. The prevailing addiction to sugar creates a variable degree of thiamine deficiency by the catatorulin effect. We further hypothesize that a mild to moderate thiamine deficiency leads to a gradual decay in the efficiency of the critical enzyme(s), insufficiently supported by the cofactor(s). Attributing the easily reversible symptoms to other causes and allowing them to continue, leads to chronic disease. This may or may not respond to pharmacological doses of cofactor, used to resuscitate the associated enzyme(s).

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

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Image by Jonny Lindner from Pixabay.

This article was first published on July 1, 2019.    

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Huntington’s Disease and Thiamine: New Research Finds Link

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Thiamine and Huntington's disease

Huntington’s disease (HD) is a genetically caused brain disease. The inheritance is an autosomal dominant gene, which means that only one individual, either male or female, can pass the gene to offspring. Albeit rare, it is a neurodegenerative condition, characterized by progressive motor, behavioral and cognitive decline, ending in death. The underlying genetic mutation for Huntington’s was discovered more than 20 years ago, nevertheless, traditional treatment remains focused on symptom management. Chorea (epitomized by an array of bodily twisting movements) is the most recognizable symptom and this does respond to one type of medication, but it is inadequate.

Neuropsychiatric symptoms may precede the classic motor symptoms of the full-blown disease by decades and this may well be extremely important in assessing a newly discovered linkage between Huntington’s disease and thiamine. In the publication, the authors discuss the prospect that megadose thiamine treatment may improve outcomes.  In the abstract, the authors provide a background. “Although promising gene silencing therapies are being tested for Huntington’s disease, no disease modifying treatments are available”. Thus, they turned to a study involving alternative molecular mechanisms that are highly technical and beyond this post. It involved the study of a great number of genes that had been damaged by this mechanism. One of the affected genes was a protein that is one of the essential factors that enable thiamine to enter cells. Because thiamine works inside body cells, its absorption requires a number of these proteins, depending on the part of the body where thiamine becomes essential to its function. They are known as transporters.

This damaged transporter gene, if genetically mutated, causes a biotin (another B vitamin) and thiamine dependent neurological disease (biotin/thiamine dependent basal ganglia [BTBG] disease). These investigators concluded that Huntington’s disease was really a BTBG-like thiamine deficiency and therefore had an easy to implement treatment. This is easier to accept, because of the dramatic publications of Costantini and his coauthors. Starting in June 2015, they published a report that they had found significant clinical Improvement in 50 cases of Parkinson’s disease with high dose thiamine. They have reported similar clinical benefits in Friedreich’s ataxia (another neurodegenerative disease), Multiple Sclerosis and Fibromyalgia, suggesting that each of these diseases, rather than having separate causes, are all energy dependent manifestations of disease.

In my own experience, I was confronted with a young woman who had been diagnosed with Multiple Sclerosis. I treated her successfully with high dose thiamine. She and her husband went to live in Italy for business purposes and she would call me annually for a resupply of nutrients.

I was impressed by the information that neuropsychiatric symptoms can appear in a person decades before the appearance of HD symptoms. It made me wonder whether, in some cases if not all, medical refusal to recognize vitamin deficiency symptoms had resulted in a gradual worsening that eventually became the symptoms of HD. There is no dispute over the genetic background of HD. What I am suggesting is that the abnormal gene requires another “stress” factor to become active like the genetic aspects of diabetes type 1 and possibly type 2.

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. 

Image created using Canva AI.

This article was published originally on November 8, 2021.

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Podcast Alert!

Yes, I have been talking about thiamine again. This time with Dr. Kurt Woeller, as part of his series: Functional

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