SIBO Archives - Hormones Matter

Exploring Manganese, Thiamine, and Calcium in Osteoporosis

Published on October 8, 2025

1.3K views

manganese, thiamine, calcium, osteoporosis

Many years ago, I wrote a short post about some unique research linking manganese deficiency in deer antlers to osteoporosis in humans. I had long since forgotten about it. Recently, someone left a comment about a connection between manganese and thiamine. It turns out that manganese deficiency diminishes tissue storage and synthesis of thiamine. So, in addition to potentially driving osteoporosis, manganese is influences thiamine availability. Given these connections, I thought I might revisit the research.

Deer Antlers, Manganese, and Osteoporosis

The dominant theory about osteoporosis in humans and animals alike, is that deficiencies in calcium and/or vitamin D drive osteoporosis. Although both impact bone density, in many circumstances, it is not clear whether these factors are causative, coincidental, or a result of some other variable. There is a growing body of evidence suggesting that while calcium and vitamin D deficiencies are problematic and can indeed induce problems with bone development and strength, another nutrient may also be involved: manganese.

Manganese, a trace metal found naturally in a wide variety of foods, including nuts, plants, and shellfish, is a cofactor for many enzymes. Deficiency is considered rare, but it is infrequently measured. Much of the research on manganese focuses on its toxicological properties when exposed to excessive amounts, usually occupationally. Since manganese accumulates in bone, excessive manganese is just as problematic for bone health as deficiency. That said, manganese is integral for normal processes of bone development and integrity. A great review can be found here.

Returning to the deer antler paper for moment, the authors posited a mechanism that I had not yet seen fully explored – that declining bone calcium observed with osteoporosis is linked to low manganese. Specifically, they argued that manganese deficiency impairs calcium uptake and integration in the bone and thus drives osteoporosis. This is claim has been repeated frequently since the work was published in 2010 but it is rarely discussed more thoroughly, at least that I could find. The actions attributed manganese in bone development include: enzyme cofactor activity; protection of osteoclasts from oxidation processes during growth and remodeling via the mitochondrial antioxidant MnSOD (manganese superoxide dismutase); cartilage and collagen synthesis; and its ability to stimulate other signaling pathways involved in bone development and integrity. Certainly, all of this is important, but I find the role it may play in calcium management is particularly interesting.

In the deer antler study, researchers found that during an especially cold winter manganese in the plant matter consumed by the deer declined. In parallel, manganese but not calcium concentrations in the antlers declined, as did antler tensile strength and bone integrity, while fractures increased. Since during development about 20% of circulating calcium is shuttled preferentially to the antlers, stable calcium concentrations in the antlers made sense. When the antlers of wild deer were compared to fed deer who survived that winter, antlers of the fed deer showed no declines in manganese or in antler integrity. This begs two questions, how does manganese influence bone calcium and is there a similar relationship between low manganese and increased osteoporosis in humans?

Regarding the first question, the research on mitochondrial manganese/calcium in bone is limited. That said, there is a fair amount of research on other tissues. A study from the 1980s showed that manganese altered the flux of calcium into and out of the rodent liver, heart, and brain mitochondria favoring influx. In other words, when manganese was present at concentrations consistent with those that might exist in real life, the mitochondria pulled in more calcium than they spit out. When magnesium was present simultaneously, the reaction was larger. More recent studies show that when manganese is present at supraphysiological concentrations, it overrides calcium influx, slows efflux, and more manganese is pulled into the mitochondria than calcium. Here, the mitochondria appear to buffer excessive manganese over calcium, but in doing so, elicit changes in mitochondrial and cellular calcium kinetics potentially leading to excitotoxic cell death – which we will discuss momentarily.

Regarding the second question, human bone contains ~40% of total body manganese and so it is possible that deficiency could lead to similar decrements in bone integrity. Several studies published since the deer antler study have linked low manganese to poor bone health and manganese supplementation to improved bone health. Interestingly, individuals with neurodegenerative disorders like Parkinson’s, Alzheimer’s, dementia, etc., show a higher propensity for osteoporosis compared to elderly patients of same age without neurodegenerative disorders. Obviously, there is a lot going on with these conditions, but I cannot help but wonder if when dietary manganese is low, bone manganese is consumed or released to favor brain manganese, thus leading to osteoporosis first, and neurodegeneration secondarily when the deficiency is prolonged. If that is the case, then osteoporosis in the elderly may be an early indicator of not only low manganese but impending brain dysfunction. This is speculative, of course, but I think a case can be made, especially when we consider the role of manganese in thiamine storage and thiamine’s role in calcium trafficking and management.

Thiamine and Calcium

Thiamine or vitamin B1, is integral to mitochondrial health. Mitochondrial health is integral to calcium management within the cell. The entry of calcium into the cell is excitatory. It tells the cell to do something; to contract a muscle, fire a neuron, migrate somewhere, grow and differentiate, etc.. This process is tightly regulated, as too much calcium or too much too fast, can cause damage or even death to the cell. This is called calcium-induced excitotoxicity.

There are multiple mechanisms to protect against this, but the primary mechanism is calcium sequestration by the mitochondria and interaction with another set of organelles called the endoplasmic reticula (ER). The mitochondria within the cell effectively mop up excess calcium, store it and then release at a more appropriate time and at a rate that is more manageable for the cell. This of course, happens only if the mitochondria have sufficient resources to function properly. What are those resources? Nutrients.

I won’t bore you with details, as I have written hundreds of articles on this topic (search here), but briefly vitamins and minerals are required for the mitochondria to perform their requisite tasks and deficiencies limit or block their activity. The tasks mitochondria are responsible for include: making energy/ATP, synthesizing other proteins involved in cell function and development, managing redox and detox processes, life/death cycles of the mitochondria but also of the cell itself, and calcium management. Thiamine is a key nutrient involved in all of these processes but is absolutely critical to the production of ATP. ATP is the energy or fuel that cells use to do all of things they need to do. What this means is that low thiamine leads to insufficient ATP, which in turn leads to poor cell function, and eventually, cell damage and death. Oh, and ultimately, our death too. We cannot even breathe without sufficient ATP. So, there is that too.

Back to thiamine and calcium. Again, I have written about this as well (here, here) as it relates to the heart, but this process is conserved across different cell populations. Briefly however, insufficient thiamine causes mitochondrial mismanagement of calcium. This, I believe happens in stages. In the early stages of deficiency, mitochondria will ramp up and store any excessive calcium to temper signals of excitation. This is a protective measure that essentially downregulates cell activity. Even so, it is an energy intensive process and so as energy wanes, so too does the ability to store and manage calcium effectively. Disordered autonomic function, also known as dysautonomia, is an indication of inadequate thiamine, which in turn means poor calcium management and disordered neural signaling in the brainstem and cerebellum (and elsewhere, but I digress).

When thiamine deficiency becomes more pronounced, either by chronicity or with a severe or overwhelming stressor, mitochondrial tempering fails and previously stored calcium is released too quickly. This causes a rapid efflux of calcium into the cell, a calcium tsunami of sorts that can be considered an internal excitotoxic event. Remember, excitotoxicity leads to cell death.

Manganese and Thiamine

While all of this is cool, the question remains, how does manganese effect thiamine? Based upon studies done many decades ago using rodents, researchers found that manganese increases the storage in multiple tissues and the synthesis of thiamine into its more active form, thiamine pyrophosphate (TPP), also called thiamine diphosphate (ThDP/TDP). A study from 1954 found that the addition of manganese to the diet increased liver thiamine and intestinal thiamine significantly. Interestingly, with low manganese, storage of thiamine in the small intestine is about 1/3-2/3 that of the liver, but with manganese, it exceeds liver storage. (Another digression: could this be a mechanism of SIBO? There is already evidence of low thiamine in SIBO, maybe low manganese is involved as well?)

A Russian study in 1985 found that total and bound thiamine content (TPP) increased in the blood, liver, heart and brain tissue while free thiamine decreased:

Addition of manganese to the diets promotes an increase of the total thiamine content in the blood and the liver, heart and brain tissues. This trace element appreciably changes the correlation between different thiamine fractions. The free vitamin B1 level in the blood and tissues decreases, while the level of its bound form (pyrophosphatic) increases. All the administered manganese doses induced a statistically significant reduction of pyruvic acid concentration in the blood.

I could not access the full study, but from the abstract it is important to note that manganese appears to increase TPP – the activated component of thiamine, which then reduces pyruvic acid content in the blood. High pyruvic acid is a key indicator of insufficient thiamine.

Other studies found similar relationships (here, here), but these relationships were not straightforward and likely to involve the interaction between other minerals and metals. Additionally, I was not able to find research untangling the thiamine>manganese relationship in humans. That said, I did find one study linking manganese to the activity of thiamine pyrophosphokinase, the enzyme responsible for phosphorylating/activating free thiamine and turning it into thiamine pyrophosphate/TPP. Granted the study was conducted in 1975, in a parsley leaf, and so, translating it to humans may be a leap, but if the human enzyme can utilize manganese, this would directly link manganese to thiamine. I should note that other enzymes accept multiple divalent cations. Pyruvate kinase (PK), for example, can substitute manganese for magnesium. The kinetic properties are different between a manganese activated versus magnesium activated PK.

Another potential mechanism at this same enzyme is via the binding to the ATP molecule. Pyrophosphokinase activity is dependent upon magnesium bound to ATP (MgATP). Manganese and magnesium share binding sites and may be somewhat interchangeable on several thiamine dependent or adjacent enzymes including a number of cytosolic and mitochondrial enzymes involved in bioenergetics. The determining kinetics of when an enzyme binds with manganese versus magnesium and to what end is unclear, at least to me, and at this point in time and so all of this is just speculation. Despite needing more research, I believe that manganese and thiamine are important components of bone integrity and when deficient create problems via the pattern below.

Low manganese →low TPP→ altered cellular calcium handling → impaired bone metabolism → osteoporosis

Final Thoughts

Barring the 1975 study mentioned above and few other studies by that same group, there seems to be very little research on the interactions between thiamine and manganese at the enzyme level. Similarly, aside from the few studies conducted in early part of the 20th century through about 1985 on how manganese affects thiamine concentrations in rodents, not much else has been done. All work since seems to have focused exclusively magnesium. Obviously, magnesium is important, however, if manganese and magnesium bind interchangeably on a variety of enzymes, including those that influence thiamine activity, it would seem to me that these are things we ought to be exploring too. I would venture that there is a whole compendium of important interactions we have missed that influence thiamine activity, and thus, mitochondrial capacity.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Photo by Markus Winkler on Unsplash

Thiamine Deficiency: A Slow Road to Dementia

by Jo Dixon

Published on June 18, 2025

17.7K views

‘Jo, you’ll be relieved to hear the tests are all normal.’

I’d heard this line so many times, and it wasn’t reassuring. Each time it became less likely that I had an illness that could be defined, diagnosed, and consequently cured, or even treated. If there was nothing wrong with me, why did I feel so awful? I had been gradually deteriorating over months, perhaps longer.

Fatigue and Other Seemingly Innocuous Symptoms

It’s difficult to say when I first felt unwell. One of the initial symptoms was terrific fatigue – struggling to find the energy to carry on each day at work. I was taking longer and more frequent tea breaks and relying on sugar to give me the buzz to carry on. Of course, it didn’t help that I didn’t sleep well. I would fall into a deep sleep early evening and then wake feeling strangely on edge with a racing heart, unable to sleep for most of the night. Even if I could sleep, it didn’t make me feel any better.

There were several other symptoms, which I could explain away, but one odd symptom was muscle twitches or fasciculations. These were worse when I was tired or had been more active. I also had dodgy guts – more about this later.

Even though I was exhausted I could continue working, being a mother to our four children – albeit a rather terrible one that repeatedly fell asleep in the middle of bedtime stories, until I developed brain fog. I felt like my thinking was occurring at less than half the usual speed. I struggled to hold a conversation, as this required listening, interpreting the other person’s words, formulating an answer, and talking. I would have to really concentrate to think about anything. I would forget things unless I wrote them down, which just meant I had unfinished lists scattered everywhere.

After falling on the ward where I had been working as a doctor, I finally acknowledged that I was sick, even if there was nothing apparently wrong with me. Once I stopped working, I deteriorated further, such that I was unable to recognize people and even places.

A Slow Road to Dementia

This was over 10 years ago. Clearly, I’ve improved since then. I’ve written a book to try to characterize my symptoms, explain what caused them, and why it was difficult to make a diagnosis. This seems even more pertinent since a lot of the symptoms I suffered with then resemble long Covid now.

My main concern was that I had developed dementia. I had many of the features: I struggled to remember recent events, I had problems following conversations, I was forgetting the names of friends and even commonly used objects, and I was repeating myself and having problems with thinking and reasoning. I also had difficulty recognizing where I was — this is visuospatial disorientation — a key marker of dementia.

Since the medical profession seemed to have no idea how to treat me I decided to try to work it out for myself. What choice did I have? Away from work, I had time to slowly read through medical papers, whilst I rested. I recognized that my symptoms improved after taking antibiotics for a gum infection. Any exertion made me markedly worse, but not immediately afterward, it would be the following day and last for several days. I improved if I rested. My other symptoms included pains in my hands and feet. I thought this was arthritis initially, but when I developed pins and needles and subsequently numbness, I realized this was a peripheral neuropathy – a problem with the sensory nerves in my extremities.

Some months earlier a close colleague had told me I was thiamine deficient, mainly because I had lost a lot of weight. I was taken aback, assuming he thought my diet was poor, or that I was drinking alcohol. I hadn’t drunk any alcohol for years as it made me feel rough after a few sips. I investigated thiamine deficiency and found that it causes loss of sensation as well as loss of balance; I already knew it affected memory from treating alcoholics under my care.

My friend kindly agreed to try high-dose intravenous thiamine on the ward. Neither of us really thought it would work, but it was worth a shot. I was astounded when after a few minutes of the infusion I started to be able to think clearer and even the pains in my hands and feet disappeared. I practically skipped off the ward to buy oral thiamine and dose up. Sadly, thiamine tablets didn’t work and two days later I was back on the unit begging for more shots. This thrice-weekly dosing of thiamine infusions continued for months.

The Gut Connection

I trained in Gastroenterology and General Medicine. They say doctors make the worst patients. For as long as I could remember I had suffered from intermittent severe central abdominal pains, which usually occurred after eating quickly on an empty stomach. According to my mother, I had been a colicky baby and had also returned to the hospital as a new baby with uncontrollable vomiting. Nothing abnormal was found.

In fact, not all the tests I had were normal. After several second opinions, I had a few abnormal tests. I had a CT scan of my abdomen, which showed that I had gut malrotation. The severe pains I had experienced throughout life were due to small bowel volvulus – twisting. I learned that if I stopped eating and lay down on my back the pain would gradually subside. Each time my guts twisted scar tissue formed adhesions, slowing down my gut movements.

My guts had been noticeably abnormal for many years. I had noisy guts and passed very loose, frequent motions. I don’t know many slim 20-year-olds who suffered from severe gastro-esophageal reflux as I did. As this progressed, I developed recurrent chest infections and required multiple courses of antibiotics. Eventually, I worked out that I was aspirating gut contents into my lungs each night, and I stopped eating in the evening and propped myself up with many pillows. All sorted – no more chest infections – no more antibiotics.

One of the other abnormal tests was an incredibly low vitamin D. Through late-night searches of anything vaguely relevant and my gastroenterology knowledge I worked out that a low vitamin D occurred in bacterial overgrowth. This made sense. I had developed bacterial overgrowth in my small intestines — the part of the gut responsible for the absorption of nutrients from food.

Small intestinal bacterial overgrowth or SIBO is due to an excess of bacteria in the small intestines. There are many risk factors including sluggish guts from adhesions, previous surgery, medications that slow the gut, but also multiple courses of antibiotics, poor immune system, and use of drugs that block acid production in the stomach, as well as pancreatitis. I’m sure that a diet high in sugar didn’t help.

I had another test specifically looking for bacterial overgrowth, which the nurse (a colleague I’d worked with many times) and I interpreted as abnormal. The consultant I saw thought the machine must have broken. This was frustrating; after so many normal tests to have a wildly abnormal test attributed to faulty equipment. I decided it was better to treat the patient (me) rather than a dubious test result. After starting antibiotics, I no longer needed the thiamine infusions. The diarrhea also improved.

I worked out that I had bacterial overgrowth from mal-rotated guts, obstructed from adhesions, which improved with antibiotics and were eventually treated with corrective surgery. I also had severe vitamin D deficiency, which was corrected with injections, and thiamine deficiency, which I subsequently managed with a fat-soluble thiamine analogue — benfotiamine. I found a paper online reporting thiamine deficiency in extremely obese patients who had undergone surgery on their small intestines to aid weight loss. Many of these patients had thiamine deficiency; they also had high folate, which was thought to be a marker of bacterial overgrowth. Oral thiamine had no effect on their thiamine levels, but after taking antibiotics the patients’ thiamine returned to normal. Interestingly, my folate was high.

What was less well known was that some bacteria produce an enzyme called thiaminase, which destroys thiamine. I can only assume that I had these kinds of bacteria in my gut. Interestingly these bacterial enzymes do not destroy benfotiamine.

I followed up on my theory of the underlying cause of dementia: that too many bacteria, producing a lot of thiaminase enzyme, destroy the thiamine in our food rendering us thiamine deficient. I found out that thiamine is essential for all living things, and it is necessary for the release of energy from food, particularly sugar or glucose. The brain only uses glucose as an energy supply. There are reports of low thiamine levels in the brain in patients who have died of dementia. Glucose metabolism in the brain is never normal in dementia. Benfotiamine has been shown to improve mild cognitive impairment. I speculated that this was the cause of my brain fog.

Thiamine Deficiency: The Missed Diagnosis

Why was it so difficult to make a diagnosis? I believe there are several reasons. Firstly, thiamine levels are rarely tested in the UK. Even though I had worked in the NHS for over 20 years I had never requested a thiamine test. Secondly, thiamine deficiency is known to present in widely differing ways. This is like many of the mysterious syndromes — a constellation of recognizable symptoms and signs with largely normal tests: irritable bowel syndrome, fibromyalgia, etc., and also long Covid. Thirdly, I wasn’t listened to. I’m not sure whether this is because I’m female, but I became extremely sick before anyone really tried to help, and even then I was reliant on friends I have in the medical profession.

I’m remarkably well now. I regained my memory and ability to think, although it probably took a couple of years. My guts still aren’t completely normal, but bacterial overgrowth is often a chronic condition. I still take supplements and I’m careful with my diet, avoiding sugar and alcohol. My diet is quite restrictive, but it’s worth it. I wouldn’t want to go back to how I was.

[atkp_product id=’49246′ template=’bestseller’][/atkp_product]

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 Katie Moum on Unsplash.

This article was published originally on June 30, 2022.

Atomic Imprint: A Legacy of Chronic Illness

by Genie

Published on May 21, 2025

16.5K views

In a sense, my complicated health history began a decade before I was born. In 1951, on a chilly pre-dawn morning in Nevada, my father-to-be crouched in a trench with his Army comrades and shielded his eyes with his hands. Moments later, an atomic blast was detonated with a light so brilliant that he could see the bones in his hands through his eyelids, like an x-ray. The soldiers were marched to ground zero within an hour, exposing them to massive amounts of radiation. My father suffered many physical issues and died of chronic lymphocytic leukemia at 61 – a far younger age than usual with this disease.

Many of the soldiers exposed to atomic tests and military radiation cleanup efforts paid dearly with their health, and the legacy was passed on to their offspring in the form of miscarriages, stillbirths, deformities, retardation, childhood cancers, and chronic health issues. I never wanted children, in part because I was concerned that my own genes were affected by my father’s radiation exposure.

Early Markers of Ill Health

Physically, I didn’t feel right as a child. I had mononucleosis as a baby and needed a prednisone shot to get well. I was sick often and lacked stamina. I had mono again in high school and relapsed in college.

I fared well as a young adult, but then hit a wall in my mid-30s when I suddenly became chronically ill with digestive issues, insomnia, brain fog, and fatigue. A hair test revealed off-the-charts mercury poisoning, so I had ten fillings replaced and detoxed. All my hormone levels crashed, so I went on bioidentical hormone replacement therapy for a time. I recovered quickly but adrenal and thyroid hormone support were still necessary. I even fared poorly with the ACTH cortisol stimulation test to assess for adrenal insufficiency (“adrenal disease” beyond so-called “adrenal fatigue”).

In 2001, a DEXA scan revealed I had osteopenia at just 40 years old and I tested positive for elevated gliadin antibodies, a marker for celiac disease, the likely cause of the bone thinning. I went gluten-free and began lifting weights – thankfully, my bone density resolved. I shifted away from a vegetarian diet and gained muscle mass and energy.

Over the next several years, I had bouts of “gut infections,” resolving them with herbal antimicrobials. About a decade ago, the dysbiosis flares became more frequent and difficult to resolve. I tested positive again for mercury. This time I did the Cutler frequent-dose-chelation protocol and reduced my mercury burden to within normal levels according to hair tests.

A Labyrinth of Health Issues

My health issues were becoming more numerous, complex, and difficult to manage as I grew older. Besides the persistent sleep and digestion issues, I often had fatigue, pain, bladder pain, urinary frequency, restless legs, migraines, Raynaud’s, chilblains, and more. Managing all these symptoms was a real juggling act and rare was the day that I felt right.

As I searched for answers, I turned to genetic testing, starting with Amy Yasko’s DNA Nutrigenomic panel in 2012 and then 23andMe in 2013 to learn which “SNPs” (single nucleotide polymorphisms) I have. A Yasko-oriented practitioner helped me navigate the complexities of the nutrigenomics approach – that is, using nutrition with genetic issues.

I learned that genes drive enzymes that do all the myriad tasks to run our bodies (which don’t just function automatically), and that certain vitamins and minerals are required to assist the enzymes, as specific “cofactors.” Genetic SNPs require even more nutritional support than is normal to help enzymes function better. So my focus shifted toward using basic vitamins and minerals to support my genetic impairments. I now understood that I needed extra B12, folate, glutathione, and more. I began following Ben Lynch’s work in elucidating the MTHFR genetic issue, as I had MTHFR A1298C.

Also in 2013, given my struggle with diarrhea, I was diagnosed with microscopic colitis via a biopsy with colonoscopy. In 2014, I learned about small intestinal bacterial overgrowth (SIBO), which gave me a more specific understanding of my “gut infections,” and tested positive for methane SIBO. I worked with a SIBO-oriented practitioner on specific herbal treatments with some short-lived success.

At the end of 2014, I learned that I have Ehlers Danlos Syndrome (EDS, Hypermobile Type), confirmed by a specialist. I came to understand that my “bendiness” likely had implications in terms of chronic illness, and I saw my bunion and carpal tunnel surgeries in a new context, as part of this syndrome.

Even with these breakthroughs in understanding, I still relentlessly searched deeper for root causes.

Genetic Kinetics

In 2018, Ben Lynch published Dirty Genes, focusing on a number of common yet impactful SNPs.

I learned that I had NEARLY ALL of these SNPs – NEARLY ALL as “doubles” and even a “deletion.” (Deletions are worse than doubles; doubles are worse than singles.) Researching further, I had doubles in many related genes with added interactive impacts. Typically people might have just a few of these SNPs.

Understanding my “dirty gene” SNPs revealed that I could be deficient in methylation, detoxification, choline synthesis, nitric oxide synthesis, neurotransmitter processing, and histamine processing. Each of these SNPs could potentially impact sleep, digestion, and much more in numerous ways. Now I potentially had a myriad of root causes.

Lynch warns people to clean up their health act before supplementing the cofactors, whereas I’d cleaned mine up years prior. Sadly, I found only limited improvements in adding his nutritional protocol. Suffice it to say I felt rather overwhelmed and disheartened.

But at the same time, I gained vital and necessary insights. I now understood why I had mercury poisoning twice: detox impairments. I understood why I had Raynaud’s, chilblains, and poor circulation: nitric oxide impairments. My migraines could be histamine overload. I needed high levels of choline for the PEMT gene to prevent fatty liver disease and SAMe for the COMT gene. Much was yet still unexplained. So I relentlessly soldiered on, following every lead, clue, and a new piece of information.

Later in 2018, a friend who also has EDS encouraged me to learn about Mast Cell Activation Syndrome (MCAS), as many with EDS also have this condition. A few weeks later, I had a three-day flare of many issues, which prompted me to delve into the MCAS world, which was just as complex as the genetic approach. In working with an MCAS specialist, I honed in on three supplements, quercetin, palmitoylethanolamide, and luteolin, to help stabilize mast cells, which improved my bladder pain, bone pain, migraines, fatigue, and generalized pain. This was the culmination of months of research and work. All of this points to further genetic involvement, even though I lack specifics.

Downward Spiral

Twenty-nineteen brought further insights. I integrated circadian rhythm entrainment work. I tried a low-sulfur diet, suspecting hydrogen sulfide SIBO, which made me feel worse; and I began taking dietary oxalates somewhat more seriously after testing positive on a Great Plains OAT test. I did glyphosate and toxicity testing, which provided a picture of my toxic load. Testing also indicated high oxidative stress and mitochondrial issues (very interrelated). Hair Tissue Mineral Analysis (HTMA) testing, with the assistance of a specialist, helped me understand my mineral status and to begin rebalancing and repleting.

In 2020, I took a hiatus from all this effort, during which time I turned my attention towards personal matters, but 2021 has been a doozy in redoubling my health efforts. My digestion had worsened, so I focused on this area. I learned about sucrase-isomaltase deficiency, a lack of certain enzymes to digest sucrose and starch. I hadn’t tolerated sugar and starch for years, and I found I had a SNP for this condition. In January, a zero-carb trial diet helped me feel much better, so I continued. I tested positive for hydrogen sulfide SIBO, and I wrestled with this “whole-other-SIBO-beast” – in February trying again the low-sulfur diet and again feeling worse. Combining the zero-starch and low-sulfur diets left few options. Despite all my best efforts, I experienced a downward spiral with a loss of appetite, nausea, and vomiting every few days.

Discovering Thiamine

Around this time, I read an article about low thiamine (Vitamin B1) lowering intracellular potassium – I had been trying unsuccessfully to raise my potassium level in my HTMA work. I began following author Elliot Overton’s articles and videos on thiamine deficiency and oxalates. I was finally persuaded to take oxalates seriously. I then read the definitive book “Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition” by Drs. Derrick Lonsdale and Chandler Marrs. I learned how B1 was key in many processes involving energy, digestion, and much more. I found that I had multiple SNPs in the B1-dependent transketolase gene, which is pivotal in several pathways. I gained some understanding of how all this related to some of my other genetic impairments, and why I might need high dose thiamine to overcome some issues.

All this was quite a revelation for me. It fit perfectly with my emphasis on vitamins and minerals to assist genes…but why hadn’t I learned of B1’s significance sooner?

In early March, I began my thiamine odyssey with 100 mg of thiamine HCL, upping the dose every couple of days. At 300mg HCL, I added 50 mg of TTFD, a more potent and bioavailable form of B1, then continued to up the TTFD dose every few days.

Similar to my experience with other vitamins, I was able to proceed rather quickly in dose increases. Many other people are not so fortunate and must go much more slowly. I already had in place most of thiamine’s cofactors (such as glutathione, other B vitamins, and methylation support) – so perhaps this helped me proceed more readily. Without these cofactors, peoples’ thiamine efforts often fail.

Magnesium is one of the most important thiamine cofactors, and for me, the most challenging. My gut cannot handle it, so I must apply it transdermally two or more times a day. At times, I had what I interpreted as low magnesium symptoms: racing and skipping heart, but these resolved as I continued.

Additionally, one must be prepared for “paradoxical reactions.” Worse-before-better symptoms hit me the day after thiamine dose increases: gut pain, sour stomach, headache, fatigue, and soreness.

My symptoms improved as I increased the dosing. When I added 180 mg of benfotiamine early on, my bit of peripheral neuropathy immediately cleared. This form of B1 helps nerve issues. As I increased my thiamine dosing, the nausea abated, my appetite came roaring back, and gastritis disappeared. Diarrhea, fatigue, and restless legs improved. I was able to jog again. My digestion improved without trying to address the SIBO and inflammation directly; the strict keto and low oxalate diets may have also helped.

In June, I attained a whopping TTFD dose of 1500 mg but did not experience further resolution beyond 1200mg, so I dropped back down. At 1200mg for a month, a Genova NutrEval test revealed that I was not keeping pace with TTFD’s needed cofactors, especially glutathione and its substrates. Not too surprising, given my malabsorption issues and my already high need for these nutrients. I dropped the TTFD to 300 mg, but quickly experienced fatigue. I’m now at 750 mg, which is still a large dose, and clearly, there is more to my situation than thiamine can address. I still have diarrhea and insomnia, and continue working to address these.

The Next Chapter

With TTFD, its cofactors, and my new gains in place, I’ve turned my attention towards a duo of genetic deletions that I have in GPX1 (glutathione peroxidase 1, one of Lynch’s dirty genes) and CAT (catalase). Both of these enzymes break down hydrogen peroxide (H2O2), a byproduct of numerous bodily processes. This unfortunate double-whammy causes me a build-up of damaging H2O2 and lipid peroxides – in other words, oxidative stress, a major factor in mitochondrial impairment, many diseases, and aging. This might be one of my biggest and yet-unaddressed issues, and I am digging deep into the published medical literature. This new chapter is currently unfolding.

I believe these two deletions are related to my father’s radiation exposure, for reasons beyond the scope of this article. But what about all the other SNPs? Many questions remain unanswered.

All my gains have been so hard-won, involving much research, effort, and supplementation. Yet what other options do I have, besides playing whack-a-mole and spiraling downward? Looking back, my improvements have been substantial, given the multitude of issues I’ve had to deal with. Perhaps now at 60, my life can start to open again to more than just self-care.

I hate to think of where I would be now, had I never come across the thiamine deficiency issue. I believe a number of factors had driven my thiamine status dangerously low earlier this year, such as malabsorption, oxidative stress, and hydrogen sulfide SIBO. I’m forever grateful to Lonsdale, Marrs, and Overton for their invaluable thiamine work that helped guide me back from the brink, and to the numerous doctors and practitioners who have helped me get this far. Perhaps my story can help others struggling with chronic health issues.

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 credit: First U.S. nuclear field exercise conducted on land; troops shown are a mere 6 miles from the blast. Nevada Test Site, 1 November 1951. This image is a work of a U.S. military or Department of Defense employee, taken or made as part of that person’s official duties.

As a work of the U.S. federal government, the image is in the public domain in the United States.

This article was published originally on September 23, 2021.

SIBO, IBS, and Constipation: Unrecognized Thiamine Deficiency?

by Elliot Overton, DipCNM CFMP

Published on May 13, 2025

161.1K views

In many of my clients, chronic upper constipation and gastroesophageal reflux disease (GERD) are misdiagnosed as bacterial overgrowth. Unfortunately, they are often non-responsive to antimicrobial treatments. Yet, sometimes the issues are fixed within a few days of vitamin B1 repletion. This has shown me that often times, the small intestinal bacterial overgrowth (SIBO) is simply a symptom of an underlying vitamin B1 or thiamine deficiency.

GI Motility and Thiamine

The gastrointestinal (GI) tract is one of the main systems affected by a deficiency of thiamine. Clinically, a severe deficiency in this nutrient can produce a condition called “Gastrointestinal Beriberi”, which in my experience is massively underdiagnosed and often mistaken for SIBO or irritable bowel syndrome with constipation (IBS-C). The symptoms may include GERD, gastroparesis, slow or paralysed GI motility, inability to digest foods, extreme abdominal pain, bloating and gas. People with this condition often experience negligible benefits from gut-focused protocols, probiotics or antimicrobial treatments. They also have a reliance on betaine HCL, digestive enzymes, and prokinetics or laxatives.

To understand how thiamine impacts gut function we have to understand the GI tract. The GI tract possesses its own individual enteric nervous system (ENS), often referred to as the second brain. Although the ENS can perform its job somewhat autonomously, inputs from both the sympathetic and parasympathetic branches of the autonomic nervous system serve to modulate gastrointestinal functions. The upper digestive organs are mainly innervated by the vagus nerve, which exerts a stimulatory effect on digestive secretions, motility, and other functions. Vagal innervation is necessary for dampening inflammatory responses in the gut and maintaining gut barrier integrity.

The lower regions of the brain responsible for coordinating the autonomic nervous system are particularly vulnerable to a deficiency of thiamine. Consequently, the metabolic derangement in these brain regions caused by deficiency produces dysfunctional autonomic outputs and misfiring, which goes on to exert detrimental effects on every bodily system – including the gastrointestinal organs.

However, the severe gut dysfunction in this context is not only caused by faulty central mechanisms in the brain, but also by tissue specific changes which occur when cells lack thiamine. The primary neurotransmitter utilized by the vagus nerve is acetylcholine. Enteric neurons also use acetylcholine to initiate peristaltic contractions necessary for proper gut motility. Thiamine is necessary for the synthesis of acetylcholine and low levels produce an acetylcholine deficit, which leads to reduced vagal tone and impaired motility in the stomach and small intestine.

In the stomach, thiamine deficiency inhibits the release of hydrochloric acid from gastric cells and leads to hypochlorydria (low stomach acid). The rate of gastric motility and emptying also grinds down to a halt, producing delayed emptying, upper GI bloating, GERD/reflux and nausea. This also reduces one’s ability to digest proteins. Due to its low pH, gastric acid is also a potent antimicrobial agent against acid-sensitive microorganisms. Hypochlorydria is considered a key risk factor for the development of bacterial overgrowth.

The pancreas is one of the richest stores of thiamine in the human body, and the metabolic derangement induced by thiamine deficiency causes a major decrease in digestive enzyme secretion. This is one of the reasons why those affected often see undigested food in stools. Another reason likely due to a lack of brush border enzymes located on the intestinal wall, which are responsible for further breaking down food pre-absorption. These enzymes include sucrase, lactase, maltase, leucine aminopeptidase and alkaline phosphatase. Thiamine deficiency was shown to reduce the activity of each of these enzymes by 42-66%.

Understand that intestinal alkaline phosphatase enzymes are responsible for cleaving phosphate from the active forms of vitamins found in foods, which is a necessary step in absorption. Without these enzymes, certain forms of vitamins including B6 (PLP), B2 (R5P), and B1 (TPP) CANNOT be absorbed and will remain in the gut. Another component of the intestinal brush border are microvilli proteins, also necessary for nutrient absorption, were reduced by 20% in the same study. Gallbladder dyskinesia, a motility disorder of the gallbladder which reduces the rate of bile flow, has also been found in thiamine deficiency.

Malnutrition Induced Malnutrition

Together, these factors no doubt contribute to the phenomena of “malnutrition induced malnutrition”, a term coined by researchers to describe how thiamine deficiency can lead to all other nutrient deficiencies across the board. In other words, a chronic thiamine deficiency can indirectly produce an inability to digest and absorb foods, and therefore produce a deficiency in most of the other vitamins and minerals. In fact, this is indeed something I see frequently. And sadly, as thiamine is notoriously difficult to identify through ordinary testing methods, it is mostly missed by doctors and nutritionists. To summarize, B1 is necessary in the gut for:

Stomach acid secretion and gastric emptying
Pancreatic digestive enzyme secretion
Intestinal brush border enzymes
Intestinal contractions and motility
Vagal nerve function

Based on the above, is it any wonder why thiamine repletion can radically transform digestion? I have seen many cases where thiamine restores gut motility. Individuals who have been diagnosed with SIBO and/or IBS and are unable to pass a bowel movement for weeks at a time, begin having regular bowel movements and no longer require digestive aids after addressing their thiamine deficiency. In fact, the ability of thiamine to address these issues has been known for a long time in Japan.

TTFD and Gut Motility

While there are many formulations of thiamine for supplementation, the form of thiamine shown to be superior in several studies is called thiamine tetrahydrofurfuryl disulfide or TTFD for short. One study investigated the effect of TTFD on the jejunal loop of non-anesthetized and anesthetized dogs. They showed that intravenous administration induced a slight increase in tone and a “remarkable increase” in the amplitude of rhythmic contractions for twenty minutes. Furthermore, TTFD applied topically inside lumen of the intestine also elicited excitation.

Another study performed on isolated guinea pig intestines provided similar results, where the authors concluded that the action of TTFD was specifically through acting on the enteric neurons rather than smooth muscle cells. Along with TTFD, other derivatives have also been shown to influence gut motility. One study in rats showed an increase in intestinal contractions for all forms of thiamine including thiamine hydrochloride (thiamine HCL), S-Benzoyl thiamine disulphide (BTDS -a formulation that is somewhat similar to benfotiamine), TTFD, and thiamine diphosphate (TPD). A separate study in white rats also found most thiamine derivatives to be effective within minutes.

Most interestingly, in another study, this time using mice, the effects of thiamine derivatives on artificially induced constipation by atropine and papaverine was analyzed. The researchers tested whether several thiamine derivatives could counteract the constipation including thiamine pyrophosphate (TPP), in addition to the HCL, TTFD and BTDS forms. Of all the forms of thiamine tested, TTFD was the ONLY one which could increase gut motility. Furthermore, they ALSO showed that TTFD did not increase motility in the non-treatment group (non-poisoned with atropine). This indicated that TTFD did not increase motility indiscriminately, but only when motility was dysfunctional. Finally, severe constipation and gastroparesis identified in patients with post-gastrectomy thiamine deficiency, was alleviated within a few weeks after a treatment that included three days of IV TTFD at 100mg followed by a daily dose of 75mg oral TTFD. Other symptoms also improved, including lower limb polyneuropathy.

To learn more about how thiamine affects gut 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.

Yes, I would like to support Hormones Matter.

Photo by Johannes Krupinski on Unsplash.

This article was first published on HM on June 1, 2020.

Post Concussive Metabolic Dysfunction in a Dancer

by Broken Mom

Published on June 22, 2023

7.9K views

post concussive thiamine deficiency in a dancer

A Concussion, an Infection and the Slow Spiral of Declining Health

Our daughter started ballet at 2.5 years old, and by 5 years old she had started competitions and had decided she was going to become a professional ballerina. She was talented, had an amazing work ethic and completely loved her life of ballet, friends and school. She was a very happy child, bright and bubbly and she woke up everyday super excited about what was going to be happening that day. From a very early age, our daughter showed determination, stubbornness and a quiet, but strong competitiveness.

In October 2016, when she was 12 years old, she got a severe concussion, and her whole life stopped for nearly 3 months. She stayed in her bedroom in the dark, couldn’t read, slept for most of the day and even trying to tie her shoelaces gave her an intense headache. After months of no improvement, we took her to a chiropractor, who told us her neck was out and she wouldn’t have gotten better until it was put back in properly. Our daughter floated out of that appointment so happy that she nearly felt back to her normal self. The chiropractor gave us an information sheet about Thiamine/B1 Vitamin at the time, but we didn’t really take any notice apart from trying to give her some more marmite (yeast spread) as it suggested.

Then in September 2017, both our daughter and our older son suddenly became very ill with vomiting, diarrhoea, rashes, headaches, stomach pain, joint pain, and bright red palms. Our older son had more intense symptoms, and also had extreme nose bleeds and petechial rashes – he was admitted to hospital where they found his liver and spleen were enlarged but they couldn’t work out what was wrong. Our son had recently come back from a school trip to Vietnam – we were trying to find if there was a link to Vietnam but he had already been home for a couple of weeks so the hospital didn’t test for any illnesses from Vietnam. After weeks of this illness, we were told our daughter had Mono/Epstein Barr Virus and that this was causing her illness and it was completely unrelated with our son’s illness. We found this extremely odd that they could have mostly the same symptoms at exactly the same time, but as our son was more acute and in hospital, we were just concentrating on trying to get both of them well.

Since then, our daughter has never fully recovered. She started not sleeping, and constantly having body pains and headaches. She was sent to a paediatrician who diagnosed her with Child Migraines and told us she would outgrow them and was given melatonin for sleep. The melatonin worked for 3 nights and then completely stopped working. Our daughter started to put on weight, and would look puffy in the face, and she lost her menstrual period even though she was gaining weight. She was always tired, always had body pains and slowly but surely lost her sparkle.

Declining Metabolic Function and Weight Gain

At the end of 2017 when she was 13 years old, she lost her place in the national ballet training program. Our daughter was extremely stoic at this point, and was determined to get a professional career without the training academy’s help. Throughout 2018 she continued to put on weight, no matter how healthy she ate or what she ate, and still didn’t have a menstrual period. We saw doctors and nutritionists, but they couldn’t explain why her weight continued to increase or they would tell us there was nothing wrong. Our daughter became quiet, withdrawn, easily irritated and frustrated and stopped being interested in anything or anyone. She continued to work at her ballet, and the only time she would ‘light up’ would be on stage, as she was still trying to compete. During 2018, she gained 10kg/22lbs while being on a very strict nutrition plan. She auditioned for a ballet academy to start at the beginning of 2019 and was accepted; she was happy but in a tired way, and she knew that she would need to stop gaining weight but had no idea how she was going to do that when she had already been trying so hard.

In February 2019 we saw a naturopath who diagnosed our daughter with Adrenal Fatigue, and said her thyroid needed support, and that she still had lingering Epstein Barr Virus in her system. The naturopath pointed to our daughter always wanting salt as an indicator of adrenal fatigue. She was put on some herbal remedies for her immune system, inflammation and liver, adrenal and thyroid support, and relaxation/sleep support as well as Epstein Barr Virus liquid drops to help her immune system recognise the lingering EB virus in her system.

The weight started to instantly melt off, her sleeping improved and we felt we finally had some answers and a solution. Our daughter was happy with the weight loss, but still struggled with her other symptoms: dizziness, dry/gritty eyes, chest pain, tiredness, muscle and joint pains, extremely sore lower and upper back pain, brain fog, very low blood pressure, daily headaches, daily sore throat, complete lack of energy and occasionally sore under her right ribs (later on she told us that she couldn’t sweat, no matter how hard or long she exercised).

A month after starting the herbal remedies, she had her first panic attack during rehearsal for a school production – she had no idea what was happening and it took a long time to calm her down. Her mental and emotional state continued to decline, it was a daily struggle to do anything; she always had to push through every single day. We continued to take our daughter to the doctors for the sore throats, tiredness, headaches etc. but we were always told there was nothing wrong with her. During this time she got an infected toenail, and ended up being on antibiotics for twice as long as usual as it wouldn’t heal. The naturopath added in additional supplements to help, and eventually her toe got better.

Even though she was still losing weight, our daughter became very apathetic and would stay in her room – we would try to talk to her every day, try to reach her but she was shut off emotionally. Then we ran out of one of the herbal supplements, and suddenly she began to gain weight again – she gained 2.8kg/6.2lbs in 2 weeks. Once we got her back on the herbal supplement she began to lose weight again, but it seemed to be slower and less effective. Our daughter got to 51.3kg (she is 5ft7 inches tall) and she was happy, and her ballet teachers told her to not lose any further weight as she was fine at the weight she was.

Hair Loss, Pale Skin, and Skyrocketing Weight

Halfway during 2019, our daughter’s hair started to fall out in clumps, it got to the point where she was too scared to wash or comb it, as it was falling out so much. We noticed our daughter was extremely pale, and at times she looked translucent. The naturopath put her on iron pills and told us to massage her scalp, but it didn’t really make a difference. The naturopath didn’t think she needed to be on the adrenal/thyroid support any longer, and was changing her supplements. Our daughter’s weight then skyrocketed, and our relationship with the naturopath started to deteriorate as she kept implying that we were starving our daughter and we felt she wasn’t able to answer our questions on why one particular supplement seemed to be the only one that would help our daughter lose weight, but she still had the other symptoms that were getting worse.

We took our daughter to other GP doctors, trying to explain her symptoms and asking for her thyroid to be checked, but we were continuously brushed off and they would look at our daughter and say it was just normal teenage hormonal stuff and there was nothing wrong. In our gut we felt there was something drastically wrong, but nobody would listen to us. We started to hate going to the doctors, going through her symptoms only to be told again and again there was nothing wrong with her, and being looked at like we had the problem, not our daughter. We started trying to research things ourselves, started tracking and monitoring everything she ate/did/sleep patterns. The naturopath would change the supplements and our daughters weight would skyrocket – we would then put her back on the original supplements and again she would start to lose weight, but every time it was less effective.

Low Metabolic Rate, Low Estradiol, Yeast and Bacterial Overgrowth, Constipation and Parasites

At the beginning of 2020, our daughter’s weight was going back up significantly and it seemed that the original supplement was no longer working at all. We realised that our daughter’s face and neck seemed to be more swollen on the left side, but couldn’t find any reason why it would be like this. Our daughter started to get new symptoms around this time as well – from not being able to sweat at all, she started to have extreme sweating everywhere, and started to get hot flushes and night sweating. We noticed that the hair on her upper lip was more noticeable/darker, and she started to get a small patch of hair just under the middle of her lower lip as well. She also started to get a very bloated around her stomach area, and couldn’t pull it in no matter how hard she tried.

In February 2020, we decided to try and get testing done ourselves, and found a functional doctor who supplied a variety of tests. We got a hormone and thyroid test, as well as a MTHFR gene mutation test. We thought if we could show our doctor some factual data, we might be taken more seriously. The functional doctor advised us to also do an Organic Acid urine test, which we did as well. The test results came back saying that our daughter’s total estrogen was so low that it was at the level of a post-menopausal woman, but the functional doctor thought that was because she was a dancer. The organic acid test picked up that she was in a hypometabolic state; again with the reason given that this was because she was an athlete. The organic acid test also showed that she had a significantly high amount of yeast and bacterial overgrowth in her gut, which would cause inflammation system wide and insulin resistance.

The functional doctor wanted to test for parasites as well, so we did a complete microbiome mapping test using a stool sample. While taking the stool sample, we were surprised that our daughter could only produce tiny, rock-hard little pebbles and we questioned her about it, we then found that she was constipated but she thought passing tiny pebble-type stools only every 3-5 days was normal.

While we were waiting for the microbiome mapping results, the functional doctor prescribed a total of 30 supplements/remedies as well as adrenal support liquid drops – these were to cover supporting biochemical pathways, weight management, cognitive support, anti-inflammatories, detoxification, liver support, hormonal metabolism, adrenal and energy support, amino acids to support cellular energy, mitochondrial NRG multivitamins to support cellular health, l-tryptophan to support sleep and neurotransmitter mood support. During this time she was also advised to stop all dairy (she was already gluten/sugar free and very low carb). We did take all of these tests results to our GP doctor, but were advised that they didn’t recognise these tests.

After a week of the new supplements, we noticed a complete shift in our daughter’s energy level and emotional/mental state. We were relieved to have our daughter’s personality back – it was literally like a heavy, suffocating blanket had been taken off her and she could finally think, feel and breathe again – it was a huge difference seeing her not having to mentally struggle through every single day. We did a lot of talking with her and she finally admitted just how numb she had felt to everything, but also scared that this was how she was going to be for the rest of her life. The supplements did nothing for her weight, which continued to increase, and some of the other physical symptoms, but we were now clinging to the information that we knew she could lose the weight, and that now she could also be better emotionally and mentally with higher energy levels – we just had to figure out what was stopping her from having all of these things at the same time.

In May 2020, the microbiome mapping results came back, and we were surprised to find that our daughter an extreme level of a parasite in her system, called Blastocystis hominis, as well as an overgrowth of Rhodotorula fungi and a couple of other opportunistic bacterial overgrowths. The functional doctor immediately put her on a parasite/bacterial/yeast eradication protocol that was to be for two months, and then we were supposed to follow that with 6 months of a rejuvenation program.

When our daughter found out it was a parasite that was making her sick, she was absolutely ecstatic. She had loved ballet her whole life, but thought it was ballet making her sick so had been pushing it away which had been hurting her emotionally – it hurt her to think that the thing she loved the most was hurting her. Now that she knew it was instead a parasite making her sick, she felt she could allow herself to love ballet again. While waiting for the herbal remedies for the eradication protocol, we started to research the parasite, and started to become very concerned at just how difficult it was to get rid of it, and the devastating symptoms/damage that it could do.

Looking at other protocols that were used to get rid of this particular parasite, the remedies weren’t the same as the ones prescribed by our functional doctor, so we questioned if these particular remedies had been used for this parasite before and if they were successful. We were assured that these remedies had been used and were definitely successful.

Failed Treatments and Inconclusive Diagnoses

Our daughter started on Australian Oil of Oregano, 6 capsules a day totalling 900mg of essential oil each day, as well as 6 capsules of a GI-Microbe remedy for worms. After a week she noticed she had a very itchy bottom and a sore stomach. Our GP doctor wanted to check for PCOS because of the lack of menstrual period and her hair falling out, so our daughter had a pelvic ultrasound 6 days after starting the Oil of Oregano. The sonographer couldn’t see anything in the ultrasound because of the amount of gas (it looked like billowing black clouds on the screen), so after a lot of discussion due to our daughter’s age, she had an internal ultrasound. The sonographer was surprised that it was still hard to see anything due to the amount of gas, so could only see one ovary and a small piece of her uterus, which the sonographer said looked good and didn’t indicate there was PCOS.

During the following week our daughter’s stomach pain became more intense, and her weight was skyrocketing. We started to get very concerned at her escalating reactions but kept being reassured by the functional doctor that this was normal. After 20 days of being on the Oil of Oregano we decided to take our daughter off all of the supplements as we felt they were just making her worse. All of the literature on the parasite Blastocystis advises that you need to wait 8 weeks before doing PCR stool testing to see if the parasite has been eradicated or not. We are currently waiting until 10 August 2020 at the earliest to be able to test to see if the parasite is gone. Since this Oregano treatment, her stools are now every day and better consistency (they were floating which we think is fat malabsorption issues?) and her menstrual period has returned. Her appetite has also reduced, and she isn’t craving carbs and sugar as she has now revealed she used to.

Since then our daughter’s weight has continued to increase at a rapid rate – in total from 27 January 2020 to 31 July 20202 she has gained 14.5kg/32lbs, with 10kg/22lbs being in the last 2.5 months. She can physically no longer do ballet, so she sits and watches in class instead. After joining a Facebook group for the parasite Blastocystis, we have been seeing a naturopath in Australia via Zoom who had the parasite themselves. We are currently waiting on a SIBO breath test results as the naturopath thinks our daughter also has SIBO. We spend all of our time trying to research all of our daughter’s symptoms, while watching her physically deteriorate. It has totally consumed our family.

Where We Are Now: Was It Thiamine All Along?

Our daughter is in a better mental/emotional space, but doesn’t physically recognise her body at all. Even our daughter’s orthodontist asked why she was so swollen in her face, especially the left side – but the doctors still don’t think there is anything wrong. Our daughter’s physiotherapist is too scared to touch her, as she is so swollen. We spend every day crying at some point. While researching SIBO symptoms, we came across a comment about Thiamine deficiency, so started to research and bought the book “Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition”. Reading about the swelling of the face, and that it is fluid retention in the body was a revelation. But because of what happened with the Oil of Oregano, we are too scared to try doing something on our own and potentially making it worse, and the more we research, more of the other co-factors, we keep finding and things to be careful of. We have been to our GP doctor asking them to investigate if it could be beriberi, so they have started doing blood tests, but then we found in the appointment notes that the doctor still thinks our daughter looks well, so we are disappointed that it looks like they are not taking this potential diagnosis seriously.

Currently we’re waiting on Allithiamine and Lipothiamine to arrive from Australia, as we can’t purchase it here in New Zealand, but with Covid-19 there are huge delays in postage. We have started our daughter on 150mg of Benfotiamine (even that was extremely difficult to find in New Zealand) but at this stage we are hesitant to just ramp up the dosage to see instant results. We took our daughter back to the chiropractor who now advises that her kidneys/bladder aren’t working properly, and also that her vagus nerve isn’t working either. Just this week, we have taken her to an acupuncturist to try and help with the fluid retention, and they’re concerned about her heart and liver and just how swollen she is. We have added in legumes to her diet to help with bile function/detoxification and her stools are now increasing and no longer floating. We are now wondering if maybe she was hypoglycaemic as well.

Reading the comments on the Thiamine Deficiency Facebook group, we should also be looking at potassium supplementation, but conversely you shouldn’t supplement with potassium if there is something wrong with your kidneys. With the doctors not believing us, alternative practitioners wanting to potentially only push their own agenda/supplements or not fully understanding the full consequences of their remedies, or not being able to find out what the root cause of the problem is, and the conflicting information all over the internet, we are completely lost/scared/petrified/confused and feel a huge pressure to fix our daughter and it feels like time is rapidly running out. The stress on us as parents is completely overwhelming, and financially we feel like we are throwing money at this ever-increasing problem and the money is fast running out. We feel that every day is getting worse than the day before, and our hope has faded to a tiny pinprick of light. Gathering all of the information together for the doctors/alternative practitioners/supplements/nutritionist plans/tests looks absolutely ludicrous, but when you’re in the thick of it you’re completely desperate to find anything that could potentially fix your child. Then when it doesn’t work, or it makes the symptoms worse, the guilt is huge.

We’re hoping that by publishing her story on Hormones Matter, others might look at our daughter’s case history, and confirm what is wrong, explain it to us so that it makes sense, and help us fix her in a safe way.

Current Diet and Supplements

Below is a snapshot of our daughter’s typical diet and supplement regime. Please note, the Benfotiamine was begun only recently.

Breakfast	Morning Tea	Lunch	Afternoon Tea	Dinner	Water/Teas and Remedies before bed
Douglas Labs Ultrazyme x 1	1 large gold kiwifruit	Douglas Labs Ultrazyme x 1	50gm Coconut Yoghurt	105gm Roast Beef	3 x Magnesium Citrate (Pure Encapsulations)
2 Egg Muffins – Bacon/Veg	2 teaspoon sunflower seeds	90gm tin pink salmon	with probiotics	0.5 cup roast pumpkin
2 Tablespoons Pumpkin Seeds	1 cup Almond Milk	1 cup green Kale/Pak Choi (homegrown)	10 almonds	0.5 cup broccoli
1 Tablespoon Apple Cider Vinegar	2 x Tran-Q	1 cup tomatoes	1 Apple	0.5 cup peas
2 Brazil Nuts		0.5 cup cucumber	2 x Tran-Q
1 scoop Orthoplex Gut Rx		0.5 cup grated carrot
1 X HPA Essentials Tablet		0.25 cup brown rice
** 1 x Doctors Best Benfotiamine 150		1 Tablespoon mashed Avocado
		1 teaspoon flaxseed oil
		1 tablespoon lemon juice
		1 X HPA Essentials
		1 scoop Orthoplex Gut Rx

** Benfotiamine was just recently added as of July 25, 2020.

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 by Dimitris Doukas from Pixabay.

This story was published originally on August 10, 2020.

Dysautonomia and Chronic Illness Post Brain Surgery

by Silvi Si

Published on April 19, 2023

10.5K views

I wanted to share my experience going through thiamine paradox and my journey to heal. I am 27 year old girl from Italy and have been suffering from various health problems since I was 14 including a brain tumor that necessitated surgery, followed by Epstein Barr Virus, Hashimoto’s thyroiditis, multiple parasitic infections, antibiotic reactions, extreme and chronic fatigue, fibromyalgia, dysautonomia, SIBO, and gastroparesis. I have begun thiamine therapy six months ago and while some of my symptoms have improved, others have remained or worsened. I am not sure what to do next and am writing this in the hope that someone will have some answers.

Dysautonomia and Illnesses Post Brain Surgery

In 2008, I underwent neurosurgery to remove a benign tumor in my temporal lobe. It was very large, near the hypothalamus and on the optic tract. After that surgery, I was in sympathetic mode for about a year and a half. It was intense. I was always alarmed and anxious with school performance anxiety. I was exhausted, but at the same time, I had the energy to do more than I could afford. Furthermore, I gained 20kg in 6 months despite eating well. This was traumatic for me. Even though I did everything I could to not gain weight, the weight still went up. I felt powerless and I was pissed off. I did a thousand diets and I still fight to lose weight. I have been on a diet ever since.

In 2010, I got an Epstein-Barr viral (EBV) infection. Next, I developed Hashimoto thyroiditis and lost a lot of hair. My beautiful hair that was soft and silky, became sparse, few and very thin. I also had pain in my neck for two years. After that EBV infection, I started to feel tired all the time, but still managed to go out and go to school

In 2011, after a month and a half of pain in the lower back and abdomen, I had a fecal analysis done and found that I had parasitic infection called blastocystis hominis. The doctor gave me metronidazole (Flagyl) in a very high dosage. When the pain in my right leg appeared, the suspicion that it was appendicitis became certain and they operated on me. The surgeon told me my appendix was was 12 centimeters, inflamed and had two abscesses.

In 2012, I had some months of extreme fatigue and abdominal pain. The seizures I had before my brain surgery returned, as did my inability to study due to lack of concentration. I then discovered that I had another parasitic infection, this time giardia. I was treated with Flagyl again. After Flagyl, I was infection-free for 6-7 months.

In March of 2013, I developed an acute onset case of what the doctor’s called a severe case of chronic fatigue, fibromyalgia, and dysautonomia. I had brain fog and was unable to focus. I had tingling in my neck arms. I started gaining again. I have episodes of dysautonomia with vagal crises that include palpitations and tachycardia so strong that even moving around in bed accelerates my heartbeat. Add to all of this a plethora of other minor symptoms. In particular, I have become unbearably cold. Previously, I was the the person who was always in half sleeves. I have also mood swings that sometimes make me feel crazy (such as unexplained nervousness attacks). I felt I had no energy in my muscles and that I could not do anything. Even though and above all I was a girl full of energy and always very cheerful.

Failed Attempts at Healing

Since then, I have done many different types of therapies (homeopathy, mineral and vitamin integrations, neural therapy, micotherapy, osteopathy) with small and short improvements. In 2017, I did probably one of the stupidest things I’ve ever done before, I fasted for 16 days. I was convinced of the idea that it could cure my thyroiditis. After that, I started not digesting well, so much so that if I ate a little more than I should, I was throwing up, and the cold in my body became even more unbearable.
A few years later in 2019, after years of GI problems, that included gastroparesis/delayed stomach emptying, bloating and pain, I was diagnosed with SIBO (sulfur). I was given Rifaximin. I also tried a herbal therapy for SIBO, and for candida, which I also had, and NAC. Nothing worked.

Where I Am Now

I still have most of these conditions. Some symptoms have passed but new ones have emerged. Overall, I am better than in 2013 when CFS started and I just couldn’t get out of bed.

A few months ago, I discovered Dr. Lonsdale’s work on thiamine deficiency and I bought his and Dr. Marrs’ book: Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition. I believe many of health issues involve thiamine deficiency.

I began with 15mg thiamine HCL injections daily for about two weeks and then increased it to 30mg per day. I also take B complex, magnesium, seleniomethionine, molybdenum, vitamin C, vitamin D, omega 3, zinc and copper because they were low in my blood exam. The first month I also took SAMe with many benefits, but now it seems to make things worse.

I eat only organic food. I don’t eat sugar, processed food, junk food, gluten, milk or dairy products, or alcohol. I have only one or two espressos per day and I eat a lot of apples because they are low in oxalates.

Thiamine Reaction or Something Else?

When I woke up on day 2 of thiamine, I saw that my eyes were swollen like balloons, there were some itchy blisters on my eyelids and around the eyes. In the morning other blisters appeared on my elbow and behind my neck under my hair. The morning of day 4, I woke up with a skin rash near the hip.

At the beginning, I had thought these reactions were relative to the thiamine, but I later realized that the hives and swelling were linked to the inositol hexanicotinate, a niacin substitute in the B complex. I have no problems with niacin though, just the inositol hexanicotinate form. From that episode forward, I began taking all the B vitamins separately.

After 2 months of thiamine HCL, I added allithiamine. I began with 1 pill, 50mgs, and I added another 50 mg pill every week, until I reached 300mg. Initially, all the symptoms I had at the beginning of the disease reappeared: severe myalgic attacks in the leg or abdomen, abdominal pain, other pains and unbearable cold in the whole body, especially in the hands. The chills are so severe that I am often shaking. It is so severe that it paralyzes me. This shaking disappeared in a few weeks, but sensation of being cold still persists. And I am still very tired.

After Six Months of Thiamine Therapy

There are some improvements from since I started with allithiamine. For example, my fatigue has improved. Although I always have chronic fatigue, there are times when I feel better for a few hours. Before starting the thiamine, I had frequent attacks of voracious hunger during which I never felt full. I’ve always tried to ignore them, because if I’m not on a strict diet, I am gaining weight. Since taking thiamine, this happens much more rarely and my sense of fullness has improved. Finally, I have fewer nervous attacks. My digestive system seems to be little better. What I am currently taking:

Allithiamine – 300mg
Riboflavin – 320mg
Niacin – 100mg
Pantothenic acid – 200mg
Pyridoxine – 20mg
Myo inositol – 2gr
Biotin – 5000mcg,
B12 – until a few months ago. It was low and now it is high.
Zinc – 30mg
Copper – 2mg
Omega 3
Inulin – 2gr
Keppra – 250mg x2 a day
Molybdenum – 200mcg
Seleniomethionine – 200mcg
NAC – 1200mg
Magnesium malate – 1800mg
Magnesium citrate – 1500mg
Vit C – 2gr x5 a day
Lysin 1gr
Vit D – 10000 UI
M2MK7 – 100mcg
DHEA – 50mg
Maca powder – 5gr
CoQ10 – 100mg
LDN therapy – since March 2020

I still have the symptoms of the paradox effect. It has been almost 6 months since I started thiamine, how is it possible? The worst symptoms now are fatigue, frozen hands, shivering. Is the thiamine not working or is something else going on? Could it be that the thiamine revealed some other deficiency that is causing me this reaction? I’d like to know whether I should continue to take it.

A warm hug from Italy.

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 May 17, 2021.

Lessons Learned About Recovering From Thiamine Deficiency

by AMZ

Published on February 1, 2023

40.9K views

lessons learned with thiamine deficiency

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.

Yes, I would like to support Hormones Matter.

Image created using Canva AI.

This article was published originally on December 9, 2021.

Solving the Medically Unsolvable: Thiamine, Oxalates, and Other Complicated Health Issues

by Elaine Sullivan

Published on January 12, 2023

55K views

solving the medically unsolvable thiamine

Welcome to a very complex tale of connecting dots between life long symptoms and a current state of severe food intolerances and vitamin deficiencies. Outside of the food safety zone, my symptoms become so severe that I cannot function. Within, there are some symptoms but very tight regimes of high maintenance food prep, supplements and lifestyle strategies keep life manageable, gratefully, without medications.

I learned how to keep these symptoms under control through health groups on Facebook, not a place one would expect to find health answers, but when doctors fail, patients like me are left with little recourse. We either remain ill or we figure it out ourselves. It seems there are many of us in the same situation, saddled with complex conditions for which doctors have little input. Modern medicine seems to have little to offer in disordered energy metabolism (affecting every system), ailing mitochondria, and vitamin deficiencies. My doctor trained in GI disorders missed the fact that my gut was causing migraines for the same reason my neurologist did, compartmentalization. Neither considered mitochondrial dysfunction. Neither considered thiamine or other nutrient deficiencies. I had to figure that out myself.

Early Childhood Memories: Longstanding Symptoms

As a little girl there was no need for me to speak because I got everything I needed through my sister. This resulted in a spell at Easter Seals, an institution for those on the autism spectrum. When I hear of delayed speech in children today I think, “Oh, the Feingold website and diet”. Delayed speech, hyperactivity, red ears or flushing—a low salicylate diet can help. I wish my mom had known about the Feingold organization, but they didn’t yet exist.

During gym class, my teacher running cold water over my wrists in the bathroom to try to turn the color of my face back to a lesser shade of crimson. An EKG revealed nothing and I was told to drink more fluids.

There was also walking and talking during sleep and then the dreaded sleep paralysis. I had a fabled allergy to a chocolate Easter basket. Then dyslexia showed up when I first tried to draw my letters.

In school, I struggled to hide my loud stomach gurgles and painful hiccups. Semi regular digestion disasters ruined some special occasions, but all was still under the radar. Painful calf muscle cramps were in the middle of the night, so no one knew and they wouldn’t have been recognized as a mineral deficiency anyway. As an adult my calf muscles were extremely tender to the touch, which, I now know, points to thiamine deficiency.

The most obvious harbinger of future troubles was motion sickness. Struggling to not barf in the back seat of our station wagon. Should I look at my coloring book, at the road, at my legs? Those symptoms haven’t changed in 40 years, I noted on a recent windy drive up to Kings Canyon. That same reaction, tunnel vision, dizziness, and nausea, has been triggered for me on perfectly level ground. It comes from chemicals called amines found in common foods such like bananas.

Persistent and Increasingly Complex Symptoms in Adulthood

Alcohol Intolerance and Arrythmia

I often witnessed my intolerance to alcohol, but didn’t think of it as a symptom. That facial flushing happened multiple times every day and it was impossible to pinpoint all the triggers until I learned about histamines. It didn’t actually hurt, but left me exhausted, because along with it came “The Throb”. This is a feeling of my heartbeat all over the upper half of my body, but different and with a broader reach than my usual variety of heart arrhythmias. I remember a physical therapist refused to work on me until I saw a doctor because my carotid artery was pulsing so visibly that it scared her. The ultrasound came back normal. I still have the throb intermittently everyday and now I understand it, like disordered sleep, to be a symptom of dysautonomia, another sign of thiamine deficiency.

Post Food Coma

I used to fall asleep while driving, always post-snack. I fell asleep while talking to my fiancé’s parents—after a meal of pizza. If I were to eat dairy right now, I would be asleep within 30-40 minutes. Unlike a nap, it feels like I have been drugged. Richard Deth is the doctor whose studies showed why casein and grain-free diets work for the autistic population, and thus, many in the chemically sensitive population as well. It has something to do with peptides crossing the gut barrier (leaky gut) and hitting opioid receptors. I trusted that his research spoke to my symptoms when a Google of opioids showed somnolence and constipation are the first two symptoms. There are other competing theories, though. That thiamine deficiency has created a state of hypersolomnence well described in this article due to pure lack of ATP. It has also been suggested that I’m so low in B2 and B12 that I can’t make melatonin, so one hit of dairy is a shock and the newly created melatonin suddenly makes me sleep. I’m not sure how that could tie into the constipation, though. Yet another connection to my known low folate status is that cow’s milk down regulates folate receptor autoantibodies (FRAs), so going dairy free is very important. It may be that all of these items contribute. Whatever, the cause however, falling into a dead sleep upon eating is not healthy and something I had to figure out.

From High Grain Pescetarian to Low Carbs and High Fat

In an effort to overcome some of my symptoms, in 2010 I went from a high grain, mostly vegetarian diet, to a more primal or Paleo diet. With this diet change, I thought I was finally on the right path to health because so many of my symptoms suddenly disappeared. The one I was happiest to leave behind was a painful condition called Interstitial Cystitis (IC). My skin was perfectly clear for the first time in adulthood. I was less anxious, with no panic attacks or depression like before. I felt full all the time and lost weight easily. I attribute those positive changes to removing grains (for my SLC19A1 glitch), processed foods (my latent salicylate sensitivity) and some improvement in B12 levels (depression) due to the addition of red meat.

Unfortunately, some darker changes were happening that took me years to connect to this diet. Terrible neck and shoulder pain and new insomnia with an “electric vibration” lead me to a diagnosis of spinal stenosis. PMS symptoms and migraines were suddenly more frequent and worse. It took me years to figure this out, but what I finally determined was that I was making and storing a lot of oxalates, the mineralized crystals best known for kidney stones.

This all makes sense to me now in terms of oxalates. Susan Owens, from the Trying Low Oxalates (TLO) group often talks about how IC can be the oxalates “speaking to us” and although painful, it is better that they are moving out rather than moving into cells or into bones for storage. I believe that my body switched from “excrete mode” for oxalates and into “storage mode” due to something about my diet change. It could be that the higher fat content created oxidative stress which started or increased the endogenous production of oxalates that I tested positively for years later. I never would have guessed my bone spur was from nutrition or disordered metabolism. My doctor and I had blamed some unremembered injury from yoga practice. I have a PubMed case study of spinal stenosis with photographs inside the bone spur showing millions of oxalate crystals. When I dump oxalates, and when I am not doing well in general, I have right side nerve pain (the side of the stenosis) that could additionally be demyelination from low B12. I’ve found topical magnesium is magical for this, thanks to the TLO group.

The increase in PMS symptoms was also oxalate related. I had always come down with IC right before my period and it makes sense that the body would take advantage of the cyclic aspect of menstruation to ditch oxalates and many other TLO group members confirmed this experience. I recognized all my PMS symptoms in a TLO file about the variety of ways our bodies “dump” oxalates.

2012 1^st Health Crisis: SIBO, Migraines, and More

After 6 years of eating “Primal”, I moved out of state and had a disabling increase in migraines, insomnia, flushing, dizziness, light sensitivity, fatigue, and heart palpitations. Doctors and normal test results were not helpful. I ended up on low dose Amitriptyline (a strong antihistamine), which put my sleep back in order and allowed me to work again. The worst of the problem was solved until I learned that anticholinergic has the word choline in it, so this drug is terrible for the mitochondria. This 3 year long mistake is so typical of what can happen when laypeople have to take charge of their own health.

Another diet-induced problem: After years of eating like this, I was only able to go to the bathroom once every 5 days, with tears in my eyes. I saw myself in a description of SIBO—Small Intestinal Bowel Overgrowth. A GI doctor agreed and I tested positive. I found thousands of people on SIBO Facebook groups not getting better with antibiotics, so I waived off his recommendations. Reintroduction of potatoes and supplementing with resistant starch corrected the problem—thanks, Internet. If only I had read Paul Jaminet’s warning about low carb diets years earlier. Later, I noted that my GI doctor’s recommendation of Miralax for constipation would have made me so much worse, as it contains polyethylene glycol, a derivative of ethylene glycol, the main ingredient in antifreeze, and a quick way to fill your body with oxalates.

At this time though, I had no idea what histamine, oxalates or salicylates were. I had tried a food journal for migraines, but my neurologist told me to only watch for cheese and wine. Well, there are a whole lot more foods than that in a histamine foods list, not to mention other chemical categories. Foiling my journal attempts was also the bucket theory. Once emptied, by a migraine for example, I was able to consume high histamine foods without any problem. It is the build up over time that leads to the bucket “spill over”. Hence, my pattern of fine health and digestion at wedding rehearsals, but then sick at the actual wedding the next day—my bucket had filled.

I was eating very “clean” and I thought healthfully. I enjoyed avocado, cactus paddles, eggs, onions, bell peppers spinach, sausage etc. for breakfast. Assorted root vegetables roasted in duck fat. 2 iced coffees per day. Snacks of Greek yogurt with fresh berries and local dates. Sweet potato roasted in orange peels, braised meats, dark chocolate and nuts. Ninety percent of my food was homemade. I always had frozen homemade soups and chili on hand plus I dabbled in fancier recipes from magazines. Although I had cut out grains and processed foods, the variety I was eating and my cooking skills were growing every year. In the next three months, my out of control reactions would cause me to take a quick but deep slide down the elimination diet rabbit hole, and land with only 12-15 safe foods.

The 2015 Crash: Salicylate Sensitivity, Tinnitus and Migraine

With the notion that my migraines, flushing and stomach gurgles were tied to the SIBO, and that natural antimicrobials were safer than antibiotics, I embarked on a high dose oil of oregano (a high salicylate) treatment to kill the SIBO with a Registered Dietitian. I can’t blame her, as neither of us knew that my previous occasional ear ringing and swollen eyelids were signs of latent salicylate sensitivity, nor that it was common in those with early speech delay. I had a terrible time on the oil of oregano, but stuck with it through the abnormally long protocol, because I was told to expect symptoms of “die off”. That period was like one long migraine with breaks only for prodromes, in which tiny flashing lights in my peripheral vision combined with distinct feelings of disassociation. I was poisoning myself, taking in chemicals that my body could not detoxify quickly enough. During the last week of treatment, I connected one stomach reaction to a high histamine meal and read everything I could about Histamine Intolerance. Immediately I stopped eating all high histamine foods and began to take supplements known to help—vitamin C and quercetin. I stopped the Amitriptyline once I read that it suppressed DAO production, an enzyme that degrades histamines. I continued to eat dates and raw honey until I tied the honey to another massive migraine (salicylates). A dear stranger on the Histamine Group pointed out to me that tinnitus is usually a salicylate symptom and not a histamine symptom.

I joined the salicylate group and started lowering salicylates in my diet. It seemed impossible to tell what I was reacting to. I stopped all supplements, I quit all caffeine and started eating from the “Fail Safe” diet lists. I changed all personal care products to salicylate-free. This started to calm my system down. The thing they don’t seem to know or mention at the Failsafe is that when you start dropping foods and you don’t know that you have an oxalate issue then you can accidentally trigger an oxalate dump, which can be very dangerous.

Now the high dose vitamin C was kicking in and creating more oxalate problems, as it can convert to oxalates in the body within two weeks. My body was out of control. Ears were ringing off the hook. The “throb” and abnormal heart palpitations were magnified 10 fold. I was in a 2^nd full blown health crisis, unable to work. Sleep, migraines, palpitations, tinnitus became unbearable. The ear pressure felt like my ears were blocked. After a 6 year hiatus, my painful IC was back every evening.

The quercetin, a methyl donor, had been building up as well. The worst night I woke every 40 minutes or so throughout the night from night-terror-dreams with my heart pounding so strongly that it made me feel nauseous. I had one strange day where my throat tightened up, but a cold never developed. I dropped and broke three plates and two drinking glasses in 3 days. I experienced high anxiety and could not drive on a freeway. I had to go through this type of experience two more times before I learned that it was due to methyl donors. The last time it happened, I burst a blood vessel in my eye. A hard-won PSA: you can potentially stop a methylation crisis with Niacin.

On April 30th, I saw an ear/hearing/allergy specialist who said my hearing was still good, and to see my neurologist about the tinnitus. I did two things that turned the sinking ship around that day. I ate a meal of all high ox foods, which stopped my giant ox dump. The nightly interstitial cystitis symptoms disappeared. Second, I restarted the Amitriptyline and finally began to stabilize and sleep through the night.

Post Health Crisis

This is what I have learned so far:

If I eat or touch high salicylate plants, my ears get short bursts of ringing plus a different type of tinnitus at night—pulsatile, so that I cannot keep my head on the pillow. I also get swollen eyelids with dark circles underneath. It can quickly turn into styes and blepharitis. Before I learned how to control it with diet, I got peeling lips, watery, itching and red eyes, excessive thirst, and feelings of dissociation before migraines. Also, insomnia and inner ear drainage feelings.
If I eat high histamine foods I get migraines as well as stomach bloating and loud gurgles followed by hiccups, light sensitivity, heart palpitations, stuffy nose during and after eating, and dizziness upon bending over. From some chemical smells I get a spot on the back of my neck that will start itching like crazy. The same spot I scratched as a child. I found my chronic low blood pressure to be associated with migraines as well.
If I eat high oxalate foods I get a return of the interstitial cystitis and dramatic muscle cramps.
If I eat dairy I either fall asleep or suffer severe brain fog within 40 minutes, plus constipation the next day. If I eat it consistently, the interstitial cystitis returns, I think due to fat malabsorption.
If I eat white rice or raw fish, I get sciatica pain at night, due to the drop in thiamine. (Interesting that German doctors systematically prescribe thiamine for sciatica pain)
If I eat fruit or any simple sugars, I get bloating and stomach gurgles. This could be a result from the simple sugars “popping” thiamine out of cells.

“The Killer Strategy” and Another PSA

I returned to my GI doctor for help, thinking that SIBO was the root of all my food intolerances. Begrudgingly, I took his antibiotic, the standard for SIBO treatment. My last appointment with him was the day he recommended a second round of Rifaximin after the first had left my test numbers 4 times worse.

The risk with antibiotics is that each time a round is taken, good bacteria that help produce thiamine and other vitamins, get wiped out with the “bad”. What if in SIBO, the bacteria are moving from the large intestines into the small to help us? Maybe they are sent to help digest our foods because our vitamin levels are not sufficient enough? Susan Owens regularly cautions our group,

“Please remember that these microbes compete for turf and form alliances. Antimicrobials do not understand or honor those distinctions and right now we are at a place of profound ignorance.”

We do know for a fact that certain antibiotics will wipeout a specific bacteria that helps us degrade oxalates. From the TLO group, here is the list of antibiotics to avoid if you want to keep your Oxabolactor Formigese bacteria alive and degrading oxalates for you:

azithromycin, ciprofloxacin, clarithromycin, clindamycin, doxycycline, gentamicin, levofloxacin, metronidazole, tetracycline and nitrofurantoin.

Most of these are quite common. I’ve taken multiple rounds of at least four of them.

A Different Framework for Treating Complex Illness

After the failed Rifaximin treatment, I thought that if I could stop the endogenous production of oxalates, (for which I had tested positively), then I could get salicylates back. Since both ride the transsulfuration pathway, it seemed logical that oxalates, a toxin, could bump salicylates off that pathway and leave my body with a salicylate overload. Oxalates also trigger the inflammasome, which could explain my histamine symptoms. So enthusiastically, I embarked on a B-vitamin supplement protocol prescribed by an experienced practitioner based on my OAT test results. At the end of that long, bumpy and educational journey, I was still only stable enough to work, and having to walk the tightrope of restrictions plus ongoing symptoms that never resolved.

Still Searching…

Dr. Derrick Lonsdale’s work on Thiamine Deficiency (TD) had always been a part of the conversations at TLO because deficiencies in B6 and/or thiamine will cause the body to produce oxalates. That is definitely one piece of my puzzle. My many out of range plasma amino acid markers attest to this, plus OAT test results. Another piece, the genetics angle, made sense to pursue since I had experienced many of my symptoms intermittently since childhood.

I met with genetics counselor John Cantanzaro. He told me to never eat grains because I was homozygous for SLC19A1. The meaning of this genetic glitch is that I am deficient in folate (vitamin B9) and thiamine (B1) due to a transporter defect. I have so very many symptoms attributable to thiamine deficiency that I am not deterred by lack of testing. As close readers of this publication know, there is no accurate way to test for thiamine in the US because the all labs have stopped offering the transketolase test. (As of this writing, it is available in Barcelona, but good luck finding someone to interpret, I am told.)

A potential second genetic puzzle piece has also been found. The brilliant scientist and researcher Susan Owens, owner of the TLO group, has pointed out that four other SNP’s in the SLC family could also create thiamine transport issues plus many other problems pertinent to my situation. SLC’s 22A1, 22A2, and 22A3 move around neurotransmitters like serotonin and dopamine, choline and acetylcholine. Perhaps that is why I have only been asleep between 3 and 6 am a handful of times in the last few years. They also are important in immune function, regulating T cells and B cells. Perhaps that is why I have fluctuating but distinct symptoms of Babesia (faux bruising, sweating, angiomas). These transporters are related to salt intake and regulation, possibly explaining my life long salt cravings, need to pee and drink water with abnormally frequency. What really got my attention was that these transporters also move salicylate and are related to how histamine and stomach acid are handled.

It seems there is currently no test for these transporters. There is also no other competing hypothesis for why anyone would have all three chemical issues—histamine, salicylate and oxalates. There is no currently practicing M.D. who can help with this, but there are plenty of us on the FB groups who have all three. It can be very disturbing for me to witness people constantly entering the groups, with signs that they have no idea what is in store for them. Some fare better than I did, finding stability after only eliminating that one category. For most of us though, it becomes a frenzied learning journey, trying to read fast enough to keep up with our changing symptoms and to not make things worse accidentally by doing the wrong thing. There are some who end up in the hospital with anaphylaxis. Others from dumping oxalates too fast–which is potentially fatal and the hospital staff would never able to recognize what was happening. I am still not sure what type of medical ID tag I need to warn my future caretakers in case of an emergency: “No vitamin C, no salicylic acids, no benzos, no Tylenol, no “biologicals” (vaccines), etc, etc.”.

How To Fix SLC19A1, the Broken Transporter?

Lately, I have started spacing my thiamine supplements further apart, thinking that if the transport is limited then I need to load the bus more frequently with smaller amounts. I also space my B6 apart from thiamine in case one inhibits the other. I recently trialed choline and finally found a crack in the relentless insomnia. Sadly, it led to some over-methylation symptoms. For thiamine support, I eat no simple sugars, including fruit, and no diuretics or processed foods. I even gave up lentil pasta for fear thiamine would get lost in the cooking water. Additionally, bicarbonate, rutin, no D-ribose are avoided. Do I need manganese? I don’t know how to overcome the transport problems and get the vitamins into my cells. I found a mitochondrial doctor, but he charges $800 for a 1 hour visit and does not accept insurance. A local naturopath is willing to give me IV, but that seems like too much at once for the transport theory. He said an injection into muscle would last longer than IV, but are there any examples of success with this theory? I am also currently pursuing the genetics angle with a Whole Exome test whose price has recently come down from outer space.

More Dietary Approaches

In 2016, I decided to try eating the opposite of what I had been eating, so in addition to my food restrictions, I went high carb, low fat vegan. Again, there were good and bad changes. My triglycerides fell from over 300, out of range high to out of range low (indicative of thiamine deficiency). They rebounded to within normal range when I reintroduced lean meat. The keratosis pilaris on my upper thighs disappeared. But I lost too much weight, which also corrected with a reintroduction of lean pork and eggs. I tried to reintroduce low oxalate grains in June and that resulted in a week and a half of drenching sweats every 20-40 minutes both day and night as well as losing my period.

Lately, I’ve been encouraged to take a hard look at B2, B12 and iron. Test markers show them all low in spite of high supplementation and my brief stint at veganism surely did not help. A ferritin of 20, within range on my Quest report, is actually very deficient and 70 is my new target level. To raise B2, I need selenium, iodine, molybdenum and iron. For all of this, I am to dramatically increase fish and liver in my diet, plus add more molybdenum, Brazil nuts (carefully, as high oxalate) and slowly titrate in methyl B12 topical oil, then retest plasma and OAT in two months.

The roots for this plan are found in two excellent websites. This one on B12 and another here on dementia. Here my known deficiencies in iron, B2, thiamine, B12 and folate, my sensitivity to methyl donors, my out of range low 3-mehtylhistadine (muscle wasting) and my high markers for succinic acid and citric acid (wasted energy) are all described as precursors to dementia.

Have you seen the movie “The Dallas Buyers Club”? Matthew McConaughey’s character seems entirely relatable to me in his need to operate so far outside of the traditional medical system to find help. Not one of my traditional doctors, requested the tests above. I had a doctor tell me my sleep issues were from never adjusting to the time difference from Chicago to LA. I had an eye doctor tell me that there were no dietary interventions for chronic blepharitis, although it is a symptom of both salicylate sensitivity and thiamine deficiency. Before I tested positive (3 times) my main doctor told me SIBO only happened to people who had stomach surgery. I’ll stop there.

This tale ends with deepest gratitude to my “team” for sharing the maps above and how my symptoms and markers could connect to it. These people have never met each other, nor me in person. Amazingly, most have been free of charge, but required an enormous amount of time, digging and learning to find.

Susan Owens and the moderators at TLO; Chandler Marrs, who connects so many of us to Dr. Lonsdale’s work through this brilliant publication and her work on FaceBook groups; the many strangers and friends on FB who have responded to my questions and shared their insights at crucial times along the way; Tim Steele; John Cantanzaro; Donna Johnson; Dawn Tasher; local naturopath Dr. Simon Barker, the Salicylate Sensitivity FB group, wonderful websites like the Healing Histamine and the many brilliant patient/researchers at Phoenix Rising. Thank you!

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 October 11, 2017.

SIBO

Deer Antlers, Manganese, and Osteoporosis

Thiamine and Calcium

Manganese and Thiamine

Final Thoughts

We Need Your Help

Related posts:

You might be interested in

Fatigue and Other Seemingly Innocuous Symptoms

A Slow Road to Dementia

The Gut Connection

Thiamine Deficiency: The Missed Diagnosis

[atkp_product id=’49246′ template=’bestseller’][/atkp_product]

We Need Your Help

Related posts:

You might be interested in

Early Markers of Ill Health

A Labyrinth of Health Issues

Genetic Kinetics

Downward Spiral

Discovering Thiamine

The Next Chapter

We Need Your Help

Related posts:

You might be interested in

GI Motility and Thiamine

Malnutrition Induced Malnutrition

TTFD and Gut Motility

We Need Your Help

Related posts:

You might be interested in

A Concussion, an Infection and the Slow Spiral of Declining Health

Declining Metabolic Function and Weight Gain

Hair Loss, Pale Skin, and Skyrocketing Weight

Low Metabolic Rate, Low Estradiol, Yeast and Bacterial Overgrowth, Constipation and Parasites

Failed Treatments and Inconclusive Diagnoses

Where We Are Now: Was It Thiamine All Along?

Current Diet and Supplements

We Need Your Help

Related posts:

You might be interested in

Dysautonomia and Illnesses Post Brain Surgery

Failed Attempts at Healing

Where I Am Now

Thiamine Reaction or Something Else?

After Six Months of Thiamine Therapy

We Need Your Help

Related posts:

You might be interested in

Lesson 1: Magnesium Formulation Is Important

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

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

More Energy and Exercise Tolerance with the Correct Supplements

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

Restoring Normal Heart Rate

Lessons Learned

We Need Your Help

Related posts:

You might be interested in

Early Childhood Memories: Longstanding Symptoms

Persistent and Increasingly Complex Symptoms in Adulthood

Alcohol Intolerance and Arrythmia

Post Food Coma

From High Grain Pescetarian to Low Carbs and High Fat

2012 1st Health Crisis: SIBO, Migraines, and More

The 2015 Crash: Salicylate Sensitivity, Tinnitus and Migraine

Post Health Crisis

“The Killer Strategy” and Another PSA

A Different Framework for Treating Complex Illness

Still Searching…

How To Fix SLC19A1, the Broken Transporter?

More Dietary Approaches

We Need Your Help

Related posts:

You might be interested in

2012 1^st Health Crisis: SIBO, Migraines, and More