thiamine insufficiency

Beyond Deficiency: Using Thiamine as a Metabolic Stimulant

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Throughout the past few years, I have been prescribing thiamine more and more often for individuals with a range of different health conditions. I have witnessed major symptomatic improvement in some people who displayed none of the key risk factors for thiamine deficiency, and many times had been following clean, whole-food dietary regimes which contained levels of thiamine beyond what is suggested by the RDA. I began asking myself:

Why does thiamine, in sustained high doses, work so well for such a wide variety of diseases? Is it merely addressing a deficiency or is there something else going on here?

I have since come to the conclusion that one does not need to be deficient in the nutritional sense to benefit from this type of therapy; that high-dose thiamine is not simply working by correcting nutritional deficiency. Rather, thiamine is functioning as a metabolic stimulant to restore oxidative energy metabolism in cells that have been inhibited by factors unrelated to nutritional status.

Overwhelming toxicity and chronic oxidative stress have the capacity to inactivate thiamine-dependent enzymes involved in the generation of cellular energy, producing biochemical changes which are similar to clinical thiamine deficiency. This could basically be referred to as “functional” thiamine deficiency. In a functional deficiency, dietary thiamine intake is somewhat irrelevant, because the concentrations obtained via the diet are simply not sufficient to overcome enzymatic inactivation.

Instead, high concentrations of thiamine are often necessary to overcome the “metabolic block” and restore the deranged metabolism back to normal. Dr. Derrick Lonsdale has discussed this concept on many occasions and laid out the theory in his various writings. In this article, I will explain the rationale behind high-dose thiamine therapy as a tool for bypassing these metabolic blocks and examine how this can be a useful therapy for chronic health conditions.

Understanding Enzymes

To appreciate thiamine’s potential utility in mega-doses, we should first look at the very basic function of enzymes. Enzymes are a type of protein that the body uses as a catalyst to facilitate or “speed up” the rate of biochemical reactions.

Enzymes are responsible for driving the reactions involved in practically every known function of the human body, including building things up, breaking things down, modifying or changing molecules, and converting one molecule into another. Vitamins and minerals act as necessary cofactors or “helpers” for specific enzymes to work as they should. In the hypothetical diagram below, the enzyme responsible for converting substrate “A” into product “B” can only fulfill the task once it has bound its cofactor/coenzyme.

Enzyme activity

The ability of an enzyme to bind with its respective cofactor is referred to as the coenzyme affinity (km). A simple way to conceptualized this is to think of the enzyme like a magnet. Enzymes with high affinity for their coenzyme/cofactor exert a strong magnetic pull and can bind very readily with their coenzyme.

With high coenzyme affinity and more binding, the activity of the enzyme speeds up and the rate of reaction (A->B) increases. In contrast, enzymes with low coenzyme affinity exert a much weaker “magnetic” pull, meaning that they are less able to bind with the cofactor/coenzyme. Less cofactor binding means that the rate of reaction decreases.

Genetic Enzyme Defects and Nutrients

A variety of inherited, genetic conditions feature the production of defective enzymes with poor cofactor affinity. For these unfortunate individuals, the concentrations of nutrients found in food are simply not sufficient to overcome the genetically determined lack of affinity.

nutrient cofactors enzymes

A successful strategy used for these conditions is the administration of pharmacologic/mega-doses of the nutrient cofactor. By saturating the cell, one can bypass the low affinity and restore enzyme function back to its normal state. Extremely high doses are often required to achieve this effect and this therapy must be maintained lifelong.

  • Thiamine-responsive maple syrup urine disease: A genetic defect in the branched chain ketoacid dehydrogenase enzyme results in remarkably low affinity for its coenzyme TPP. Continued high doses are necessary restore the function of this enzyme complex.
  • Thiamine responsive Leigh’s disease: Inherited mutation in the gene encoding Pyruvate Dehydrogenase, with a decreased affinity for its TPP cofactor. Treated with pharmacological doses of thiamine to stimulate defective enzyme activity.
  • B12-responsive Methylmalonic acidaemia: Genetic defect encoding the methylmalonyl-CoA mutase enzyme, causing low affinity for adenosylcobalamin cofactor and a pathological accumulation of methylmalonic acid. This condition can be treated with megadoses of B12.
  • Biotin-responsive holocarboxylase synthetase deficiency: Genetic mutation renders biotin-responsive carboxylase enzymes much less able to bind with biotin cofactor due to markedly decreased affinity. Supraphysiologic doses can restore normal enzyme function.
  • B6-responsive homocysteinuria: A rare defect in the cystathionine-B-synthase enzyme reduces affinity for its coenzyme pyridoxal-5-phosphate. This leads to the toxic buildup of homocysteine. Mega-doses of vitamin B6 can return enzyme activity back to normal.

It is worth noting that these genuine genetic defects are extremely rare and are not applicable to the large majority of people. Nevertheless, similar principles can also be applied when an enzyme has been inactivated by other factors.

Prolonged Oxidative Stress, Inflammation, and Enzyme Activity

The activity of different enzymes is tightly regulated depending on metabolic requirements, energy intake, and numerous other conditions within the cell. In simplified terms, if cells need to break something down, build something up, slow a process down, speed a process up, the activity of the enzymes involved in those pathways will reflect that. Enzyme activation/inhibition is a necessary part of normal cell physiology. However, the activity of specific enzymes can also be affected by other factors including toxins. There are certain enzymes involved in energy metabolism which are particularly susceptible to inactivation by free radicals and oxidative damage. Short-term, this is most likely beneficial, but under conditions of chronic oxidative stress, such as that found in chronic disease, enzyme inactivation can become pathological.

A key enzyme involved in mitochondrial energy metabolism called alpha ketoglutarate dehydrogenase (KGDH). Several nutrients serve as cofactors for this enzyme complex, with thiamine taking center stage. KGDH is a rate-limiting step in in the TCA cycle, meaning that when this enzyme slows down, every other downstream step also slows down. Whilst a deficiency of any of the necessary cofactors will reduce the activity of this enzyme, it is also exquisitely sensitive to oxidative stress. KGDH appears to be more sensitive to disturbed homeostatic factors than other enzymes, playing the role of a metabolic redox sensor, capable of switching oxidative phosphorylation “on” or “off” depending on the cellular redox state and requirement for energy. Reactive oxygen species will selectively inactivate the KGDH complex and slow down oxidative energy metabolism. This inhibition is functionally beneficial for cells in the short-term as an attempt to avoid energy overload and oxidation. Not only is KGDH a target of oxidative inactivation, but it is also a significant generator of oxidative free radicals. Here, it plays a regulatory role which clearly serves essential functions in maintaining cell homeostasis.

Under long-term conditions of oxidative stress, chronic KGDH inhibition is thought to be a driving factor underlying many neurodegenerative diseases. In chronic fatigue syndrome, recent metabolomic analysis found that one of the few metabolites (out of 800+) elevated with statistical significance was alpha-ketoglutarate, which is perhaps also consistent with chronic KGDH inhibition. Several toxic and inflammatory factors have also been shown to inhibit KGDH. Immune cells in the brain called microglial are involved in neuroinflammation and can be activated by a variety of stressors including toxins, trauma, and infectious insult (think Lyme, or lipopolysaccharide coming from a leaky blood brain barrier). Microglia produce myeloperoxidase and downstream products including hypochlorous acid and mono‐N‐chloramine – all of which are powerful inhibitors of KGDH. Heavy metals including aluminum and arsenic, along with fungal mycotoxins inhibit thiamine-dependent enzymes including KGDH and pyruvate dehydrogenase (PDHC).

Activated microglia caused by inflammation in the brain generate excess amounts of nitric oxide and its free radical peroxynitrite, both of which further inactivate KGDH. Polyunsaturated fats lining neuronal membranes are prime targets for oxidative damage in the brain, yielding a toxic byproduct called hydroxynonenal (HNE). Once more, HNE was shown to inactivate both KGDH and PDHC, whereas other mitochondrial enzymes were unaffected.

Endogenous neurotoxins such as and isoquinolone derivatives (breakdown products of catecholamine neurotransmitters) have been associated with Parkinson’s disease, and also inactivate KGDH. These metabolites include oxidized derivatives of dopamine and norepinephrine. Other KDHC and PDHC inhibitors include the breakdown products of halogenated toxic chemicals such as Tetrafluoroethylene (TFEC).

KDGH enzyme modulation
Oxidative stress and chronic inflammation are the hallmarks of chronic disease and both factors appear to inhibit/inactivate KGDH. As the rate-limiting step in oxidative phosphorylation, the chronic inhibition of this enzyme can spell devastating consequences for cellular energy turnover. A person could be obtaining a great amount of thiamine through their diet, but the underlying inhibition of these enzymes will produce the exact same outcomes as a dietary deficiency. In other words, these changes will induce a functional deficiency.

Mega-Dose Thiamine to the Rescue

When enzyme inhibition becomes pathological, we can apply similar principles as outlined above with nutrient-responsive genetic conditions. We can use high doses to bypass or overcome the metabolic blocks caused by enzyme inhibition. This concept was wonderfully illustrated in a study titled: Thiamine preserves mitochondrial function in a rat model of traumatic brain injury, preventing inactivation of the 2-oxoglutarate dehydrogenase complex.

For this study, researchers investigated the effects of traumatic brain energy (TBI) on energy metabolism, using several groups of rats who were not deficient in thiamine. They showed that the oxidative stress associated with TBI inactivated the KGDH enzyme, causing great reductions in energy synthesis, which was coupled with brain damage. Administering massive doses of thiamine to the rats before TBI was able to completely protect the KGDH enzyme. The thiamine-treated group maintained normal activity of KGDH, mitochondrial respiration, and ATP despite being exposed to the injury. Furthermore, the restoration/protection of KGDH might have also conferred some degree of cytoprotection by combating inflammation, which was demonstrated by reduced inflammatory gene expression at three days post-TBI.

KDGH and thiamine

What this study demonstrated was that very high doses of the cofactor could provide protection against an insult which was not related to deficiency. In fact, similar results have been shown in several other studies:

  • Thiamine administration protected neurons against inflammation-induced impairments in neurogenesis caused by exposure to radiation, both in vitro and in vivo. Thiamine treatment also significantly increased lifespan. Attenuation of these inflammatory effects are thought to be due to increased stimulation of KGDH activity.
  • A more recent study also looked at traumatic brain injury (TBI) with a focus on glutamate neuroexcitoxicity. They showed that excess nitric oxide and peroxynitrite found in neuroinflammation led to the inactivation of KGDH. KGDH inhibition reduced glutamate uptake into the Kreb’s cycle, producing glutamate excitotoxicity and neuronal cell death. Once again, extra levels of thiamine reversed this issue by stimulating KGDH, increasing glutamate clearance and protecting the cells against injury. The authors concluded:

Thus, the impairment of OGDHC [KGDH] plays a key role in the glutamate mediated neurotoxicity in neurons during TBI; pharmacological activation of OGDHC may thus be of neuroprotective potential. 

Interesting choice of words, huh? They are basically telling us that the pharmacological use of thiamine might be helpful in conditions where KGDH is inactivated, and enzymatic stimulation can be protective against glutamate neuroexcitoxicity. For the reader’s reference, here are a quick list of conditions which are thought to involve neuroexcitoxicity as part of the disease-process:

Spinal cord injury leads to significant neuroinflammation similar to that found in TBI, with excess nitric oxide production and deficits in brain glutathione levels (an intracellular antioxidant). In one study: thiamine in high doses ameliorated excess nitric oxide levels and maintained brain levels of glutathione. The authors hypothesized that this was related to changes in precursor amino acid availability. However, this is likely also related to the stimulation of transketolase (TKT) activity (a thiamine-dependent enzyme involved in replenishing reduced glutathione). Under conditions of oxidative burden and increased requirement for glutathione recycling, there is a need for increased TKT activity and thiamine.

High doses of thiamine will stimulate the transketolase enzyme to maintain glutathione levels. This was shown in a different study using metabolomic analysis in cardiac ischemia, which found increased levels of ribulose-5-phosphate suggestive of increase TKT activity. Indeed, both thiamine and benfotiamine were found to increase the genetic expression and activity of the transketolase enzyme to counteractive oxidative damage and cell injury in diabetic vascular endothelial dysfunction. High doses of thiamine can also restore activity of the pyruvate dehydrogenase enzyme complex in the face of inactivation. Cardiac arrest was shown to markedly depress PDHC activity through inactivation.

In rats, high-dose thiamine post-cardiac arrest restored pyruvate dehydrogenase activity in brain, mitochondrial respiration, improved neurological function, reduced brain injury, and improved survival at 10 days. The quantity of the enzyme did not change, showing that thiamine worked by stimulating PDHC activity at high doses, thereby preventing injury-induced inactivation of this enzyme complex.

Pre-treatment with thiamine pyrophosphate protected against cardiac ischemia by maintaining mitochondrial function, ATP concentrations, and inhibiting mitochondrial fission.

Furthermore, copper toxicity was shown to inactivate the PDHC , produce mitochondrial dysfunction and neurological damage in rats. High doses of thiamine protected against the inhibition of Pyruvate dehydrogenase, markedly extended life span and protected against neuronal death.

The Use of Mega-Dose Thiamine in Clinical Practice

The late Italian neurologist A. Constantini published several case studies on the use of mega doses of thiamine for different conditions and saw impressive results. In one of the case reports on fibromyalgia, two patients saw an abrupt and immediate improvement only when they reached 1,800mg per day. At lower doses, improvements were negligible. High dose thiamine produced appreciable improvements in fatigue in 15 MS patients. Likewise, high doses were shown to produce remarkable and rapid improvement in the neurological condition essential tremor. Severe chronic fatigue in IBD patients with normal thiamine lab tests was reversed in most patients with megadoses.

Thiamine injections completely reversed gait abnormalities and motor failure in two patients with Freidrick’s Ataxia. Importantly, Constantini and colleagues concluded:

From this clinical observation, it is reasonable to infer that a thiamine deficiency due to enzymatic abnormalities could cause a selective neuronal damage in the centers that are typically affected by this disease.

Furthermore, in a case report of two patients, dystonia was reverse with thiamine administration. I have also seen this occur in several children with autism and/or neurodevelopmental abnormalities. Another case report detailed high-dose thiamine injection in patients with Parkinson’s disease, all of which had “normal” plasma thiamine levels, meaning that they were not classically diagnosed as having deficiency. The patients experienced between 30 and 77% improvement in motor coordination. We have seen from the research above that the neurotoxic metabolites which are thought to drive Parkinson’s also have the strong capacity to inhibit thiamine-dependent enzymes. It is therefore no wonder why thiamine can have such as tremendous impact on this condition.

Constantini and colleagues completed a larger study with 50 patients two years later, and found that 100mg thiamine injection twice per week produced massive improvement in both motor and non-motor symptoms, with some patients experiencing complete clinical remission.

Are these results simply addressing a deficiency or is something else going on here?

The daily recommended dietary intake of thiamine is merely 1 – 1.5 mg per day. Surely, if the benefits were simply due to nutritional repletion then we would see benefits at similar levels, or even 10x that amount? Except we do not. Rather, most people are required to consume 100 to 1000 times the daily recommended intake to see restoration of metabolism and symptomatic improvement. This is what I see in clinical practice on a frequent basis, and this is also what has been demonstrated in the case literature.

Beyond Treating A Deficit

The sheer amount of the nutrient necessary for clinical improvement is not consistent with simply addressing a deficit. Nutritional repletion is by no means an adequate explanation for this magnitude of effect. It IS consistent with stimulating enzyme activity to overcome inactivation, however.
Constantini hit the nail on the head with one quote from another paper:

We may suppose that symptoms decrease when the energetic metabolism and other thiamine-dependent processes return to physiologic levels. Our aim was not to correct a systemic deficit of thiamine, but rather to increase the activity of enzymes involved in cell production energy in selective brain regions.

Indeed, Constantini understood that thiamine could be used as metabolic enhancement to stimulate the enzymes involved in energy metabolism which had otherwise been inhibited by other factors. This is where we are dealing with a “functional deficiency” which can only be addressed by supraphysiologic concentrations to saturate the cell for improved bioenergetics. As I said mentioned previously, Dr. Derrick Lonsdale has highlighted on many occasions how thiamine’s effective is due to its pharmacological action, rather than nutritional repletion.

Rather than remaining hyper-focused on correcting a deficit, we should be using this molecule to improve bioenergetics regardless of nutrient status. This means that someone does not necessarily need to be nutritionally deficient to benefit from thiamine supplementation at high doses.

The Non-Enzyme Functions of Thiamine

It is worth noting here that there are a few other variables which I have not discussed thus far. Outside of the context of genuine inherited genetic defects, there are numerous polymorphisms in genes related to thiamine transport and metabolism. These polymorphisms can influence enzyme activity, albeit to a lesser extent, and can predispose one to developing a deficiency. Nonetheless, this does not alter the fundamental principles laid out in this article. It is also important to understand that the clinical improvements demonstrated are not just due to thiamine’s role as a cofactor to drive biochemical reactions to their completion. Rather, this nutrient exerts numerous non-coenzyme functions including allosteric regulation of other enzymes in energy metabolism, direct anti-oxidant and anti-inflammatory actions. It has been shown to influence the transcription of genes involved in modulating and dampening inflammation and oxidative stress upstream. Thiamine and benfotiamine supplements exhibit “anti-stress” properties in the brain, protecting against stress induced suppression of hippocampal neurogenesis. These effects stem from anti-oxidant, rather than coenzyme roles. A review of thiamine’s non-enzyme actions can be found here.

Thiamine as a Front Line Therapy

At this point, I hope that the reader can appreciate some of the potentially beneficial applications of thiamine therapy in high doses. Since this nutrient exhibits extremely low toxicity, is relatively cheap and easy to access, I believe that it should be considered as a front-line therapy, in conjunction with other interventions, for disorders involving mitochondrial dysfunction and chronic oxidative stress. This especially applies to neurological diseases. Whilst many people do not require pharmacological doses, there are many who DO benefit from this. I have seen it on many occasions, and I am sure that I will continue to do so in the future. As it currently stands, the therapeutic potential of this nutrient is untapped. 

Disclaimer

I should note, before beginning any type of treatment, consult your physician. The work above represents the current state of research and observations from my own clinical practice. It should not constitute medical advice. Please be aware that although this vitamin is non-toxic and one cannot overdose, some individuals with longstanding health issues exhibit negative reactions upon taking even small doses of thiamine. These reactions are often associated changes in electrolyte homeostasis, other nutrient deficiencies and/or can be associated with the formulation of thiamine administered. There are a number of articles on these reactions on this site under the search terms, paradoxical reaction, refeeding syndrome, and more recently, calcium management and heart function.

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

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Photo by Jack Carter on Unsplash.

This article was published originally on EONutrition on November 17, 2020 and edited and republished here with permission. 

The Red Thread and Thiamine

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

Unhealthy Beginnings for My Beautiful Daughter: IVF and Induction

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

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

A Truly Gifted Child

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

Early Childhood Symptoms and Triggers

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

Vaccinations, Cyclic Fevers, and Green Drinks

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

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

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

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

The Red Thread and Thiamine

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

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

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

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

Environmental Causes Of Ill-health and Longstanding Thiamine Insufficiency

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

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

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

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

We Need Your Help

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

Yes, I would like to support Hormones Matter.

This story was published first on August 31, 2020. 

HPV Vaccine Healing: A Story of Hope

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On 24 June 2019, eight months after her HPV vaccination, my 13 year old niece Rebecca was diagnosed with moderate Chronic Fatigue Syndrome (CFS).  This followed months of illness that had resulted in her being unable to attend school. Her symptoms at this time included crushing fatigue made worse by activity such as sitting up, talking or walking. Her fatigue was not relieved by rest. Indeed rest was impossible. She couldn’t sleep, and when she did, she woke frequently despite spending most of the time lying in bed in the dark. She was in pain, her muscles aching constantly and her abdomen tender and cramping. She felt sick and dizzy, had ‘brain fog’, headaches, word finding difficulties, a chronic cough, and chest pain. She  was extremely emotional and in constant need of comfort. She did not want to eat, sometimes going days with only mouthfuls of food and craved only simple carbs such as pasta. She contracted shingles and was so ill that an ambulance was called.

Fortunately, by the time of her diagnosis, my sister (her mum) and I had begun to treat her with a nutrient cocktail that included high doses of thiamine and she was already showing signs of a positive response. We had started down this path after I had come across an article by Chandler Marrs on Hormones Matter back in April 2019, I ordered Drs. Lonsdale and Marrs’, Thiamine Deficiency Disease, Dysautonomia, and High Calorie Malnutrition and read it from cover to cover in a matter of days. I am not a medic. I read with Google by my side, gradually learning what words such as syncope and pseudohypoxia meant. The more I read, the more convinced I became that thiamine deficiency and dysautonomia described perfectly what was happening with Rebecca. I noted that alongside the many symptoms described that matched Rebecca’s, HPV vaccination was thought to be a factor in precipitating full blow thiamine deficiency. Indeed, as I read, it became clear that this CFS had not come out of the blue.

Childhood History of Unrecognized Thiamine Insufficiency

Rebecca had a history of weird and seemingly unconnected symptoms throughout her childhood. As a young child, she had episodes when her lips went blue, though no heart problems. She was a sweaty sleeper. She had always had word finding difficulties, and regular mild tummy aches. She had been ‘sensitive’ to stimulus such as noise, strong tastes and smells and even as a toddler would frequently withdraw to her bedroom for downtime. She had a diagnosis of childhood migraine at age 9 and a brain scan done at 10 years old revealed lots of ‘white matter lesions’, though the doctor was unable to interpret what this might mean other than they were common in migraineurs. She had never been the most energetic child despite coming from a sporty family and needed frequent rests and naps after school and at the weekend to manage the demands of her life. When she contracted viruses, she would take longer than her peers to recover from the same virus. Aged 10, she had episodes of blurred vision, unexplained by visits to the opticians or specialist doctors. Alongside all of these symptoms, she had also been diagnosed with vitiligo and had light therapy for 6 months at age 9 years old.

Enter the HPV Vaccine

Our current understanding is that this situation of low level puzzling symptoms may have continued, however in October 2018 she had her first and only dose of the HPV vaccine. This, we think, given an existing thiamine insufficiency, may have been enough of an insult to her system to precipitate the debilitating symptoms that medicine has labelled CFS. Only weeks after the HPV vaccine, she was struggling to attend school with all the symptoms described above. Frequent visits to the doctors as the symptoms progressed led to various prescriptions for antibiotics, anti-nausea drugs, pain killers, a triptan for migraine, and on diagnosis of the CFS, Rebecca was offered anti-depressants. The antibiotics made her tummy pain and discomfort worse. The anti-nausea drugs had no effect at all. The triptan made her nausea worse. Three days of full doses of nurofen, paracetamol and codeine did not work to take the pain away either. We chose not to take the consultant up on the idea of taking anti-depressants. Instead we did our research, found, what we believe was the root cause, and began thiamine therapy. Rebecca’s recovery began soon after.

Time Course of Recovery

  • On 7 May 2019, Rebecca took her first 50mg dose of thiamine and we gradually increased the dose. Her symptoms did get worse initially, exactly like the refeeding syndrome or paradox described by Lonsdale and Marrs.
  • On 16 May, my sister had a consultation with the naturopath Elliot Overton who suggested adjustments to the type and dose of thiamine.
  • On 28 May, Rebecca started 150mg of allithiamine in three separate doses each day.
  • On 29 May, one hour after her first 50mg dose of allithiamine, for the day Rebecca got out of bed briefly and ate. Over the next few weeks we noticed her mood and activity levels went up and down with the thiamine doses.
  • On 28 June, we noted that Rebecca was more emotionally stable. She was more socially interested and her appetite and sleeping were improving.
  • On 10 July, the thiamine dose now increased to 400mg across the day.
  • By 18 July, we felt that Rebecca was turning a corner, she was waking more easily in the morning, joining in with family activities and had even been observed running in the garden with the dog. The time to recover from activity decreased and at times she became more animated and talkative than ever.

Where We Are Now

It’s now September and the start of a new school year. Rebecca is taking 900mg of allithiamine a day. In August she managed to participate gently in two family breaks, including some beach time and short walks. A couple of weeks ago she spent some time playing energetically with her family in their pool, interspersed with rests. Her mum and I are so cheered to watch her have fun and laugh again. Rebecca reports that she no longer craves pasta and her mum notices that she sleeps earlier and wakes less frequently during the night. Rebecca still needs to rest and pace herself, and sometimes she will overdo it and need a day or two for recovery, but we are confident in that recovery now. Rebecca has this week returned to school part time.

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Photo by Tj Holowaychuk on Unsplash.