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Marginally Insufficient Thiamine Intake and Oxalates

Published on January 11, 2023

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Over the last few years, it has become increasingly apparent how important thiamine is to overall health. Thiamine (thiamin) or vitamin B1, sits atop the mitochondria at multiple entry points involved in the metabolism of foods into cellular energy (ATP). It is also critical for several enzymatic reactions within the mitochondria. We have illustrated repeatedly how thiamine deficiency leads to mitochondrial dysfunction, which in turn leads to complex multi-organ system illnesses characterized by chronic inflammation, disturbed immune function, altered steroidogenesis. Each of these is related to deficient mitochondrial energetics. When serious or chronic, thiamine deficiency leads to erratic autonomic function, now called dysautonomia, and a set of disease processes called beriberi.

Long before those symptoms emerge and absent severe deficiency, marginal thiamine status evokes subtle changes in metabolic function. Among these changes, enzymes that would normally metabolize certain foods fully and into useful substrates for other functions are downregulated, shifting the metabolic pathway towards more toxic end-products. The chemistry is complicated and we will go over it in a moment, but first I would like to propose a framework for understanding metabolism. For me, it is useful to imagine metabolism visually as giant maze of right and left turns; where wrong turns lead to dead ends and dead ends lead to the build up of endogenous toxins. Among the primary variables determining the route metabolism takes is enzyme nutrition.

Enzymes require nutrient cofactors to perform their metabolic tasks. When the appropriate nutrient co-factors are present in sufficient concentrations for the enzymes to operate fully, the food we eat is successfully metabolized into end-products that are useful for all manner of processes and cellular energy is produced. Even in the case of genetic aberrations that limit enzyme function endogenously, there is evidence that nutrient manipulation can overcome inadequate enzyme activity. When nutrient co-factors are in short-supply, however, resources are reallocated. Metabolism shifts directions, it takes a right turn when it should move left or vice versa. Different enzymes are activated and metabolism eventually reaches a dead end but not before potentially toxic, unused waste products build up. As these toxins build up, other systems become disrupted, inflammatory and immune responses are activated, demanding ever more energy to resolve. It is this energy spiral, I believe, that induces and maintains many of the illnesses we see today. This means that observing how one reacts to certain foods may point us to correctable nutrient deficiencies.

The Rise in Food Sensitivities

In recent years, I have become fascinated by the growing preponderance of food sensitivities and intolerances. It seems everyone has a problem with something. Given the current practices used in industrial food production, I suppose it is no wonder. We use a staggering number of chemicals to grow and process foods; chemicals that reduce the nutrient content of supposedly healthy foods, but also, present as toxicants that must be dealt with metabolically when ingested. The double hit of low nutrients/high toxicants is disastrous for metabolism. Throw in the generally high calorie content of the western diet and one has to wonder how our mitochondria function at all. And yet they do. Well, sort of. If we don’t count the exponential growth in chronic and seemingly intractable illnesses, but I digress. I believe that food, or lack of quality food, is top among the core contributors to modern illness and food sensitivities are among the key early warning signs of poor metabolism and by definition, faltering mitochondria.

Oxalate Problems

One of the more intriguing and troubling food intolerances that has become increasingly common is to the high oxalate foods. Oxalates are natural substances found in many healthy foods, especially dark leafy greens like spinach, that bind calcium and other minerals, and when left unmetabolized, can form crystals leading to kidney stones. Approximately 10% of men and 7% of women experience at least one episode of kidney stones across the lifetime. Beyond the kidney stone, oxalate intolerance is linked to wide range of chronic health conditions largely due to the build up oxalic acid which may or may not bind calcium, but causes problems nevertheless. Poor oxalate metabolism disrupts gut health, shifting the microbiome unfavorably causing dysbiosis, damages the mitochondria and induces system wide oxidative stress, inflammation and immune reactivity. Problems with oxalate metabolism have been found in individuals with autism, multiple sclerosis, arthritis, and fibromyalgia to name but a few. A common and usually somewhat successful remedy is to avoid the consumption of high oxalate foods. Below are some of the more common high oxalates.

Figure 1. High Oxalate Foods

Absent genetic aberrations leading to poor oxalate handling, I cannot help but wondering if the avoidance diet is the correct response, especially permanently. Certainly, it would help short term, and there may be foods that result in oxalate accumulation that could or should be avoided long term, but an across-the-board and permanent avoidance of most oxalate producing foods seems problematic nutritionally. If we consider that many who suffer from oxalate issues may also be sensitive to other foods, the avoidance approach could limit dietary options considerably. What if we are approaching this issue incorrectly? My gut tells me, and research seems to back it up, that barring genetic issues with oxalate metabolism, the dietary component is not simply one of excess oxalate consumption. It is a problem with inadequate nutrient consumption in the face of excessive non-nutrient foods – e.g. it is a problem with the modern western diet in its entirety.

Other Dietary Contributors to Oxalate Buildup: Processed Foods

If we dig into the oxalate issue a little more, we see that foods resulting in excess oxalate storage are not necessarily limited to whole foods listed above in Figure 1. A number of foods classified as high oxalate, are simply processed food products, high in carbohydrates, trans fats and low in nutrients. Below is a graph of some of the higher oxalate foods as compiled by the University of Chicago via Harvard’s School of Public Health. Notice, how processed foods make this list. Sure, their oxalate status is significantly lower than other foods, but consider what portion of the average western diet these products comprise. Click the links above to see a more complete listing foods that result in high oxalate accumulation. When you search through those lists (especially, the one from the University of Chicago), it becomes apparent that virtually all processed foods can result in oxalate problems.

Figure 2. Oxalate Content in Common Foods

food-oxalate-graph

One could argue that oxalate buildup involves shifts in the metabolic pathway that are directly related to nutrient deficiencies and those nutrient deficiencies emerge from the consumption of the modern diet. Processed carbohydrates, for example, in the presence of thiamine deficiency, are metabolized quite differently than when thiamine is present, with the former resulting in oxalate build up. Since a diet high in processed carbohydrates is one of the leading causes of thiamine deficiency in the first place, this begs the question, is the issue really oxalates or a sort of high calorie malnutrition resulting in thiamine deficiency, where oxalate accumulation is just a side-effect. Similarly, when thiamine is absent, fatty acid metabolism can go awry, making highly processed, high carbohydrate, high fat foods damaging on two fronts.

Finally, there are many other foods that can lead to high oxalate production in the presence of low thiamine including: beer, wine, tea, coffee, yogurt, bread, rice, soybean paste, soy sauce, and oil, along with foods that have been fermented, roasted, baked, or fried. And just like high carbohydrate diets can lead to thiamine deficiency, as nature would have it, all alcoholic drinks, coffee, and tea decrease thiamine uptake thereby both creating and exacerbating the thiamine deficiency that leads to oxalate accumulation. It could be that problems with oxalates is simply the early sign of thiamine deficiency and it may very well be a protective mechanism of sorts, a metabolic diversion, albeit an unhealthy one, to forestall the other issues associated with insufficient thiamine intake.

I should also mention that oxalate problems may not be solely related to diet. Inasmuch as all pharmaceuticals damage the mitochondria and either decrease thiamine directly or increase the demand for the need for thiamine indirectly, regular use of pharmaceuticals may also contribute to the problem. Similarly, a number of environmental exposures increase glyoxal (a precursor to oxalate build up in the face of low thiamine), including: cigarette smoke, smoke from residential log fires, vehicle exhaust, smog, fog, and some household cleaning products.

Is Thiamine Really the Problem?

It may be. The chemistry is complicated and detailed below, but basically, marginal thiamine status, prevents the proper metabolism of certain foods leading to the build up of toxins while simultaneously crippling the natural detox pathways. The combination of increased toxins and decreased detox ability leads to all sorts of damage and illness, high oxidative stress, and as illustrated by the graphic below, can lead to cancer (to be discussed in a subsequent article). Thiamine prevents this. A paper published in 2005, (from which Figure 3., is taken) details just how many mechanisms that lead to oxalate accumulation are initiated by low thiamine.

Figure 3. How Low Thiamine Leads to Elevated Glyoxal and Cancer

glyoxal pathways

The specifics involve a metabolic diversion that leads ‘food’ metabolites down what is called the glyoxal pathway, the pathway responsible for oxalates. Each of the red ‘X’s’ indicates an impaired thiamine dependent enzyme.

With Marginal Thiamine

Elevated glyoxal and methylglyoxal
- Diminished activity of thiamine dependent enzymes (transketolase, pyruvate dehydrogenase, branched chain ketoacid dehydrogenase, and a-ketoglutarate)
  - Low transketolase = low NADPH
  - Low NADPH = low glutathione (the primary detoxification agent in the body; glutathione also requires vitamin C)
    - Low glutathione = poor detoxification of glyoxal and methylglyoxal = increased carcinogenic protein adducts
- High Oxalate Foods
  - Glyoxal >glyoxalate > oxalates
Diminished pyridoxal kinase (PK) activity*
- *This is not discussed in the aforementioned paper, but should be included. PK is the enzyme that converts the inactive form of vitamin B6 (pyridoxine 5-phosphate) into its active form, pyridoxal 5-phosphate (P5P). Low P5P prevents glyoxalate from being converted back into glycine, leading to high oxalates. Many mistakenly assume that low vitamin B6 is responsible for high oxalates. While that is possible, it is also possible, and often more likely, that low thiamine is responsible.

With Sufficient Thiamine

Thiamine dependent enzymes work appropriately
- Sufficient transketolase activity = sufficient NADPH
Glyoxal and methylglyoxal are metabolized into other substrates and/or excess is detoxified
- Sufficient NADPH = sufficient glutathione
Glyoxalate is converted to a-hydroxy-b-ketoadipate or glycine and not oxalate
- Alanine glyoxylate amino transferase (AGT), the enzyme required to convert glyoxalate into to glycine instead of oxalate has sufficient activated vitamin B6.

This is not to say that there are not other vitamin and mineral deficiencies also associated with hyperoxaluria, there are. Research has shown that low magnesium (a requisite co-factor in many of same enzymes as thiamine), along with low vitamin A, in addition to the low vitamin B6, mentioned above play a role. Vitamin E may also be involved.

Take Home

The majority of modern illnesses are the result of poor diet and environmental exposures directly, cumulatively, and generationally. Over the span of a few short generations, we have forgotten that food is fuel and that good, clean, unprocessed food is required for health. The allure of processed foods and cheap agriculture through chemistry, has left much of the population starved of nutrients, while simultaneously bearing a high toxicant load. The result is all sorts of metabolic disturbances which may manifest as food insensitivities and intolerances. It is interesting to note that the metabolic changes involved in oxalate buildup do not require what we would consider a full-scale thiamine deficiency, but rather, a sort of thiamine insufficiency initiated by marginal thiamine intake, something that is likely common across populations.

A less complicated overview of the low thiamine > high oxalate connection can be viewed below.

Is Your Body Producing too much Oxalate?

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Image: Scanning electron micrograph of the surface of a kidney stone showing tetragonal crystals of weddellite (calcium oxalate dihydrate) emerging from the amorphous central part of the stone; the horizontal length of the picture represents 0.5 mm of the figured original. Image credit: Kempf EK – Own work, CC BY-SA 3.0.

This article was published originally on August 15, 2019.

Quick Thoughts: Hyperemesis and Early Thiamine Deficiency

by Chandler Marrs, PhD

Published on January 3, 2023

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A while back, I published an article about expanding the symptoms considered to be associated with thiamine deficiency. Conventionally, we tend to look only at the end stage results of long term thiamine deficiency as being the indicators of disease, forgetting that to get to this stage there was a prodrome, which, except in rare cases, proceeds across many months, if not years. Even with a severely thiamine restricted diet, it can be weeks to months before the more traditionally recognized neurological or cardiovascular symptoms manifest. A series of studies conducted in early 1940s found that among the most common early symptom of thiamine deficiency was GI dysfunction ranging from nausea, vomiting, and constipation, to severe food intolerances and complete anorexia. The prominence of vomiting in this scenario got me thinking about hyperemesis, the severe and near continuous vomiting experienced by some women during pregnancy, but also, about the exploding numbers of illnesses that involve GI dysmotility and dysbiosis. From IBS to SIBO, gastroparesis to constipation and really everything in between, could they also be a consequence of insufficient thiamine? According to the research, yes. Indeed, these non-pregnant cases of GI dysfunction, easily fall under the umbrella of gastrointestinal beriberi – thiamine deficiency that manifests in GI system, sometimes months before the onset of the more traditional cardiovascular or neurological forms.

Pregnancy, Vomiting, and Thiamine

With pregnancy, we know that the energy demands upon the mom are enormous, which means that given its role in energy metabolism, thiamine demands are enormous as well. Some older research estimates the demand for thiamine increases by at least 5X that of a non-pregnant woman. Other research, which I seem to have lost the reference for, posited the demand increased by a factor of 10. Personally, I believe the demand and need for thiamine and other nutrients during pregnancy is higher yet.

The RDA for thiamine during pregnancy is 1.4mg per day, just a fraction over the RDA for non-pregnant women (1.1mg). A quick scan of prenatal vitamins shows that most include from 1.5mg – 3mg of thiamine, woefully below the estimated need of 5-10X non-pregnant levels. That discrepancy alone could cause problems in women who may have been borderline thiamine deficient pre-pregnancy. The pregnancy itself would tip her over into deficiency territory. This then could very easily lead to increased vomiting, which then would further hamper the intake and absorption of thiamine, exacerbating the deficiency, and cause more vomiting; a cycle that becomes especially dangerous to both mom and the baby as time progresses.

While it is easy to see how thiamine deficiency is a common consequence of hyperemesis, it is possible that it is also a contributing cause. Dr. Lonsdale and others have long asserted a role for thiamine deficiency as a causative contributor to hyperemesis. Just based upon the estimated need versus the availability in prenatals and diet, especially once vomiting has begun, this makes sense. Importantly, these types of symptoms have been observed across many case studies unrelated to pregnancy, so much so that gastrointestinal beriberi is a legitimate, though woefully under-recognized form of thiamine deficiency disease. As mentioned previously, the symptoms include GI distress in the form of vomiting, gastroparesis (delayed stomach emptying, which results in vomiting), disturbed GI dysmotility, either too much or too little, and dysbiosis. All of this is documented to be attributable to insufficient thiamine in non-pregnant people. Is it so difficult to see that pregnancy too could elicit or exacerbate gastrointestinal beriberi?

But Wait, What About Carnitine and CoQ10?

If you follow my work, a few years back I mapped one of the causes of hyperemesis to a carnitine deficiency. Carnitine is critical to the metabolism of fatty acids, and its deficiency along with another mitochondrial co-factor, CoQ10, have been linked to a condition called Cyclic Vomiting Syndrome (CVS). Supplementation with l-carnitine and CoQ10 appears to resolve the vomiting with CVS. After publishing that paper, anecdotal reports came back suggesting that l-carnitine and CoQ10 was useful in preventing and resolving hyperemesis. I believe that it is still involved in many cases, but it is possible that thiamine is involved as well and it may be a contributing factor to the carnitine deficiency. Thiamine, in addition to its role in key enzymes involved in carbohydrate and protein metabolism, is also involved in fatty acid metabolism and positionally, it sits a step above carnitine.

Here we have a few options beyond the traditional and largely ineffective anti-emetic medications given to women with hyperemesis; options that I would argue are significantly safer and healthier for mom and baby and likely far more effective. If thiamine and/or l-carnitine deficiency are at the root of hyperemesis, correcting those deficiencies early should give women a much easier and healthier pregnancy.

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This article was published originally on May 24, 2021.

Energy Loss as a Cause of Disease

by Derrick Lonsdale MD, FACN, CNS

Published on December 7, 2022

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

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

Heresy in Medicine

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

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

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

Envisioning an Alternative Approach

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

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

The Second Paradigm

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

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

The Production and Consumption of Energy

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

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

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

The Medical Revolution

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

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

Yes, I would like to support Hormones Matter.

Image by Jonny Lindner from Pixabay.

This article was first published on July 1, 2019.

Sleep Requires Energy

by Derrick Lonsdale MD, FACN, CNS

Published on October 4, 2022

17032 views

It is widely believed that almost no calories are used during sleep. That is incorrect: while the body rests during sleep and energy consumption is not high, it is a long way from zero. A convenient way to measure energy use is known as the “metabolic equivalent” (ME). This is defined as the rate of energy used by a person sitting and awake, the “resting metabolic rate”. A person riding a bicycle may be using five MEs; a runner, nine or more. A sleeping person uses about 0.9 MEs, so we burn calories when we are asleep about 90% as fast as while sitting on the couch watching television.

Energy conservation is important in sleep, but it’s expenditure is still required. It has been proposed that sleep is a physiological adaptation to conserve energy but little research has examined this proposed function. In one study, the effects of sleep, sleep deprivation and recovery sleep on the whole-body, total daily energy expenditure was examined in seven healthy participants aged 22+/-5 years. The findings provided support for the hypothesis that sleep conserves energy and that sleep deprivation increases total daily energy expenditure. I read somewhere that an enthusiastic young astronomer decided that sleep was unnecessary and used his telescope for 13 nights without sleeping during the day. He became extremely ill, thus showing the importance of sleep in survival. The recognition that sleep is one of the foundations of athletic performance is vital.

Research in the general population has highlighted the importance of sleep on neurophysiology, cognitive function and mood. In a post on Hormones Matter, we reported several young people who had a post Gardasil vaccination crippling condition that turned out to be due to thiamine deficiency. All of them had been exceptional athletes and students before the vaccination. We concluded that the brain energy requirement for exceptional people put them at greater risk of succumbing to stress if their capacity for MEs was limited, either for genetic or nutritional reasons. We assumed that their thiamine deficiency before vaccination was marginal and either asymptomatic or producing trivial symptoms ascribed to other “medically more acceptable” causes. The stress of the vaccination required an energy dependent adaptive response that precipitated fully symptomatic thiamine deficiency. You might say that they were “weighed in the balance and found wanting” as the proverb says.

The Stages of Sleep

Sleep is a complicated process. The first sensation is known as “sleep latency” and registers the time taken from eye closure to falling asleep. The sleep cycle is then divided into five stages, each cycle lasting approximately 90-120 minutes. Stage one is known as light sleep. In stage 2 the brain is resting the parts used when awake. Stages 3 and 4 are deeply restorative. Stage V is known as rapid eye movement (REM) sleep and may be the most important part. Movement of the eyes behind closed lids is observed. The autonomic nervous system is activated for unknown reasons. It is in this stage when we dream and most sleep disorders occur.

Circadian Rhythm

The word circadian means “about 24 hours”. The circadian clock is a complex, highly specialized network in the brain that regulates its day/night metabolism and is a key for metabolic health. It is modulated by behavioral patterns, physical activity, food intake, sleep loss and sleep disorders. Disruption of this clock is associated with a variety of mental and physical illnesses and an increasing prevalence of obesity, thus illustrating that it is dependent on energy balance (production/consumption). Reduced sleep quality and duration lead to decreased glucose tolerance and insulin sensitivity, thus increasing the risk of developing type 2 diabetes. In other words there is a close link between circadian rhythm and available energy . I have seen patients who were unable to take the night shift at work because they were unable to adapt. The increase in obesity has been paralleled by a decline in sleep duration but the potential mechanisms linking energy balance and the sleep/wake cycle are not well understood. An experiment was reported in 12 healthy normal weight men. Caloric restriction significantly increased the duration of deep (stage 4) sleep, an effect that was entirely reversed upon free feeding.

Sleep Apnea

This condition is fairly common in the United States and is probably generally fairly well-known by most people. The patient stops breathing during sleep and may repeatedly awaken with a start. The disease was discovered because a woman reported that her husband kept waking up with a start because “he was affected by an evil spirit”. Fortunately, the physician took her seriously and it led to the studies that determined its cause. Many patients with, or at risk of, cardiovascular disease have sleep disordered breathing (SDB). These can be either obstructive because of intermittent collapse of the upper airway, or central because of episodic loss of respiratory drive. SDB is associated with sleep disturbance, hypoxemia, hemodynamic changes and sympathetic activation. Brainstem dysfunction combined with heart disease is the hallmark of the thiamine deficiency disease, beriberi.

What that means is that there are two types of sleep apnea. In the obstructive type, the tongue falls back into the pharynx and blocks the airway. In the one where there is loss of respiratory drive, the centers in the brain stem are compromised. It is these centers that completely take over the control of breathing when we are unconscious as in sleep. If their supervisory mechanisms fail, breathing ceases. Carbon dioxide concentration increases and stimulates the brain controls that restart breathing. Occasionally these mechanisms are so sick that breathing does not restart. Hence a form of nocturnal sudden death follows. When we are awake we can override these centers and control our breathing voluntarily. Obesity and obstructive sleep apnea have a reciprocal relationship depending on the regulation of energy balance. When I was in practice I treated several patients with sleep apnea using large doses of thiamine. Because of this I hypothesized that the association of dysautonomia with so many different diagnoses is because of loss of oxidative efficiency and subsequent disorganization of controls that are mediated through the limbic system and brainstem. I came to the conclusion that energy deficiency in the brain was the core issue.

I recently had a letter from the parents of a then five-year-old child who came under my care 35 years ago. She has a genetically determined disorder that affects energy balance and I had treated her by dietary restriction and providing non-caloric nutrients. They informed me that she was doing very well. The condition is known as Prader Willi syndrome, a terminology that indicates that nothing was known about its cause when it was initially described. Today, 10 studies have provided evidence that total energy, resting energy, sleep energy and activity energy expenditure are all lower in individuals with this syndrome. Dietary discipline and nutritional supplementation had paid off.

An Explanatory Analogy

You may think that comparing the human body with an automobile is manifestly absurd, but the principles that I will use in the analogy are simple.

Fuel

First of all, both use fuel: gasoline is the fuel for a car, but it must be calibrated to the design of the engine, giving rise to the gasoline choices at the pump. Although different forms of human food may be compared to gasoline choices, the primary fuel for our cells is glucose and this is particularly true for the brain. Glucose, a carbohydrate, can be synthesized in the body from other components in the diet and different diets are sometimes used therapeutically. Unlike the car, the human body must derive its “spark plug” from the food and is the basic reason why organic, naturally occurring, food is a necessity. The food industry cannot imitate or replace it.

Engine

The engine in a car burns gasoline to create energy. It requires spark plugs to ignite the gasoline and waste gases are eliminated through an exhaust pipe.

Every cell in the human body has an “engine”. Without going into details this is known as the Krebs cycle (named after its discoverer). Its objective is to produce energy and glucose has to be “ignited” (oxidized). The oxidation process, while releasing energy, gives rise to carbon dioxide (the “ash”) that is eliminated in the breath. Energy is stored in an eletrochemical form known as adenosine triphosphate (ATP).The nearest parallel would be a battery. It releases an electrical form of energy that is then used for function. Whether we like to recognize it or not, we are electrochemical machines and the only way that we can preserve or retrieve health is by furnishing the complex of ingredients that enable food to be converted into energy.

To continue the analogy, when you put your car in the garage and turn off the ignition the car is technically “dead”. Obviously, we are unable to do that with the human body, but let us make a simple comparison. Supposing for some reason it was desirable to keep the car “alive” when it was in the garage. The engine would continue to run and it would be consuming fuel. Because the body requires energy to remain alive, the “engines” have to continue running, even when we are asleep. This does make sense for the consumption of energy when we are asleep———it keeps us alive !

Transmission

The energy developed from burning gasoline has to be transmitted to the wheels in order to produce the normal function of the car, which is the ability to move. The transmission is a series of levers that are interconnected.

The same is true in the human body, but it is biochemical in nature. A series of energy consuming enzymes use the protein, fat and carbohydrate to build the diversity of tissues that make up the body. Throughout life, cells are destroyed and replaced, so this is a continuous process of energy consumption and repair. Every physical movement, every thought and emotion, consumes energy. Like the transmission in the car, the energy produced by the citric acid cycle engine is consumed in every movement of the body, every thought occurring in the brain and every emotion.

Chassis

The body of a car is just a container on wheels designed to carry around human beings. Its sole function is to move and until we have driverless cars a human being must be the driver.

In comparison, the body of a human being is merely a chassis that carries the brain around. It might be said that the brain can be compared with the car driver and every function of the body is under the command of the brain. Another analogy that I have used is an orchestra where the brain is the conductor and the organs are banks of instruments in which the cells come under the command of the conductor.

Putting It All Together

The 2019 Nobel prize has just been awarded to three scientists who have discovered how our body cells respond to low concentrations of oxygen (hypoxia). The reaction of medical scientists is very positive since this discovery will certainly be applied to the treatment of many diseases. Apparently scientists are already trying to find drugs that will influence this effect. For example, it has long been known that hypoxia will introduce inflammation. My forecast is that the use of nutrients will often correct the genetics by epigenetic mechanisms and this is already under way.

I found the Nobel prize extremely interesting because of a little-known phenomenon that was described by the early investigators of the vitamin B1 deficiency disease, beriberi. They had found in this disease that the arterial concentration of oxygen was low while the venous concentration was relatively high. Arterial blood carries oxygen from the lung to all the tissues of the body. It has to be unloaded into the cells that then use it to produce energy. The venous blood then returns to the lung to be loaded again with oxygen. A relatively low arterial oxygen reflects an inadequate loading at the lung tissues, while a relatively high venous oxygen indicates poor utilization by the cells to which it is delivered. This means that thiamine (vitamin B1) is an essential catalyst in the delivery of oxygen to the tissues. Its deficiency induces gene expression similar to that observed in hypoxia and has been referred to as a cause of pseudo-hypoxia (false hypoxia).

The heading of this article is that sleep requires energy, but I am making the case that being alive and well simply means that oxygen is being consumed efficiently, as long as the “blueprint” of DNA is healthy. It strongly suggests that hypoxia and/or pseudo -hypoxia are the underlying causes of disease and may explain why thiamine and its derivative are such important therapeutic agents.

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

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This article was published originally on October 14, 2019.

What Is Thiamine to Energy Metabolism?

by Derrick Lonsdale MD, FACN, CNS

Published on September 15, 2022

16129 views

What Is Energy?

Energy is an invisible force. The aggregate of energy in any physical system is a constant quantity, transformable in countless ways but never increased or diminished. In the human body, chemical energy is produced by the combination of oxygen with glucose. This reaction is known as oxidation. The chemical energy is transduced to electrical energy in the process of energy conservation. This might be thought of as the “engine” of the brain/body cells. We have to start thinking that it is electrical energy that drives the human body.

The production of chemical energy is exactly the same in principle as the burning of any fuel but the details are quite different. The energy is captured and stored in an electronic form as a substance known as adenosine triphosphate (ATP) that acts as an energy currency. The chemical changes in food substances are induced by a series of enzymes, each of which combine together to form a chain of chemical reactions that might be thought of as preparing food for its ultimate breakdown and oxidation.

Each of these enzymes requires a chemical “friend”, known as a cofactor. One of the most important enzymes, the one that actually enables the oxidation of glucose, requires thiamine and magnesium as its cofactors. Chemical energy cannot be produced without thiamine and magnesium, although it also requires other “colleagues”, since all vitamins are essential. A whole series of essential minerals are also necessary, so it is not too difficult to understand that all these ingredients must be obtained by nutrition. The body cannot make vitamins or essential minerals. There is also some evidence that thiamine may have a part to play in converting chemical energy to electrical energy. Thus, it may be the ultimate defining factor in the energy that drives function. If that is true, its deficiency would play a vital role in every disease.

Energy Consumption

Few people are aware that our lives depend on energy production and its efficient consumption. A car has to have an engine that produces the energy. This is passed through a transmission that enables the car to function. In a similar manner, we have discussed how energy is produced. It is consumed in a series of energy requiring chemical reactions, each of which requires an enzyme with its appropriate cofactor[s]. This series of reactions can be likened to a transmission, consuming the energy provided from ATP and enabling the human body to function. If energy is consumed faster than it can be synthesized, or energy cannot be produced fast enough to meet demand, it is not too difficult to see that an insufficient supply of energy, a gap between supply and demand, would produce a fundamental change in function. This lack of function in the brain and body organs presents as a disease. The symptoms are merely warning the affected individual that something is wrong. The underlying cause of the energy deficiency has to be ascertained in order to interpret how the symptoms are generated.

Why Focus On Thiamine?

We have already pointed out that thiamine does not work on its own. It operates in what might be regarded as a “team relationship”. But it has also been determined as the defining cause of beriberi, a disease that has affected millions for thousands of years. Any team made up of humans requires a captain and although this is not a perfect analogy, we can regard thiamine as “captain” of an energy producing team. This is mainly due to its necessity for oxidation of glucose, by far and away the most important fuel for the brain, nervous system and heart. Thus, although beriberi is regarded as a disease of those organs, it can affect every cell in the body and the distribution of deficiency within that body can affect the presentation of the symptoms.

Thiamine exists only in naturally occurring foods and it is now easy to see that its deficiency, arising from an inadequate ingestion of those foods, results in slowing of energy production. Because the brain, nervous system and heart are the most energy requiring tissues in the body, beriberi produces a huge number of problems primarily affecting those organs. These changes in function generate what we call symptoms. Lack of energy affects the “transmission”, giving rise to symptoms arising from functional changes in the organs thus subserved. However, it must be pointed out that an enzyme/cofactor abnormality in the “transmission” can also interrupt normal function.

In fact, because of inefficient energy production, the symptoms caused by thiamine deficiency occur in so many human diseases that it can be regarded as the great imitator of all human disease. We now know that nutritional inadequacy is not the only way to develop beriberi. Genetic changes in the ability of thiamine to combine with its enzyme, or changes in the enzyme itself, produce the same symptoms as nutritional inadequacy. It has greatly enlarged our perspective towards the causes of human disease. Thiamine has a role in the processing of protein, fat and carbohydrate, the essential ingredients of food.

Generation Of Symptoms

Here is the diagnostic problem. The earliest effects of thiamine deficiency are felt in the hindbrain that controls the automatic brain/body signaling mechanism known as the autonomic nervous system (ANS). The ANS also signals the glands in the endocrine system, each of which is able to release a cellular messenger. A hormone may not be produced in the gland because of energy failure, thus breaking down the essential governance of the body by the brain. Hypoxia (lack of oxygen) or pseudo-hypoxia (thiamine deficiency produces cellular changes like those from hypoxia) is a potentially dangerous situation affecting the brain and a fight-or-flight reflex may be generated. This, as most people know, is a protective reflex that prepares us for either killing the enemy or fleeing and it can be initiated by any form of perceived danger. Thus, thiamine deficiency may initiate this reflex repeatedly in someone that seeks medical advice for it. Not recognizing its underlying cause, it is diagnosed as “panic attacks”. Panic attacks are usually treated by psychologists and psychiatrists with some form of tranquilizer because of the anxiety expressed by the patient.

It is easy to understand how it is seen as psychological, although the sensation of anxiety is initiated in the brain as part of the fight-or-flight reflex and will disappear with thiamine restoration. It may be worse than that: because the heart is affected by the autonomic nervous system, there may be a complaint of heart palpitations in association with the panic attacks and the heart might be considered the seat of the disease, to be treated by a cardiologist. The defining signal from the ANS is ignored or not recognized. Because it is purely a functional change, the routine laboratory tests are normal and the symptoms are therefore considered to be psychological, or psychosomatic. The irony is that when the physician tells the patient “it is all in your head”, he is completely correct but not recognizing that it is a biochemical functional change and that it has nothing to do with Freudian psychology.

A Sense Of Pleasure

We have known for many years that dietary sugar precipitates thiamine deficiency. A friend of mine had become well aware that alcohol, in any form, or sugar, will automatically give him a migraine headache. He still will take ice cream and suffer the consequences. I have had patients tell me that they have given up this and that “but I can’t give up sugar: it is the only pleasure that I ever get”. They still came back to me to treat the symptoms. We have come to understand that we have no self-responsibility for our own health. If we get sick, it is just bad luck and the wonders of modern medicine can achieve a cure. The trouble is that a mild degree of thiamine deficiency might produce symptoms that will make it more difficult to make the necessary decisions for our own well-being. Let me give some examples of symptoms that are typically related to this and are not being recognized:

Occasional headache, heartburn or abdominal pain
Occasional diarrhea or constipation
Allergies
Fatigue
Emotional lability
Insomnia
Nightmares
Pins and needles
Hair loss
Palpitations of the heart
Persistent cough for no apparent reason
Voracious, or loss of appetite

The point is that thiamine governs the energy synthesis that is essential to our total function and it can affect virtually any group of cells in the body. However, the brain, heart and nervous system, particularly the autonomic (automatic) nervous system (ANS) are the most energy requiring organs and are likely to be most affected.

Since the brain sends signals to every organ in the body via the ANS, a distortion of the signaling mechanism can make it appear that the organ receiving the signal is at fault. For example, the heart may accelerate because of a signal from the brain, not because the heart itself is at fault. Hence heart palpitations are often treated as heart disease when a mild degree of thiamine deficiency in the brain is responsible.

We have known for many years that sugar in all its different forms can and will precipitate mild thiamine deficiency. It is probably the reason why sugar is considered to be a frequent cause of trouble. If thiamine deficiency is mild, any form of minor stress may precipitate a much more serious form of the deficiency. An attack by an infecting organism is a source of stress imposed on the affected person and requires a boost of energy consumption. Therefore the illness that follows can be regarded as a “war” between the attacking disease producing organism and the brain/body that has to mobilize a defense. Either death, recovery, or a “stalemate” might be the expected outcome. If this is the truth, then any disease will respond to the ingestion of nutrients, particularly thiamine. It strongly suggests that Holistic or Alternative medicine could add a huge benefit to health preservation or the treatment of disease.

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

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This article was published originally on August 25, 2020.

Unraveling Symptoms and Syndromes

by Derrick Lonsdale MD, FACN, CNS

Published on September 6, 2022

10631 views

What Is a Syndrome?

A syndrome is the name given to a collection of symptoms and physical signs that have been observed in the past in a single patient or in a group of similar patients. This is often named after the first person to report this set of observations. It is called a syndrome when others have made the same observations, sometimes years later. The terminology is purely descriptive, even though there may be a constellation of abnormal laboratory tests associated with the clinical facts. Unfortunately, the underlying cause is seldom, if ever, known.

Chronic Fatigue Syndrome

Chronic fatigue syndrome (CFS) is also known as myalgic encephalomyelitis (ME). In a review, it is described as a “challenge to physicians”. Its prevalence is reported as approximately 1% in the general German population. The author states that there are no convincing models that might explain the underlying cause as an independent unique disease. A variety of conditions such as chronic infectious disease, multiple sclerosis, endocrine disorders and psychosomatic disease are suggested in a differential diagnosis. There is said to be a significant overlap with major depression.

Another review describes CFS as characterized by debilitating fatigue that is not relieved with rest and is associated with physical symptoms. In order to make the diagnosis, these authors indicate that at least four of the following symptoms are required to make the diagnosis. They include feeling unwell after exertion, unrefreshing sleep, impaired memory or concentration, muscle pain, aching joints, sore throat, or new headaches. They also say that no pharmacologic or alternative medicine therapies have been proven effective.

Fibromyalgia Syndrome

According to the American College of Rheumatology, fibromyalgia syndrome (FMS) is a common health problem characterized by widespread pain and tenderness. Although chronic, there is a tendency for the pain to fluctuate in intensity and location around the body. Deficient understanding of its true cause gives rise to the false concept that it is neurotic. It is associated with chronic fatigue and patients often have sleep disorders. It is estimated that it affects 2 to 4% of the general population and is most common in women. It affects all ages and the causes are said to be unclear. FMS patients may require psychiatric therapy due to accompanying mental problems. Gonzalez and associates concluded that the combination of psychopathological negative emotionality, interpersonal isolation and low hedonic capacity that they found in a group of patients has implications for the daily living and treatment of these patients.

Regional Pain Syndrome

Complex regional pain syndrome (CRPS) is another common and disabling disorder, characterized by defective autonomic nervous system function and inflammatory features. It reportedly occurs acutely in about 7% of patients who have limb fractures, limb surgery, or other injuries, often quite minor. A small subset of patients progress to a chronic form in which autonomic features dominate. Allodynia (pain due to a stimulus that does not usually provoke pain) and hyperalgesia (increased pain from a stimulus that usually provokes pain) are features of CRPS and require a better understanding.

Sleep Apnea Syndrome

Apnea is the term used for a temporary cessation of automatic breathing that usually happens during the night. This syndrome is described as the most common organic disorder of excessive daytime somnolence. Its prevalence is highest among men age 40 to 65 years and may be as high as 8.5% or higher in this population. It is associated with cigarette smoking, use of alcohol and poor physical fitness.

Similar Cause with Different Manifestations

Complex Regional Pain Syndrome is related to microcirculation impairment associated with tissue hypoxia (lack of oxygen) in the affected limb. Without going into the complex details, hypoxia induces a genetic mechanism called hypoxia inducible factor (HIF-1 alpha) that has a causative association with CRPS. It has been found that inhibiting this factor produced an analgesic effect in a mouse model. The interesting thing about this is that thiamine deficiency does exactly the same thing because it induces biochemical effects similar to those produced by hypoxia (pseudo[false]hypoxia). A group of physicians in Italy have shown that high doses of thiamine produced an appreciable improvement in the symptoms of three female patients affected by fibromyalgia and are probably pursuing this research. Dietary interventions have been reported in seven clinical trials in which five reported improvement. There was variable improvement in associated fatigue, sleep quality, depression, anxiety and gastrointestinal symptoms.

Dr. Marrs and I have published a book that emphasizes deficient energy metabolism as a single cause of many, if not all, diseases. The symptomatic overlap in these so-called syndromes is generated by defective function of cellular metabolism in brain. Fatigue is the best symbol of energy deficiency and the English translation of the Chinese word beriberi is “I can’t, I can’t”. Fatigue is a leading symptom in beriberi. When physicians diagnose psychosomatic disease as “it’s all in your head”, they are of course, quite right. However, to imagine or conclude that the variable symptoms that accompany the leading one of fatigue are “imaginary” is practically an accusation of malingering. The brain is trying to tell its owner that it has not got the energy to perform normally and the physician should be able to recognize the problem by understanding the mechanism by which the symptoms are produced. Every thought, every emotion, every physical action, however small, requires the consumption of energy. Obviously we are considering variable degrees of deficiency from slight to moderate. The greater the deficiency the more serious is the manifestation of disease that follows. Death is a manifestation of deficiency that no longer permits life.

Our book is written primarily for physicians, but it is sufficiently lacking in technological language to encourage reading by patients. It emphasizes, by descriptions of case after case, the details of how genetic risk and failed brain energy are together unable to meet and adapt a person’s ability to meet the daily stresses of life. Stress, genetic risk and poor diet all go together. A whole chapter discusses the functions of the autonomic nervous system and how it deviates when the control mechanisms in the lower brain are defective. This system is the nervous channel that enables the brain to communicate the adaptive body actions necessary to meet living in an essentially hostile environment. We show that an excess of sugar and/or alcohol produce deficiency of vitamin B1 and the so-called psychosomatic disease that results is really early beriberi “I can’t, I can’t”. Variability in symptoms caused by this effect is because the cellular energy deficiency distribution varies from person to person and is affected by genetically determined differences.

This is illustrated by the case of a boy with eosinophilic esophagitis whose first eight years of life were marked by repeated diagnoses of psychosomatic disease. At the age of eight, upper endoscopy revealed the pathology in the esophagus. There was a family history of alcoholism and he was severely addicted to sugar. Many of his symptoms cleared with the administration of a thiamine derivative and resulted in a dramatic increase in stature. No pediatrician or other physician whose attendance was sought through those first 8 years evidently had ever questioned diet or the gross ingestion of sweets. They simply treated each condition as a confirmation that they were “psychological”.

It is worth noting that references 1 through 4 refer to both CFS and FMS syndromes being affected by psychological issues. This implies that the patient is “inventing” the poorly understood (and often bizarre) symptoms as a result of neurosis. The unfortunate complainant may easily become classified in the mind of the attendant physician as a “problem patient”. I have become aware that this can rise to such a degree of misunderstanding that the patient is denied access to the physician and even to other physicians in the same clinic. It is indeed about time that an overall revision be made to the absurd concept that the brain can “invent” a sensation that has no importance in solving the electrochemical problem. When we see the statistics of incidence of these common syndromes we have to conclude that there is an underlying cause and effect that pervades the general population. We are very conscious that our cars need the right fuel to work efficiently but rarely take it into consideration that the quality of food is our sole source of energy synthesis.

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

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This article was published originally December 2019.

Thiamine for Fibromyalgia, CFS/ME, Chronic Lyme, and SIBO-C

by AMZ

Published on June 7, 2022

28393 views

The Road to Thiamine

In August 2020, I was at my wits end. I had developed gastroparesis in March 2020, after 10 days of metronidazole (Flagyl), for a H. Pylori infection and SIBO-C symptoms. After seven days, I developed the symptoms usually associated with the intake of this drug – nausea, confusion, anxiety, paranoid thinking and mild gastroparesis symptoms. I no longer had bowel movements initiated by my body and had to use enemas twice a week. This state continued and worsened until the end of July 2020, when I also had a surgery for stage 4 endometriosis.

I managed to stay alive those months by eating an elemental diet (90%) and a few bits of solid food such as white rice, goat cheese, or lean meat. After the surgery, however, my gastroparesis got worse. I contacted my family doctor at the end of August and told her that I could no longer eat any solid food without severe nausea and that I need to be in a hospital to be fed intravenously or with a gastric tube. She agreed that my situation demanded immediate attention and she wrote me the referral for an inpatient hospital admission.

I was lucky though that at that exact time, I stumbled upon the low oxalate diet mentioned by a member of a Facebook group. I joined the Trying Low Oxalate (TLO) group on Facebook and read what researcher Susan Owens wrote about oxalates. I started implementing it and realized that small portions of low oxalate food every 2-3 hours were accepted by my body. In a few weeks my gastroparesis symptoms were reduced and my belly pain diminished.

From the Low-Oxalate Diet to Discovering Beriberi Disease

At some point in September 2020, while researching oxalates, I found Elliot Overton’s videos on oxalates and I listened to them. I also read his articles on this website where he talks about allithiamine, a thiamine supplement that contains something called TTFD, as being something radically different in terms of its unparalleled effects on the human body. I was skeptical, because I had spent about 20,000 euro on supplements in the previous four years, each of them being promoted as health-inducing by big names in the field of chronic Lyme disease, MTHFR, CFS/ME, SIBO and so on, while their effects on my health were only partial and temporary at best.

I decided that this would be the last supplement I’d buy. The worse would be losing 40 euros and I had already spent too much on worthless treatments. I took 150 mg allithiamine + magnesium + B2 + B3 for 3 weeks and I was less tired, could move more around the house, and overall was feeling much better, even my extreme light sensitivity was subsiding. Then I stopped taking it, not sure it was doing anything. That’s when I knew that it had worked and that I needed it badly. I took the same dosage for another 2 weeks. The next three weeks I had to wait to receive it from the USA, and I was again completely bed ridden.

However, I used this time to read most of Dr. Derrick Lonsdale’s book on thiamine deficiency. I became convinced that I had dry beriberi and that most of my neurological symptoms were caused by thiamine deficiency. I also noticed that the dosage is highly individual and some individuals needed very high doses of thiamine per day in order to function.

I now understood, why 2015 was the year I became bedridden for most than 90% of the time: I spent 6 months in a very hot Asian country, as part of my master degree studies. The energy requirement to deal with the hot weather and the demanding job depleted my already low thiamine levels. At that time, I was on my way to diabetes as well. I had fasting blood sugar levels of 120 mg/dl. I could no longer assimilate/use carbs in the quantities my body required (70% of the daily caloric intake) and I was always hungry and always thirsty. Looking back on my childhood and my ever-declining health from 2008 onwards, it was clear to me that I had problems with thiamine.

The Astonishing Effects of Thiamine

In December 2020, I increased my thiamine dosage to 300 mg per day and I was astonished at the changes I experienced – an 80% reduction across all my symptoms and some even completely disappear.

Mid-January, I decided to increase my allithiamine dosage to 450-600 mg because I felt like my improvements were stagnating. I also noticed that during the days I was more physically active (meaning: I cooked food for longer that 10-15 minutes, my energy levels were higher when I was taking more allithiamine and I didn’t experience the typical post-exertional malaise I was used to in the past). I also noticed that taking allithiamine alone in high doses doesn’t work so well and that the active B complex capsules and the B3 I was taking did have an important part to play in how I felt.

In the beginning of February, I was craving sugars so badly, that I gave in and bought a cake for my birthday. I ate two slices and discovered that my mental confusion, the brain fog and generally poor cognitive skills improved “overnight”. I was astonished, since I had been led to believe that “carbs are bad”, “sugar is bad” and “gluten is bad” and that the problem was with the food itself rather than with my body missing some vital nutrients. I didn’t experience any side effects from the gluten either, even though my food intolerance test shows a mild reaction to gluten containing cereals.

By February 20th, this high-dose allithiamine ‘protocol’ and the ability to eat carbs again, eliminated all of my symptoms of SIBO-C/IBS-D/slow transit constipation, endometriosis, CFS/ME, fibromyalgia, constant complicated migraine with aura, severe food intolerances, including a reversal of my poor cognitive skills. I was able to discuss highly philosophical concepts again, for one hour, without suffering from headaches and insomnia.

Early Metabolic and Mitochondrial Myopathies

On February 21^st, I decided to go for a walk. I walked in total that day 500 meters AND walked up four flights of stairs, because I live on the 4th floor without an elevator. By the end of that day, my disease returned and I became bedridden again. I could not believe it. This was the only thing I did differently. I just walked slowly.

And so I searched the internet for “genetic muscle disease”, because my sister shares the same pattern of symptoms. A new world opened before my eyes. I found out that in the medical literature, exercise intolerance, post-exertional malaise and chronic fatigue are well known facts and are described in conditions known as “myopathies”. That there are several causes for myopathy and that they can be acquired (vitamin D or B1 deficiency, toxic substances impacting the mitochondria, vaccines and so on) or inherited. It was also interesting to find out that while doctors manifestly despise and disbelieve CFS/ME symptoms, they are not utterly unknown and unheard of or the product of “sick” minds.

When I read this paper, although old and maybe not completely accurate in the diagnostics, I understood everything about my health issues.

I remembered my mother telling me that my pediatrician said he suspected muscular dystrophy when I was one years old, because I could not gain weight. I weighed only 7 kg at the age of one year, but he wasn’t convinced and so no tests were done in communist Romania. In addition to being overly thin, throughout my childhood, I always had this “limit” that I couldn’t go past when walking uphill or if I ran up a few flights of stairs, no matter how fit and in shape I was. Otherwise, I would develop muscle weakness such that my muscles felt like jelly. I would become completely out of breath, which I now know is air hunger. I couldn’t climb slightly steeper slopes without stopping 2/3 of the way up. My heart would beat very hard and very fast. I would feel like I was out of air and collapse. I first experienced this at the age of 5-6 and these symptoms have been the main feature of my physical distress since.

Because of these symptoms, I have led a predominantly sedentary lifestyle with occasional physical activity, never daily, apart from sitting in a chair at school. I didn’t play with classmates for more than 5 minutes. I couldn’t participate in physical education classes. Any prolonged daily physical activity led to general weakness, muscle cramps, prolonged muscle “fever”, and so I avoided them.

Now, I know why. Since reading this article, I was able to present my entire medical history to a neurologist and my symptoms were instantly recognized as those of an inherited mitochondrial or metabolic myopathy. I am currently waiting for the results of the genetic tests ordered by the neurologist, which will make it possible to get the right types of treatments when in a medical setting.

Before Thiamine: A Long History of Unexplained Health Issues

In addition to the problems with gaining weight and inability to be active, I had enuresis until 9 years old, along with frequent dental infections, and otitis. I had pain in my throat every winter, all winter and low blood pressure all the time. At 14 years of age, I weighed about 43-45 kg. I remained at that weight until age 27. I had a skeletal appearance. I also had, and continue to have, very flexible joints. For example, my right thumb is stuck at 90 degrees, which I have to press in the middle to release. I can feel the bone repositioning and going into the joint. This happens at least once a week.

My diet was ovo-lacto-vegetarian diet, with 70% of the calories coming from carbohydrates from when I was able to eat until 2015. In 2015, I could no longer process carbohydrate due to severe thiamine deficiency.

Since the age of 18, I have had quasi-constant back pain in the thoracic area. I have stretch marks on thighs, but have had no sudden weight gain/loss. Among the various diagnoses I had received before the age of 18 years old:

Idiopathic scoliosis – age 18. No treatment.
Iron deficiency anemia – at 18. Treatment with iron-containing supplements. No result.
Frequent treatments for infections (antibiotics)
Fasting hypoglycemia (until 2015).

The Fibromyalgia Pit

In 2008, my “fibromyalgia” symptoms began, although looking back at my history, many of these symptoms were there all along. I made a big change in my physical activity levels and this began my 12 year decline in health. In 2008, I started my philosophy studies at the university and decided to get more “in shape” by walking daily to and from the university. A total of 6 km per day.

Constant fatigue, no energy.
Worsened back pain.
Weak leg muscles at the end of the day.
Frequent nightmares from which I could never wake up. I felt like I couldn’t find my way out of sleep. After waking up, I would sit down and after 10 minutes I found that my head had fallen on my chest and I had fallen asleep involuntarily, suddenly.
Sensations of waves of vibrations passing through me from head to toe, followed by the sensation of violent “coming out” of the body and out-of-body experiences.
Heightened menstrual symptoms.
Fairly frequent headaches.

Over the summer, I recovered completely as I resumed my predominantly sedentary lifestyle. Then, in the fall, I began walking to and from university again, and my symptoms just got worse. This cycle continued for the next few years. My symptom list expanded to include:

Migrating joint pains.
Frequent knee tendinitis.
Pain in the heels.
Generalized pain, muscles, joints, bones.
Frequent headaches.
Sleep disturbance with insomnia beginning at 2-3am every night.
Frequent thirst, increased water intake (3-4 l/day).
Frequent urination, especially at night (woken 2-3 times).
Bumping my hands on doors/door frames.
Unstable ankles.
Painful “dry” rubbing sensation in hip/femur joint.
Prolonged angry spells.
Memory problems (gaps).
Difficulty learning new languages.

I underwent a number of tests including, blood tests, X-ray + MRI of the spine, and a neurological consultation. All that came back was high cholesterol (180 LDL, 60 HDL), low calcium, iron deficiency anemia, scoliosis, and hypoglycemia. No treatment was offered.

From February 2010-August 2010 I had a scholarship in Portugal. Philology studies interrupted. I was using public transport to go to classes, which were about only 3 hours a day. I required bed rest outside classes with only the occasional walk. I had a complete remission of all symptoms in July 2010 when I returned home and resumed my sedentary lifestyle. This was the last complete remission.

From August 2010 – December 2010, I resumed day courses at both universities and resumed the walking.

All of my symptoms were aggravated enough that by December I was bedridden. I stopped attending classes due to back pain in sitting position. I wrote two dissertations lying in bed. Once again, I sought medical advice and had a number of tests and consultations with specialists. I was diagnosed with peripheral polyneuropathy and “stress intolerance”, fibromyalgia. The treatment offered included:

Medical gymnastics: aerobics, yoga and meditation presumably to get me in shape and calm me down.
Calcium and iron supplementation, gabapentin, and low-dose mirtazapine.

The physical activity worsened symptoms, as it always does. The mirtazapine improved my sleep. I took it for 2 weeks and then stopped because I was gaining weight extremely fast.

From 2011 – October 2012, I was almost completely bedridden. I had to take a year off because I couldn’t learn anything, my head hurt if I tried. The physical symptoms improved after about a year, as did the deep and total fatigue. I tried to get my driver’s license in 2012, but failed. I couldn’t remember the maneuvers and the order in which to perform them. I couldn’t concentrate consistently on what was happening on the road. There was too much information to process very quickly.

From 2012-2015, I was getting my master’s in France. This aggravated all of my symptoms of exertion, both physical and intellectual. In 2013, I underwent general anesthesia for a laparoscopic surgery due to endometriosis, after which something changed in my body and I never fully recovered to previous levels of health. I took another year break between the two years of master’s studies. I couldn’t learn anymore. Symptoms relieved a bit by this break. After three months in Thailand for a mandatory internship, in one of the most polluted cities in the world, I got sick and developed persistent headache, with very severe cognitive difficulties. At this point, 90% of my time was spent in bed.

A general anesthetic in the autumn of 2015 for a nose tumor biopsy was the “coup de grâce”. Since then, I only partially recovered a few hours after a fluid infusion in the emergency ward and a magnesium infusion during a hospital stay in Charites Berlin in 2016. Other improvements: daily infusions of 1-2 hours with vitamins or ceftriaxone.

How I Feel Since Discovering Thiamine

In order to recover from the crash I experienced in February, I increased my B1 (TTFD) intake mid-March and made sure I was eating carbs every three hours, including during the night. I need about 70% of my total caloric intake to come from carbs.

I am currently taking 1200 mg B1 as TTFD, divided in 4 doses, 600-1200 mg magnesium, 500 mg B2/riboflavin, 3 capsules of an active, methylated B vitamin complex, 80-200 mg Nicotinamide 3X per day and 1-2 capsules of a multi-mineral and a multi-vitamin. I make sure I eat enough proteins, especially from pork meat, because it contains high amounts of BCAAs and helps me rebuild muscles.

I walked again the last week of April 2021, 500m in one day, because of a doctor’s appointment. I did not experience a crash that day or the following days. I did not have to spend weeks recovering from very light physical activity.

I can now use my eye muscles again, and read or talk with people online. I can cook one hour every day without worsening my condition.

After 5 years of constant insomnia, only slightly and temporarily alleviated by supplements, I can finally sleep 7.5 hours every night again. I no longer wake up 4-5 times a night.

My wounds are healing and my skin is no longer extremely dry and cracked.

My endometriosis, SIBO-C, gastroparesis, food intolerances, “fibromyalgia” pain, muscle pain due to hypermobility, are all gone.

And to think that all of this was possible because of vitamin B1 or thiamine, in the form of TTFD and that I almost didn’t buy it, because I no longer believed in that ONE supplement that would help me!

I will always be grateful for the work Dr. Derrick Lonsdale, MD, researcher Chandler Marrs, PhD and Elliot Overton, Dip CNM CFMP, have done so far in understanding, treating and educating others about chronic illnesses. More than anything, more than any physical improvement I experienced so far thanks to their work, what I gained was truth. Truth about a missing link, multiple diseases being present at one time and about why I have been sick my entire life.

Physical Symptoms and Diagnoses Prior to Taking Thiamine

Fibromyalgia and polyneuropathy diagnostic and mild, intermittent IBS-C since 2010;
Endometriosis symptoms aggravating every year, two surgeries, stage 4 endometriosis in 2020;
Surgeries under general anesthesia severely worsened my illness and set my energy levels even lower than they were before;
CFS/ME symptoms, hyperglycemia/pre-diabetes, constant 2-3 hours of insomnia per night and constant 24/7 headache since 2015, following an infection and during my stay in a very hot climate;
POTS, Dysautonomia, Post Exertional Malaise Symptoms from minor activities, starting with 2016;
Increased food intolerances (gluten, dairy, sugar/sweets, histamine, FODMAPs, oxalates, Sulphur-rich foods), to the point of eating only 6 foods since 2018;
Chronic Lyme disease diagnostic based on positive ELISA and WB test for IgM, three months in a row, in 2017;
Weight gain and inability to lose weight after heavy antibiotic treatment, skin dryness, cracking, wounds not healing even for 1.5 years, intolerance to B vitamins and hormonal preparations, since 2017;
Complicated migraine symptoms and aura, light intolerance, SIBO-C and IBS-D, slow intestinal transit, following a 4 month period of intermittent fasting that made me lose 14 kg, living in bed with a sleep mask on my eyes 24/7, severe muscle weakness, since 2018;
Two weeks recovery time after taking a 10 minute shower;
Gastroparesis, living on an elemental diet, in 2020;
All my symptoms worsened monthly, before and during my period.

Treatments Tried Prior to Thiamine

Gluten, dairy, sugar/sweets, FODMAPs, histamine, oxalate, Sulphur-rich foods/supplements free diets; AIP, SCD, Wahl’s protocol, candida diets; high dose I.V. vitamins and antibiotics, oral vitamins and antibiotics, liver supplements and herbs, natural antibiotics (S. Buhner’s protocol), MTHFR supplements, alkalizing diet, essential oils, MCAS/MCAD treatment, SIBO/dysbiosis diets and protocols, insomnia supplements, and any other combination of supplements touted as helpful for such symptoms.

And this is just what I remember top of my head. Their effect was, at best: preventing further deterioration of my body, but healing was not present.

Additional Literature

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

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Image by Gordon Johnson from Pixabay.

This case story was published originally on May 11, 2021.

Refeeding Syndrome in the Context of Thiamine Deficiency

by Derrick Lonsdale MD, FACN, CNS

Published on June 6, 2022

27510 views

Refeeding syndrome in thiamine deficiency

Although this has been mentioned many times in posts and in the comments of readers on this website, there still seems to be a lack of understanding. The commonest complaints have been that “thiamine caused side effects” or “I was allergic to thiamine”, inevitably causing the complainant to discontinue it. I want to emphasize the important meaning of these seemingly adverse effects by illustrating a typical case in my own experience. First of all, please understand that thiamine deficiency has its major effects in the lower part of the brain. It is this part of the brain that controls the automatic (autonomic) nervous system that orchestrates the functions of all the organs in the body. Thiamine deficiency has its dominating effect by damaging this system and the result is known as dysautonomia.

Recognizing Thiamine Deficiency Syndromes

One day I was in conversation with a young woman and was trying to describe the huge number of symptoms that result from dysautonomia. When I finished listing them, I was surprised when she said that I had exactly described the symptoms that she had suffered for years. I had no prior knowledge of this, believing that she was completely healthy. She told me that this polysymptomatic condition had been present for as long as she could remember. Apparently it had never been understood by any physician that she had consulted and she had come to accept that it was “just the way that I am made”. She was in her early thirties and it must have required a lot of courage to do the work for which she was employed. Unrelenting fatigue dominated her life, and this is a major clue to her problem.

Symptom Exacerbation: Refeeding Syndrome

I advised her to start taking thiamine and magnesium supplements, starting with a low dose and advising her that the symptoms would become worse for an unpredictable period of time (refeeding syndrome). Note that this individual was known to be intelligent, was fully employed and that nobody was apparently aware that she had any health problems. Later she told me that after she started the supplements, for a month or more she had suffered an excruciating exaggeration of her many symptoms. Trusting that I knew what I was talking about, she persisted with the supplements. This is of great importance because without this information it might be interpreted as “side effects” and the nutrients withdrawn. It also would probably accompanied by anger and the ultimate symptomatic relief never experienced. Using her own words she then said “after about a month of taking the supplements, all my symptoms disappeared and my energy was better than any that I had experienced in my whole life”.

I will try to interpret what was happening here as an example of refeeding syndrome. It is important to understand that the many symptoms experienced by this woman were due to cellular energy deficiency in the brain. Their variability may have included emotional symptoms such as anxiety, depression, or anger without obvious cause because they would be the result of exaggerations of normal brain activity. The lower part of the brain is highly sensitive to energy deficiency and because it organizes all bodily functions, it can give rise to heart palpitations, chest pain, unusual sweating, pins and needles in the extremities, nausea, abdominal pain, vomiting, insomnia, constipation, diarrhea, or abnormal sense of balance including vertigo. Body pain that has no observable cause (hyperalgesia) or a pain response from a stimulus that does not usually cause pain (allodynia) may occur.

Refeeding Syndrome in Children

A 14-year old boy with sugar induced thiamine deficient eosinophilic esophagitis suffered agonies of hyperalgesia and screamed when I touched his abdomen (allodynia). Postural Orthostatic Tachycardia Syndrome (POTS) is quite a common variant which is particularly frightening to the patient. Let me emphasize once and for all, when symptoms like this go unrecognized, sometimes for years, they become temporarily exaggerated if the necessary nutrients are provided in too high a concentration. Whether this be a single vitamin, a group of vitamins or whole nutrition, this syndrome must be expected. A gradual introduction of the appropriate nutrients is mandatory. Because thiamine is so integral to energy metabolism, I found over the years that it was the most important. Because young children have not been exposed to malnutrition for too long because of their age, refeeding syndrome is seldom if ever encountered. The syndrome is directly related to the time of exposure to malnutrition and its severity. It is therefore an effect in adults and occasionally in adolescents..

Whether intelligence is a genetically determined gift or whether it is acquired during life, the brain consumes a disproportionate degree of energy that can only be met by an appropriate ingestion of food and water. If this is inadequate, symptoms begin to register the inadequacy by producing a sense of fatigue as the dominant one. It is the way that the brain signals its lack of cellular energy. The symptoms are easily removed if the underlying cause is recognized early. Because in many cases they are not recognized and the malnutrition may continue, it is not very surprising that cellular damage would be expected gradually to accrue. Perhaps chronic neurodegenerative disease may follow.

From Catabolic to Anabolic Metabolism

The normal states of damage and repair (anabolic metabolism) would be inadequate and a state of gradual breakdown and inadequate repair would be predicted (catabolic metabolism). Because thiamine deficiency causes the condition known as beriberi, I would like to state once more that the English translation of this Chinese word is “I can’t, I can’t”, severe, intractable fatigue being the dominating effect. Although the refeeding syndrome is poorly understood according to current medical literature it is apparently related to a rapid change from catabolic to anabolic metabolism. The misguided attempts to re-nourish the victims in concentration camps at the end of World War II resulted sometimes in their death. It is at least understood that correcting catabolic to anabolic metabolism, whatever produced the abnormal state, demands low doses of food in starvation and low doses of supplementary vitamins in the long term effects of high calorie malnutrition.

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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.

Yes, I would like to support Hormones Matter.

This article was published originally on January 6, 2020.

thiamine deficiency - Page 6

The Rise in Food Sensitivities

Oxalate Problems

Figure 1. High Oxalate Foods

Other Dietary Contributors to Oxalate Buildup: Processed Foods

Figure 2. Oxalate Content in Common Foods

Is Thiamine Really the Problem?

Figure 3. How Low Thiamine Leads to Elevated Glyoxal and Cancer

With Marginal Thiamine

With Sufficient Thiamine

Take Home

Is Your Body Producing too much Oxalate?

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Putting It All Together

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Generation Of Symptoms

A Sense Of Pleasure

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From the Low-Oxalate Diet to Discovering Beriberi Disease

The Astonishing Effects of Thiamine

Early Metabolic and Mitochondrial Myopathies

Before Thiamine: A Long History of Unexplained Health Issues

The Fibromyalgia Pit

How I Feel Since Discovering Thiamine

Physical Symptoms and Diagnoses Prior to Taking Thiamine

Treatments Tried Prior to Thiamine

Additional Literature

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Recognizing Thiamine Deficiency Syndromes

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From Catabolic to Anabolic Metabolism

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