thiamine Archives - Page 5 of 13

Huntington’s Disease and Thiamine: New Research Finds Link

Published on October 9, 2024

11109 views

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

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

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

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

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

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Image created using Canva AI.

This article was published originally on November 8, 2021.

Rest in peace Derrick Lonsdale, May 2024.

Bactrim: An Anti-Folate, Anti-Thiamine, Potassium Altering Drug

by Chandler Marrs, PhD

Published on September 10, 2024

31011 views

A few weeks back we published a case story of young man who developed serious cardiac and neurological symptoms after beginning a course of two antibiotics, Bactrim and Keflex. His symptoms immediately reminded me of beriberi induced by an acute thiamine deficiency. After some digging, I found that at least one of the antibiotics, Bactrim, likely does indeed induce thiamine deficiency by potently blocking both thiamine transporters. This had been only recently and accidently discovered and is clearly not common knowledge. What is common knowledge, however, is that Bactrim is also an anti-folate. This was by design, as blocking bacterial folate metabolism makes for a potent antibacterial, which also just so happens, makes it a viable chemotherapeutic. While it is impossible to rule out the Keflex in his sudden illnesses, as this drug too carries potentially serious side effects, or the combination of the two drugs, I would like to focus on Bactrim for this post, and specifically, its anti-folate and anti-thiamine properties. I believe these aspects of the drug may underlie many its adverse reactions in addition to, and perhaps compounding, those associated with its propensity to induce hyperkalemia.

A Medical Workhorse with a History of Adverse Events

Bactrim, a combination of two antibiotics, trimethoprim and sulfamethoxazole, was first approved in 1968 and 1973 in Canada and the US, respectively and has become a mainstay in pharmaceutical medicine. It is prescribed for everything from acne and UTIs to prophylactic treatments associated with HIV. On average, there have been between 6-7 million prescriptions of this drug written annually from 2007-2017, except for in 2015, where almost 12 million prescriptions were written.

It is one of those antibiotics, that because it has been around for so long, is considered safe and benign. In reality, however, there are a number of serious side effects associated with it including:

Aseptic meningitis – inflammation of the meninges (outer layer of the brain) absent bacterial involvement.
Hemolytic anemia – the destruction of red blood cells more quickly than they can be made particularly in folks with glucose-6-phosphate dehydrogenase (G6PD) deficiency. One study of hospitalized patients found 6 per 100,000 prescriptions resulted in hemolytic anemia.
Methemoglobinemia – decreased blood oxygen saturation via increase methemoglobin.
Delirium, gait disturbances and other CNS symptoms – owing to the ease in which it crosses the blood brain barrier. In one study of elderly patients, cerebral spinal fluid concentrations were ~50% of that in serum.
Stephens – Johnson Syndrome and toxic epidermal necrosis – a potentially life-threatening reaction where the lining of the skin and mucous membranes blisters and necrolyses.
Acute respiratory distress syndrome (ARDS), requiring mechanical ventilation, sometimes leading to organ transplant, often with poor outcomes, including death. This is particularly troubling, as it has been identified in children.
Renal disorders including: hyperkalemia and hyponatremia, and an acute interstitial nephritis, but also, hypertension and cardiac events, sometimes fatal. In immunocompromised patients, the rate of hyperkalemia with Bactrim hovers around 20%. Case studies suggest Bactrim induced hyperkalemia in non-immunocompromised patients as well, though its incidence is neither studied nor reported. In patients who also use spironolactone, a potassium sparing diuretic known for inducing hyperkalemia that is widely prescribed for hypertension, heart failure and for acne, but also as birth control (drospirenone is a spironolactone analog used in the oral contraceptive brands such as Yas, Yasmin and others), the risk of sudden death doubles. Although, the spironolactone + Bactrim > sudden death relationship is studied typically only in the elderly, both drugs are increasingly common in adolescents and young women and may account for a good percentage of the adverse events in these populations that are considered idiopathic. Similarly, the popular angiotensin enzyme inhibitors (ACE) and angiotensin II receptor blockers (ARB) used for hypertension, when combined with Bactrim carry 7-fold increased risk of potentially deadly interactions involving hyperkalemia.

A review published in 2011, identified 925 papers on the adverse effects of trimethoprim and sulfamethoxazole through 2011. Considering that the vast number of medication adverse reactions are rarely identified much less published, almost 1000 papers published suggests something is going on with this medication. While most of the adverse effects of this drug are attributed to its induction of hyperkalemia – high potassium levels via its blockage of the sodium channels in the kidneys, I think that is only part of the story. Another component, as I mentioned previously, involves its ability to block critical nutrients; first as an anti-folate, per its original design, and next quite incidentally, at least as far the published research is concerned, as a thiamine transporter antagonist. The blockade of the metabolism and uptake of these two critical nutrients is key to understanding the spectrum of adverse events associated with it, particularly those not directly induced by the sodium channel blockade that causes hyperkalemia. Although I would argue, deficiencies in these two nutrients would exacerbate Bactrim’s effects on sodium-potassium balance.

Bactrim Blocks Bacterial Folate Metabolism

Folate, or vitamin B9 is essential for DNA synthesis and repair. As such, it is critically important during reproduction for all organisms from bacteria to human. Folate deficiency during pregnancy is associated with serious neurodevelopment aberrations including neural tube defects like spina bifida and thus Bactrim should be strongly contraindicated for pregnant women, but at least one small study found that 3.2% of the pregnant women sampled were prescribed Bactrim.

Folate deficiency at any point across the lifespan may be equally problematic, though less frequently observed, as it provokes an array of symptoms that may attributable to any number of factors. Nevertheless, folate deficiency is linked to immune system dysfunction, dermatological issues, cardiovascular dysregulation, and neurologic problems, including sensory neuropathies with axonal damage. This is addition to a spectrum of neuropsychiatric manifestations from depression to dementia that are associated with this critical nutrient. Importantly, folate and folate products are linked to almost every other metabolic pathway through shared ATP, NAD, and NADP pools inasmuch as they both contribute to the production of NADPH and ATP, and are directly affected by the ratios of these molecules. Folate and vitamin B12 share a particularly close relationship, where deficiency in one, creates a functional deficiency in the other via alterations in methionine pathway leading to megaloblastic anemia. All told, folate is integral for healthy cell function and proliferation, mitochondrial respiration and epigenetic regulation.

Each of the two drugs that make up Bactrim block microbial folate synthesis precipitating complete folate deprivation in bacteria, capable of resulting in folate deficiency non-bacterial cells.

The trimethoprim component of Bactrim binds to a critical enzyme in the metabolism of folate, called dihydrofolate reductase (DFT). This inhibits the reduction of folate into cofactors necessary for DNA synthesis. By binding DHT, dihydrofolic acid (DHF) and then tetrahydrofolic acid (THF) are blocked. THF is essential in one carbon metabolism and the transfer of methyl, methylene, and formyl groups from one molecule to another during the production of nucleotides and amino acids e.g. DNA synthesis and repair.

Sulfamethoxazole also blocks folate metabolism, albeit at a different junction. It is a structural analog of the vitamin-like compound para-aminobenzoic acid (PABA) found in several foods and involved in the metabolism of folic acid. In bacteria, it is a required growth factor. As a structural analog to PABA, sulfamethoxazole binds to and blocks a key enzyme in the folate pathway (dihydropteroate synthetase) thereby inhibiting the conversion of PABA and downstream metabolites critical for folate synthesis and metabolism.

Neither trimethoprim nor sulfamethoxazole alone kill bacteria. They simply prevent bacterial replication. Taken together, however, the combination yields potent bactericidal effects. Bactericidal antibiotics, as a class of drugs and irrespective of specific mechanisms of action, fundamentally and sometimes irrevocably, damage mitochondria.

…it has been demonstrated that major classes of bactericidal antibiotics, irrespective of their drug-target interactions, induce a common oxidative damage cellular death pathway in bacteria, leading to the production of lethal reactive oxygen species (ROS) (4–12) via disruption of the tricarboxylic acid (TCA) cycle and electron transport chain
The overall importance of these observations relates to an expanded mechanism of action, whereby bactericidal antibiotics promote complex redox alterations that contribute to cellular damage and death, while also underlining a common evolutionary and developmental linkage between primordial bacteria and mitochondria (56,57).

Damaged mitochondria, in turn, imperil human health and no doubt, contribute to the vast array of post-antibiotic health issues that have become increasingly common and associated with a number of antibiotics.

Bactrim Blocks Thiamine Uptake

In addition to blocking folate metabolism, the trimethoprim component of Bactrim also blocks thiamine uptake. This was only recently discovered by accident. As part of a study on a cancer drug called Fedratinib, which is known to induce a severe form of thiamine deficiency called Wernicke’s encephalopathy, researchers tested the thiamine blocking capabilities of several drugs that were structurally analogous to Fedratinib. Trimethoprim was among the drugs tested and found to potently block both thiamine transporters. Absent the ability to transport thiamine from diet into the cells, deficiency ensues.

Like folate, thiamine or vitamin B1, is an essential cofactor for key enzymes involved in one carbon metabolism and energy production in all living cells. Thiamine acts as a catalyst and cofactor to all of the enzymatic reactions that participate in oxidative metabolism yielding ATP (see figure 1) and is absolutely critical for glucose metabolism. It also occurs twice in the pentose phosphate pathway (PPP), the alternative glucose oxidation pathway that provides nicotinamide adenine dinucleotide phosphate (NADPH) and ribose 5-phosphate (R5P) for glutathione, nucleic acid, and fatty acid synthesis and steroid hydroxylation, respectively, making thiamine necessary for not only ATP production, but required for duplication and detoxification processes. It is also involved at the alpha oxidation phase of fatty acids, at the HACL1 enzyme and is critical for the metabolism of the branched chain amino acids, leucine, isoleucine, and valine.

mitochondrial nutrients — Figure 1. Mitochondrial Nutrients from: Thiamine Deficiency Disease, Dysautonomia and High Calorie Malnutrition

Importantly, thiamine sits atop these processes, as a gatekeeper of sorts. Its absence or insufficiency thus, derails downstream functions associated the conversion of food into ATP in each of the substrate pathways, glucose, protein, and fats, creating a biological energy deficiency that imperils human health. Insofar as thiamine is only stored in the body for about 18 days, it must be consumed regularly to avoid insufficiency and outright deficiency. Insufficient consumption and/or ingestion of pharmaceutical compounds that block intestinal thiamine transporters responsible for bringing thiamine into the cells, pose a serious health risk that includes death. Mitochondrial ATP is requisite for cell functioning globally, as such decrements to ATP affect every organ and tissue in the body, but are most damaging where a consistent supply of ATP is requisite for survival – in the heart and the brain. That is why, the most serious conditions associated with thiamine deficiency are wet and dry beriberi and Wernicke’s encephalopathy, the condition for which Fedratinib contains a black box warning. More commonly, thiamine insufficiency is associated with a litany of dysautonomic syndromes, although it is not widely recognized as such.

The case story that compelled my investigation into Bactrim included clear symptoms of both wet and dry beriberi, marked by serious dysautonomic function. The bradycardia, chaotic heart rhythm and blood pressure changes were the most acutely dangerous for this individual, particularly if this was accompanied by disrupted sodium and potassium balance, as we can suspect was the case. Had he been older and/or carried additional comorbidities, he might not have survived. He did survive, however, but remains chronically symptomatic of thiamine deficiency 6 years later.

The question one must ask is how presumably healthy individuals develop thiamine insufficiency upon the usage of drugs like Bactrim. That is, how are Bactrim and other thiamine depleting drugs capable of provoking such a rapid decline into fulminant deficiency? Thiamine is, after all, in most enriched and fortified foods. A similar question, how then, even after cessation of the drug do these individuals develop unremitting health issues indicative of longstanding thiamine deficiency?

Absent outright thiamine starvation, most folks consume sufficient thiamine from food to avoid the more acute thiamine deficiencies, but not enough to prevent the more gradual and often chronic thiamine insufficiency syndromes that mark modern medicine and certainly not enough to offset the direct blockage of thiamine transporters from pharmaceuticals like Bactrim, the mitochondrial damage initiated by modern medications (here, here, here, here, and more), environmental chemical exposures and industrial food based toxicants to which we are all exposed. If one’s diet is high in sugars, supplemented with coffee or tea, and/or if alcohol is consumed regularly, the path to thiamine deficiency is expedited.

From this perspective, it is not inconceivable that a significant portion of the population is thiamine insufficient, if not outright deficient. Across different research projects, estimates suggest from 30-70% may have insufficient thiamine intake to meet the demands of daily living and given the corresponding rise in chronic health issues of metabolic e.g. mitochondrial origins, it is not surprising that many are just one medication away from full blown deficiency. To the extent that thiamine is connected to the synthesis of downstream metabolites like folate synthesis, it is not unexpected either, that a background insufficiency in both nutrients would be exacerbated and potentially become deadly with the addition of Bactrim to the mix. Moreover, absent nutrient repletion post antibiotic usage, it is entirely likely that the mitochondrial ill-effects imposed by this drug would become longstanding.

Of Bacteria and Men: A False Dichotomy

Although trimethoprim’s thiamine blocking capability was not known until 2017, had anyone bothered to look at the structure of the compound relative to that of thiamine, it would have been obvious. As far as I can tell, in the 50 years this drug has been on the market, its conformational similitude to thiamine was not considered. Nevertheless, it was well known that Bactrim blocked folate, that folate was critical to human health, and that its deficiency could wreak havoc on health. Why was its actions on folate metabolism not considered problematic? The answer to that question has to do in part to shoddy research and in part to an economically self-serving framework for understanding human physiology that has since become institutionalized into medical dogma. In other words, it was easier and more economically prudent not to question potential problems in the research or the assumptions driving said research than risk losing a useful and lucrative antibiotic.

When trimethoprim was originally discovered and yet still, medicine believed that bacteria were somehow entirely separate from the organism in which they resided. The otherness of potential drug targets holds true to this day.

Although trimethoprim inhibits dihydrofolate reductase in bacteria, it is estimated that an approximately 50,000 times increased concentration of the drug is required to inhibit the human form of this enzyme.”

This notion appears to be based upon a study in 1965, where uptake of the drug and subsequent DHT enzyme binding activity in lab grown bacteria (escherichia coli, staphylococcus aureus, proteus vulgaris), in other animal tissue, and in pulverized human liver cells post autopsy from one individual, were compared. The bacteria won. When trimethoprim was present, folate to DFT was not reduced, even when extra folic acid was added to the media. Remember, in order to get to usable folate – THF, we need the DFT enzyme to work. So, based upon the blockage of the DFT>THF pathway in bacteria, trimethoprim was deemed ‘strongly antibacterial’. Furthermore, it was deemed safe by its apparent inability to block folate in ‘human cells’. It should be noted that the stability of the enzymes from the animal and the human liver cells varied significantly from 25-60%, calling into question the very results upon which this medication was eventually developed and approved. No matter, a potential antibiotic was born and no one was the wiser.

The fallacies upon which trimethoprim safety was based were that bacteria are completely separate from the humans in and on which they reside, that they are solely responsible for illness, and that pharmaceuticals designed to attack said bacteria would affect only their intended targets. None of which are true. While it is true that some of the enzymes within the metabolic pathways in bacteria are different from those in other cells, they still share a degree of similarity, some 30% sequence homology, suggesting enzymes in these cells will also be affected, though perhaps not as strongly as those in the bacterial populations.

More importantly, however, and this speaks to the fallacy of separateness that medicine holds dear, at any given time, we carry with 3–6 pounds of commensal bacteria that are responsible for a myriad of functions, including “protective responses that prevent colonization and invasion by pathogens,” the inhibition of “growth of respiratory pathogens by producing antimicrobial products/signals and competing for nutrients and adhesion sites” and importantly, for our purposes, the synthesis and metabolism of vitamins to be used by the host; the very pathways blocked by these antibiotics.

Several intestinal bacteria in the colon, but also in the small intestine, are capable of biosynthesis of natural forms of folate as well as vitamin B12 and other B-vitamins (Camilo et al. 1996; Magnusdottir et al. 2015; Rossi et al. 2011). It has been shown that specific transporters in the colon actively absorb folate (Said 2013) and as such contribute to folate levels in peripheral tissues and the circulation (Aufreiter et al. 2009; Lakoff et al. 2014; Pompei et al. 2007b). These findings indicate that intestinal bacteria contribute to folate metabolism and that colonic contents represent a substantial and natural source of folate.

We are neither separate from our bacterial communities nor are our vitamin synthesis pathways sufficiently distinct from bacteria that we can target a pathway in one without affecting the other. We carry vast microbial ecosystems whose functions are critical to human survival; vitamin synthesis among them. Indeed, bacterial folate synthesis genes are ubiquitous across the gastrointestinal tract, 13% of which, contain all of the required for complete de novo folate synthesis and almost 40% have the genetic capacity to synthesize folates in the presence of PABA, the upstream intermediate blocked by the sulfamethoxazole component of Bactrim. Importantly, bacterial synthesis of folate and other B vitamins, represents a critical pathway not only for nutrient availability of the human host, but for managing the vast microbial ecosystems in a manner favorable to host survival. Disruption of these ecosystems involving nutrient depletion results in pathogenesis both of the infectious and oncogenic varieties.

Given the large number of gut bacteria in comparison to eukaryotic cells, which also contain evolutionary derived mitochondria (mitochondria are believed to originate from bacteria and as such share similar enzymes and metabolic pathways with them), it would seem that the blockade of these critical nutrient pathways while effectively antibacterial, may also, induce unintended harm. Materially,

…the summated populations of ‘simple’ organisms may in fact regulate the ultimate fate of our genetic material. In sum, it has become compellingly apparent that eukaryotic cells and complex organ systems cannot survive without the synergistic complex interactions of competent enteric bacteria and evolutionarily fashioned mitochondria…

but “go ahead and just cover him with some Bactrim. How can it hurt?”

Postscript

Bactrim is also sold under the names: Septra, Sulfatrim, Septrin, Apo-Sulfatrim, SMZ-TMP and cotrimoxazole.

Although I did not spend any time covering Keflex, the second drug prescribed to this individual, I would like to note that it too damages mitochondria, albeit by different mechanisms. Briefly, Keflex can cause a deficiency in leucine, an amino acid that regulates something called the mTOR receptor, which, when blocked or, in this case, absent its cognate ligand, would downregulate mTOR and deregulate mitochondrial function. The mTOR pathway regulates the balance between protein anabolism and catabolism critical for cell growth and division. Its down-regulation shifts towards catabolism resulting in muscle wasting.

If you experienced a negative reaction to Bactrim and would like to share your story, contact us.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Photo by Haley Lawrence on Unsplash.

This article was published originally on October 20, 2020.

Kawasaki Disease

by Derrick Lonsdale MD, FACN, CNS

Published on September 3, 2024

7993 views

Some years ago, I was confronted with a four-year-old girl as a patient. She had experienced repeated unexplained fever accompanied by a cough, sore throat, diarrhea, and croup. When she came to my attention she had an unusually severe episode of fever with an itchy rash, pain behind the knees and elbows, loss of appetite and abdominal pain. Her respirations were accelerated and the palms and soles were reddened and swollen. Her heart rate was 160 bpm and the blood pressure was 140/80, an extremely high blood pressure for a four-year old child. The laboratory changes were those that are generally associated with inflammation and there were changes in the electrocardiogram, indicating that the heart was affected. Chest X-rays chest showed inflammation in the lung. My interest in diet caused me to make specific inquiries and I found that she had been indulged with ad lib ingestion of sweets. I, therefore, requested the laboratory test known as red cell transketolase, a test for thiamine (vitamin B1) deficiency. It was strongly positive, clearly indicating deficiency of this vitamin. She was subjected to pharmacological doses of vitamin B1 to which she responded clinically.

Kawasaki Disease

The changes in the electrocardiogram, indicating some effect in the heart, the itchy rash and particularly the swollen and red palms and soles, suggested that the disease was a manifestation of that described by a Japanese doctor named Kawasaki in 1974. Today the condition is called Kawasaki Disease. Although it is now known to be associated with inflammation of blood vessels and is often characterized by incomplete and atypical forms, the cause of the disease is still a medical riddle that has eluded scientists for some 50 years. It is reportedly the most common cause of acquired pediatric heart disease in developed countries and the number of cases continues to rise in many parts of the world. In the United States it is estimated that there are 5 to 6 thousand new cases a year, but its true incidence may be unknown. It is also said to be increasing decade by decade in Japan, where there are 12,000 new cases a year.

Febrile Lymphadenopathy and Eosinophilic Esophagitis

The search for a cause in Kawasaki Disease is reminiscent of two cases in children that I encountered. They were both close to the age of six years and had had recurrent episodes of fever, sore throat and swollen glands in the neck, going on for several years. Would anybody in today’s concept of disease believe that it was due to something other than recurrent infection? Both of these children had been subjected to antibiotic treatment, in spite of the fact that there had never been any laboratory evidence of infection. One of the boys had been admitted to a prestigious hospital during a febrile episode and a lymph node in the neck had been removed. It was reported to be swollen, but with a normal structure. No previous questions had been asked concerning diet, but when this subject was addressed, it revealed that both children had been heavily indulged with sweets. Each had overt evidence of an abnormality in thiamine metabolism and no evidence of infection. One child was studied in detail and aside from laboratory evidence of thiamine deficiency he was found to have elevated levels of folate and vitamin B12 in the blood, both of which returned to the normal level when he was treated with thiamine, indicating the metabolic complexity that needed to be addressed. Both responded to pharmacologic doses of thiamine. The recurrent episodes ceased.

Another patient that I reported on this website was a 14-year-old boy whose symptoms for his first eight years of life were diagnosed as psychosomatic. Finally, at the age of eight, upper endoscopy had revealed eosinophilic esophagitis, an increasingly common disease throughout the world, marked inflammatory infiltration of the esophagus. He was addicted to sugar and his red cell transketolase test was highly abnormal, revealing severe thiamine deficiency. He responded clinically to pharmacologic doses of thiamine.

Discussion

We have three different conditions with widely varying symptoms, each nominated as a specific disease entity, but all coming under the umbrella of thiamine deficiency. At first sight this is so illogical in the light of our present understanding about disease that it would be considered a touch of madness. If, however, we look at it in a different light, it may begin to make sense. It is the cells in our bodies that cooperate to form a living person. Each cell has a vital responsibility within the group of similar cells that make up a given organ. I have used an orchestra as an analogy. Each instrumentalist knows exactly what he or she has to do in playing a Symphony. Each has to conform to the musical script and play according to the signals delivered from the conductor. If the conductor sends out the wrong signals, the performance could be a disaster. Conversely, if enough individuals in the first violin section or any other group of instrumentalists are absent or sick, the Symphony would also be a disaster.

To return to the subject of disease, the brain, particularly its lower part, is the conductor of the interplay between body organs and the brain that results in healthy action. It sends and receives signals from the body that enable us to function. A breakdown of energy metabolism in brain cells as depicted by thiamine deficiency, would create a chaotic distribution of signals to the body that might be likened to a breakdown of “the Symphony of Health”. Thiamine deficiency in the brain is exactly like being deprived of sufficient oxygen and it makes the “conductor” abnormally irritable. Some form of mild stress, such as a rapid change in environmental temperature gives a false impression that the subject is being attacked and it orders a full defensive reaction exactly like that initiated by the attack of a microorganism. In a sense, we might describe the whole thing as a “delusion” perpetrated by a sick brain driving the body to defend itself against a ghost.

We have known now for a long time that sugar is a dangerous substance that results in different manifestations of disease. We have also known from experiments that were done by Sir Rudolph Peters in Cambridge in 1936 that adding glucose to live pigeon brain cells caused these cells to start respiration (using oxygen). If those cells had been made thiamine deficient experimentally there was no respiration. Peters called this the catatorulin effect that shows how dangerous it is to take sugar in the presence of cellular thiamine deficiency. Is the explosion in these diseases seen in children a reflection of their being indulged with sweets, often starting in infancy?

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Image credit: Kawasaki_symptoms.jpg: Dong Soo Kimderivative work: Natr, CC BY 2.0

This article was published originally on November 16, 2016.

Rest in peace Dr. Lonsdale.

Poor Nutrition Stress: The Enemy of Health

by Derrick Lonsdale MD, FACN, CNS

Published on August 14, 2024

9107 views

In previous posts, I have indicated that stress can initiate or exacerbate disease and medication or vaccine adverse reactions. Read that statement, you might think I am attributing the onset of serious disease and adverse reactions to a psychosocial cause. That is not the case. Stress comes in a myriad of forms, some external, some internal, and although much of what we call stress relates to psychosocial responses to perceived threats, I think stress encapsulates so much more. At its most fundamental level, stress represents a physical state where the body is performing less than optimally. Let me explain.

What is Stress?

I define the word “stress” as a physical or mental force that is acting upon you. An example of mental or psychosocial stress might be an insult from a person, meaning that the stress comes from a source outside the body. On the other hand, it might be the realization that a deadline has to be met, a mental source from within. Any form of injury is an obvious source of physical stress. Physical action such as shoveling snow is another form of stress, demanding energy consumption imposed by the individual who wishes to get rid of the snow. Being infected with a virus or by bacteria is a form of stress that demands a defensive reaction. In each of these instances, the body reacts to the inflicting stressor. Sometimes, when the resources are available, it reacts efficiently. Other times, when the resources are not available or when additional factors intercede, the body’s response to the stress is ill-adapted.

Your Body is Your Fortress, Your Immune System the Soldiers

Perhaps an analogy might help to provide an explanation for the remarks that follow. I imagine the body as being like an old fashioned fortress. The people living within it go into action when the fortress is attacked by an enemy from outside. It would be of little use if the defense soldiers went to the eastern battlements if the attack came from the west and so there had to be a central figure that would coordinate the defensive reaction. The nature of the attack would be spotted by a guard on duty and the central figure informed by messenger.

The body represents the fortress and the lower part of the brain represents the central figure that coordinates the defense. The cells in the blood known as white cells can be thought of as soldiers, armed with the necessary weapons to meet the nature of the enemy. Suppose, for example, a person’s finger is stuck by a splinter carrying a disease bearing germ. The pain, felt in the brain, recognizes its source and interprets it as a signal that an attack has occurred. White cells in the area can be regarded as the “militia under local command” and a “beachhead” is formed to wall off the attack. The white cells sacrifice themselves and as they die, they form what we call pus. If the beachhead is broken and the germs manage to get into the bloodstream, it is then called septicemia and the brain/body goes into a full defensive reaction where high fever is the most obvious result. Such an illness is an attack/defense battle.

The symptoms that develop from such an infection represent the evidence for this defense, feeling ill, pain and developing a fever are excellent examples. Micro-organisms are most efficient at 37° C, the normal body temperature. The rise in body temperature, initiated by the brain, makes the microorganisms less efficient and may kill some of them. One therefore has to question the time honored method of reducing the fever, during illness, as being an example of good treatment. While reducing fever improves the symptoms caused by the infection, it also reduces the efficiency of the immune battle raging within.

The outcome against the stressor is death or recovery; although it is possible sometimes to end up in a kind of stalemate, represented by prolonged symptoms of ill health. Chronic illness may be viewed as the immune system’s inability to eradicate fully the stressor.

Poor Nutrition and Stress

As I have emphasized in previous posts, the autonomic (automatic) nervous and endocrine systems are used to carry the messages between the body and the brain that enable the defense to be coordinated. This demands a colossal amount of cellular energy, no matter the nature of the stress. That energy to fight stress comes from oxidation of the fuel that is provided from nutrition. Of course, the greater the stress the greater the energy demand, but in the end the equation is quite simple. If the energy required to meet the stress is greater than the energy that is supplied, there must be a variable degree of collapse within the defensive system. That collapse presents as intractable symptoms, where the body is unable provide the energy needed to sustain health. This is the secret of the autonomic dysfunction in the vitamin B1 deficiency disease, beriberi. It is also the secret behind the initiation of POTS because both conditions are examples of defective oxidation. You can read more details regarding thiamine deficiency, beriberi, POTS and other health issues from previous posts on this website

High Energy Demands Equal High Nutritional Demands

Nutrient density of diet might appear to be perfectly adequate for a given individual, but inadequate to meet the self-initiated energy demands of a superior brain/body combination in a highly active individual such as an actively engaged student or athlete. Our genetic characteristics, the quality of nutrition and the nature of life stresses each represent a factor that all combine together to give us a profile for understanding health and its potential breakdown.

Epigenetics and Mitochondria: The Stress of Our Parents

Epigenetics, the science of how our genes are influenced by diet and lifestyle, is relatively new. Epigenetics considers the possibility that genes can be activated and deactivated by nutrition and lifestyle. Stress can come in many forms, from psychosocial trauma, poor nutrition, environmental and medical toxin exposures, to infections. Stress impacts how our genes behave. Even though one may inherit a hard-coded genetic mutation from a parent, that mutation may not be activated unless exposed to a particular type of stress. Similarly, an individual who may have no obvious illness-causing genetic abnormalities but stress, in the form of nutritional depletion, exposures or trauma, can turn on or turn off a set of genes that induce illness. What is remarkable about epigenetics is the transgenerational nature of the stressors. The memories of stressors affecting our parents and even our grandparents can affect our health by activating or deactivating gene programs.

We also have to consider the state of our mitochondria, the “engines” in each of our cells that produce the energy for cellular function (to learn more about mitochondria and health, see previous posts on this website). Mitochondria have their own genes that are inherited only from the mother. Damage to the DNA that makes up these genes sometimes explains the similarity of symptoms that affect a given mother and any or all of her children. For example, although this damage may be inherited, we also have scientific evidence that thiamine deficiency, known to be the result of poor diet, can damage mitochondria. A bad gene might be the solitary cause of a given disease, but even where this is known as the cause, the symptoms of the disease are sometimes delayed for many years, suggesting that other variables must play a part. A minor change in cellular genetic DNA might be alright to meet the demands of normal living, but impose a risk factor that could be impacted by prolonged stress or poor nutrition, and disease emerges.

Nutrition is the Only Factor that We can Control

The imposition of stress on any given individual is variable, most of which is accidental and out of our control. Therefore, if we represent these three factors, genetics, stress and nutrition as three interlocking circles, all of which overlap at the center of such a figure, there is actually only one circle over which we have control and that is nutrition. We now know from the science of epigenetics that nutritional inadequacy can affect our genes. By examining the mechanism by which we defend ourselves against stress, we can also see the effect of poor nutrition.

Poor Nutrition Equals a Poor Stress Response

Using these three variables, perhaps we can begin to understand several unanswered questions. Why does a vaccination negatively affect a relatively small percentage of the total population vaccinated? Or why do some medications negatively impact only some individuals? It might be because of a genetic risk factor or because of a collapse of the coordinated stress response related to quality of nutrition or a combination of both. Why does a vaccination tend to “pick off” the higher quality students and athletes? Again, the same kind of answer; high quality machinery demands high quality fuel. Since the limbic system of the brain has a high energy demand and represents the computer that coordinates a stress response we can understand the appearance of beriberi or POTS and cerebellar ataxia, all examples of a deviant response to stress. Nutrition, therefore, should not be looked at as supplement to good health, but as the foundation of health. When disease or medication and vaccine reactions emerge, efforts to identify and then restore nutritional deficiencies must be the first line of immune system health. Without critical nutrients, the body simply cannot mount a successful stress response and the battlefield will expand and eventually fall.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Image by Pedro Figueras from Pixabay.

This article was published originally on May 6, 2014.

Sleep Requires Energy

by Derrick Lonsdale MD, FACN, CNS

Published on July 23, 2024

25645 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.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Image by freestockcenter on Freepik.

This article was published originally on October 14, 2019.

Recurrent Fever With Swollen Glands: Febrile Lymphadenopathy and Thiamine

by Derrick Lonsdale MD, FACN, CNS

Published on July 10, 2024

14362 views

fever swollen glands - Febrile Lymphadenopathy.

Every profession has its jargon and the medical profession is no exception. Perhaps it is even more addicted to jargon than other professions. The title used here refers to an extremely common disease, particularly in children. Febrile is the word used to describe fever. Lymphadenopathy simply means that lymph glands are swollen. The mechanism is as follows: the throat becomes infected, often with streptococcus and may affect the tonsils or adenoids. A message is sent from the throat to the brain that reacts to cause the body temperature to be raised. We will see why later. The lymph glands in the neck are stimulated to get bigger as part of the immune response. The child feels sick and accepts bed rest and these essentially defensive reactions are referred to as the “illness”. Often a treatment such as aspirin is given to the child to bring the temperature down under the mistaken concept that this is the dangerous part of the illness. A previous post on this website described a case of Reye’s syndrome, a deadly disease known to occur as a result of giving aspirin to bring the fever down. It is of course true that a very high temperature such as 106°F is considered to be dangerous. But this is because the brain mechanism that initiates this temperature is itself in an abnormal state and may be the actual source of the danger.

Understanding Fever as an Immune Response

If we look at this situation in the cold light of day, we can come to false conclusions. Yes, this is the expected situation with an infected throat and it is invariably treated with antibiotics. But let us see what is really happening in all cases of this common affliction. The brain has received a message from the throat that an attack by a microorganism is occurring. The brain sets up a defense mechanism and I refer to the microorganism as a “stressor” (the enemy). The brain is programmed to recognize the attack as dangerous to the organism. The physical aspects of the infection and the brain mechanisms that receive the message and activate the defense are in constant communication. The body temperature is raised by the brain as part of this defense.

Microorganisms, the stressors, are programmed by Mother Nature to operate at maximum efficiency at 37°C, the normal temperature of the human body. By raising the body temperature, the environment for the microorganisms is detrimental to its action and decreases its virulence. No rise in body temperature indicates that the brain is sick!

Inflammation Is an Immune Response: Resting Boosts Immune Function

The inflammation of the throat makes it harder for the microorganism to gain entrance and is also part of the defense. Strangely enough, we now know that inflammation is controlled and governed by the brain. A message to the lymph glands in the neck increases their size to cope with the expected passage and trapping of bacteria from the infected area and is part of the immune response.

The bed rest or fatigue that occurs with illness is yet another part of the immune mechanism. Bed rest conserves the cellular energy needed to activate the defense mechanisms.

You can readily see that all of these reactions that we call sickness are scripted and controlled completely by the brain. It may come as a surprise to many readers, but fever, inflammation and energy conservations are necessary immune reactions. Diminishing or overriding those reactions, usually by trying to reduce fever with a drug or failing to rest rather than assisting the body’s defense systems, may only prolong the illness and perhaps even create new ones.

The modern method of treatment is, of course, to kill the organism. Little thought is given to whether the supply of energy in the brain is sufficient to run the complex organization of defense. It also assumes that the genes that oversee the immune response are intact and functionally healthy.

Nutrient Interactions With Immune Response

Now I must tell you about two children, both of whom had suffered from repeated episodes of febrile lymphadenopathy (Lonsdale D. Recurrent febrile lymphadenopathy treated with large doses of vitamin B1: report of two cases). Each child had been treated by antibiotic therapy with their recurrent episodes over a two or three-year period on the assumption that they were caused by bacterial infection. Both were medical puzzles because evidence of bacterial infection was lacking and it was assumed that the recurrent episodes were viral in nature. I had the opportunity to study one of them in detail.

The child had been admitted to a prestigious hospital and a swollen gland in the neck had been biopsied under the impression that it might explain the disease. The pathologist had reported an enlarged but otherwise perfectly normal gland structure. The mother told me that at this hospital he had also had the concentrations of vitamin B12 and folic acid measured in the blood, presumably because they were looking for evidence of deficiency. She volunteered that “the doctors told me that I was giving him too many vitamins”, apparently because the two vitamins had been found to be in an unusually high concentration. She also volunteered that this was very strange to her “because I had not been giving him any vitamins at all. The doctors didn’t believe me”. This naturally intrigued me.

Without going into the technical details, I found that he had evidence of abnormal thiamine metabolism. The folic acid and B12 concentrations were indeed extremely high. When I gave him the big daily doses of thiamine, these two vitamins each fell into its range of normal blood concentration. I discharged him from the hospital where these studies had been carried out, continuing the high dose treatment with thiamine. Two or three months later, the mother called me to say that her child had not had any episodes of fever and was extremely well. I responded to her by asking if she was interested in stopping the thiamine in the interests of science. She did stop it and three weeks later he had an episode of sleep walking, spontaneous urination as he went down the stairs and another episode of febrile lymphadenopathy.

You may well ask how the sleep disturbance could possibly be associated with the throat problem, so continue reading. I readmitted him to the hospital and clinical examination revealed the sore throat and a very large lymph gland in the neck. The folic acid and B12 concentrations were once more elevated. I restarted the thiamine and the two vitamin concentrations again fell into the normal range. The enlarged lymph gland disappeared and I discharged him from the hospital with instructions to continue the high dose thiamine. About a year later she reported that the episodes had begun again. I told her to add a multivitamin to the thiamine and again the episodes ceased. The other child also had evidence of abnormal thiamine metabolism that was resolved by the administration of large doses of thiamine, but unfortunately, I was not able to study him further. Please note that both children had been indulged with ad lib candy and soft drinks.

Nutrient Deficiency in the Face of High Sugar Intake: Altered Immune Responses

The explanation is construed from a rational approach to the genius of Mother Nature. I have already described the normal mechanism of defense to infection organized by the brain. Think of the body as being like an old-fashioned fortress. When an approaching enemy is spotted by soldiers on the Eastern battlements, a message is sent to the commander. The commander is then able to plan the defense and off duty soldiers are deployed to the scene of impending attack. Imagine that the commander is drunk and he sends the reserve soldiers to the Western battlements. Or perhaps the commander imagines falsely that he has received a message and deploys his defensive soldiers throughout the fortress unnecessarily, a “May Day” without reason. Obviously the commander would be to blame.

This is an analogy for the brain/body response to infection. Messages throughout the body are automatically relayed through the autonomic (automatic) nervous system and by the hormones released from the endocrine glands. Hormones, carried in the blood stream, are messengers. White blood cells are “the defending soldiers”. Both the autonomic and endocrine systems are under the control of the more primitive lower part of the brain, the commander in the analogy and the part of the brain that is known to be peculiarly sensitive to thiamine deficiency. There is good scientific evidence that thiamine deficiency will make the “commander” much more sensitive to incoming signals from the “battlements”. Like the “drunk commander”, it organizes a complete defensive reaction without there being any need.

To be a little more scientific, thiamine deficiency causes reactions in the lower brain that are exactly like a mild to moderate deprivation of oxygen. That is why thiamine deficiency is reported scientifically to cause pseudo-hypoxia (pseudo, false: hypoxia, deficiency of oxygen). These children had been indulged with ad lib. candy and soft drinks. Even if they had had the average intake of thiamine from the diet, essential to the processing of sugar, it was insufficient to metabolize the sugar. You might say that this was an increased sugar/thiamine ratio, equivalent to dietary thiamine deficiency with a normal healthy diet.

Microorganisms Attack: The Immune Response Defends

Each case of the usual form of febrile lymphadenopathy can be visualized as a hostile attack by a microorganism (a stressor) requiring a defense response. However, in the case of these two children, when the brain ”commander” was exposed to thiamine deficiency (pseudo-hypoxia), itself imposing brain stress, it became hypersensitive to virtually any form of incoming signal from the environment. It is therefore possible that a change such as ambient temperature was being perceived falsely as a dangerous threat to the organism (the patient). Hence, it is hypothesized that any proposed minor form of stress initiated the defensive response, mediated and organized by the lower brain that is programmed to perceive danger. It is possible that a virus in each case may or may not have been responsible for being the “stressor” but it is more likely that the “commander” was initiating an unnecessary defense based on a false perception of a non-existent attack such as ambient temperature change.

I have to turn to analogy once more. A car has an engine. Its essential function is to produce energy. The energy has to be transmitted to the wheels through individual mechanical parts that are connected together to form an energy consuming transmission. In the human body each cell has its own engines and they are called mitochondria. Their function is also to produce energy that has to be converted into mental and physical action. Thiamine is essential to energy production from the mitochondria and a series of enzymes are the equivalent of the mechanical parts of the transmission in a car and therefore can be thought of as an energy consuming biochemical device. Therefore, mitochondria produce energy; the transmission consumes it in mental and physical action. Folate (folic acid) and vitamin B12 are essential to this biochemical transmission. Because thiamine deficiency depletes cellular energy, the enzyme dependent (energy hungry) transmission developed problems. Folate and B12 accumulated in the blood simply because they were not being used. When thiamine was given to this boy, cellular energy improved and the two vitamins were consumed in their actions and their concentrations decreased in the blood.

Sleepwalking: An Example of Brain Dysfunction?

Sleepwalking has always been a puzzle. A sleepwalker is not consciously aware of what he or she is doing. I remember the case of a man who drove his car for 70 miles and had no recollection of doing it. I had found from my clinical experience that sleepwalking children would stop doing this with the administration of nutrients, particularly thiamine and magnesium. The fact that the subject of this discussion urinated as he descended the stairs indicated abnormal automatic autonomic nervous system activity. This was pretty good evidence that it was oxidative deficiency in the brain that was responsible for both physical and mental abnormal activity after therapeutic thiamine had been withdrawn.

The Use of a Multivitamin: Completing the Nutrient Team

As the story above indicated, the episodes of febrile lymphadenopathy began to return about one year after he had been discharged with instructions to take only thiamine. There is a particular relationship between thiamine and magnesium because both of them are cofactors together for the same enzymes. However, vitamins and minerals are non caloric nutrients that work as a complex team. There might still be nutrients in naturally occurring food that await discovery. Mother Nature knows how they all should be balanced. The further we move from our biologic origins by the introduction of artificial foods in our hedonistic pursuit of pleasure, the more illness can be expected. Our present medical model is concerned only with killing the attacking agent. Rather simple clinical research revealed an anomaly of this nature in the organization of defense, without knowing how common it is. It should surely focus our attention on the role of nutrition in providing the raw materials for this organization. An infection gives rise to a battle. There are only three possible outcomes: the enemy wins: the defense wins: there is stalemate. The stalemate possibility suggests that chronic long term infection can be tackled by the use of energy producing nutrients that improve the efficiency of a defensive program.

Unfortunately, there are problems with what appears to be a simple solution. Even natural food does not have the nutrient density that it used to have because of changes in farming practices. Also, whether we like it or not, evolution is going on all the time and in the modern world, the smartest brains have the greatest evolutional advantage. Those interested in following the numerous posts on this website will note that post Gardasil thiamine deficiency appears to affect the brightest and the best. I have suggested that relatively poor nutrition, coupled with a smart brain, creates a greater risk of succumbing to a risk from vaccination, mild infection or trauma.

I have seen several articles that state the uselessness of dietary supplements, claiming that the numerous vendors are cheating the public. My own library research reveals numerous papers on the subject of supplementary nutrients coming from many parts of the world other than America. Although they are not cheap, the expense is very much less than the drugs issued by pharmaceutical companies and their curative or preventive properties are huge. Humanitarian research in this area of relative ignorance is a modern necessity.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Photo by Kelly Sikkema on Unsplash.

This article was published originally on April 19, 2016.

A Question of Responsibility in Health and Disease

by Derrick Lonsdale MD, FACN, CNS

Published on June 5, 2024

5768 views

Self-responsibility is much needed in the quixotic culture that surrounds us today. It should begin to be acquired even in infancy as we learn to navigate life. The difficult job of parenthood, perhaps the most important one of all, has to be undertaken without previous experience or training. In former years the wisdom of grandparents was sought avidly when families tended to remain in the same locality. Geographic separation has caused them to be largely discarded.

This post states that there is no more important example of self-responsibility than in maintenance of health. When we are struck down by disease, we have been taught that it is purely an act of nature: that it has nothing to do with our own actions. It is regarded as bad luck or an inevitable effect of genetic predisposition. We have also been taught that when we get sick, whatever the cause may be, that the wonders of modern medicine will take care of it. We accept a prescription as a birthright, often without seeking why it is being prescribed or how it is expected to cure us. Is that really how we want to live?

Self-Responsibility is Critical to Health

When I emphasize dietary indiscretion as the harbinger of ill health, some readers will say, “oh yes, we’ve heard all that stuff before. It is so boring”, not even bothering to read further. So let us use an analogy that I have used before in posts on this website. You have bought a car and the owner’s manual tells you that the engine uses regular gas. However, a friend has told you that high octane gas increases acceleration and makes the car livelier. You have decided that the feel of the car with high octane gas appeals to you, even though you have also been told that it increases the wear-and-tear on the engine, possibly leading to an eventual breakdown. With that knowledge, you are faced with a choice. If your decision is to continue using a fuel for which the engine has not been designed, it might be referred to as indiscretion, or even lack of self-responsibility. When the forecast of breakdown becomes a reality you might even blame the car maker. Cursing the necessary expenditure, you might expect a skilled mechanic to repair the damage, even forgetting that it may have been your own fault. Could this be compared with dietary indiscretion? Of course, you need to have the knowledge of how and why the “wrong choices” do, in fact, result in health breakdown. If you persist in making those “wrong choices”, are you in fact exercising self-responsibility towards your own health?

Natural Sugars versus Sugary Sweets

However we arrived on the face of the earth, we could not have survived if the fuel had not been available to us. Anthropologists tell us that our ancestors were “hunter gatherers”. The food (fuel) was provided by Mother Nature in the form of nuts, seeds, roots, leaves and fruits. In particular, there was no such thing as sugar in a free state. It was locked up in the fruit and leaves. There are at least 40 or more nutrients in natural food that are mandatory to the maintenance of health and many may not even have been discovered yet. None of them are contained in the highly processed, heavily sweetened substances we call food.

Where did we go wrong? Believe it or not, sugar is the villain. We can now go on the Internet and are told repeatedly that it is more addictive than cocaine and yet 80% of the artificial foods on the shelves of a groceries store contain sugar. In fact, these “foods” would not sell unless they were sweet to the taste. People are so bored with hearing this that it is virtually ignored. Because the characteristic symptoms develop slowly and do not produce abnormal conventional laboratory studies, the connection is almost invariably lost. When symptoms do emerge, they are often mistakenly diagnosed as psychosomatic, for which the standard treatment is a prescription for one of the many tranquilizer pills. Self-indulgence as the cause is never considered by patient or physician.

Of Different Fuels

Let’s try to keep it simple by turning once again to analogy. Gasoline in a car engine has to be ignited. The explosion that occurs represents a union of gasoline with oxygen. The resultant energy has to be captured in a cylinder in order to drive a piston. This connects with a flywheel that transmits the energy to the wheels through a transmission. Our bodies have exactly the same problems but the mechanisms are widely different. Glucose, derived from simple sugars, is the primary fuel of our cells, particularly in the brain. It is “ignited” by uniting it with oxygen and this is done by means of an enzyme. In order to function properly, this enzyme requires the presence of vitamin B1 (thiamine) and magnesium. You could say that thiamine and magnesium “ignite the glucose”, releasing energy in the form of electrons. The energy from electrons synthesizes a kind of energy currency known as ATP. This works a little like a battery. Chemical energy derived from “burning” (oxidizing) glucose must be transduced to electric energy for physical or mental function. If those nutrients are not present, the sugars remain unprocessed, free to evoke the host of modern disease processes that fall under the rubric of Type 2 diabetes.

Returning to our engine analogy, many car owners will remember that they had to use a mechanism called a choke when starting the cold engine. This resulted in a temporary high concentration of gas. Perhaps it will be remembered that if and when the choke was not released or discontinued when the engine had warmed up, the engine would run distinctly badly and black smoke would emerge from the exhaust pipe. The black smoke represents inefficient combustion of the gasoline. Therefore, there should be a much lower ratio of gasoline to oxygen when the engine has warmed.

Cellular Engines Need Fuel

Each of all our cells have “engines” called mitochondria that generate energy. They work constantly, do not have to be started like a car engine and are always warm. They do not need a choke. When we take an excess of calories that do not contain the necessary vitamins and minerals, it is exactly like choking our mitochondria, creating inefficiency of energy production. This is particularly true of sugar that overwhelms the ability of vitamin B1 to “ignite” it. Inefficient combustion (oxidation) gives rise to organic acids that are the equivalent of black smoke in the car exhaust and they can be found in the urine. This inefficiency of energy production affects the part of the brain that is responsible for our ability to adjust ourselves (adapt) to the changes that occur in our environment. We develop functional changes such as “brain fog”, palpitations of the heart, unusual or excessive sweating and “goosebumps” may appear on the skin. We may have a drop in blood pressure, associated with a fainting attack. Because the standard laboratory tests are normal, it is concluded that the symptoms are psychosomatic.

I remember the case of an adolescent whose diet contained a lot of “junk foods”. He climbed a rope in the gymnasium, entailing the consumption of energy. When he came down he passed out and was removed to the nearest hospital. Without knowing that he had vitamin B1 deficiency, they gave him intravenous fluids containing glucose. He had eleven bloodstained bowel movements and died. Giving sugar to somebody who is deficient in vitamin B1 is extremely dangerous and the trouble is that ingestion of sugar leads to vitamin B1 deficiency. There is considerable evidence that dietary indiscretion of this nature, continued over years, may eventually give rise to a brain disease that is given a name. Alzheimer’s, senile dementia, Parkinson’s disease and other well-known scourges may well be the legacy in your later years.

What We Eat and Drink Matters

In light of this discussion, who is responsible for the current health crisis? While it is tempting to blame others, and certainly the food and pharmaceutical industries benefit greatly from our incessant need to indulge, the blame ultimately must reside with each of us. We have abdicated our responsibility to manage our own health. Like the car owner who ‘likes the feel’ he gets from his car with high octane gas, we like the feel we get from when we eat sweets and other junk foods. Ultimately though, without the correct fuel, engines clog and sputter. Whether those engines reside in our vehicles or in our bodies, absent the correct fuel, damage accrues. It is a relatively simple equation, but one that requires a modicum of self-awareness and responsibility. Unfortunately, I am afraid self-responsibility seems to have disappeared from modern concepts of health and disease. I suspect that until it is found and embraced again as core human value, diseases of consumption and indulgence will continue to flourish.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Image by Tumisu from Pixabay.

This article was published originally on December 7, 2016.

Dr. Derrick Lonsdale passed away on May 2, 2024. He will be missed.

Hyperglycemia and Low Thiamine: Gateways to Modern Disease

by Chandler Marrs, PhD

Published on May 2, 2024

4682 views

Thiamine deficiency, hyperglycemia gateway to disease

In Thiamine Deficiency in Modern Medical Practice and Threats to Thiamine Sufficiency in the 21^st Century, I introduced the concept that thiamine deficiency underlies many common conditions plaguing modern healthcare and identified exposures and mechanisms threatening thiamine stability. In this document, I will tackle the pattern of metabolic changes associated with the modern dietary practices leading to thiamine insufficiency, and resulting in, and sustaining hyperglycemia.

Hyperglycemia Through a Different Lens

Hyperglycemia, and the metabolic dysfunction it initiates, is a worldwide problem that has reached epidemic proportions. Due in part to overconsumption of sugary foods and in part to decrements in mitochondrial capacity that drive cravings for sugars, hyperglycemia fuels the metabolic derangements underlying obesity, type 2 diabetes, cardiovascular disease, and more recently, research suggests Alzheimer’s disease as well. These interconnected disease processes represent the top leading contributors to morbidity and mortality.

Conventional wisdom attributes these disease processes to over-nutrition and the solutions that follow involve the restriction of calories and/or the medical manipulation of the pathways initiated by hyperglycemia. Admittedly, excess caloric intake is a component, but this nomenclature suggests an overly simplified concept of nutrition; one where all that matters is calories consumed relative to calories burned. This view obfuscates the role of micronutrients in the conversion of these calories/foods into adenosine triphosphate (ATP), the energy source for all cells. It ignores the fact that the aberrant cascades so commonly associated with hyperglycemia, are merely adaptive responses to the lack of micronutrient availability and consequent reduction in ATP. Finally, through this lens, the entirety of the blame for overeating is placed upon the individual.

In reality, while the initial choices that precipitated the hyperglycemia may have been the individual’s responsibility, once these patterns become entrenched molecularly, the resulting decline in ATP drives the cravings for high-calorie foods to compensate. In a very real way, these patients are starving despite sufficient or even excessive caloric intake. It is high-calorie malnutrition, but malnutrition nevertheless. Viewed from perspective, hyperglycemia is not a disease of excess, per se, but rather, one of deficiency. As such, the opportunities for treatment are expanded beyond the typical trend to reduce, block, or otherwise override a particular pathway, and shifted towards a rebalancing of metabolic health. Here, the question is not so much which pathways should be blocked to stave off the associated deleterious effects of hyperglycemia, but rather, what does the patient need to more effectively metabolize foods into energy? What is missing from his/her diet that will reduce the body’s drive for sugars as its primary energy source? In other words, what does he or she need to be healthy?

To answer those questions, one has to look more closely towards bioenergetics and ask what micronutrients are needed to convert consumed foods into ATP and whether or not the patient’s diet provides those nutrients. Research suggests that the energy metabolism enzymes from the cytosol through the mitochondria require at least 22 micronutrients to utilize the macronutrients from consumed foods to produce ATP. Many of these micronutrients are in short supply with high carbohydrate diets (see Threats for details). Thiamine is top among them, and because of its gateway role in energy metabolism, thiamine insufficiency is a significant contributor to the disease processes currently attributed to hyperglycemia.

Thiamine, Sugar, and Energy Metabolism

Thiamine is a required and rate-limiting co-factor to five enzymes involved in energy metabolism, including those at the entry points for the glucose, fatty acid, and amino acid pathways (transketolase, pyruvate dehydrogenase complex [PDH], 2-Hydroxyacyl-CoA lyase [HACL], and branched-chain alpha-keto acid dehydrogenase [BCKAD] and alpha ketoglutarate dehydrogenase [a-KDGH]. Insufficient thiamine leads to poor glucose handling resulting in hyperglycemia. It also induces poor protein and fatty acid metabolism resulting in the elevated branch-chain amino acids and dyslipidemias common to patients with hyperglycemic metabolic syndrome.

Conversely, high carbohydrate diets increase the demand for thiamine, which, if left unchecked, ultimately leads to thiamine deficiency, hyperglycemia, disturbed protein, and fatty acid metabolism. In healthy, thiamine-sufficient adults, high carbohydrate consumption results in a significant reduction of mean plasma thiamine concentrations in just over three weeks. Over the longer term, a high carbohydrate diet initiates many changes in thiamine and energy metabolism that ultimately result in reduced thiamine availability, higher circulating glucose, and poor energy metabolism. Thus, whether by cause or consequence, low thiamine and hyperglycemia are inextricably intertwined. One eventually leads to the other.

Altered Metabolism and Mechanisms of Damage

Under normal glycemic conditions and where thiamine is sufficient, excess sugars from glycolysis are shuttled through the pentose phosphate pathway via the thiamine-dependent enzymes transketolase to PDH and onward through the mitochondria. Under conditions of high carbohydrate intake/low thiamine, however, these sugars are diverted away from the primary metabolic pathways used for ATP production, inducing a net decline in ATP, and away from the synthesis of ribonucleotides and NADPH, substrates for RNA/DNA, and fatty acid metabolism and ROS detoxification respectively, to secondary metabolic pathways, specifically, the polyol/sorbitol, hexosamine, diacylglycerol/PKC, advanced glycation end product (AGE) pathways. Research suggests the upregulation of these pathways underlie the macro-and microvascular cell damage attributed to hyperglycemia, related cardiovascular and neural damage, while the decrements in ATP drive the general metabolic dysfunction associated with obesity and a host of other inflammatory conditions.

The high carbohydrate/low thiamine diet disturbs amino acid and fatty acid metabolism as well. Elevated branched-chain amino acids (BCAA) are common with hyperglycemia. Indeed, elevated BCAA may predict impending diabetes. Underlying the elevated BCCA is impaired catabolism due to a genetic or environmentally triggered defect in the BCKAD enzyme. BCKAD is dependent upon thiamine and elevated BCCAs are a manifestation of deranged energy metabolism precipitated by thiamine insufficiency. Genetic aberrations of BKCAD display similarly elevated BCAA, though typically much earlier, and respond favorably to thiamine supplementation.

With chronic hyperglycemia, the increased branched-chain keto acids, a secondary effect of poor BCAA catabolism, lead to excess short and medium-chain acylcarnitines. Surplus acylcarnitines increase the flux of fatty acids through the b-oxidation pathway beyond its capacity. This results in incomplete fatty acid metabolism, the dyslipidemias noted with hyperglycemia, and the formation of the pro-inflammatory diacylglycerol and ceramides that reinforce insulin resistance.

All of this, of course, comes against the backdrop of declining ATP capacity. Under conditions of insufficient thiamine/hyperglycemia, ATP production may be reduced up to 70% depending upon the severity and chronicity of disordered metabolism, the organ or tissue in question, and the model used to test. Decrements in the brain and heart, because of their high energy demands are the most severe, while reductions in the GI system and musculature present most noticeably in the early stages. Fatigue, weakness, and GI disturbances are among the earliest and most common unrecognized symptoms of the initial stages of insufficient thiamine.

Correcting Metabolic Dysfunction With Micronutrients

Ideally, ill-health would precipitate dietary changes, but in the case of hyperglycemia, particularly when it is chronic, the altered metabolic pathways and reduced capacity to synthesize ATP from consumed foods make this prospect difficult to impossible for some. Based upon thiamine’s role in this process, a more amenable approach might be to address thiamine and other micronutrient deficiencies first. Research from multiple disciplines demonstrates the remarkable improvement in metabolic capacity with thiamine repletion suggesting that simply replenishing this and other micronutrients may slow or reverse the progression of disease in these populations. Below are a few of the hundreds of studies published on this topic.

Thiamine reduced or reversed hyperglycemia-related activation of the secondary glucose pathways (polyol/sorbitol, hexosamine, diacylglycerol/PKC, AGE) via upregulation of the PDH enzyme. It improved cardiac contractility, reduced cardiac fibrosis and decreased the expression of the mRNA-associated proteins (thrombospondin, fibronectins, plasminogen activator inhibitor 1, and connective tissue growth factor), and prevented obesity in the overfed arm of an experiment using streptozotocin-induced diabetes in rats.
In streptozotocin (STZ)-induced diabetic rats, high-dose thiamine and benfotiamine (a synthetic S-acyl derivative of thiamine) therapy increased transketolase and PDH activity increasing ribose-5-phosphate and reduced microalbuminuria and proteinuria by 70-80%. PKC, AGE, and oxidative stress were all reduced significantly.
In STZ-induced diabetic/leptin mutant type rats, benfotiamine improved heart function and prevented hyperglycemia-induced, left ventricular end-diastolic pressure increase and chamber dilatation in both models.
Benfotiamine administration 150mg thiamine daily thiamine significantly reduced blood glucose within a month, in a randomized, placebo-control trial of 24 drug naïve T2D diabetics.
In a three-month randomized placebo controlled trial, 50 T2D patients in the experimental arm were given 3X 100mg thiamine per day. Thiamine therapy significantly improved microalbuminuria, glycated hemoglobin, while decreasing PCK levels. Markers of oxidative stress and fibrinolysis were non-significant.
After 45 days of benfotiamine and vitamin B6 supplementation, 19 of the 22 patients enrolled in the study saw statically significant reductions in pain, symptom scores, neurophysiological and biological markers of diabetic neuropathy.
A 6 month randomized trial with 60 T2D with medication-controlled blood sugar and 26 age – and BMI-matched controls found that 100mg thiamine daily, significantly corrected lipid profiles and creatinine levels.
One time administration of 100mg IV thiamine, improved endothelium-dependent vasodilatation in 10 patients with TD2 during an acute glucose tolerance test.
One week of IV thiamine administration at 200mg/day in six patients with heart failure (HF) and who were also receiving diuretics (diuretics deplete thiamine) improved left ventricular ejection fraction (LVEF) in four of those patients from 24% to 37%.
A randomized, double-blind, placebo controlled study of HF patients on diuretic treatment found that 300mg/day oral thiamine improved LVEF significantly.

Thiamine Insufficiency Versus Deficiency

Among the more common misperceptions about thiamine is that deficiency is delineated by laboratory testing. While this is true for severe deficiency and when the appropriate laboratory tests are utilized, far too often, the insufficiency syndromes that present months to decades before frank deficiency is detected, are missed completely. This owes in part to the variability of testing methodologies and in part to the very framework from which we determine sufficiency and deficiency. Thiamine testing, like the tests for many micronutrients, carries a high false-negative rate and fails to consider the nature of micronutrient deficiency relative to need. The next paper in this series will addressing testing methods.

As outlined above and in the Threats document, several environmental variables increase the demand for nutrients, a diet high in carbohydrates is top among them. The increased demand will not necessarily or immediately test positive for deficiency. Rather, it will present symptomatically and must be suspected based upon the symptoms of deranged energy metabolism. In these cases, thiamine supplementation is done to support and correct reduced enzyme activity so that consumed foods may be more efficiently metabolized and converted into ATP. This then reduces the use of the less efficient and generally deleterious secondary metabolic cascades linked to the constellation of negative health effects associated with hyperglycemia.

Consider Thiamine

Thiamine is a safe, non-toxic, essential nutrient that has become increasingly difficult to maintain in the face of modern dietary practices and chemical exposures. Thiamine sufficiency is fundamental to energy metabolism, mitochondrial capacity, and thus, health. Consider thiamine in your practice.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

Image created using Canva AI.

thiamine - Page 5

We Need Your Help

Related posts:

You might be interested in

A Medical Workhorse with a History of Adverse Events

Bactrim Blocks Bacterial Folate Metabolism

Bactrim Blocks Thiamine Uptake

Of Bacteria and Men: A False Dichotomy

Postscript

We Need Your Help

Related posts:

You might be interested in

Kawasaki Disease

Febrile Lymphadenopathy and Eosinophilic Esophagitis

Discussion

We Need Your Help

Related posts:

You might be interested in

What is Stress?

Your Body is Your Fortress, Your Immune System the Soldiers

Poor Nutrition and Stress

High Energy Demands Equal High Nutritional Demands

Epigenetics and Mitochondria: The Stress of Our Parents

Nutrition is the Only Factor that We can Control

Poor Nutrition Equals a Poor Stress Response

We Need Your Help

Related posts:

You might be interested in

The Stages of Sleep

Circadian Rhythm

Sleep Apnea

An Explanatory Analogy

Putting It All Together

We Need Your Help

Related posts:

You might be interested in

Understanding Fever as an Immune Response

Inflammation Is an Immune Response: Resting Boosts Immune Function

Nutrient Interactions With Immune Response

Nutrient Deficiency in the Face of High Sugar Intake: Altered Immune Responses

Microorganisms Attack: The Immune Response Defends

Sleepwalking: An Example of Brain Dysfunction?

The Use of a Multivitamin: Completing the Nutrient Team

We Need Your Help

Related posts:

You might be interested in

Self-Responsibility is Critical to Health

Natural Sugars versus Sugary Sweets

Of Different Fuels

Cellular Engines Need Fuel

What We Eat and Drink Matters

We Need Your Help

Related posts:

You might be interested in

Hyperglycemia Through a Different Lens

Thiamine, Sugar, and Energy Metabolism

Altered Metabolism and Mechanisms of Damage

Correcting Metabolic Dysfunction With Micronutrients

Thiamine Insufficiency Versus Deficiency

Consider Thiamine

We Need Your Help

Related posts:

You might be interested in