mitochondria Archives - Hormones Matter

Energy Loss as a Cause of Disease

Published on March 4, 2026

18.3K views

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

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

Heresy in Medicine

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

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

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

Envisioning an Alternative Approach

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

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

The Second Paradigm

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

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

The Production and Consumption of Energy

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

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

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

The Medical Revolution

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

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This article was first published on July 1, 2019.

Rest in peace Derrick Lonsdale, May 2024.

Food Composition and Hyperglycemia

by Chandler Marrs, PhD

Published on March 2, 2026

10.4K views

Over the last few months, I have written a number of white papers on thiamine for contract. They may or may not be published in part or in full at some future date. Among them, I was contracted to write separate papers about thiamine in diabetes, cardiovascular disease, and Alzheimer’s disease. As I began writing the first article, I realized that these were not separate topics. Rather, each disease process was simply a different manifestation of the same core problem: persistent hyperglycemia. This, in turn, was a direct response to our current ultra-processed, chemically-laden, refined sugar, garbage-food environment; a problem we all seem reticent to confront.

The garbage foods that we consume lead to metabolic dysfunction marked by, among other things, hyperglycemia. Hyperglycemia, in turn, leads to specific metabolic adaptations that result in the inability to efficiently convert consumed foods, not just sugars, but amino and fatty acids as well, into energy. (See here for details.) Poor energy metabolism then drives cravings and overeating as a compensatory reaction to increase metabolic energy, which in turn, further entrenches hyperglycemia and its metabolic cascades. It is a deadly spiral, the likes of which are evident in skyrocketing rates of metabolic ill-health. A recent study found that only 12% of the population, 20% if the authors were generous in their description, could be considered metabolically healthy.

From my perspective, it is this shift in metabolic capacity, in the pathways used to metabolize food that drives much, if not all, modern illness. Importantly, many of the disease processes we now consider to be separate entities, like diabetes, the various cardiovascular diseases, the neurodegenerative diseases like Alzheimer’s and dementia, cancer, and even the litany of chronic autoimmune, inflammatory, or pain and fatigue related disease processes, may not be separate at all. They may just represent the way the consumption of ultra-processed foods and the resulting hyperglycemia mix with the individual’s unique genetic and environmental circumstances to form disease. In other words, food provides the spark, hyperglycemia is the kindling, and how and where the flame burns is determined by the individual’s genetics and the totality of his or her life, lifestyle, and environmental exposures. It all begins with food though.

What Are Ultra-processed Foods?

Just about everything in the middle aisles of a super market or purchased from a fast food establishment would be considered ultra-processed. These products are:

…formulations of several ingredients which, besides salt, sugar, oils and fats, include food substances not used in culinary preparations, in particular, flavours, colours, sweeteners, emulsifiers and other additives used to imitate sensorial qualities of unprocessed or minimally processed foods and their culinary preparations or to disguise undesirable qualities of the final product.

In other words, most of the American diet. These products are highly palatable, densely caloried (because of all of added sugars and fats), and loaded with synthetic chemicals, but have no discernable endogenous nutrient content. Sadly, almost 60% of the American diet for adults and close to 70% for kids aged 2-19 years is comprised of ultra-processed food products.

Processing is not the only problem though. Conventionally grown and raised food and livestock have all but bred out of their products any semblance of nutrition in favor of bigger, faster-growing, and more attractive products. In the place of nutrients, we get excess sugars (yes, conventionally grown produce has a higher sugar content than organic or that was grown in the past), along with lots of herbicides, pesticides, hormones, antibiotics and veritable laundry list additional mitochondrial poisons. From farm to table, the composition of modern food products is lacking nutrients while rich with potential anti-nutrient and toxicant compounds. Is it any wonder only 12-20% of the population can be considered metabolically healthy or that hyperglycemia drives modern illness?

Why Hyperglycemia?

Backing up just a bit, let us talk about how discussions of hyperglycemia are framed conventionally and what that has to do with the composition of the foods we ingest. Most discussions of hyperglycemia involve either the absence of sufficient insulin as in the case of Type 1 diabetes or a developed resistance to insulin as in the case of Type 2 diabetes. In either case, there is insufficient insulin available, either absolutely or relative to need, to transport glucose from the bloodstream into the cells and this results in hyperglycemia. Much of the research involves defects in pancreatic islet cell function, glucose receptors and transporters relative to these diseases. In general, diet exacerbates hyperglycemia. With type 2 diabetes, however, diet accounts for almost all of the disease process itself. In many, but not all cases of type 2 diabetes, diet also induces obesity and may provoke a host of additional disease process affecting the heart and the brain. Indeed, Alzheimer’s disease is now considered an outgrowth of persistent hyperglycemia and has been categorized as type 3 diabetes.

This linkage of diabetes with obesity leads many to conclude that if the individual just reduces his/her calories and/or increases activity and loses weight, the diabetes, the obesity, and the assortment of other disease processes that ensue, would resolve and/or be prevented. For some this may be true, but if the persistent rates of obesity, despite reductions in caloric intake are any indicator, this aspect of diet is only indirectly related to the disease at hand. My research involving the some of the metabolic pathways associated with hyperglycemia, leads me to believe that hyperglycemia represents more than just an excess of calories, carbohydrate or otherwise, and that changes to pancreatic islet function, and glucose receptors and transporters are simply adaptive response to ailing mitochondrial metabolism. What is causing metabolism to fail? The American diet of ultra-processed food-like products that are high refined sugars, trans fats and chemical toxins, but low in usable macronutrients and micronutrients – that is the root of these illnesses.

Micronutrient Deficiency Underlies Hyperglycemia

Adenosine triphosphate (ATP), the fuel source for cellular function, the energy currency that all organisms require to survive, is derived entirely from food. The foods we eat provide the macronutrients – protein, fats, and carbohydrates, and the micronutrients –vitamins and minerals – that, with a little oxygen, are then processed by the mitochondria into ATP. Absent frank starvation, the key variables in this process are the micronutrients. Thiamine and its activating partner magnesium are especially important because they manage the gates to this process. Micronutrients derived from foods allow for the catabolism of consumed macronutrients so that it may be turned into ATP. Vitamins and minerals fuel the enzymatic machinery that allows energy factory to work. Insufficient micronutrients slow down enzyme capacity (the energy machinery), causing a backup of macronutrients (a supply excess), at the gates. That excess has to be dealt with. Some of it is forced through alternate pathways that, through a variety processes, break down and salvage some of the macronutrients as a way to temper the backup, but most of the excess either just floats around in the blood or is stored in the fat cells. The glucose that floats around in the blood and desensitizes the glucose receptors and transporters and re-regulates pancreatic islet function – that is hyperglycemia. The glucose that is stored as fat – that is obesity.

Those macronutrients that cannot be processed because of absent micronutrients, not only lead to the hyperglycemia cascades and the various diseases processes associated therewith, but their consumption produces little to no energy or ATP and, in most cases, consumes it. In other words, despite ingesting an excess of calories, the mitochondria, and thus the human in which they reside, are starving. If macronutrients cannot get into the factory, the factory cannot produce ATP. The result is cravings and overeating, which no amount of willpower will overcome. This is why a simple reduction of caloric intake, absent recognition of food composition, does not work for many with type 2 diabetes. They are already starved for energy. Proteomic studies in rodents fed comparable diets illustrate this pattern of poor energetic capacity with reduced expression of the proteins involved in energy metabolism and increased expression of those marking oxidative stress and aberrant cell proliferation (cancer pathways).

A Technical Aside

In more technical terms, when the excess sugars cannot be processed via oxidative phosphorylation or through the pentose phosphate pathway – processes that ultimately produce ATP and other important substrates – they are diverted through salvage pathways like the polyol/sorbitol, hexosamine, diacylglycerol/PKC, AGE pathways. This leads not only to decrements in ATP production but the macro- and microvascular cell damage associated with persistent hyperglycemia leading to heart disease and neurological dysfunction.

Similarly, in the absence of sufficient micronutrients, thiamine in particular, the catabolism of branched chain amino acids suffers, resulting in increased branched chain keto acids, especially short and medium chain acylcarnitines. Surplus acylcarnitines then overwhelm the b-oxidation pathway involved in fatty acid metabolism. This, in turn, leads to incomplete fatty acid metabolism (dyslipidemia) and the formation of the pro-inflammatory diacylglycerol and ceramides associated with metabolic dysfunction. The hyper-activation of ceramide synthesis expedites cell death, blocking complex 3 of the electron transport chain in the mitochondria.

Inadequate micronutrient availability, and again, thiamine and magnesium especially, further imperials the alpha oxidation of fatty acids. This is the step before beta-oxidation. Poor alpha-oxidation results in increased phytanic acid and disrupted sphingolipid homeostasis; two patterns with linked with a variety of neurological sequelae. All of this is linked to persistent hyperglycemia, which evolves from inadequate micronutrient content relative to demands.

Coincidently, COVID death is linked to both increased ceramide synthesis and disturbed sphingolipid homeostasis.

We postulate that SARS[1]CoV-2 causes endothelial damage by binding ACE2 and misbalancing the renin-angiotensin pathway, dysregulating sphingolipids and activating the ceramide pathway, known to mediate endothelial cell apoptosis in the setting of radiation damage. Such injury also generates reactive oxygen species, vasoconstriction and hypoxia, and ultimately the deposition of platelets on an exposed vessel basement membrane initiating the intravascular coagulopathy and multi-organ failure, pathognomonic of severe COVID-19 and death.

Underlying both processes are micronutrient deficient patterns of hyperglycemia, e.g. insufficient thiamine, magnesium and likely other nutrients, but most have not been investigated. Inasmuch hyperglycemia accounts for much of the risk for COVID severity, it is difficult not wonder if these pathways were not already entrenched pre-virus and the virus simply escalated the negative adaptations beyond rescue.

Food Composition Matters More Than Caloric Intake

From this perspective, it is clear that it is not solely an excess of calories that causes hyperglycemia, or even an excess of carbohydrates, although both play a large role. It is the quality or composition of the food that is the problem. Modern foods are calorie dense, sure, primarily because of the use of refined sugars and added fats. They are also loaded with chemical poisons, which we all seem to disregard as important. Carbohydrates derived from natural, organic, and unadulterated fruits, vegetables and grains, carry with them vitamins, minerals, fiber, and proteins that allow the body to convert the macronutrient substrates into useable energy. Indeed, a diet rich in these types of foods is unlikely to induce hyperglycemia or obesity. In contrast, processed foods, while high in carbohydrates, fats, and chemicals that are toxic to the mitochondria, carry few to no micronutrients, little to no fiber, or other compounds that can be used by the body to produce ATP all the while carrying an abundance of chemical toxins. From a metabolic standpoint, ultra-processed foods are nothing more than edible poisons. They demand more energy to process than they add and wreak havoc with far more systems than were illustrated here. The hyperglycemia and associated damage that ensues is evidence of this process. If we are to tackle these health issues, the entirety of modern food landscape relative to metabolic health must be addressed.

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

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This article was published originally on October 28, 2021.

Mitochondrial Capacity and Thiamine: Notes from a Presentation

by Chandler Marrs, PhD

Published on January 15, 2026

2.6K views

Mid December, I gave a talk on mitochondrial capacity and thiamine’s role therein (included below). My argument was that mitochondrial capacity e.g. their capacity to produce ATP efficiently from the foods we consume, and to meet the demands of living, drives health or illness. I also argued that thiamine drives mitochondrial capacity, and thus, is implicated in modern illness.

It is an argument I have made for years now, and of course, I wrote a book about it, together with the late Dr. Derrick Lonsdale. It is not something readily considered by western medicine, however. Even as our understanding of the molecular mechanisms and pathways connected to mitochondrial functioning has expanded over the last century, the fundamental nature of mitochondrial energetics remains underappreciated. We look to everything else the mitochondria do as somehow more important to health and disease than simple energetic capacity, forgetting that these other processes do not happen without sufficient energy.

Energy is the most basic unit of life. It is the capacity to transform something into something else. Absent this, we are nothing more than rocks.

That said, I did learn a few things when preparing for this talk. Namely, I learned how many discrete disease there are. Did you know that we now have over 26,000 separate disease entities recognized by the medical profession and over 18,000 ‘global’ or ‘systemic’ disease entities? I did not and was shocked. Before I looked this up, I thought we had maybe a few thousand, ten thousand if I were being generous. Never once did I contemplate 26,000. That is absolutely insane. Worse yet, apparently there are over 20,000 pharmaceutical products currently on the market. A pill for every ill – almost.

With all of this knowledge, one might think we have advanced in our capacity for health and healing. One would be wrong. According to the latest research, 76% of the population deals with at least one chronic condition. And quite unironically, despite the endless discrimination of discrete diseases, most symptoms, from 25-75% according to one report, remain medically unexplained. We are drowning in distinctions where perhaps there should be none, or at least far fewer, and we are none the wiser or healthier for it.

From my perspective, I cannot help but wonder how many of these discrete diseases are not simply expressions of poor mitochondrial capacity? Sure, there are potentially millions of combinations of interactions between genetics and the lived environment that are likely to affect disease presentation, but is each set of symptoms really representative of a separate disease? From a mitochondrial perspective, probably not.

Moreover, if mitochondrial capacity is the key to health, then instead of searching for and naming each permutation of disease expression and creating new drugs for each, we could go back to the basics and ask ourselves – what do I need to be healthy and am I getting it? If I am ill, chances are I am missing something, probably lots of somethings and those missing components to health, along with the long list of environmental toxicants and genetic interactions that lessen mitochondrial capacity, are what is driving illness. Perhaps if we support the mitochondria and view health from that perspective, we can reduce the burden of disease while culling the impossible and growing list of supposedly discrete diseases.

Alas, none of that will happen, at least not on a scale that would make a difference. That said, perhaps my lectures and articles might help a few people reclaim their health and their family’s health. For me, that is a win.

Here is the latest.

Mitochondrial Capacity, Thiamine, and Dysautonomia

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

Yes, I would like to support Hormones Matter.

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ASD, Seizures, and Eosinophilic Esophagitis: Could They Be Thiamine Related?

by M Albert

Published on December 10, 2025

7.9K views

My 18 year old son has ASD and has had a seizure disorder since he was 6 years old. He has tried virtually all anti-epileptic drugs. Either the side effects were unbearable, they made his seizures worse, or had no effect on his seizures. He was diagnosed with Eosinophilic Esophagitis. He is underweight and of short stature, and always has been. Mitochondrial tests show that complex II is working at 26% capacity. He is also autistic. He has tested positive for folate receptor antibody.

Over the years he has done several rounds of antibiotics, including Flagyl, which I have since learned that it significantly depletes the body of thiamine. He has also taken several rounds of Diflucan, Azithromycin, Vancomycin, Augmentin, Amox for various issues including candida, clostridia, gram negative gut bacteria, etc.

He is currently on Lamictal and just started Briviact for seizures. The Briviact causes anger and aggression issues. He currently deals with OCD tendencies. He was recently found to have bone density of 2.8 standard deviations below normal. This falls in the range of osteoporosis, but he has not been diagnosed with it because of his age.

He eats fresh and a lot of dried fruit, meats, raw and cooked greens, white rice, lots of cooked veggies, eggs. He also takes Lipothiamine 100 mg/day, Magnesium 550 mg, a multi-vitamin, calcium, vitamin D, and K, all at the direction of his doctors.

Childbirth and Infancy

M was born on July 9th 2005 7lbs 9oz. He was full-term. I had high blood pressure at 41 weeks and labor was induced. He would not drop into position and he became distressed and so was delivered via cesarean while I was under general anesthesia.

He spent 4 days in the NICU because he aspirated meconium and would not latch to feed. While in the NICU, he was administered antibiotics. He was formula-fed, not breast-fed.

As an infant, the large size of his head was somewhat of a concern for the pediatrician. He was administered vaccinations according to the CDC guidelines for the first 12 months. He had infantile spasms off and on. He spiked a fever for every vaccination. Tylenol was administered. He received 3 doses of flu vaccine, accidentally, within 3 months.

He did not sleep well, and still doesn’t.

Initially, he was very precocious. As an infant, he would put puzzles together that were for much older children. He would complete sorting activities that were well beyond his age range. He did not babble and eye-contact was fleeting.

After his 18 month vaccination, he lost just about everything within 2 weeks. After these vaccinations, he couldn’t do his puzzles, bring food to his mouth, smile, couldn’t stand to be read to when he previously loved to be read to. He also developed a sensitivity to light and sound and cried a lot.

At 24 months, he was diagnosed with profound autism.

PANDAS/PANS and Eosinophilic Esophagitis

At age 10 years, he abruptly lost skills again and it was thought he had PANDAS/PANS as he had several strep infections treated with antibiotics. He did a several month long courses of Augmentin or Azithromycin to treat PANDAS/PANS. He had a severe trauma at age 11. He was horrifically abused by a school employee.

He has always been of short-stature nearing 5th percentile for height, and slightly overweight for his age, until age 14 when he started having symptoms of Eosinophilic Esophagitis. He was diagnosed with EoE at 15 and has struggled to keep his weight high enough as he dealt with the intense pain, fatigue, and esophagus issues with this condition. He is currently taking Dupixent for his Eosinophilic Esophagitis as the PPI and Budesonide slurry were not addressing the issues. So far Dupixent is allowing him to eat. His diet remains very restricted due to having so many trigger foods and he has almost no appetite.

He eats a lot of dried and fresh fruit. He loves greens, raw and cooked. He also eats meat, white rice noodles. He eats mostly an organic diet. He does occasionally enjoy candy.

Seizures

He developed seizures at age 6. These were controlled for a while on Depakote, but the side effects of Depakote were too much for him and so we had to stop. His seizures are now not controlled. He has 1-2 tonic-clonic seizures per week, plus several staring spells all throughout the day. Recent EEG showed abnormal spikes and discharges in the frontal and temporal lobes. It indicated his seizures involved many places on his brain. Brain surgery was being considered for seizures at this time, but ruled out as an option due to the nature of his seizures.

He has failed several other seizure meds including Vimpat, Zonegran, Aptiom, Topamax, Onfi, and others. He is currently on Lamotrigine and Epidiolex for his seizures. He also takes trazadone and gabapentin for sleep, although these do not consistently help him sleep. He is so consumed by fatigue and can hardly get out of bed even to walk across the room. With tons of encouragement he can do brief periods of school work. The meds cause him to lose focus and become frustrated. He seems to almost always be lost in a fog and unable to participate in basic conversations without losing focus or becoming too exhausted to continue. Each seizure will cause him to be in bed for 2-3 days. He has fallen many times going into a seizure and is now afraid to leave the safety of his bedroom. He will come out, but rarely.

He has intermittent issues with nystagmus. He had a bad case of COVID 2 years ago, which caused clusters of seizures and constant nystagmus.

He has an exaggerated startle response.

Despite It All

M is a sweet young man. He is brilliant. He loves animals. He tells everyone he sees that he is so happy to see them. He is working with a local legislator on how to improve rights for non-speaking people, especially in the court room. He is completing all of his high school courses at home with straight A’s and he is a published poet.

He does not speak, but he communicates by pointing to letters on an alphabet board. This is a skill that took him years to learn. He communicates at an age-appropriate level or higher. He is working, slowly, toward a standard high school diploma.

Postscript

Based upon what I have learned from this website, I discussed thiamine with our physician. It turns out, she heard Dr. Lonsdale speak years ago. She recommended 50mg of Lipothiamine. The entire time he was taking it, he had no seizures. I was not sure that it was thiamine or the meds until we ran out for about a week. The seizures returned, but as soon as we resumed the Lipothiamine, they disappeared again. He has been taking it again and now it has been 2 weeks without seizures. I don’t want to get my hopes up, but it could definitely be a piece of the puzzle. Are there others out there with similar experiences?

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

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This story was published originally on January 2024.

Hormones, Hysterectomy, and the Aging Brain

by Chandler Marrs, PhD

Published on November 18, 2025

19.1K views

Everything slows down as we age. For some lucky folks, aging happens gracefully with nary a disease in sight. For others, the springs start popping off around 40 and by the time we reach ‘old age’ our bodies and brains are barely functioning. Arguably, diet and lifestyle have something to do with how well or how poorly we age, and of course, genetics contribute mightily, but beyond that, we really have no idea what’s happening with aging.

Sure, there are all sorts of physiological systems that become progressively less efficient over time. Wear and tear plays a huge role, but the relationships aren’t linear. There are always outliers. There are folks who, on a diet of smokes and scotch, live well into their nineties with all their faculties intact. Then there are the poor souls who are prodigiously healthy, who eat right and exercise, but yet, whose bodies seem set on wide-scale destruction, where the slightest change in lifestyle risks sending them into a morass of cascading illness. Somewhere in the middle, the rest of us live – sometimes healthy, sometimes not – aging in fits and spurts. What the heck?

From a physiological standpoint, aging is marked by two opposing factors: decreasing hormones and increasing inflammation. Where they intersect, age-related illnesses seem to accrue. Called endocrine senescence, researchers have long noted a relationship between declining hormones and declining immune function (marked by increased and inefficient inflammatory responses). Might there be some truth to the ever-young, hormone peddlers? Could hormones be the key to offsetting the age-induced inflammatory cascades? Possibly.

Hormones and Mitochondria

I just finished writing an extensive paper on acquired mitochondrial illness. Throughout the research, I stumbled upon a short essay linking mitochondrial structure and function to estradiol. More specifically, the rapid estradiol decline common post oophorectomy (ovary removal), fundamentally alters the shape, and ultimately, the function of mitochondria. Researchers found that a rapid decline in estradiol evokes significant damage in the brains (and presumably other organs) of female monkeys. Additional studies using estradiol starved mitochondria from female rodents showed similar shape alterations and consequent declines in brain bioenergetics. Interestingly though, with natural menopause, where estradiol declines more gradually, no such structural changes were observed. In fact, with the more gradual decline in estradiol, the mitochondria appear to increase their production of the lifesaving ATP as a compensatory reaction.

All Paths Lead to the Mitochondria

Recall, from previous posts, that mitochondria take dietary nutrients and oxygen, and change them into the chemical energy (ATP) that is used by every cell in the body. Without ATP, cell function grinds to a halt. So, anything that derails the mitochondria, imperils cell function and initiates cell death. Lack of nutrients, sedentary lifestyle, pharmaceutical, and environmental toxicants, all derail mitochondrial function. Cluster too much cell death together in one tissue or one organ and disease happens. Since mitochondria are in every cell of the body, mitochondrial damage induces disease broadly, but especially in regions with high energy demands like the brain, the heart, the muscles, and the GI system.

The cardinal symptoms of mitochondrial damage include fatigue, weakness, muscle pain, and depression. These are followed by dysregulated systems; a GI system, for example, that overreacts or under reacts or temperature dysregulation (hot flashes, cold insensitivity), insulin/sugar dysregulation, emotional volatility, migraines, seizures, syncope (fainting), and so on. It’s not a pretty picture.

In addition to providing the fuel for cellular respiration, e.g. life, mitochondria control a host of other functions, steroidogenesis is one of them. This means that if we fail to feed the mitochondria or hurl insults at them, hormone dysregulation is inevitable. Ditto for inflammation, as the mitochondria regulate inflammatory cascades. Every woman knows when her hormones are out of whack. Well, now we know that hormone dysregulation emerges from the mitochondria.

From a systems perspective, consider the mitochondria as central regulators of organismal health. Mitochondria both send and receive signals from all over the body and then adjust their functioning accordingly. With their role in hormone synthesis, we would expect there to be cross-talk between the mitochondria and circulating hormones. Indeed, there is. All steroid hormones have receptors on the mitochondrial membranes. When hormone concentrations increase or decrease, the mitochondria will initiate the synthesis of new hormones and send signals throughout the body to adjust other hormone-responsive systems as well.

No Estradiol Equals Misshapen Mitochondria: Donuts and Blobs

Removing the ovaries starves the mitochondria of one of its many feedback mechanisms and damages the brain mitochondria in the regions of the brain responsible for executive function and memory – the frontal cortex and the hippocampus. The mitochondria change shape, from spheres (healthy) to donuts and blobs, which represent early and late-stage mitochondrial damage, respectively. Misshapen mitochondria cannot provide the energy (ATP) needed to perform critical brain functions such as neural communication or the antioxidant tasks needed to clean up toxicants. Neurodegeneration ensues. In layman’s terms, and in the early stages, brain fog and memory loss. Researchers believe that it is this loss of functional mitochondria that contribute to the onset of neurodegenerative disorders like Alzheimer’s and other dementias. And, this loss of function is precipitated by an unnatural loss of estradiol.

Ovary Removal is Common with Hysterectomy – Now What?

For the millions of women who have had their ovaries removed with hysterectomy, this presents a problem. Amid the myriad of other side effects associated with ovary removal, and perhaps, the root cause of these effects, we can add mitochondrial damage and brain mitochondrial damage, specifically. The rapid decline of estradiol, and other hormones, places many women at risk for neurodegenerative disorders like Alzheimer’s. How could this be mitigated?

In animal research, hormone replacement with 17B – estradiol immediately after the ovaries are removed seems to temper the damage, at least in the short term. There are no long-term studies. Similarly, epidemiological studies in human women suggest hormone replacement immediately after open menopause and/or hysterectomy with oophorectomy reduces clinical symptoms associated with the diseases of aging – e.g. the cognitive decline of Alzheimer’s and other dementias. However, since the synthetic estrogens used pharmacologically are different compounds than those produced endogenously (and used in basic and animal research) and because there are no mitochondrial imaging or even mitochondrial function tests done with human females given hormone replacement, it is difficult to compare the two sets of literature.

Some data suggest that the use of synthetic estrogens damages mitochondria and further diminishes the synthesis of remaining endogenous estrogens (the adrenals continue to produce estradiol and other estrogens after the ovaries are removed). Women who have used synthetic estrogens such as those in oral contraceptives and hormone replacement therapies have lower concentrations of endogenous estradiol, estrone, androstenedione, testosterone, and sex hormone-binding globulin. Based upon the aforementioned research, the decline in endogenous hormones would suggest a commensurate derangement in mitochondrial structure and function, but there are no data either way. At the very least, caution is warranted when contemplating the use of synthetic estrogens, particularly in the current environment that is rife with estrogenic chemicals. There are no data on the use of ‘natural’ or ‘bioidentical’ hormones and human mitochondrial function. So, although the animal data are fairly clear, estradiol replacement begun early enough appears to offset the decline in endogenous estradiol, how this translates to human females is not known.

Other Hormones and Additional Pathways

A flaw common to most research in this field is the failure to address the other hormones involved in modulating health. Estradiol is but one of many estrogens produced endogenously. It is also one of many steroid hormones produced in the ovaries and regulated by mitochondrial function. How estradiol removal or add-back affects progesterone, the androgens, or even the glucocorticoids (cortisol) – is not known. Compensatory reactions are likely. Understanding how those reactions mediate mitochondrial function might determine a viable workaround for the depleted estradiol. The beauty of human physiology is a mind-blowing breadth and depth of compensatory reactions to maximize survival. So I would think, and this is purely speculative, that even if one has lost her ovaries, and even if estradiol treatment was not initiated immediately, or if synthetic estrogens were used instead, there should be other mechanisms to tap into and compensate for this loss. That is, there should be multiple pathways to help maintain mitochondrial function. What those are, I do not know, but they are worth exploring.

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

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This post was published originally in January 2015.

It’s Just ATP

by Chandler Marrs, PhD

Published on August 11, 2025

7.1K views

A while back, I wrote an article called ‘Just a Vitamin Deficiency‘ in an effort to dispel the notion that vitamin deficiencies are inconsequential to health. Truth be told, I have written dozens of similar articles hoping to change the tide of disregard. A few weeks after publishing the vitamin article I began this one. I wanted to address the growing body of research suggesting that ATP production is somehow immaterial to health and healing. The two ideas are connected, of course, because without vitamins and minerals we cannot produce ATP and without ATP we cannot catabolize nutrients from the foods we consume into more ATP. In health, medicine, and research, we seemed to have lost sight of these connections in favor of ever more complicated, and indeed, bifurcated explanations of our ill health.

I decided not to publish this article originally. It seemed redundant. Then, lo and behold, another article hit social media once again bemoaning how energy production was unimportant relative to all of the other cool functions overseen by the mitochondria.

The analogy of mitochondria as powerhouses has expired. Mitochondria are living, dynamic, maternally inherited, energy-transforming, biosynthetic, and signaling organelles that actively transduce biological information.

To be fair, the article is exceptionally detailed and very well done and I agree with the authors overall. They clearly demonstrate the complexity of mitochondrial function. Where I have a problem though, is in the failure to recognize the primacy of ATP over all other functions. This is among my top pet peeves in the world of mitochondrial research and medicine. It is as if the simple act of making energy is not sexy enough to consider in health or disease. While I understand that the mitochondria are central regulators of just about everything and I understand that there are dozens or more cool pathways that are managed directly by the mitochondria and their various signaling proteins, what I do not understand is how we seem to miss the fact that all of these functions, and I mean all of them, require ATP. Indeed, decrements in ATP capacity often initiate, and certainly sustain, many of the negative reactions we see outlined in the annals of mitochondrial research.

In this particular article, the authors concede that defects in oxidative phosphorylation (OXPHOS) impact all of the functions they so eloquently describe.

Because most biochemical reactions taking place within mitochondria are directly or indirectly linked to OxPhos and Δψm [mitochondrial membrane potential], including substrate and ion uptake, mtDNA perturbations have widespread consequences for several metabolic pathways.

For the uninitiated, OXPHOS is the process by which the metabolized products of the foods we consume are shuttled through various enzymatic reactions within the mitochondria to ultimately produce ATP. Defects in OXPHOS not only imperil energy production but also set into motion a cascades of negative reactions. From an article published earlier this year:

OxPhos defects trigger mtDNA instability and cell-autonomous stress responses associated with the hypersecretory phenotype, recapitulating findings in plasma of patients with elevated metabokine and cell-free mitochondrial DNA (cf-mtDNA) levels. These responses are linked to the upregulation of multiple energy-dependent transcriptional programs, including the integrated stress response (ISR).

OXPHOS is clearly important to mitochondrial function, and why wouldn’t it be? The synthesis of energy, of ATP, is the foundation of life. Think about it for a moment. Energy is fundamental to survival, not incidental, but fundamental. So, if energy wanes all of the functions dependent upon said energy become disturbed. Sure, there are other mechanisms by which a particular pathway may become unfavorably altered, and sure, delineating those mechanisms is important, but each and every one of those patterns requires energy to execute. The degree to which energy metabolism is inadequate to the task will influence, if not determine, the pattern of response, irrespective of the other variables that may be at play.

Breathing, for example, requires energy and not just the mechanical act of inhalation and exhalation, but the absorption, trafficking and metabolism of oxygen (O2). Of course there are a lot of factors that can impede breathing and oxygen management that seem outside of the purview of mitochondrial influence, but in reality, they are not. Energy or ATP is required at every step, including arguably the most important step – the utilization of O2 to create more ATP.

For O2 to be used, we need ATP.

For ATP, we need functional mitochondria.

For functional mitochondria, we need macro- and micronutrients.

Food provides the substrates that allow the mitochondria to produce ATP. It provides macronutrients like protein, fats, and carbohydrates, and perhaps most importantly, food provides the micronutrients to utilize that fuel. It’s that simple, or at least it used to be, before industrial food manufacturing so thoroughly decimated the food supply leaving vast swaths of the population starved for vitamins and minerals.

The ills of modern food production notwithstanding, without sufficient micronutrients to metabolize food into fuel and ultimately into ATP, alternate processing pathways are used; pathways that consume more ATP than they produce, and pathways that burn dirtier and emit more toxins than the body has the energy/ATP to deal with. This is the root of all metabolic disorders and more often than not, most modern illness, regardless of diagnosis.

So, while detailing all of the cool things that mitochondria are responsible for is important to understand, especially if we are ever to move medicine away from the compartmentalized model that it has so fixated on, let us not forget ATP is the basis of life.

Perhaps, in our investigations mitochondrial function, we ought to examine ATP capacity, not just output but capacity, and the pathways therein used to produce this ATP and manage the metabolism of foods. Perhaps then we will finally understand how critical the right nutrients are to mitochondrial health. Perhaps we also ought to look at how to support native mitochondrial function, not by blocking aberrantly altered pathways, but by providing the mitochondria with the most basic building blocks for optimal ATP production – nutrition. If we can get the mitochondria to more efficiently produce ATP, would that not then favorably influence everything else?

From that perspective, it seems obvious that ATP, the energy cells consume to do all of the things that cells do, would be fundamental to health, and to life itself. Like all of the other things that should be obvious to modern medicine though, it is not. Sadly, it does not appear to be obvious even to those who research and treat mitochondrial illness. ATP capacity is not something we can ignore, but we do, and this, I believe, is one of the biggest failings of modern medicine and modern mitochondrial research.

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

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This article was published originally on August 16, 2023.

Energy Medicine

by Derrick Lonsdale MD, FACN, CNS

Published on July 30, 2025

16.3K views

I have written many posts on Hormones Matter and have tried to answer the questions arising from each post. These questions and my answers have been so repetitive that I decided to try to make it clear what “energy medicine” is all about and why it differs from conventional medicine. It is only natural that the posted questions are all built on our present ideas about health and disease. What I am about to say is that the present medical model has outgrown its use. Therefore it is obvious that I must discuss what this means. First of all, why do we need a “medical model”? In fact, what is the difference between complete health and its lack? The Oxford English dictionary gives the definition of disease as “a serious derangement of health, disordered state of an organism or organ”

The American Model of Medicine

As I have said before, the present American medical model was aimed at making a diagnosis of one of many thousand described diseases. It was devised from the Flexner report of 1910 that was initiated by Rockefeller. Rockefeller wanted to make medical education adhere to a common standard, thus creating the present “medical model”. The Flexner report used the methodology of diagnosis that was current in Germany. This stated that the patient’s report to a physician is called “history”, involving the patient’s description of symptoms and their onset. From this, the physician may or may not have an idea what is wrong. The next part is the physical exam where a hands-on search of the patient’s body is made for evidence of disease. This is extremely complex when put fully into clinical operation and also may or may not provide clues to a diagnosis. The third operation is laboratory testing and it is this constellation of abnormal tests that provide scientific evidence for the nature of the disease. Each test has been researched and aside from one that is either positive or negative, others have a normal range reported in numerical terms. Perhaps, as an example, the test for cholesterol level is the best known. Each test has to be interpreted as to how it contributes to arriving at a diagnosis. Finally, the physician has to try to decide whether medical or surgical treatment must be offered. Please note that the surgical removal of a sick organ may be the signature of medical failure, for example, removing part of the intestine in Crohn’s disease, for it represents a missed opportunity to treat earlier in the disease process.

Laboratory Tests and A Drug For Every Disease

It is the constellation of symptoms described by the patient and the abnormalities found by the physical examination that constitute a potential diagnosis to formulate what laboratory tests should be initiated. It is the constellation of laboratory tests that may or may not provide the proof. There are problems with this. For instance, there may be test items in the constellation that create confusion, such as “it might be disease A or disease B. We are not sure”. Tests that are “borderline” positive are particularly confusing. The diagnosis finally depends often on who was the first observer of these constellations. For example a person by the name of Parkinson and another person by the name of Alzheimer, each described clinically observed constellations that gave rise to Parkinson’s disease and Alzheimer’s disease. Since they were first described, the pathological effects of each disease have been researched in painstaking detail, without coming to the conclusion of the ultimate cause. Finally, the pharmaceutical industry has indulged in complex research to find the drug that will reverse the pathological findings and produce a cure. Because this concept rides right through the objective, each disease is thought to have a separate underlying cause and a separate underlying cure in the shape of a new “miracle drug”. Witness the recent revival of a drug that was initially found to be useless in the treatment of Alzheimer’s disease. This revival depends on the finding of other pathological effects discovered in the disease, suggesting new clinical trials. When you take all these facts into consideration, it is a surprisingly hit and miss structure. For example, we now have good reason to state that a low cholesterol in the blood is more dangerous than a high one. Why? Because cholesterol is made in the body and is the foundation material for building the vitally important stress hormones. Cholesterol synthesis requires energy and is a reflection on energy metabolism when it is in short supply.

The Physicians Desk Reference, available in many public libraries, contains details concerning available drugs. Each drug is named and what it is used for, but often there is a note saying that its action is poorly understood. Just as often, there may be one or two pages describing side effects. In fact, the only drugs whose action is identified with cause are the antibiotics. The rest of them treat symptoms but do not address cause. Antibiotics affect pathogenic bacteria but we all know that the bacteria are able to become resistant and this is creating a problem for the near future. It is interesting that Louis Pasteur spent his career researching pathogenic microorganisms. However, on his deathbed it is purported that he stated “I was wrong, it is the defenses of the body that count”.

It must be stated that the first paradigm in medicine was the discovery of pathogenic microorganisms and their ability to cause infections. Many years were spent in trying to find ways and means of killing these organisms without killing the patient. It was the dramatic discovery of penicillin that led to the antibiotic era. I like to think that Louis Pasteur may have suggested the next paradigm, “assist the body defenses”.

Energy Medicine: A New Paradigm for Understanding Health and Disease

When a person is seen performing on a trampoline, an observer might say “hasn’t he got a lot of energy!” without thinking that this represents energy consumption. Energy has to be captured in the body and is consumed in the physical action on the trampoline. Many people will drink a cup of coffee on the way to work believing that it “creates” energy. The chemical function of caffeine stimulates action that consumes energy, giving rise to a false impression. Every physical movement, every passing thought, however fleeting in time, requires energy consumption. The person who has to drink coffee to “get to work”, is already energy insufficient. He/she can ill afford this artificial consumption of the available energy.

I am going to suggest that the evidence shows “energy medicine” may indeed be the new paradigm, so we have to make sure that anyone reading this is conversant with the concept of energy. In physics, “energy is the quantitative property that must be transferred to an object in order to perform work on, or heat, the object. Energy is a conserved quantity, meaning that the available energy at the beginning of time is the same quantity today. The law of conservation of energy states that “energy can be converted in form but not created or destroyed”. Furthermore, Einstein showed us that matter and energy are interconvertible. That is why the word “energy” is such a mystery to many people. What kind of energy does the human body require?

We are all aware that the electroencephalogram and the electrocardiogram are tools used by physicians to detect disease in the brain and the heart. If that means that our organs function electrically, then where does that energy come from? We do not carry a battery. We are not plugged into a wall socket and the functional capacity of the human body is endlessly available throughout life. The only components that keep us alive are food and water. Everyone knows that foods need to contain a calorie-delivering and a non-caloric mixture of vitamins and essential minerals. The life sustaining actions of these non-caloric nutrients is because they govern the process of energy capture by enabling oxygen consumption (oxidation). They also govern the use of the energy to provide physical and mental function.

The calorie bearing food, consisting of protein, fat and carbohydrate is used to build body cell structure. This is called anabolic metabolism. If body structure is broken down and destroyed, weight is lost and the patient is sick. This is called catabolic metabolism. In healthy conditions, food is metabolized to form glucose, the primary fuel.

Thiamine (vitamin B1), together with the rest of the B complex, governs oxidation, the products of which go into a cellular “engine” called the citric acid cycle. This energy is used to form adenosine triphosphate (ATP) that might be referred to as a form of “energy currency”. Without thiamine and its vitamin colleagues in the diet, ATP cannot be formed. Research for the next stage of energy production has yielded insufficient information as yet concerning production of electrical energy as the final step. The evidence shows that thiamine may have an integral part in this electrification process, although much mystery remains. Suffice it to say that we are electrochemical “machines” and every physical and mental action requires energy consumption.

Maybe the Chinese Were Right

In the ancient Chinese culture, an energy form called Chi was regarded as the energy of life itself. Whether this really exists or not and whether it is in some way connected to the auras purported to surround each person’s body is still conjectural. It would not be too absurd to suggest that it might be as yet an undiscovered form of energy and that it is truly a reflection of good health. My personal conclusion is that some form of electromagnetic energy is the energy that drives our physical and mental functions and that it is transduced in the body from ATP, the storage form of chemical energy. There is no doubt that acupuncture does work and certainly encourages the conclusion that the meridians described by the ancient Chinese thinkers are an important evidence of electrical circulation. There is burgeoning evidence that energy is the core issue in driving the complex process of the body’s ability to heal itself. The idea that the physician or anyone else that purports to be a “healer” is a myth, because we have the magic of nutrients that are capable of stimulating energy production as already described. The “bedside manner” is valuable because a sense of confidence and trust results in energy conservation. Remember the proverb “worry killed the cat”.

Illness and the Lack of Energy

As essentially fragile organisms, we live in a situation of personal stress. We are surrounded by micro-organisms ready to attack us. We have built a culture that is enormously stressful in many different ways, I turn once again to the writings of Hans Selye, who advanced the idea that we are suffering from “the diseases of adaptation”. He recognized that some form of energy was absolutely essential to meet any form of physical or mental stress. One of his students was able to produce the general adaptation syndrome in an animal by making the animal thiamine deficient. Energy metabolism in Selye’s time was poorly understood. Today the role of thiamine is well known. As I have described in other posts and in our book, the lower part of the brain that controls adaptive mechanisms throughout the body is highly sensitive to thiamine deficiency. Alcohol, and sugar in all its forms, both overload the process of oxidation. Although energy metabolism depends on many nutrients, thiamine is vital to the function of mitochondria and its deficiency appears to be critical. Because the brain and heart are the dominant energy consumers it is no surprise to find that beriberi has its major effects in those two organs. Symptoms are just expressions of oxidative inefficiency of varying severity. This is the reason why 696 medical publications have reported varying degrees of success in the treatment of 240 diseases with thiamine. Its ubiquitous use as a drug depends on its overall ability to restore an adequate energy supply by stimulating mitochondrial function. It is also why I propose that energy deficiency is the true root of modern disease.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

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This article was published originally on November 19, 2019.

Rest in peace Derrick Lonsdale, May 2024.

Gastrointestinal Disease and Thiamine

by Derrick Lonsdale MD, FACN, CNS

Published on June 9, 2025

19.8K views

The gastrointestinal (GI) tract, long thought to be specific only to the process of digestion, starts at the mouth and ends at the anus. Modern research has revealed that it has a very complex relationship with the rest of the body, especially the brain, and this post is aimed at giving the reader a glimpse of this research.

The Impact of Medication on the GI Tract

Every year many new medications are approved for clinical use, several of which can cause clinically significant GI tract toxicity. An article in the medical literature describes the drug-induced injury to the fragile lining of the tract. A drug by the name of Flagyl is used for resistant bacterial infections. Its chemical name is metronidazole and occasionally it results in the complication of encephalopathy (brain disease). It has been proposed that the adverse effects of the drug may be due wholly or in part to its conversion to a thiamine analog (the drug has a similar formula to thiamine and acts as an antagonist to the action of the vitamin). It seems that this happens enough that a Metronidazole Toxicity group has been formed online and has a considerable number of people with complaints regarding the use of this drug. Because the encephalopathy is said to be uncommon, it is apparently accepted as an occasional side effect, even though many people have been crippled from its use. The number of people reporting serious symptoms in the Toxicity group tends to negate the conclusions of officialdom that this encephalopathy is “uncommon, if not rare”.

Thiamine Deficiency and Obesity

This is defined by a formula known as the body mass index. Obesity is a growing worldwide epidemic currently affecting one in 10 adults. In the United States the incidences is as high as 40%. A publication claims that the only proven long-term treatment of severe obesity is surgical modification of the gastrointestinal anatomy, termed bariatric surgery. Complications are seen in patients who fail to follow the recommended changes in lifestyle. They include nausea, vomiting, so-called dumping syndrome, acid reflux and nutritional deficiencies. The authors note that “despite caloric density, the diet of patients prior to bariatric surgery is often of poor nutrient quality“. Unfortunately it needs to be pointed out that it is exactly why they became obese in the first place. Bariatric surgery is “shutting the stable door after the horse has gone”. Although obesity has been viewed traditionally as a disease of excess nutrition, the evidence suggests that it may also be a disease of malnutrition. Thiamine deficiency (TD) was found in as many as 29% of obese patients seeking bariatric surgery. They can present with vague signs and symptoms. In many posts on this website it has been pointed out that high calorie malnutrition is a widespread scourge in America and is responsible for the high incidence of obesity. The “vague signs and symptoms” are typical of early TD (beriberi) and are often misdiagnosed as psychosomatic.

Constipation or Diarrhea

The commonest form of bypass surgery for obesity, without going into the details, is known as Roux-en-Y. I do not know the reason for this nomenclature, but for surgeons it defines the technique. A publication in the medical literature described thiamine deficiency after gastric bypass and hypothesized that this is common. Of 151 patients, 27 met the criteria for thiamine deficiency, a prevalence of 18%. Eleven of these patients reported constipation after the surgery and treatment with thiamine improved it.

A 29-year-old patient has been described who had experienced sudden blindness and a disturbance of consciousness after two months of chronic diarrhea and minimal food intake. Amongst other physical signs, hemorrhages were seen in the eye. Leaking of blood from capillaries has long been recognized as a phenomenon that might be found in thiamine deficiency. It is of particular interest that the examination of cerebrospinal fluid revealed it to be normal, but magnetic resonance imaging showed changes that were interpreted as typical of thiamine deficiency. After administration of intravenously administered thiamine, both visual acuity and the visual field rapidly improved with the simultaneous recovery of consciousness. No indication was provided to explain a two-month period of diarrhea, although it was accompanied by “minimal food intake”.

A patient with Crohn’s disease and long-standing diarrhea resulted in combined thiamine and magnesium deficiency. Despite massive doses of thiamine given intravenously the symptoms of the deficiency could not be suppressed until the magnesium deficiency was also corrected. Many posts on Hormones Matter have discussed the relationship of magnesium with thiamine. Both of them work together as cofactors for a number of vitally important enzymes that govern energy metabolism. Obviously, literally any lapse of health can occur if energy is insufficient to meet the demands of living. Therefore, it is possible to understand that fatigue and other disorders related to ulcerative colitis and Crohn’s disease are the manifestation of an intracellular mild thiamine deficiency.

It is important to note that, in spite of finding the levels of thiamine and thiamine pyrophosphate in the blood to be normal, 10 patients out of 12 showed complete regression of fatigue and 2 patients showed partial regression when thiamine was administered. Note the doses of thiamine that were given. They ranged from 600 to 1500 mg/day given by mouth. The thing to understand here is that this was not simple vitamin replacement. These authors were using thiamine as a completely non-toxic drug, revealing genuine pioneering. Other authors have noted that micronutrient deficiencies occur in Crohn’s disease. They reported two patients with Crohn’s disease who complained of sudden-onset eye and brain dysfunction and confusion while receiving prolonged total parenteral nutrition. Magnetic resonance imaging allowed definitive diagnosis of Wernicke encephalopathy, a well-known brain disease occurring as a result of thiamine deficiency.

The Gut – Brain Connection

Within the last decade, the complement of bacteria living in the human bowel, now known as the gut microbiome, has become a focus of attention. The GI tract was once regarded simply as a digestive organ, but recent research has led to finding that the microbiome may have an impact on human health and disease. Surprisingly, it has become a focus of research for those interested in the brain and behavior. Multiple routes of communication between the gut and the brain have been established. Recently the gut microbiota (the complement of bacteria) has been profiled in a variety of conditions, including autism, major depression and Parkinson’s disease. Of course, there is still debate as to whether or not the changes observed are primary in causing the disease or merely a reflection of it. Other authors have raised the question of the importance of the microbiota in the pathology associated with autism, dementia, mood disorders and schizophrenia. It is interesting that the GI microbiome has been regarded as a complex ecosystem that reportedly establishes a symbiotic mutually beneficial relation with the host. It is said to be rather stable in health, but affected by age, drugs, diet, alcohol and smoking. Smoking leads to modifications of the bacterial complement and is linked with absence of a protective effect toward ulcerative colitis, and deleterious for Crohn’s disease.

An interesting slant has been placed on this problem of relationship between the host and the bacteria which make up the microbiome. It is pointed out that thiamine is an essential cofactor for all organisms, including bacteria and the role that gut microbes play in modulating thiamine availability is poorly understood. Little is known about how thiamine impacts the stability of microbial gut communities. In order to study this, a model gut microbe (Bacteroides thetaiotaomicron) was chosen. The study showed that thiamine acquisition mechanisms used by this microorganism not only are critical for its physiology and fitness but also provide the opportunity to model how other gut microbes may respond to the shifting availability of thiamine in the gut. Importance of this means that the variation in the ability of gut microbes to transport, synthesize and compete for thiamine is expected to impact on the structure and stability of the microbiota. The authors conclude that this variation may have both direct and indirect effects on human health.

The Role of Energy Metabolism

The question of whether bacterial changes in the gut are primary or secondary makes us think of which is the “chicken” and which is the “egg”. Bacteria are complex one-celled organisms and they require energy to perform their normal function, just the same as our body cells. Therefore, thiamine is as important to bacteria as it is to us, bringing us back to considering the frontier of medical thinking that energy metabolism is the core issue of health and disease.

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Image by Andrew Martin from Pixabay.

This article was published originally on May 6, 2019.

Rest in peace Derrick Lonsdale, May 2024.

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