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Understanding Mitochondrial Energy, Health and Nutrition

Published on March 2, 2023

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I live in a retirement community. In my everyday discussions with fellow residents, I find that the idea of energy metabolism as the “bottom line” of health is almost completely incomprehensible. Since my friends are all well-educated professional people, I came to the conclusion that few people really have an idea about energy. For example, we talk about people who indulge in physical sports being energetic, while people sitting behind a desk are classed as sedentary. What we fail to realize is that mental processes require even more energy than physical processes. Both physically and mentally active people consume energy, so it is obvious that some kind of attempt must be made to talk about energy as it applies to the human body.

Hans Selye and the Stress Response

I will begin by giving an outline of the work that was performed many years ago by a Canadian scientist by the name of Hans Selye. Originally he was a Hungarian medical student. Some of the teaching was done by presenting individual patients to the class of students. The professor would describe the details of the disease for each person. What interested Selye was that the facial expression of each patient appeared to him to be identical. He came to the conclusion that this was the facial expression of suffering, irrespective of the nature of the disease. He referred to this as the patient’s response to what he called “stress”. He decided to study the whole concept of stress. He immigrated to Canada and in Montréal he set up a research unit that came to be called “The Research Institute of Stress”.

Of course, Selye could not study human beings and his experiments were performed on literally thousands of rats. He subjected them to many forms of physical stress and detailed the laboratory and histological results. He found that each animal would begin by mustering the well-researched fight-or-flight reflex. If the stress was continued indefinitely, the metabolic resistance of the animal gradually decayed. He called this ability of the animal to resist stress the “General Adaptation Syndrome” and came to the conclusion that it was driven by some form of energy. If and when the supply of energy was exhausted, he found laboratory changes in blood and tissues that were listed carefully. Although extrapolating this information from animal studies, he ended up by saying that humans were suffering from “diseases of adaptation” and that they were the result of a failure to adapt to the effects of life stresses.

My addition to this is that it would have been better to describe them as “the diseases of maladaptation”, meaning that humans have to have some form of energy to meet life. If there is energy failure, disease will follow. The remarkable thing is that energy production in the human body was virtually unknown in Selye’s time, so his conclusion was a touch of genius. The mechanism by which energy is produced in the cells of the body is now well-known. We know that energy consumption is greatest in the lower part of the brain and the heart, organs that work 24 hours a day throughout life. The lower part of the brain that organizes and controls our adaptive capabilities is particularly energy consuming. So before we begin to think about energy as a driving force, let us consider what we mean by stress and how we adapt to it.

Human Stress: Surviving a Hostile Environment

We all live in an environment that is essentially hostile. We have to adapt to natural changes such as cold, hot, wet and dry. We are surrounded by enemies in the form of microorganisms and when they attack us, we have to set up a complex mechanism of defense. Add to this the possibility of trauma and the complexity of modern civilization, involving business and life decisions. We possess the machinery that enables us to meet these individual stresses, meaning that we are adapting. Health means that we adapt successfully and that is why “diseases of maladaptation” makes a lot of sense. Obviously, the key is that the machinery requires energy.

Energy Metabolism, Physics, and Chemistry

First of all, let us begin by trying to define energy. The dictionary describes it as “a force” and the only way in which we can appreciate its nature is by its effects. It is not a substance that we can see but the effects of light energy enable us to have vision. The old riddle might be mentioned; “Is there a sound in the forest when a tree falls?” The answer is of course that the only way that the resultant energy can be perceived is when it is felt by the human ear. Even that is not the end of the story, because the ear mechanism has to send a message to the brain where the sound is perceived. Thus, there is no sound in the forest when a tree falls. It is the perception of a form of energy, a force that impacts on the ear of any animal endowed with the ability to hear. Energy can be stored electrically in a battery or as heat energy in a hot water bottle, but the inevitable process is that the energy drains away. A hot cup of coffee cools. A battery gives up its stored energy and becomes just “another lump of matter”.

For example, if a stone is rolled up a hill, its natural tendency would be to roll down the hill again. Whatever force is being used to roll the stone up the hill is known as “potential energy”. In other words, there has to be a constant supply of energy as long as the stone is moving up a gradient against gravity. When it reaches the top, we say that the potential energy is being stored in the stone. It is the equivalent of electricity being stored in a battery. The “potential energy”, however, requires an electrical force to “electrify” the battery. The potential energy in the stone can be released by allowing it to roll down the hill and Newton called this kind of energy “kinetic” (the use of a force to produce movement). The force that is being used is of course the effect of gravity and the stone becomes stationary when it gets to the bottom of the hill. The use of gravity as the source of energy is simply wasted, but note that gravity has not changed. It is still available for use. Let us take a simple example of this energy being used for a purpose. Suppose that there is a wall at the bottom of the hill and a farmer wishes to create a gate. In a fanciful way he could use the stone to create a gap in the wall. The gap in the wall is the observable mark of the effect produced by consumption of kinetic energy.

The body consists of between 70 and 100 trillion cells, each of which has a special function. Each is a one-celled organism in its own right and in order to perform their function they need a constant supply of energy. This is developed by complex body chemistry. The “engines” in each cell are called mitochondria and one of their many different functions is to synthesize energy. The energy that is developed is stored in a chemical substance known as adenosine triphosphate (ATP) and in order to understand this a little more, perhaps we should think of the Newtonian analogy for comparison. The Newtonian hill is replaced by an electronic gradient and the stone by the chemical ATP

Of Mitochondria and ATP

Cellular energy is produced in the mitochondria by oxidative metabolism. This simply means that a fuel (glucose) combines with oxygen but, like any fuel, it has to be ignited. The best way to analogize that is to say that thiamine can be compared with a spark plug that ignites gasoline in a car. It “ignites” glucose. The resultant energy is used to add a phosphate molecule to adenosine three times to make ATP (the electronic gradient). We have “rolled an electronic stone up an electronic hill”. As the adenosine donates phosphate molecules, it becomes adenosine monophosphate (AMP) that must be “rolled uphill again”. As it is “rolling down the electronic hill”, it is transferring energy. Therefore, ATP can be thought of as an energy currency. Note that there must be a continuous supply of fuel (food) that must contain the equivalent of a spark plug (thiamine) in order to maintain an energy supply with maximum efficiency.

The loss of any one of a huge number of components in food that work in a team relationship with thiamine, lowers the energy maximum. That is why thiamine deficiency has been earmarked as the major cause of a disease called beriberi that has haunted mankind for thousands of years. Its deficiency particularly affects the lower part of the brain and the heart because of their huge energy demand. Since the lower brain contains the control mechanisms that enable us to adapt to the environment, as depicted above, it is easy to see that we would be maladapted if there is energy deficiency, just as Selye predicted. In fact, one of his students was able to produce a failure of the General Adaptation Syndrome by making his experimental animals thiamine deficient. It also suggests that a lot of heart and brain disease is really nothing more than energy deficiency that could be easily treated in its early stages. If the energy deficiency is allowed to continue indefinitely because of our failure to recognize the implications, it would not be surprising that changes in structure would develop and produce organic disease.

Health and Disease in the Context of Energy

With this concept in view, the present disease model looks antiquated. There are only three factors to be considered. The first one is obviously our genetic inheritance. If it is perfect, all it requires is energy to drive it. However, DNA is probably never perfect in its formation. It may not be imperfect enough to cause disease in its own right, but a slight imperfection would constitute what I call “genetic risk”, causing disease in association with a stressor such as an otherwise mild infection or trauma.

Suppose that a given patient died from an infection (think of the 2018 flu).The present medical model would place the blame on the pathogenic virulence of the virus without considering whether malnutrition played a part by failing to produce sufficient energy for the complex immune response. Therefore, the second factor to be considered is the perfection of the fuel supply and that obviously comes from the quality of nutrition. Stress (the viral attack or non-lethal trauma) becomes the third consideration, since we have shown that an adequate energy supply is required for adapting on a day-to-day basis. There is even a new science called epigenetics in which it has been shown that nutrient components can be used to upgrade genetic mistakes in DNA. A fanciful interpretation of these three factors, genetics, nutrition and stress can be portrayed by the use of Boolean algebra. This is a mathematical representation as interlocking circles. The area of each circle can be easily assessed, marking their relative importance. The interlocking area between any two of the three circles and that of the three circles together completes the picture. It becomes easy to perceive how a prolonged period of stress can impact health. The present flu epidemic may be an example of the Three Circles of Health in operation, explaining why some people have only a mild illness while others die. Could the appalling nutrition in America play a part?

Why Thiamine

The pain produced by a heart attack has always been a mystery in explaining why and how it occurs. The answer of course is that pain is always felt by sensory apparatus in the brain. The brain is able to identify the source of the signal as coming from the heart but cannot interpret the reason. I am suggesting that in some cases, the heart is having difficulties from energy deficiency and notifying the brain. A coronary thrombosis would introduce local energy deficiency, but other methods of producing energy deficiency would apply. It is logical to assume also that brain disease is a manifestation of cellular energy deficiency. That is why I had found that so many children referred to me for various mental conditions responded to megadoses of thiamine. It is also why I had found that so much emotional disease was related to diet and not to poor parenthood.

I recently came across a patient that I had seen many years ago when he was a child. He had a diagnosis of Tourette’s syndrome, made elsewhere. I treated him with megadoses of thiamine and his symptoms resolved completely. Medical skepticism would answer this by calling it a placebo effect, but since this effect is well-known, it must have a mechanism. For many years I have believed that therapeutic nutrition “turns on” this effect by enhancing cellular energy. A small group of physicians known as “Alternative Medicine Practitioners” use water-soluble vitamins, given intravenously, irrespective of the acceptable clinical diagnosis. For example, I remember a young woman who came to see me with a diagnosis of “Thrombocytopenic Purpura”. This disease is a loss of cellular elements known as platelets and it had resisted orthodox treatment for years. I gave her a series of intravenous injections of water soluble vitamins with complete resolution of the problem. I must end by stating that healing is a function of the body. The only way that a healer can be justifiably recognized is by supplying the body with the ingredients that it requires to carry out the healing process. Perhaps spontaneous healing, as for example initiated by religious belief, is an ability to muster those ingredients that are present, but hitherto unused.

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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 February 14, 2018.

Food Composition and Hyperglycemia

by Chandler Marrs, PhD

Published on February 14, 2023

5164 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.

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.

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This article was published originally on October 28, 2021.

Problems With the Medical Model of Disease

by Derrick Lonsdale MD, FACN, CNS

Published on December 19, 2022

6274 views

The use of the word model is supposed to describe the nature of disease as it differs from that of health. Hippocrates was the first person to offer a solution to the preservation of health by saying “Let food be your medicine and let medicine be your food”. Throughout most of history there was no model and treatment was based on largely futile ideas. The present age of medical thinking was ushered in by the discovery of disease producing microorganisms. The model became “kill the microorganism, the bacterium, the virus, the cancer cell”. If no microorganism or cancer cells could be found, the remaining diseases were long considered to be a mystery.

Recent research has advanced the model by discovering that the brain controls inflammation through the vagus nerve by the use of metabolites called cytokines. However, the present medical model still dictates that the various symptoms that signify loss of health are put together in collections. Each is considered to represent a particular disease that has to be named for diagnostic purposes and that a cure for each is to be found from detailed research. So we now have literally thousands of different diseases, often being called after the person who first observed a particular symptom/sign collection, such as Parkinson or Alzheimer. Each of the named diseases is supposedly recognized by a collection of laboratory tests that are “diagnostic”. What is even worse, is that this collection is often called a syndrome and the first observer has his/her name appended. From that time on, this particular collection is known as “Joe Soap’s syndrome”. Fortunately, there is change on the horizon as we gradually realize that the human body is a “machine” whose function is metabolic in nature.

The Stress of Life

When I was in active practice, I discovered that thiamine could be used as a “drug” for many of the situations that I encountered, seemingly irrelevant to the diagnostic category with which I was supposedly dealing. I was thought of by my colleagues as a medical heretic. Since it had long been known that thiamine deficiency was responsible for the disease called beriberi, I studied the history of the early attempts to find its cause. Beriberi had existed for thousands of years and was still largely a mystery at the end of the 19th century. I found how easy it was for the investigators to be misled. In Eastern cultures rice had been a staple for centuries. At that time, factories had been built in China in which buildings had been separated by a corridor. In the summer months the workers would congregate in them to take their lunch. As the sun moved around, it would shine on the congregated workers and several of them would come down simultaneously with the first symptoms of beriberi. The obvious conclusion for the investigators was that this was some kind of infection since several of them had succumbed at the same time. When it was found that thiamine deficiency was responsible, an explanation was required for this simultaneous incidence of the disease.

We now know that ultraviolet light is a source of stress. It can be concluded that the affected workers had been marginally deficient in thiamine. They were either asymptomatic or had mild symptoms attributed to other causes. The stress caused by sunlight had provoked symptoms of the disease simply because the required energy was unavailable to achieve homeostasis. This intriguing discovery caused me to seek the work of Hans Selye, whom I visited in Canada. As I have written in several posts on this website, he had determined from the study of rats that each form of stress had to be resisted and required energy. He called it the General Adaptation Syndrome (GAS) and offered the idea that human disease was a lack of sufficient energy required for adapting to the more severe environmental influences encountered on a daily basis. This included severe trauma and infections. The energy deficiency conclusion of Selye was later backed up by one of his students who was able to produce the GAS experimentally in a thiamine deficient rat without using any form of experimental stress.

It seemed to me to be obvious that I had to study the way energy is produced in the human body if I were to understand the reality of health and disease. In Selye’s time energy metabolism was poorly understood and it was a mark of his genius that enabled him to suggest that it was energy deficiency that caused the collapse of the GAS. The reason that all animals, including humans, are living is because they construct energy from food and this creates a chemical called adenosine triphosphate (ATP). From there, electrical energy has to be created and that is the energy that we use for functional activity. The transition from chemical to electrical energy is not precisely known but there is some evidence that thiamine in the form of thiamine triphosphate (note the parallel with ATP) plays an important part. This triphosphate form is exceptionally high in the electric organ of the electric eel, capable of producing a paralyzing shot of electrostatic electricity to zap its prey. The electric organ is an adaptation of a nerve ending just like ours. It is obviously important to understand that this is an evolutional adaptation and does not mean that we can produce a high energy output from our nerve endings. Indeed, the evidence is strongly in favor of the energy being in microvolts. We are identifying the electrical potential when we perform an electroencephalogram or an electrocardiogram and a recent test has been devised using the electrical potential of a person with Chronic Fatigue Syndrome (Open Medicine Foundation April 2, 2021).

Many of the people reading the information on this website are themselves patients seeking help for their misunderstood disease. The history recorded in their posts is repetitive and in each case their reported symptoms are usually thought to be bizarre by the physicians that have been consulted. In the present medical model a “real” disease is called organic and is marked by a series of abnormal laboratory tests. When these tests are reported to be normal, the conclusion is nearly always the same. The symptoms are considered to be imaginary in a person who is thought to be psychologically abnormal. They are referred to as psychosomatic and the patient is told that “it is all in your head”. It is always surprising to me that the physician seems to have the belief that the bizarre nature of the symptoms is generated in the patient’s brain without consumption of energy, that thought processes or imagination are not the result of energy consumption by brain cells.

Distorted Truth

The real trouble is that the disease model represents a distortion of the truth. To make a diagnosis, it is inherently necessary that some of the presently used laboratory tests must be abnormal. No thought is given to the possibility that energy deficiency in the brain might be the cause of the symptoms. Therefore no effort is made to obtain the right laboratory tests. It demands a totally different way of thinking about health and disease. People affected by this kind of brain energy deficiency disease are often working and living ostensibly normal lives but suffering greatly. They are in fact experiencing early beriberi, a disease that has a long morbidity and a low mortality. They can go on experiencing these symptoms for years, but if they are completely ignored as psychological misfits, one can easily imagine that permanent damage will develop. Perhaps Alzheimer’s and Parkinson’s disease are really reflections of this permanent damage and that there will never be a “cure” for them. Attention to relatively simple symptoms, usually diagnosed and treated as variable named conditions such as “allergy” may be the only way in which these named diseases can be prevented.

To give an example of this kind of thinking, I was confronted by a 12-year-old African-American girl with extremely severe asthma occurring in individual attacks. Physical examination revealed that her body was covered with “goose bumps”. Because of this I came to the conclusion that her autonomic nervous system was dysfunctional and the cause of her asthma. I had already come to the conclusion that thiamine deficiency caused the energy failure that resulted in dysautonomia and that sympathetic/parasympathetic imbalance could affect the bronchial tubes. Without further testing, I gave her thiamine in pharmacological doses. It resulted in a complete disappearance of the asthma. This patient, at the age of 30 years, contacted me to let me know that she had only experienced two mild attacks of asthma in her 20s.

Health Requires Energy

What is important to remember is that any situation involving physical or prolonged mental stress requires energy in the brain, used to organize the complex defenses of the body. The recent discovery by Dr. Marrs and myself that thiamine deficiency in America is common, suggests that brain energy is insufficient in many people. If and when they are attacked by a microorganism such as Covid-19 it is possible their symptoms and their continuation reflect brain energy deficiency. Consequently perhaps they are unable to adapt and overcome the stress of the viral attack. It also suggests that symptoms expressed by so called Longhaulers might be helped by the administration of pharmacological doses of thiamine.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

This article was published originally on April 7, 2021.

Image by Joshua Nicholas Vanhaltren from Pixabay.

Energy Loss as a Cause of Disease

by Derrick Lonsdale MD, FACN, CNS

Published on December 7, 2022

11215 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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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 first published on July 1, 2019.

The Winnowing of the Western Diet: Reconsidering Food Sensitivities

by Chandler Marrs, PhD

Published on May 3, 2022

6157 views

A few weeks ago, I posted some articles on Facebook regarding the need for protein in one’s diet (here, here). I believe that the lack of protein in the modern diet and the subsequent substitution with processed carbohydrates is one of the leading contributors to metabolic disease. Over the last 50 years or so, we have become increasingly afraid of eating protein and fat. Convinced by industry-sponsored advertising and ill-conceived medical science postulating that only calories matter and that eating fat makes one fat, we avoided the higher calorie foods like meat and shifted our diets towards lab manipulated but lower calorie and lower fat, ultra-processed carbohydrates. This has left much of the population starved for both macro (protein, fats, and plant-based carbohydrates) and micro (vitamins and minerals) nutrients. Ironically, the push to avoid high-calorie foods has resulted in higher calorie intakes in those who regularly consume ‘low-calorie’ foods than those who consume the higher calorie whole foods.

Similarly ironic, a corresponding form of malnutrition develops as a result of the low nutrient content in these industrial foods – this despite nutrient fortification. We have labeled this type of malnutrition as high calorie malnutrition. It is a metabolic starvation of sorts that develops concurrently with obesity, but also, with many disease processes including, I would suspect, food sensitivities. With the choice of highly processed foods, excessive calories must be consumed to meet the minimum nutrient requirements. Sugar is metabolically easy energy. So too is fat. Protein, by comparison, is not. Unfortunately, sugar, though technically energy-rich, is nutrition poor, and therein lies much of the problem. Worse yet, the fats used in most processed foods are hydrogenated, and thus, provide few health benefits but carry many risks.

When I bring up the notion of eating more protein, fat, or simply eating more nutrient-dense foods in general, I am met with resistance, sometimes philosophical, but oftentimes, based upon long-entrenched food sensitivities that develop over time, eventually winnowing the number of non-triggering foods down to almost nothing. Over the last several years, the breadth and depth of individual food sensitivities has exploded. Sensitivities to protein and fats, in particular, seem to be growing, but also to fruits and vegetables and, of course, grains. These are not allergies in the traditional sense, though there may be an altered histamine response involved. Rather, they may represent a complicated response to a lack of particular nutrients that results in the inability to digest or metabolize certain foods.

In response to the aforementioned posts on protein, a reader asked:

Chandler Marrs, what about the inability to absorb protein? …About 17 years prior to my husband’s death, he started eating all kinds of junk food (carbs). Every piece of crap he could pick up at Dollar General…he had never had a sweet tooth or liked junk food till then. Visiting with his neurosurgeon after my husband’s death…on diet and progression of his issues, he told me that when [my husband] went to junk food it was for energy, that he was no longer able to absorb protein. He told me that my husband was doing what his body dictated he do, the only thing he could do for energy…

I don’t know the history behind this gentleman’s illness, nor any of the details beyond what was posted above, but I would not be surprised if cancer were involved, perhaps in the brain, either originally or one that metastasized. The reason behind my suspicions is that cancer involves a switch in energy metabolism, wherein sugars are no longer used effectively in the manufacture of ATP – cellular energy – creating a sense of starvation, particularly when other fuels are absent and/or the machinery used to convert the other fuels to energy is deranged. Even if cancer was not part of this gentleman’s illness, the craving for sugars and the suspected inability to absorb or utilize proteins and fats for energy production points to a common metabolic adaptation to a longstanding nutrient-poor diet. It is a chemical conditioning of sorts, much like a drug addiction, that nets cravings for the foods/fuels that maintain the new normal, whatever that state may be.

What is often missed in the discussions of food sensitivities is that to digest and metabolize foods and convert them into usable and beneficial substrates for health, the machinery responsible requires nutrient co-factors e.g. vitamins and minerals. Absent those co-factors, food cannot be processed into ATP in the mitochondria. And absent ATP, none of the other processes in the body work. Since those co-factors come from the foods themselves, it is a reciprocating process. Nutrient dense foods provide the cofactors to process more micro-and macronutrients while effectively producing the requisite ATP. In contrast, nutrient poor foods provide an excess of sugars – potential energy – that can never fully be converted to actual energy or ATP because the machinery responsible for processing those foods is starving for nutrients, and thus, does not work very well. When one is not able to convert the food to energy nor to derive what few nutrients may come with these foods, cascades of ill-health begin. One of those cascades involves storing the excess as fat. To the extent one is able to store this fat, though unsightly, I imagine is a highly adaptive response, as individuals with similarly poor diets who do not or cannot store fat, risk a comparatively higher rate of all-cause mortality.

Returning to the question of food sensitivities, or more appropriately, the inability to digest and metabolize particular foods, I suspect that longstanding dietary factors, along with genetic and/or environmentally induced epigenetic variables, create and then maintain nutrient deficiencies that inhibit one’s ability to ‘eat’ certain foods. Across time and as those foods are avoided, nutrient availability continues to decline. Mitochondrial function is perturbed but adapts to the new environment, resulting in chemical reactions that induce inflammation and the other patterns so common with metabolic disturbances. This may include intense cravings for certain foods that are metabolically more accessible, like sugars. Admittedly, sugars are exactly what a body in this state does not need, but much like the cravings for drugs in an addiction model, I suspect the body has adapted to having this substance present in high concentrations. It has re-regulated itself accordingly, and because of this, both the absence of the substance and the addition of other, metabolically less well-adapted substances, cause great distress chemically. These changes are then experienced symptomatically.

We know from addiction models, that when a substance is present continuously and in high concentrations, the body adapts so that it can maintain some sort of homeostasis and survive. Receptors, transporters, enzymes, and the like, are reregulated. Some upregulate, others downregulate. As this reregulation occurs, the body becomes chemically conditioned to its new state, seeking to maintain it at whatever cost. When what is in excess carries no nutritional value, as it so often does, we have the bonus of starving the enzymes that make metabolism possible, further imperiling health. At the root of much of this reregulation is nutrition or lack thereof. Every enzyme in the body requires nutrient co-factors to function. Absent these nutrients, metabolism falters; not just the metabolism of foods to energy but the metabolism of drugs, the metabolism of neurotransmitters, hormones, and the like. Absent nutrients, we have widespread changes in the totality of our biochemistry. How those changes manifest is dependent upon the individual’s genetic makeup and environment, but make no mistake, they are occurring.

While it is clear that one can avoid many of these problems by eating a nutrient-dense diet, it is not as clear how one recovers these functions once they are lost. Do we simply feed the offending substance until tolerance develops? Or do we tackle the enzyme issues first, supplying the requisite nutrients in the form of supplements so that they function more effectively and then re-introduce the offending foods? I don’t know the answer, but my instincts tell me that enzyme issues have to be addressed first and the vitamin and mineral deficiencies corrected before the offending foods can be reintroduced. What I do know, however, is that something must be done. Human beings cannot live well or for very long without protein and fat. Those are requisite substrates for health.

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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 article was first published on June 20, 2019.

Beriberi: The Great Imitator

by Derrick Lonsdale MD, FACN, CNS

Published on April 12, 2022

32988 views

Because of some unusual clinical experiences as a pediatrician, I have published a number of articles in the medical press on thiamine, also known as vitamin B1. Deficiency of this vitamin is the primary cause of the disease called beriberi. It took many years before the simple explanation for this incredibly complex disease became known. A group of scientists from Japan called the “Vitamin B research committee of Japan” wrote and published the Review of Japanese Literature on Beriberi and Thiamine, in 1965. It was translated into English subsequently to pass the information about beriberi to people in the West who were considered to be ignorant of this disease. A book published in 1965 on a medical subject that few recall may be regarded in the modern world as being out of date and of historical interest only, however, it has been said that “Those who do not learn history are doomed to repeat it”. And repeat it, we are.

Beriberi is one of the nutritional diseases that is regarded as being conquered. It is rarely considered as a cause of disease in any well-developed country, including America. In what follows, are extractions from this book that are pertinent to many of today’s chronic health issues. It appears that thiamine deficiency is making a comeback but it is rarely considered as a possibility.

The History of Beriberi and Thiamine Deficiency

Beriberi has existed in Japan from antiquity and records can be found in documents as early as 808. Between 1603 and 1867, city inhabitants began to eat white rice (polished by a mill). The act of taking the rice to a mill reflected an improved affluence since white rice looked better on the table and people were demonstrating that they could afford the mill. Now we know that thiamine and the other B vitamins are found in the cusp around the rice grain. The grain consists of starch that is metabolized as glucose and the vitamins essential to the process are in the cusp. The number of cases of beriberi in Japan reached its peak in the 1920s, after which the declining incidence was remarkable. This is when the true cause of the disease was found. Epidemics of the disease broke out in the summer months, an important point to be noted later in this article.

Early Thiamine Research

Before I go on, I want to mention an extremely important experiment that was carried out in 1936. Sir Rudolf Peters showed that there was no difference in the metabolic responses of thiamine deficient pigeon brain cells, compared with cells that were thiamine sufficient, until glucose (sugar) was added. Peters called the failure of the thiamine deficient cells to respond to the input of glucose the catatorulin effect. The reason I mention this historical experiment is because we now know that the clinical effects of thiamine deficiency can be precipitated by ingesting sugar, although these effects are insidious, usually relatively minor in character and can remain on and off for months. The symptoms, as recorded in experimental thiamine deficiency in human subjects, are often diagnosed as psychosomatic. Treated purely symptomatically and the underlying dietary cause neglected, the clinical course gives rise to much more serious symptoms that are then diagnosed as various types of chronic brain disease.

Thiamine Deficiency Related Mortality. The mortality in beriberi is extremely low. In Japan the total number of deaths decreased from 26,797 in 1923 to only 447 in 1959 after the discovery of its true cause.
Thiamine Deficiency Related Morbidity. This is another story. It describes the number of people living and suffering with the disease. In spite of the newly acquired knowledge concerning its cause, during August and September 1951, of 375 patients attending a clinic in Tokyo, 29% had at least two of the major beriberi signs. The importance of the summer months will be mentioned later.

Are the Clinical Effects Relevant Today?

The book records a thiamine deficiency experiment in four healthy male adults. Note that this was an experiment, not a natural occurrence of beriberi. The two are different in detail. Deficiency of the other B vitamins is involved in beriberi but thiamine deficiency dominates the picture. In the second week of the experiment, the subjects described general malaise, and a “heavy feeling” in the legs. In the third week of the experiment they complained of palpitations of the heart. Examination revealed either a slow or fast heart rate, a high systolic and low diastolic blood pressure, and an increase in some of the white blood cells. In the fourth week there was a decrease in appetite, nausea, vomiting and weight loss. Symptoms were rapidly abolished with restoration of thiamine. These are common symptoms that confront the modern physician. It is most probable that they would be diagnosed as a simple infection such as a virus and of course, they could be.

Subjective Symptoms of Naturally Occurring Beriberi

The early symptoms include general malaise, loss of strength in knee joints, “pins and needles” in arms and legs, palpitation of the heart, a sense of tightness in the chest and a “full” feeling in the upper abdomen. These are complaints heard by doctors today and are often referred to as psychosomatic, particularly when the laboratory tests are normal. Nausea and vomiting are invariably ascribed to other causes.

General Objective Symptoms of Beriberi

The mental state is not affected in the early stages of beriberi. The patient may look relatively well. The disease in Japan was more likely in a robust manual laborer. Some edema or swelling of the tissues is present also in the early stages but may be only slight and found only on the shin. Tenderness in the calf muscles may be elicited by gripping the calf muscle, but such a test is probably unlikely in a modern clinic.

In later stages, fluid is found in the pleural cavity, surrounding the heart in the pericardium and in the abdomen. Fluid in body cavities is usually ascribed to other “more modern” causes and beriberi is not likely to be considered. There may be low grade fever, usually giving rise to a search for an infection. We are all aware that such symptoms come from other causes, but a diet history might suggest that beriberi is a possibility in the differential diagnosis.

Beriberi and the Cardiovascular System

In the early stages of beriberi the patient will have palpitations of the heart on physical or mental exertion. In later stages, palpitations and breathlessness will occur even at rest. X-ray examination shows the heart to be enlarged and changes in the electrocardiogram are those seen with other heart diseases. Findings like this in the modern world would almost certainly be diagnosed as “viral myocardiopathy”.

Beriberi and the Nervous System

Polyneuritis and paralysis of nerves to the arms and legs occur in the early stages of beriberi and there are major changes in sensation including touch, pain and temperature perception. Loss of sensation in the index finger and thumb dominates the sensory loss and may easily be mistaken for carpal tunnel syndrome. “Pins and needles”, numbness or a burning sensation in the legs and toes may be experienced.

In the modern world, this would be studied by a test known as electromyography and probably attributed to other causes. A 39 year old woman is described in the book. She had lassitude (severe fatigue) and had difficulty in walking because of dizziness and shaking, common symptoms seen today by neurologists.

Beriberi and the Autonomic Nervous System

We have two nervous systems. One is called voluntary and is directed by the thinking brain that enables willpower. The autonomic system is controlled by the non-thinking lower part of the brain and is automatic. This part of the brain is peculiarly sensitive to thiamine deficiency, so dysautonomia (dys meaning abnormal and autonomia referring to the autonomic system) is the major presentation of beriberi in its early stages, interfering with our ability for continuous adaptation to the environment. Since it is automatic, body functions are normally carried out without our having to think about them.

There are two branches to the system: one is called sympathetic and the other one is called parasympathetic. The sympathetic branch is triggered by any form of physical or mental stress and prepares us for action to manage response to the stress. Sensing danger, this system activates the fight-or-flight reflex. The parasympathetic branch organizes the functions of the body at rest. As one branch is activated, the other is withdrawn, representing the Yin and Yang (extreme opposites) of adaptation.

Beriberi is characterized in its early stages by dysautonomia, appearing as postural orthostatic tachycardia syndrome (POTS). This well documented modern disease cannot be distinguished from beriberi except by appropriate laboratory testing for thiamine deficiency. Blood thiamine levels are usually normal in the mild to moderate deficiency state.

Examples of Dysfunction in Beriberi

The calf muscle often cramps with physical exercise. There is loss of the deep tendon reflexes in the legs. There is diminished visual acuity. Part of the eye is known as the papilla and pallor occurs in its lateral half. If this is detected by an eye doctor and the patient has neurological symptoms, a diagnosis of multiple sclerosis would certainly be entertained.

Optic neuritis is common in beriberi. Loss of sensation is greater on the front of the body, follows no specific nerve distribution and is indistinct, suggestive of “neurosis” in the modern world.

Foot and wrist drop, loss of sensation to vibration (commonly tested with a tuning fork) and stumbling on walking are all examples of symptoms that would be most likely ascribed to other causes.

Breathlessness with or without exertion would probably be ascribed to congestive heart failure of unknown cause or perhaps associated with high blood pressure, even though they might have a common cause that goes unrecognized.

The symptoms of this disease can be precipitated for the first time when some form of stress is applied to the body. This can be a simple infection such as a cold, a mild head injury, exposure to sunlight or even an inoculation, important points to consider when unexpected complications arise after a mild incident of this nature. Note the reference to sunlight and the outbreaks of beriberi in the summer months. We now know that ultraviolet light is stressful to the human body. Exposure to sunlight, even though it provides us with vitamin D as part of its beneficence, is for the fit individual. Tanning of the skin is a natural defense mechanism that exhibits the state of health.

Is Thiamine Deficiency Common in America?

My direct answer to this question is that it is indeed extremely common. There is good reason for it because sugar ingestion is so extreme and ubiquitous within the population as a whole. It is the reason that I mentioned the experiment of Rudolph Peters. Ingestion of sugar is causing widespread beriberi, masking as psychosomatic disease and dysautonomia. The symptoms and physical findings vary according to the stage of the disease. For example, a low or a high acid in the stomach can occur at different times as the effects of the disease advance. Both are associated with gastroesophageal reflux and heartburn, suggesting that the acid content is only part of the picture.
A low blood sugar can cause the symptoms of hypoglycemia, a relatively common condition. A high blood sugar can be mistaken for diabetes, both seen in varying stages of the disease.

It is extremely easy to detect thiamine deficiency by doing a test on red blood cells. Unfortunately this test is either incomplete or not performed at all by any laboratory known to me.

The lower part of the human brain that controls the autonomic nervous system is exquisitely sensitive to thiamine deficiency. It produces the same effect as a mild deprivation of oxygen. Because this is dangerous and life-threatening, the control mechanisms become much more reactive, often firing the fight-or-flight reflex that in the modern world is diagnosed as panic attacks. Oxidative stress (a deficiency or an excess of oxygen affecting cells, particularly those of the lower brain) is occurring in children and adults. It is responsible for many common conditions, including jaundice in the newborn, sudden infancy death, recurrent ear infections, tonsillitis, sinusitis, asthma, attention deficit disorder (ADD), hyperactivity, and even autism. Each of these conditions has been reported in the medical literature as related to oxidative stress. So many different diseases occurring from the same common cause is offensive to the present medical model. This model regards each of these phenomena as a separate disease entity with a specific cause for each.

Without the correct balance of glucose, oxygen and thiamine, the mitochondria (the engines of the cell) that are responsible for producing the energy of cellular function, cannot realize their potential. Because the lower brain computes our adaptation, it can be said that people with this kind of dysautonomia are maladapted to the environment. For example they cannot adjust to outside temperature, shivering and going blue when it is hot and sweating when it is cold.

So, yes, beriberi and thiamine deficiency have re-emerged. And yes, we have forgotten history and appear doomed to repeat it. When supplemental thiamine and magnesium can be so therapeutic, it is high time that the situation should be addressed more clearly by the medical profession.

We Need Your Help

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

Yes, I would like to support Hormones Matter.

This article was published originally on November 4, 2015.

Hormones, Hysterectomy, and the Aging Brain

by Chandler Marrs, PhD

Published on April 7, 2022

11495 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.

Digging Deeper into Mitochondrial Dysfunction

by Chandler Marrs, PhD

Published on April 5, 2022

15036 views

When you have a hammer, everything becomes a nail, or so they say. I worry about this as I dig deeper into mitochondrial dysfunction. Could all of these disparate symptoms and conditions have their roots in the mitochondria? Could it be that simple? Perhaps. More and more, as I search for explanations for the devastating symptoms that so many of our readers report, the research I find points to mitochondrial dysfunction. Sure, changes in gut microbiota and function are apparent and often related and certainly immune dysregulation is a component of these illnesses, but the underlying connection among these disturbances seems inevitably and inextricably linked to dysfunctional mitochondria as the central hub of illness. Heal the mitochondria, heal the body is quickly becoming my new mantra.

Mitochondria as Danger Sensors

Some researchers argue that the mitochondria are the danger sensors for host organisms; having evolved over two billion years to identify and communicate signs of danger to the cells within which they reside. The signaling is simple and yet highly refined, involving a series of switches that control cellular energy, and thus, cellular life or death. When danger is present, energy resources are conserved and the immune system fighters are unleashed. When danger is resolved, normal functioning can resume.

If the danger is not resolved and the immune battles must rage on, the mitochondria begin the complicated process of reallocating resources until the battle is won or the decision is made to institute what can only be described as suicide – cell death. Cell death is a normal occurrence in the cell cycle of life. Cells are born and die for all manner of reasons. But when cell death occurs from mitochondrial injury, it is messy, and evokes even broader immune responses, setting a cascade in motion that is difficult to arrest.

And, if the on the battlefield, the host army is understaffed and under-resourced, no matter how hard the immune fighters battle, the fight will be lost, maybe not immediately, but eventually. All sorts of mechanisms will be employed to reallocate and reinforce needed battlements, but they will be for naught, further depleting already scarce host resources, until the decision is made, within the mitochondria, to begin pulling back, withdrawing, and ultimately casting the final orders of cell death.

It’s not Autoimmunity, but Impaired Immunity

I never much liked the war model of health and disease, but it seems to work well as metaphor for immune functioning, as it is far more illustrative and useful than the self-versus non-self-characterization. Really, what army with two billion years of experience, one that contains all of the memories and skills of battles past, would misidentify itself and begin broad scale fratricide – kill itself and its brethren for no other reason but mistaken identity and do so for years on end? Sure, there can be errors, over compensation and other weaknesses in the immune system, but not continued aggression towards itself in some maladaptive response. That makes no sense and contradicts the very notion and function of an immune system – to keep the host organism alive and well. Indeed, when we consider the trillions of microbes – clear non-self entities – that live inside and upon us, the idea that the immune system evolved simply to kill the non selves seems laughable. And so, I reject the concept of autoimmunity, not because the patients who suffer from continued immune system activation are not ill, they are, but because the concept of autoimmunity belies the very nature of immune function and severely limits possible approaches to recovery.

The Naming of Things

Many of you might be thinking ‘what the heck does what we name things have to do with understanding illness?’ Well, the language and the characterization of disease impacts therapeutic choices. In a system where autoimmunity dominates the discussion, survival is predicated on suppressing the invading immune army. Consequently, most therapeutic options for autoimmune disease are immunosuppressant, and mostly they fail. In contrast, if one characterizes immune function by its ability to protect and sustain life by fending off dangers or threats to survival, be they self or non-self, it does not matter, then we can be open to finding causes for those failed battles. We can ask questions like: what resources are missing that would allow the immune army to fend off the danger once and for all or what could heal the damaged cells, scavenge toxicants and oxidants or re-calibrate mitochondrial energy production? When we re-frame the discussion in this way, we open the door to a deeper understanding of health and disease. It is from this perspective, one that says chronic immune activation is not a disease itself but a symptom of an on-going and failing immune battle, that we can get to the mitochondria as the central hub for chronic ill-health.

Evolution and the Mighty Mitochondria

Mitochondria are interesting little buggers, having evolved from the very parasites our immune system sought to protect us against. Called symbionts, the mitochondria were microbial intruders swallowed by the host. In a brilliant move of survival, they somehow convinced the host organism not only not to kill them but to let the mitochondria, a parasitic intruder, run the host’s energy supply. The mitochondria proved their utility and developed a symbiotic relationship with the cells within which they resided. Over time, mitochondria developed a myriad of intricate communication and resource allocation mechanisms to ensure not only their survival but that of their host organism. And so, in many ways, the mitochondria evolved as part of a cooperative and collaborative ecosystem; one in which they sense and communicate danger to the rest of the organism, and if need be, initiate the final death programs; something, they should be loath to do, since their survival depends entirely on host survival.

Clearly though, and from the very beginning, the mitochondria positioned themselves as the brains of the operation. Mitochondria control energy. There is no other resource more important to the living organism than energy. Consider the most consistent sickness behaviors across all illness include, lethargy, fatigue, sleepiness, often followed by muscle and body aches, anorexia or the loss of interest in eating. The reduction in energy is purely a function of mitochondrial resources. The achy muscles are moderated by mitochondrial retractions of energy and the loss of appetite too, mitochondrial diminishments – recall the orexin/hypocretin system. By whatever pathway, declining mitochondrial energy production arises when danger signals, or more appropriately, cell damage signals are communicated. It is then that the immune armies are activated and inflammation sequences unleashed.

What Does Mitochondrial Dysfunction Look Like?

Everything and nothing at the same time. Mitochondrial dysfunction doesn’t lead to one, clear cut disease, even when there are clear genetic markers, but predisposes one to everything. Where mitochondrial damage is felt and the subsequent immune events present is complex and dependent upon the interactions among the host organism’s innate predispositions, environmental exposures and nutritional status, with the latter two significantly influencing each other. The microbial composition of the host, especially in the gut, but also on the skin and the various mucous membranes that interface with the outside world, can also moderate or trigger the danger signals that lead to mitochondrial dysfunction. More often than not though, mitochondrial damage is felt where oxygen demands are greatest, the brain, the heart, the gut, the muscles. Diseases that are currently identified discretely might all have common symptoms – the mitochondria.

Certainly, chronic fatigue should be considered mitochondrial in nature. I don’t think there is a more clear-cut example of mitochondrial dysfunction than severe fatigue, muscle pain and weakness. The question becomes, from where does the dysfunction originate and how can it be fixed or healed?

Migraine, seizures, ataxias and other neurological disorders are emerging as mitochondrial, particularly was more work is done on the hypocretin/orexin system.

Autonomic dysregulation, recognized under the umbrella as dysautonomias are mitochondrial in nature.

Thyroid dysfunction is likely mitochondrial in nature; the interaction between thyroid hormones and mitochondria is direct. Given the mitochondria’s role in steroidogenesis, other hormone systems are likely modulated by mitochondrial functioning.

Research is emerging suggesting that gastrointestinal disturbances, particularly those of dysmotility like IBS, gastroparesis, constipation and pseudo obstruction but also anorexia are mitochondrial in nature. Indeed, the GI system has its own nervous system, called the enteric nervous system. Only 10-15% of GI motility is controlled from brain’s autonomic system. The rest is controlled on site by the enteric system, mostly from cells called the interstitial of cells Cajal – the smooth muscle cells that propagate contractility and rhythm and form the gut barrier between the inside contents and the rest of the body. The mitochondria control energy usage and production here. Mess with these cells, diminish oxygen usage, pull back energy production and all sorts of things go wrong. We can get ill-timed contractions or no contractions at all, making the movement of food stuffs through the GI impossible. Poor absorption and metabolism of nutrients, and increased permeability of the tight junctions allowing for the leaky gut scenario common in many chronic conditions, become prominent and are also symptoms of mitochondrial dysfunction. Even anorexia, the will to eat, can be disturbed significantly by mitochondrial damage.

And I suspect, although I have no evidence to support this claim, in women, mitochondrial damage can express itself in the reproductive organs, especially when oxygen demands are greatest, menstruation and pregnancy. Consider the increasingly painful muscle contractions for some women involved in shedding the uterine lining during menstruation, just as diminished oxygen and energy in other muscles begins the cycle of lactate production and buildup that initiates pain, so too might this happen in the uterus. As mitochondrial deficiencies persist, uterine dysfunction would grow and compensatory immune system mechanisms increase until the compensatory mechanisms take a life of their own. When we consider the mitochondrial influence on GI motility, their influence on uterine function is not difficult to imagine. I have an inkling that endometriosis, the excessive growth of endometrial cells first within the uterus and then in regions of the body where they ought not be, is a protective mechanism, albeit an aberrant and problem causing one, that indicates increased mitogenesis and cell growth as a compensatory reaction to some original mitochondrial inadequacy. How this might happen molecularly provides some intriguing possibilities.

Immune function and inflammatory reactions are directly controlled by mitochondrial signals of danger and so to the extent we see chronic inflammatory conditions, one can look towards mitochondrial resources and the ensuing danger signals for clues towards reducing these reactions. While much of the clinical research is nascent, more and more clinicians, often from disparate specialties and sometimes without recognizing the immune-mitochondrial connections, have made great inroads towards healing and restoring mitochondrial function through diet and nutritional supplementation paired with the reduction and removal of environmental and medical toxins and dietary inflammasomes.

Is Everything a Nail, When One has a Hammer?

Maybe, but I can’t help but thinking that this mitochondrial hammer might be the one to hit the nail on the head and finally make some inroads towards reducing the suffering and burden of chronic disease. Only time will tell. For the moment, however, this is a hammer that deserves more recognition and whether it turns out to be the final clue or not one thing is clear, mitochondrial health is critical for human health. Deny the mitochondria their due and chronic, complicated illness will persist.

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: OpenStax, CC BY 4.0, via Wikimedia Commons

This article was published previously on Hormones Matter in June 2014.

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