pseudo-hypoxia

Mitral Valve Prolapse and Dysautonomia

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Anatomy of the Heart

As everyone knows, the human heart has four chambers. The two upper chambers are the atria and the two lower ones are the ventricles. The left atrium receives oxygenated blood from the lung and passes it into the left ventricle through the mitral valve. The left ventricle then pumps oxygenated blood through the arterial system, delivering nutrients and oxygen to the entire body. The deoxygenated blood goes into the venous system and a central venous channel known as the inferior vena cava delivers this blood into the right atrium. The right atrium passes the venous blood through the tricuspid valve into the right ventricle which then pumps the blood to the lung where oxygen is extracted from the air to oxygenate the blood, thus completing the circulation.

Understanding the Heart Valves

The mitral and tricuspid valves have been described as “watch pocket” valves because their construction reminds us of the kind of pocket in the waistcoats of gentlemen that were used for carrying a watch. They are made of tissues that respond to the increasing pressure caused by the contraction of the ventricles, thus closing the respective apertures between the atria and the ventricles. It is not too difficult to imagine that the pressure generated particularly in the left ventricle is enormous, thus producing “wear and tear” on the tissues that make up the mitral valve. However, it is not that simple and we shall see in this post why mitral valve prolapse is surprisingly common and how it affects health. Prolapse means that the valve is not closing properly. This is because degeneration has occurred in one of the leaflets of the valve and it prolapses into the atrium as the pressure in the ventricle increases. This causes regurgitation of blood from the ventricle to the atrium.

Mitral Valve Prolapse: Incidence and Sex Distribution

Mitral valve prolapse (MPV) is the most common condition affecting the heart valves. Some studies show that it affects 2-3% of all women. It is interesting that it is diagnosed in young women, but the incidence decreases markedly in older women. This decrease in incidence is not seen in the male population which is consistent in both young and old men. As the result of a large study known as the Framingham study, the incidence of MPV is known to affect equal numbers of men and women. The cause for the difference in age distribution in women is unknown. Occasionally, MVP is associated with other heart conditions but it is generally considered that these diseases would have been present with or without MVP. The outcome differs for men and women. Recent studies have indicated that, for men, the requirement for surgical intervention to repair the valve is higher than for women and increases with age.

Mitral Valve Prolapse and Dysautonomia

Patients with MVP frequently have chest pain of undetermined cause. In 1975, 23 patients with deformity of this valve underwent metabolic studies. Chest pain occurred in five of these patients while being tested and in 2 patients a change in the electrocardiogram indicated myocardial ischemia. Lactate (lactic acid production in tissues is related to energy metabolism) abnormalities were reported in 30% of these patients, indicating abnormal metabolic changes. As early as 1979 it was recognized that MVP was associated with defective function of the autonomic nervous system (ANS). It will be remembered that the ANS is automatic and is the nervous system by which the lower part of the brain exercises control over body organs. This introduces a complex association that begs explanation.

In 1994, it was reported that recent research had shown that subsets of patients with MVP had a number of related symptoms that included fatigue, heart palpitations, chest pain, exercise intolerance, breathlessness, dizziness, headache, sleep disorders, gastrointestinal disturbances, cold extremities and panic attacks, classified as MVP syndrome. The lack of a proven cause-and-effect relationship between MVP and panic disorder does not diminish the clinical significance of the high rate of co-occurrence between the two conditions. In 1991, it was suggested that the nonspecific symptoms “with no discernible objective cause who fail to respond to medication” should be ascribed to panic disorder as a possible explanation for symptoms. This illustrates that this polysymptomatic disorder with an unknown explanation and little or no laboratory evidence is often ascribed erroneously to psychosomatic symptomology.

Increased activity of the sympathetic branch of the ANS has been reported in association with MVP, promoting “myxomatous degeneration” in the mitral valve. This branch of the ANS is the system that promotes brain/body action and has a high energy consumption. Sleep apnea, a common disease, is associated with repeated episodes of hypoxemia (reduced blood oxygen) and is considered to be the primary stimulus for sympathetic over activity in these patients.

Hypoxia and Pseudohypoxia

The prevalence of MVP was found to be significantly higher in people living at moderate altitude compared with those living at sea level. The difference is because of the decrease in oxygen concentration in the air. A common disorder occurring at altitude in people that are often regarded as being “unfit” is mountain sickness. Postural phenomena, cardiac arrhythmias and autonomic dysfunction are responsible for pre-syncope (dizziness) and syncope (short passing out spells) in patients with MVP. Of some interest, evidence has been reported that hyperglycemia (high blood sugar) as might be found in a poorly controlled diabetic, produces cellular chemical changes, mimicking the effects of hypoxia on vascular and neural function. This effect has been referred to as pseudohypoxia. The resulting dysfunction in cellular metabolism and accumulation of pyruvate and lactate during thiamine deficiency has been referred to as pseudohypoxia. Low levels of magnesium were found in the blood of some children with MVP and a five week treatment with magnesium chloride decreased the incidence of chest pain. In 1980, 7 patients with neurologic and cardiologic abnormalities in association with MVP were studied. Abnormal muscle biopsies revealed a peculiarity known as “ragged red fibers” (a characteristic of staining for histological examination). The manuscript was later withdrawn, but serum alanine and pyruvate levels were abnormal and clearly showed evidence for thiamine deficiency. “Ragged red fibers” in muscle have been shown to be the result of thiamine deficiency in an animal study.

Oxygen Deprivation and Mitral Valve Prolapse

It appears that some form of deprivation involving inefficient oxygen metabolism is well established as a constant relationship with the incidence of MVP. In order to affect 2-3% of women, the underlying cause must be common. Its polysymptomatic association is clearly produced by inefficient mitochondria that should certainly be recognized for what it is rather than proposing psychologic dynamics. In the large number of patients whose cases I experienced in my practice, with proven thiamine deficiency, I was often puzzled by a complaint of chest pain. It was almost invariably over the left side of the upper chest, reportedly in most cases to be intermittent and disappeared after treatment with thiamine. Because thiamine deficiency was invariably associated with evidence of dysautonomia, I had concluded that this chest pain, sometimes referred to as pseudo-angina, was in some way related to dysfunctional activity of the autonomic nervous system.

We may be making a common mistake by making the wrong associations. The underlying cause of panic attacks, chest pain and all the other symptoms recorded in MVP syndrome are really the result of poor oxidation (pseudohypoxia) similar to oxygen lack (true hypoxia). Oxidation is the consumption of oxygen in the synthesis of cellular energy. Therefore I am proposing here that the reason for the common appearance of MVP syndrome is because of the massive ingestion of sugar throughout the population. This induces an imbalance between the carbohydrate calories and the availability of vitamins involved in their oxidation, particularly thiamine. The symptoms recorded in MVP syndrome are exactly the same as those recorded in beriberi, known for years as the thiamine deficiency disease. Perhaps the reason for an age discrepancy in the diagnosis of MVP in women is a lesser degree of sympathetic nervous system over activity with increasing age.

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BruceBlaus, CC BY-SA 4.0, via Wikimedia Commons.

This article was published previously on July 4, 2018. 

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Why Do We Use Nasal Oxygen?

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I live in a retirement home and I see many residents who are receiving nasal oxygen, so I am going to try here to address the reason. They may have been diagnosed with either heart disease or lung disease and they have probably been observed clinically to be “short of breath”. Of course, I do not know the specific reason for a given individual receiving this treatment, but does the average patient understand why he or she has to tolerate this inconvenience? I strongly suspect that they have merely been told that they need oxygen administration without explaining the underlying reason. Generally speaking, most people take for granted that they are alive and have little interest in why or how, unless their health becomes threatened. Obviously, when nasty things start to occur, they ask a physician why it is happening to them and the physician tries to diagnose the affliction. It usually winds up by the patient being told that it is disease A or B and a superficial description of the disease is provided. Each disease is regarded as having a specific treatment and a specific cure that is usually being sought by a drug company. The most up-to-date drug is offered. Unfortunately, with the exception of bacterial infection, most drugs only treat the symptoms and do not address the underlying cause. Modern research focuses almost exclusively on genetics and for the most part little consideration is given to prevention other than making a diagnosis of early disease. So why are these people receiving nasal oxygen?

Why Do We Need Oxygen?

Of course, we all understand that our environment must supply us with oxygen, water and food, without any of which we die. Although I have written about oxygen utilization in many posts on this website, it bears repetition because of what I want to say about nasal oxygen administration as described above. First of all, it must be stated that the main three gases in air are nitrogen, oxygen and inert gases. Seventy-eight percent of air is made up of nitrogen, 21% is oxygen, just under 1% is argon and the remaining part is made up of other gases such as carbon dioxide and water vapor. In other words, our oxygen intake is dosed. Too much oxygen is as lethal as none at all, illustrating the wisdom that was propounded in ancient China called Yin and Yang, not too much and not too little. The thing that always amazes me is the concise nature of the natural world and how we should fit into it. The more I get to know about the human body the more I realize how little we know. However, we do know what we do with oxygen. It is called oxidation.

Understanding Oxidation

It is surprising to me that many people appear not to understand that when a fuel burns, it is because the fuel is combining with oxygen. The result is the production of energy in the form of heat, the simple physics that we learned in school. The word oxidation is defined as “cause to combine with oxygen”. But consider that a piece of newspaper will not burst into flame by itself. It has to be ignited. If we use a match, the heat generated from striking it on a rough surface is enough to make it burst into flame and that energy in the form of the flame is transferred to the newspaper. What we are looking at is simply the transfer of energy from one action to another. Even striking the match requires the energy of the individual who performs it. But there is another factor that comes into play here. The newspaper will produce what we call ash, representing the fact that the newspaper has not been completely consumed (oxidized). I am providing these simple principles to explain now that this is exactly what happens in the body. The principles are identical: the mechanisms are different.

Cellular Oxidation

Starting with first principles, as we breathe, our lungs are taking in air and extracting oxygen from it. The oxygen is transferred into the bloodstream and picked up by combining with hemoglobin that coats red cells. This represents a transport system and the oxygen has to be delivered to each of the 70 to 100 trillion cells. This in itself is an amazing representation of the blood circulation. The deoxygenated blood is transferred to the venous circulation and transported back to be re-oxygenated. It is now that the process of oxidation takes place in the cells that have received the oxygen. To put it as simply as possible, glucose, the primary fuel, combines with oxygen to yield energy that drives the function of the cell in which the oxidation takes place. Just like the analogy of the newspaper, the combination of glucose with oxygen has to be “ignited”. Thiamine and other vitamins and minerals are the equivalent of a match. Carbon dioxide and water are the equivalent of ash from the newspaper. They have to be got rid of and so they are expired in the breath. Gasoline in a car engine has to be ignited so the explosion in a cylinder might be referred to as oxidation. The smoke in the exhaust pipe is the “ash”.

Nasal Oxygen and Hypoxia

It is my experience is that the use of nasal oxygen, although completely correct in itself, seems to be associated with ignorance of the fact that the sufferer is probably lacking the vitamins and minerals that enable the oxygen to be utilized in the body. Indeed, the lack of vitamins and minerals may be the main issue in the underlying cause of the disease, a fact that is flatly denied by the vast majority of physicians. The word for lack of oxygen in medical literature is hypoxia. The effects of thiamine deficiency, because it causes exactly the same symptoms, is referred to as pseudo-hypoxia (false lack of oxygen). In reality, the symptoms of the patient are caused by lack of oxidation, resulting in lack of cellular energy and consequently, their loss of function. Using the above analogy, it would be like holding a piece of newspaper and expecting it to burst into flame spontaneously. The most recent medical literature is full of manuscripts reporting the relationship of thiamine deficiency with chronic disease, even cancer, and various forms of traumatic surgery. It is not sufficiently recognized that the widespread ingestion of empty carbohydrate calories easily induces inefficient oxidation. This is but another reason why Dr. Marrs and I have written our book “Thiamine Deficiency Disease, Dysautonomia and High Calorie Malnutrition“, available at Amazon books. ‘

Conclusion

Why do so many individuals require nasal oxygen? With the present thought process, the patient is considered to have a condition that would benefit from its administration, perhaps heart or lung disease, operating on the present disease model. Physicians are not really thinking in terms of oxidative metabolism as the underlying mechanism. The point that we are trying to make here is that no amount of extraneously supplied oxygen will be effective unless the vitamins and minerals are present in sufficient quantity for the oxygen to be used in the creation of energy. Oxidation requires the presence of glucose, oxygen and the requisite vitamins and minerals and deficiency of any one of the three will be responsible for the symptoms.

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This article was published originally on April 5, 2018. 

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Hypertension, the Autonomic System, and Thiamine

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Physiological studies have long demonstrated the vital role of the autonomic nervous system in controlling blood pressure values. Beriberi, the classical disease due to thiamine deficiency, is the prototype example of dysautonomia in its early stages. The limbic system and brainstem are peculiarly sensitive to thiamine deficiency. Hypoxia is known to initiate sympathetic nervous system activity. Because thiamine deficiency has effects similar to those of hypoxia, these effects have been referred to in the literature as arising from pseudo-hypoxia.

There is much evidence that the common indulgence of empty calories, particularly those derived from simple carbohydrates and processed fats, is producing pathophysiologic brain effects due to what has been termed high calorie malnutrition. This form of malnutrition is totally different from that produced by starvation, the traditional form of malnutrition. Although the concentration of thiamine in the blood may be considered to be normal, it is only normal in the presence of a healthy diet. The excess of empty calories results in a high calorie/thiamine ratio that overwhelms the normal oxidative capacity associated with the presence of thiamine.

Patients suffering from high calorie malnutrition represent the “walking sick” of America. In its early stages it results in a polysymptomatic disease that defies our present concept of diagnosis. Traditional laboratory results may be quite normal or nonspecifically abnormal and the symptoms “written off” as psychosomatic. It may well be that some cases of hypertension, affecting millions, is part of the clinical effect produced by the dysautonomia of thiamine deficiency. The text that follows provides support for this hypothesis. It may also be true that failure to recognize the true etiology may lead over time to chronic brain disease in the untreated patient.

Autonomic Control of Blood Pressure

It has been well documented that the autonomic nervous system plays a key role in controlling blood pressure values. The hypothesis has been put forward that the origin, progression, and outcome of human hypertension are related to dysfunctional autonomic cardiovascular control, especially to abnormal activation of the sympathetic division. There is a consistent association between hypertension and pro-inflammatory cytokines of the innate and adaptive immune system. The sympathetic nervous system, a major determinant of hypertension, is pro-inflammatory, whereas the parasympathetic nerve activity dampens the inflammatory response through α7-nicotinic acetylcholine receptors. In the Goldblatt model of renal hypertension and the use of renal denervation in the treatment of drug-resistant hypertensive patients, autonomic mechanisms underpin the maintenance of this hypertension. Autonomic mechanisms initiate the development and maintenance of renal vascular hypertension. Obesity-associated overnutrition leads to neural inflammatory molecular changes, particularly in the hypothalamus, leading to elements of the metabolic syndrome. Increased sympathetic activation is a critical mediator.

Children, Hypertension, and Obesity

There are an increasing number of children diagnosed with primary hypertension, mainly in association with obesity. One of the factors considered is dysregulation of the autonomic nervous system. Emerging evidence suggests that the sympathetic branch plays a much broader role in the regulation of blood pressure, including the development and maintenance of sustained hypertension by a chronically elevated central sympathetic tone. A recent study examined the relationship between the autonomic nervous system dysfunction, anxiety and depression in hypertension. The sympathetic nervous system and arterial baroreceptor reflex control of renal sympathetic nerve activity has been proposed to play a role in long-term control of arterial pressure.

Abundant evidence supports the role of the sympathetic nervous system in the pathogenesis of obesity -related hypertension. The mechanisms are incompletely understood. A study supports the concept that increased renal sympathetic activity is the critical mechanism by which increased central sympathetic outflow initiates and maintains reductions in renal excretion function, resulting in obesity hypertension. Hypertension and obesity are risk factors for coronary heart disease in adults. Childhood weight problems and high blood pressure increase the risk of subsequent obesity and hypertension as an adult.

The Role of Hypoxia in Blood Pressure Regulation

Obstructive sleep apnea is one of the most common causes of hypertension in Western societies, causing chronic intermittent hypoxia. The normal homeostatic balance between HIF-1α-dependent pro-oxidant and HIF-2α dependent antioxidant enzymes is disrupted. Hypertension affects one in three United States adults and involves the integration of the actions of multiple organ systems, including the central nervous system, driving enhanced sympathetic outflow and increased blood pressure. There is increased understanding of hypothalamic activity in hypertensionChanges in the baroreflex and chemoreflex may contribute to the development of chronic hypertension observed in obstructive sleep apnea patients. Animal studies have identified induced hypoxic hypertension, but this is still conjectural in humans.

Thiamine Deficiency and Pseudo-hypoxia

Because mild to moderate thiamine deficiency results in pseudo-hypoxia in the limbic system and brainstem, emotional and stress reflexes of the autonomic nervous system are stimulated and exaggerated. Like chronic intermittent hypoxia that activates HIF-1 and suppresses HIF-2-mediated transcription, thiamine deficiency induces HIF-1α mediated gene expression similar to that observed in hypoxic stress. Thiamine deficiency induces an early, functionally significant central muscarinic cholinergic lesion that may be at least part of the reason for sympathetic overdrive. Details of the genetic determination in hypertension are poorly understood. A novel blood pressure locus that encodes a previously uncharacterized thiamine transporter has been reported, again perhaps emphasizing the importance of thiamine deficiency in hypertension. Evidence supports the likelihood that an increased cytosolic ratio of NADH/NAD+, caused by hyperglycemia, results in playing an important role in the pathogenesis of diabetic complications. Thiamine deficiency occurs in individuals with diabetes, leading to hyperglycemic-induced damage and oxidative stress. The potential benefit of long-term replacement is not yet known but may well reduce the cardiovascular risk and angioplasty complicationsThiamine deficiency should be considered in all patients with pulmonary hypertension of unknown origin.

Maternal hypertension is the most common medical disorder of pregnancy, varying from 4 to 6% of all pregnancies. The daily dose of 100 mg of thiamine has been given to over 1000 non-selected prenatals starting in the second and third trimesters. The expected number of toxemia patients in this group was well over 150, but the actual occurrence was zero.

Hypertension and High Calorie Malnutrition

Optimum nutrition is the level of intake that should promote the highest level of health. A deficit in nutrition may result in tissue depletion of essential nutrients that can lead to biochemical changes and eventually to clinical signs and symptoms. Adverse conditions prenatally increase the risk of cardiovascular disease, including hypertension. Obstructive sleep apnea increases over the course of pregnancy and is common during the third trimester. These adverse conditions have reportedly been completely prevented by the use of 100 mg of thiamine beginning even before pregnancy is confirmed. Thiamine deficiency, resulting in impaired oxidative metabolism, leads to a multifactorial cascade of events in the brain that include focal decreases in energy status, oxidative stress, blood-brain barrier disruption, glutamate-mediated excitotoxicity, amyloid deposition, immediate-early gene induction and inflammation.

Thiamine Tetrahydrofurfuryl Disulfide and Hypertension

This disulfide derivative of thiamine is the synthetic counterpart of allithiamine that occurs naturally in garlic. Allithiamine was discovered in Japan in 1951 and extensively researched by Japanese scientists. Experimental work in animals and human subjects revealed that its metabolic effect was much more powerful than the thiamine from which it was derived. Almost unknown in America, its therapeutic actions have been reviewed.

SHR rats are widely studied as a model of hypertension, exhibiting metabolic abnormalities that share features with the human metabolic syndrome. The SHR rat becomes hypertensive early in life and blood pressure continues to increase with age, often resulting in a cardiovascular event. Over the course of four months, blood pressure and body weight of two groups of SHR rats were monitored. The control group was fed normally and the TTFD group was given increasing doses of TTFD from 5 to 15 mg. There was a statistically significant reducing effect on the treated rats as compared with the controls. Of the 13 TTFD-supplemented rats, five showed a definite response with no rise in the expected blood pressure measurements, while the control group showed a 20 to 25 mm Hg increase in blood pressure across the experiment. The results showed that TTFD has a preventive effect on blood pressure in these genetically abnormal rats.

Thiamine Deficiency > Hypoxia > Hypertension

It has been shown in the above text that hypoxia and pseudo-hypoxia have virtually identical effects in the area of the brain that is peculiarly sensitive to thiamine deficiency. Since any phenomenon that causes inefficient oxygen consumption is dangerous to the organism, activation of the fight-or-flight reflex seems to be entirely logical. Repeated hypoxia in sleep apnea syndrome induces persistent chronic sympathetic dominance and is obviously an abnormal state of metabolism. It is possible that sleep apnea represents a combination of brainstem thiamine deficiency and recurrent obstructive hypoxia. Lonsdale and Marrs have published evidence that thiamine deficiency is widespread in the American population and that its effects in the brain are diverse and the resulting morbidity prolonged. Evidence could be accumulated by proving thiamine deficiency and attempting clinical trials with TTFD.

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This article was published originally on November 17, 2020. 

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Are Seizures Due to Hypoxia?

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Some years ago I was invited to speak at the Institutes for the Achievement of Human Potential in Philadelphia. This is a wonderful institution that takes children with intellectual and developmental disabilities in a residential program and provides them with a complex physical training program. Many doctors have given their time as consultants and one of them was a neurosurgeon who had voiced the principle that seizures, so common in these children, were due to hypoxia in the brain. So what did he mean?

Hypoxia is the technical word used for deficiency of oxygen affecting cellular metabolism. Although it applies to all tissues in the body, it is particularly devastating to brain tissues because of their rapid consumption of oxygen. This did make sense to me because I had become aware that brain cells become irritable when they are partially deprived of oxidation. Oxidation is the technical term used for consumption of oxygen by combining with a fuel to produce energy. It is to be noted, as I have repeatedly stated in these posts, that the administration of oxygen is totally useless unless oxidation can take place. Those that have read these posts are aware that thiamine is an absolute necessity in the process. Although it involves other vitamins and minerals, thiamine appears to be a dominating factor.

Treatment of Seizures

As most people know, epileptic seizures are treated by means of drugs and each patient is given one of these drugs on clinical trial. If it is clear that a particular drug does not work, another drug is tried. This process continues until success is achieved, meaning that the patient is free of seizures. Unfortunately, many of the seizures witnessed in children fail to respond to any of the assortment of drugs tried. Pharmaceutical companies are always trying to find yet another drug that has to go through the process of approval by the FDA before it can be prescribed.

One of the awful traps for the treatment of seizures is switching from one drug to another. When a drug is withdrawn, the other one must be substituted rapidly. This is because withdrawal from any of these drugs threatens to cause a dramatic situation known as status epilepticus. When this happens, the patient just goes on seizing indefinitely and it is often hard to get it under control and it is potentially lethal. Pediatric neurologists are the doctors for treating seizures in children and I was not usually involved until an incident occurred that gave me a chance to see whether the neurosurgeon was correct in suggesting hypoxia. So here I must digress.

What is Pseudo-Hypoxia?

Deficiency of thiamine causes what is sometimes referred to as pseudo-hypoxia (pseudo, false). This means that its absence is really equivalent to deprivation of oxygen. As many readers of these posts know, I have had an absorbing interest in thiamine for many years. In particular, I had an independent investigator license for studying the action of a derivative of thiamine known as thiamine tetrahydrofurfuryl disulfide (TTFD). Without going into the technical details, this particular derivative has exactly the same action as thiamine from which it is derived, but is much more biologically active.

Could it be that seizures were due to pseudo-hypoxia rather than deficiency of oxygen? We know from the history of beriberi, the classic thiamine deficiency disease, that arterial oxygen concentration was low while it was higher than normal in venous blood. This demonstrates that thiamine has an important action in the ability of hemoglobin to pick up oxygen in the lung, deliver it to tissues and cause its consumption in the process of oxidation. Seizures could therefore possibly be a mixture of true hypoxia and pseudo-hypoxia.

A Patient in Status Epilepticus

I had my chance to test TTFD. A 12 year old boy with intractable seizures had been admitted to the hospital under a neurologist. A number of drugs had been tried without success and he had been admitted to try to find yet another. The neurologist had to be out of town for a few days and evidently inadvertently, the medication that this boy was receiving was discontinued without the new drug being substituted. He went into the condition of status epilepticus, the potentially serious situation already described. Because I was the doctor on duty, I was called to handle the emergency. I had some vials of TTFD that could be given intravenously and several of these vials were administered. Within a short time the seizures had stopped. Next morning he was seen walking around the ward, free of seizures and talking to other patients. I began to give him TTFD in the form of pills. Was this evidence that the neurosurgeon, mentioned above, may be right, that seizures were due to oxygen deprivation? I believe it was. However, I believe the mechanism was akin to the pseudo-hypoxia that is induced with thiamine deficiency.

Why Was This Case Not Published?

Unfortunately, the neurologist was completely antagonistic to any concept of vitamin therapy. He was neither interested in the administration of TTFD, nor the reason for its experimental use. So ingrained is this in the minds of so many physicians, he concluded that the use of “a vitamin” was neither justified nor was it the explanation for this boy coming out of a serious and potentially lethal situation. The oral dose of “the vitamin” was discontinued and the neurologist went back to finding whether the proposed new drug was effective. Because of his lack of interest and failure to discuss the situation with me, it was impossible to put the facts together and set up a research situation that might have led to a new way of looking at epileptic seizures in children.

We know that there is a particular form of seizure known as hypsarrhythmia that is sometimes sensitive to the administration of vitamin B6 and one would have thought that this would set off an exploratory research into the use of other members of the vitamin B complex. Without data, however, medical publication is impossible and so this particular case has laid on my conscience ever since. I am sure that most people would believe that a clue of this nature would be picked up, examined closely, presented to a group of interested physicians and lead to further research. It is unfortunately quite typical of the mindset of any group of contemporary physicians at any age in the history of man and may well be a surprise to many. It certainly applies to other professions, businesses and indeed to virtually any human activity. Having used this vitamin to treat literally hundreds of patients without any sign of toxicity, surely it would be worth a trial.

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This post was first published on May 18, 2016.

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Dysautonomia and Hypoxia

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Every profession has its jargon that enables its practitioners to communicate relatively easily but is incomprehensible to those outside the indicated profession. This is most true in the medical profession, so I am about to explain a disease condition that has become extraordinarily common. I will begin by defining the word dysautonomia. “Dys” is a prefix meaning abnormal and “autonomia” refers to the autonomic nervous system. The autonomic system is the part of the nervous system that controls autonomic functions and behaviors that ensure survival. This includes, heart rate, respiration, digestion, temperature, even libido.

The autonomic system operates largely involuntarily and without conscious consideration. Many people are not aware that we have two types of nervous system. The one that we all understand is called “voluntary”, enabling us to carry out willed actions. This nervous system is controlled by the upper part of the brain known as the cortex, the latest part to be evolved, capable of thought and giving us those human abilities that are unique within the animal kingdom. In contrast, the lower part of the brain controls an involuntary “messenger system” that enables us automatically to adapt to the conditions of environment that we meet on a daily basis throughout life. The messenger system does not think. It acts automatically. The autonomic system is a “three channel system” that sends and receives signals to and from all parts of the body.

The Three Channels of the Autonomic System

The first channel connects with a bunch of glands known as the endocrine system. These are the glands that produce hormones, messengers borne by the blood to the body organs. This is a complex messenger system that adjusts, influences and modifies behavior. The other two channels are known as the sympathetic and parasympathetic systems. Between them, they provide direct communication that enables a given organ to react and participate in the symphony of adaptation. All work in a coordinated manner. Thus, the action of the autonomic nervous system, either by direct communication with an organ or by means of releasing a hormone, activate or deactivate all the organs in the body selectively.

Sympathetic System. This is best thought of as the action stimulating mechanism. Its best known reflex is known as “fight-or-flight”, activated by any form of mental or physical stress or threatened danger. It will accelerate the heart, deactivate the intestine, produce a sense of anxiety or panic, dilate the pupils in the eyes and raise the blood pressure, all things that you desire to happen if you are either fighting or fleeing from an enemy. It is designed for short-term action and consumes energy at an accelerated rate, particularly in the brain. It is important to note that this is a reflex, not a thought process. It is activated by a visual, auditory or tactile stimulus that is interpreted as danger. I think of this as a “stress input” that is answered by either physical or mental action in some form of self-preservation.

Reading a telegram that provides bad news triggers an emotional reflex that does not necessarily require physical action but is an obvious source of stress and the mental response is sympathetic and energy consuming. It may well induce accelerated heart rate, pallor and pupillary dilatation as a modification of a fight-or-flight reflex. Emotions are reflex, engineered by the lower brain and programmed according to the nature of the incoming stimulus perception. This in turn stimulates the thought processes of the higher brain that is capable of modifying the reaction. Sympathetic action of this nature is also activated by the release of adrenaline from its appropriate gland “and gives rise to what is sometimes called the ”adrenaline rush”.

Parasympathetic System. This is best thought of as “the rest-and-be-thankful” mechanism. It will decelerate the heart, activate the intestine, produce a sense of peace, constrict pupils of the eye and lower blood pressure, the very opposite of that produced by the other system. Our primitive ancestor could now roll a stone over the mouth of his cave and carry out the functions of the body after he has escaped from danger. He can now sleep, eat, indulge in bowel activity and experience a sense of peace. This also is not a thought process.

Dysautonomia: Autonomic Chaos

It is obvious that if the sympathetic and parasympathetic systems were activated together there would be chaos. Reflex sympathetic action under normal circumstances is balanced by a withdrawal of the parasympathetic action and vice versa. Thus, for example, accelerated heart rate is partly produced by withdrawal of the parasympathetic at the same time as it is accelerated by the sympathetic. This coordination is computed by the lower part of the brain. Under normal circumstances its action is modified by the upper brain that provides willpower under what might be called “advice and consent”. On the other hand, under urgent necessity, when danger is life threatening, the sympathetic system takes over the action completely, explaining why a soldier in battle may not be consciously aware that he has lost a finger until the action is completed.

If the reflex coordinated mechanism of the autonomic system is lost for any reason, it is referred to as dysautonomia. A medical textbook entitled “Dysautonomia” was edited by Sir Roger Bannister, then a London physician who was the first athlete to run the four-minute mile. The book describes many examples of this condition and deals with the genetic aspect. It never addresses the subject of nutrition, an oversight that introduces the clinical blindness of the modern physician to nutritional deficiency disease. This is in spite of the fact that the best example of dysautonomia is beriberi, long known to be caused by deficiency of thiamine (vitamin B1) by the ingestion of empty carbohydrate calories.

Hypoxia and Pseudo-hypoxia in Dysautonomia

The word hypoxia refers to lack of oxygen. Its most devastating effect is in the brain and particularly the lower brain that never sleeps. This is because the cells in that part of the brain have a heavy requirement for oxygen. As we all know, oxygen is delivered to all the 70 to 100 trillion body cells by the bloodstream and they consume it in the synthesis of energy. This consumption of oxygen is in turn dependent on the presence of thiamine and other vitamins. A deficiency of thiamine therefore produces the same clinical effect as hypoxia. For this reason, its deficiency causes what is sometimes known as pseudo-hypoxia (pseudo meaning false).

Since the lower brain controls the autonomic nervous system, we can now see how thiamine deficiency results in dysautonomia. Of course, as we all know, a complete lack of oxygen means death. We are here discussing the effects of a mild to moderate hypoxia or pseudo-hypoxia. The so-called TIA (transient ischemic attack) is an example of hypoxia because of a temporary failure of blood delivery to the brain. In most cases it is probably a brief contraction in the muscular wall of a major artery resulting in constriction of the artery. The irony is that I believe a common mechanism for TIA may involve arterial artery spasm from magnesium deficiency. It might well be obviated by taking a supplement of magnesium as a preventive. Thiamine and magnesium deficiency both produce the same effect by preventing the consumption of oxygen, thus stopping energy synthesis: hence the term pseudo.

Clinical Effects of Pseudo-hypoxia

There are many papers published in the medical literature in which a particular disease (for example lung cancer) is associated with dysautonomia. Each one of these manuscripts offers a case report in which the cause of this interesting but baffling association is unknown. My hypothesis is that pseudo-hypoxia gives rise to the dysautonomia whose symptoms are not recognized for what they represent, are ignored, or treated symptomatically and lead eventually to more cellular damage within a body organ that becomes an organic disease. If recognized in the early stages, diet correction and a few supplementary vitamins are all that is needed. If not, it is hypothesized that symptoms increase and reflect irreparable cellular damage. The constellation of symptoms is then referred to as disease A or B, e.g. Parkinsons’s or Alzheimer’s.

It has now been shown that a common condition called “panic attacks” can be induced in a patient by the inhalation of air enriched with about 30% carbon dioxide, producing hypoxia. Therefore, this condition has nothing to do with Freudian psychology. It is a purely biochemical phenomenon, induced by hypoxia or pseudo-hypoxia. I recently met a friend with a story that I hear repeatedly. He was suddenly overcome by faintness while at work. It was associated with dizziness, lack of control and unconsciousness. He was conveyed by ambulance to the nearest emergency room where all the tests were negative and he was allowed to go home. Almost automatically this is referred to as psychosomatic disease as though the unfortunate patient is imagining or even inventing the obvious brain caused symptoms. There is little doubt that this represents a temporary period of hypoxia or pseudo-hypoxia that is extremely threatening to the individual for his or her future, since it indicates a state in the brain that can result in a recurrence, perhaps of greater severity.

I learned later that this friend had received heart surgery many years before this incident. Since the primary organs affected by the pseudo-hypoxia of beriberi are the brain, the nervous system and the heart, perhaps pseudo-hypoxia was the underlying cause of the heart problem that led to surgery. I doubt that it was ever considered. The trouble is that I cannot tell a friend that perhaps all he has to do is to take a few vitamin supplements. He simply would not believe me. My credibility would be lost, possibly with the loss of friendship and my proffered advice, like the proverbial seed falling on stony ground. The concept is “outside the box” and does not conform to the medical model that exists in the minds of all of us.

What is particularly important to understand is that mild to moderate hypoxia or pseudo-hypoxia is itself a form of stress and triggers the fight-or-flight reflex. This is quite logical since a decreased oxygen concentration is dangerous and even life-threatening. Under these conditions the lower brain is more easily activated and the resulting action fails to heed the advice and consent provided by the upper brain. Thus, a child or adolescent consuming empty calories, will be thiamine deficient and his brain susceptible to periods of pseudo-hypoxia, particularly when experiencing other energy demanding stressors. The hypoxia will affect autonomic regulation, which will manifest in a number of seemingly unrelated symptoms, that include digestive issues, attentional deficits, unexplained aches and pains and perhaps most notably in children, behavioral difficulties represented by extreme emotional lability.  The easiest way to produce pseudo-hypoxia is by the widespread consumption of carbohydrate and fatty foods (e.g doughnuts) representing empty calories, so commonly associated with the consumption of high sugar content beverages. Sugary foods are not only devoid necessary nutrients, but the sugar itself forces what thiamine stores that exist out of the cells. Could high calorie malnutrition be responsible for some of the otherwise inexplicable violence reported almost daily in the news media? It is biochemically possible. Perhaps an easier question to answer, could thiamine deficiency and the resultant hypoxia be responsible for the myriad of autonomically controlled systems currently labeled dysautonomia? Possibly.

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