thiamine oxygenation

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. 

Recovery from Reye’s Syndrome: A Case Report

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In a number of posts on this website I have mentioned the technical term “oxidative metabolism” in relationship to thiamine. I have tried to explain it by analogy, using the consumption of gasoline in a car. Gasoline is mixed with oxygen and ignited by a spark. In the human body glucose is the equivalent of gasoline and thiamine is the equivalent of the spark. This case tells us that thiamine has other effects of equal importance.

Many years ago, I learned of a naturally occurring derivative of thiamine that had been discovered in garlic. It had a more powerful clinical action than the original thiamine from which it had been derived. The Japanese investigators who discovered it had done many experiments with both animal studies and human subjects, with some remarkable results. For example, they had found that mice could be partially protected from cyanide poisoning by treating them with this derivative before the cyanide was given. It had been synthesized and is used in Japan as a prescription item (Alinamin) in many different diseases. I became intrigued by its potential and since it was totally unrecognized in the United States, I applied to the FDA for an Independent Investigator License (IND) that was granted to me in 1973. Because it has a long and complicated chemical name I shall call it TTFD. I used it in treating many patients, usually with great benefit and never saw the slightest sign of toxicity.

Reye’s Syndrome, the Flu, and Thiamine

In order to introduce its potential, I am going to describe the case of an 18-month-old girl who was admitted to our hospital with Reye’s syndrome. Some people reading this will remember that this disease kept cropping up in association with epidemics of “flu”. Many of the children died and although it has now been discovered that it was due to aspirin given to the child to bring down the fever, at the time that I treated this case, this fact was not known.

The infant was admitted to the hospital in a coma which had begun 48 hours previously with repeated vomiting. The initial treatment was given by neurologists, using exchange blood transfusion and as in other cases, was a complete failure. The coma deepened rapidly. Pupils became fixed and dilated and she was judged to be in a terminal state. The respirator that had been used to keep her alive was withdrawn. One week after her admission there was no change in her condition. She was deeply comatose and all treatment other than normal life support was withdrawn. In short, her case was considered to be hopeless.

High Dose Thiamine (TTFD) for Reye’s Syndrome?

Because from that point on the treatment was to be experimental, I obtained full consent from the parents. I gave 100 mg of TTFD by nasogastric tube every four hours and 150 mg by intravenous injection, a total of 750 mg in 24 hours. This was repeated daily. When you consider that the daily intake of thiamine under normal healthy circumstances is 1 to 1.5 mg a day, this was truly a humungous dose. Please understand that this is not vitamin replacement. It is clearly the use of a vitamin as a drug.

The first thing that happened was the lip vermilion became bright red, whereas it had previously been dusky, the color of deoxygenated blood. There was healthy flushing of the cheeks. Two days later there was some spontaneous movement of the limbs, her pupils responded to light and she developed a cough reflex. After one week the daily dose of intravenous TTFD was discontinued and the oral dose decreased to 300 mg a day. After nine days from the beginning of this treatment TTFD was decreased to 150 mg a day.

On the 15th day, eye contact could be established and she responded to sounds but was still unconscious, a state known as coma vigilum. Subsequently she began to take Jell-O from a spoon and began to show primitive crying responses. By the 21st day she was able to chew and could support her own weight with help. She began to walk with her hand held and self feeding began. Speech returned and gradually improved. She was discharged from hospital one month after this treatment had been started. The TTFD was continued at the same dose and three months later she was clinically well, although muscular tone was diminished. Not surprisingly, as she grew there was evidence of some permanent damage.

Thiamine, the Mitochondria and Oxygen

We now have reason to believe that Reye’s syndrome is mitochondrial in nature. Mitochondria are organelles within our cells that generate energy from oxidative metabolism. In this disease the mitochondria are affected in that part of the brain that maintains life. The return of lip vermilion and flushed cheeks was the first indication that oxygen was being picked up by the blood in the child’s lungs and conveyed to the tissues. The return of function in the brain indicated that oxidative metabolism had been restored. Hemoglobin is a protein that coats our red cells and combines with oxygen in the lungs to become what is called oxyhemoglobin. It is bright red in color and that is why oxygenated arterial blood is bright red. When arterial blood gets to the tissues, it delivers the oxygen to the cells and the hemoglobin loses its red color, becoming bluish, the color of venous blood and the color of hemoglobin after it has delivered the oxygen. The first indication of this transformation was the change in the color of the lips and the appearance of flushed cheeks.

Thiamine, Oxidative Metabolism and Reye’s Syndrome

The administration of TTFD to this child had resulted in the formation of oxyhemoglobin, enabling the delivery of oxygen to the brain. Because function increased we also have to assume that the oxygen was unloaded to the cells that needed the oxygen. It also explains why the low concentrations of oxygen in arterial blood and high concentrations in venous blood were recognized by early investigators in beriberi. This is important new information because it indicates that thiamine has some effect on the ability of hemoglobin to pick up oxygen and even deliver it.

In 2004, Japanese scientists showed that the injection of a compound similar to TTFD could actually increase the concentration of oxyhemoglobin. This ability has never been recognized for the chemical functions of thiamine and TTFD has an action that is identical to that of thiamine. It forces us to wonder whether TTFD might be a benefit to those people with bluish lips and poor color attributed to heart disease and other situations labeled with the term cyanosis (deoxygenated blood). Using it at the time of hospital admission would probably have prevented permanent damage.

Reference

  1. Ishimaru T, et al. Hemodynamic response of the frontal cortex elicited by intravenous thiamine propyl disulfide administration. Chem. senses 2004;29(3):247-51.

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This post was published originally on Hormones Matter on March 16, 2016. 

Photo: Histopathology of Reye’s syndrome, liver Histopathology of autopsy liver from child who died of Reye’s syndrome. Hepatocytes are pale-staining due to intracellular fat droplets via Wikipedia and CDC/ Dr. Edwin P. Ewing, Jr., the Centers for Disease Control and Prevention‘s Public Health Image Library.