Dyspnea, Air Hunger, and Molecular Oxygen Consumption

What is Dyspnea?

This is the medical term for shortness of breath. The word is derived from the Greek, dys meaning abnormal + pnein, to breathe. We are aware, of course, that we get “out of breath” when we exercise and that this is perfectly normal. We are also aware that exercise breathlessness is less acute after physical training. Dyspnea is applied to breathlessness at rest and when it is greater than expected with the degree of exertion. It is a symptom of disease. Chronic dyspnea is defined as resting shortness of breath that lasts more than one month. Most cases of dyspnea result from asthma, heart failure, myocardial ischemia (shortage of oxygen containing blood to the heart), chronic obstructive pulmonary disease, pneumonia and is even related to “psychogenic” disorders (meaning that there is no evidence of  physical disease). Associated symptoms and risk factors such as smoking, chemical exposures and medication use also need to be considered and the examination of the patient by a physician, together with laboratory studies, may lead to an obvious conclusion. However, this does not necessarily lead to appropriate treatment.

The Anaerobic Threshold

We all know, of course, that we need oxygen for life and that we die quickly without it. However, most people tend to take it for granted and have little or no interest in what we do with it or why. Heart and lung activity depend on efficient breathing to provide the continuous influx of oxygen that is delivered in the blood. The functions of both the heart and lung are controlled by a network of neurons located within the lower brainstem, the part of the brain that connects with the spinal cord. The basic rhythm of breathing is generated by these nervous mechanisms. This means, of course, that damaged mechanisms in the brain can be responsible for failure to breathe. An example of this is opioid poisoning. The common condition of sleep apnea is also an example of brainstem disease.

The use of oxygen in our cells is called oxidative respiration (also known by the technical term, redox) and refers to the complex mechanisms that yield cellular energy. This activity takes place within mitochondria that exist inside all our cells. Perhaps we can refer to this as the action of the primary engine, the engine that requires oxygen to function. If for any reason this mechanism is exhausted for lack of one or more of the components that enable it to function, another form of energy production automatically comes into play. This does not depend on the presence of oxygen to function. Perhaps we can refer to it as the secondary (backup) engine. The function of this secondary engine comes into play automatically and is referred to as “the anaerobic threshold”. This form of energy is less efficient and causes a sustained increased in lactic acid and metabolic acidosis. A person may notice, for example, that when climbing steps the legs become fatigued but that after resting for a short while, recovery occurs. This is because the lactic acid generated in the muscles is consumed and normal oxidative metabolism is restored. It is much more noticeable in older individuals, because the efficiency of oxidative metabolism gradually declines with age. Undue or prolonged physical or mental stress requires huge amounts of energy to perform the essential adaptive response and may cause it to run out of one or more of the necessary components that are used in the primary “engine”.

Thiamine, Dyspnea, and Cellular Energy

Carbohydrate from food is broken down to glucose and converted to glycogen where it is stored in the liver. When any cellular activity is mobilized (e.g. a run in the park), an enzyme in the liver converts glycogen to glucose which is then oxidized (burned) as fuel. Fatty acids are also used as fuel and thiamine (vitamin B1) is the vital component for the oxidation of both fatty acids and glucose. Glucose is the only fuel used by the brain.

Muscle Weakness and Dyspnea

As already indicated, dyspnea is a common, disabling symptom in chronic heart failure. Weakness in the muscles used for breathing is important in the dyspnea experienced by some patients with pulmonary disease and studies have shown that patients with stable chronic heart failure have weakness in these chest muscles. The cellular energy deficiency that gives rise to dyspnea also gives rise to weakness in the muscles, thus aggravating the clinical situation.

There is a serious lethal disease known as Amyotrophic lateral sclerosis (sometimes known as Lou Gehrig’s disease) that leads to chronic respiratory failure from failure of the diaphragm (the large muscle that separates the chest cavity from the abdominal contents and used in breathing). This is a major driver of dyspnea and mortality. In this disease, energy expenditure is known to be often abnormally high and this may be an important observation. If energy expenditure exceeds its production, the deficit must be a cause of the dysfunction.

Energy Synthesis Versus Expenditure

I live in a retirement home and of course it is not uncommon to see people being pushed around in a wheelchair and being treated with nasal oxygen. The question that always occurs to me is whether the sole administration of oxygen is considered to be effective. The mechanism of oxidation requires oxygen of course, but proper fuel (glucose) and vitamin B complex are both necessities. If the patient is consuming a normal diet, the glucose will be available but there is generally nothing to indicate whether an adequate supply of B complex is part of that diet. Often sick people do not eat very well and I would insist on a supplement of B complex to such an individual if I were in charge.

Although ALS is relatively rare, if energy expenditure exceeds synthesis as the underlying cause, perhaps a method of accelerating its synthesis might be a logical approach and there is some precedent for approaching it this way. Without going into the technical details, redox (reduction/oxidation) is the technical word used to describe the essential reactions of oxidation in the synthesis of energy and I came across two manuscripts that suggest the need for research into thiamine metabolism in this disease.

Why Thiamine?

In our book “Thiamine Deficiency Disease, Dysautonomia and High Calorie Malnutrition“, we describe the case of an eight-year-old child who had suffered from chronic asthma from the age of four years. She was so allergic to virtually any mattress that she had to sleep on a plastic lawn chair. The bronchial tubes are closed and opened under the influence of the autonomic nervous system (ANS), so asthma is really an example of dysautonomia (abnormal action of the ANS). This means that the bronchial tubes shut down abnormally, making breathing exquisitely difficult. The controls of the ANS in the brain are energy dependent and dysautonomia results from lack of energy in those control centers. The signaling mechanisms become distorted. Since thiamine sits astride the chemistry of energy production, this girl was given large doses of thiamine to which she responded dramatically. It is an example of drawing a logical deduction from understanding the actions of the brain when oxidative metabolism is compromised. I am not suggesting that large doses of thiamine would be beneficial to all cases of asthma, but I am suggesting that an imbalance of nervous control is responsible for a lot of poorly understood disease.

How We Got Here: The Flexner Report

In 1910, a study of American medical schools resulted in the Flexner report, written by Abraham Flexner under the aegis of the Carnegie Foundation. Many aspects of the present-day American medical philosophy stem from this report and its aftermath. Homeopathy and natural medicines were derided and some doctors were even jailed. Colleges in electrotherapy were closed. Flexner obtained his information by visiting Germany where the laboratory was supposed to prove the exact nature of the disease. It is this model that persists in America today, resulting in the collision between Orthodox and Alternative medicine (the use of nutrients to assist the natural process of healing by stimulating energy production). It is also the reason why Orthodox physicians refuse to recognize that abnormal electrochemical reactions in the brain are responsible for symptoms. Because they do not look for evidence of nutrient deficiency and the present standard laboratory tests are negative, they refer to the symptoms as psychosomatic. For many years it has always been a mystery to me why a patient with long-suffering problems of health can be accused of inventing symptoms “to hide behind some form of reality”. There is every reason to replace this idea with a mild disruption of brain chemistry as the underlying cause. It is also the reason why psychogenesis is included as one of the causes of dyspnea. The word psychosomatic should be abolished.

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Photo by Mick Haupt on Unsplash.