Chronic fatigue syndrome (CFS) has symptoms similar to neurally mediated low blood pressure, and treatment for this kind of low blood pressure helps some with CFS (J. Am. Med. Assc. 1995; 274: 961). If you are in the treatable group, good for you. For those with CFS who read this, I would like to propose an explanation of CFS that may lead to an alternative treatment.

My explanation depends on my work with cycling of the hormones melatonin and dehydroepiandrosterone (DHEA). My idea is that melatonin and DHEA levels determine blood pressure. If DHEA is too high, blood pressure is too high; the opposite occurs with melatonin. For example, melatonin is very high in children, but melatonin begins a steady decline following childhood (puberty) to very low levels in old age. Blood pressure is lowest in children and increases thereafter. Problems with neurally mediated hypotension (low blood pressure) are more common in the young than old. Melatonin is highest at night, and blood pressure decreases slightly at night. I suggest melatonin reduces blood pressure by reducing DHEA production. Exercise increases DHEA and blood pressure. Excitement, according to my work, also increases DHEA; excitement increases blood pressure. In this case, I think DHEA stimulates the smooth muscle of blood vessels and makes them constrict; this increases blood pressure. In people with normal DHEA, exercise also uses DHEA. The increased blood pressure of exercise, therefore, is temporary. People with CFS exhibit lingering tiredness after exercise. They burn their small supply of DHEA during exercise, but do not replenish it in sufficient quantities to produce the sense of well-being, I attribute to DHEA.

I suggest chronic fatigue syndrome results from a disruption of this cycle that increases melatonin, while DHEA declines. My work suggests this cycle is increased by viral infection. The majority of patients in the JAMA study reported an abrupt onset of symptoms in association with an infectious illness that resembled influenza or mononucleosis. I think the first response of this cycle to viral infection is an increase in melatonin, which then increases DHEA. (These cycle to produce the chills and fevers of viral infections.) It is known that DHEA increases dramatically in response to HIV infection, then declines thereafter. I suggest the same mechanism is at work in AIDS and chronic fatigue syndrome. That is, a virus attacks these people who cannot maintain their DHEA response. One group dies, the other live miserable lives. DHEA is necessary for normal mental and physical health.

My work suggests melatonin is our natural narcotic. In the JAMA tilt tests, people with CFS, experienced symptoms quiet similar to those of people who have taken narcotics, i.e., nausea and vomiting, sweating, light-headedness, etc. These are also symptoms of syncope caused by neurally mediated hypotension. They are also symptoms of viral infection. I suggest they all are produced by too much melatonin. Narcotics mimic the effects of melatonin. (Melatonin is our way of maintaining day/night rhythms, and narcotics (derived from plants) are used by plants to maintain this rhythm.) People with CFS are not producing the DHEA response of the cycle; the virus has probably harmed their adrenal glands, which make DHEA. A symptom of CFS is unrefreshing sleep. In normal people, melatonin (sleep) leads to increased DHEA in the morning.

I suggest chronic fatigue syndrome results from DHEA insufficiency. DHEA taken orally in the morning may alleviate these symptoms. DHEA is currently available in a specific form that produces physiological levels of DHEA in the blood, and is available upon prescription. Surely this should be better than the complicated drug regimen currently being used for CFS.

(This short article was published in The Morning News of Northwest Arkansas, Springdale, Arkanasas, Nov. 26, p. 3F, 1995.)

Added in Support of Above
Int. J. Mol. Med. 1998 Jan; 1(1):143-146
"Dehydroepiandrosterone sulfate deficiency in chronic fatigue syndrome"
Kuratsune H, Yamaguti K, Sawada M, Kodate S, Machii T, Kanakura Y, Kitani T

"The chronic fatigue syndrome (CFS) is a condition of unknown etiology, characterized by a persistent debilitating fatigue, the muscle-related symptoms and the neuropsychiatric symptoms. Recently, it has been reported that the patients with CFS might have impaired activation of the hypothalamic-pituitary-adrenal axis, and suggested that a part of the patho-genesis of CFS might be associated with abnormalities of the endocrine system. Herein, we show that the majority of Japanese patients with CFS had a serum dehydroepiandrosterone sulfate (DHEA-S) deficiency. Serum DHEA-S is one of the most abundantly produced hormones which is secreted from the adrenal glands, and its physiological function is thought to be a precursor of sex steroids. DHEA-S has recently been shown to have physiological properties, such as neurosteroids, which are associated with such psychophysiological phenomena as memory, stress, anxiety, sleep and depression. Therefore, the deficiency of DHEA-S might be related to the neuropsychiatric symptoms in patients with CFS."