New Theory of Reflex Sympathetic Dystrophy

Copyright ã 1997 by James Michael Howard.

 (January, 2007:  Something to try:  5-HTP may be beneficial as it is a precursor to serotonin and melatonin.  Increasing serotonin and melatonin may increase the “melatonin – DHEA cycle” by increasing sleep (melatonin), increase mood (serotonin), and decrease pain (serotonin).

This is a new theory of reflex sympathetic dystrophy (RSD). My theory of RSD assumes that some people are genetically disposed to develop RSD. My explanation involves circumstances that a number of people experience, but only some develop RSD. This is not unusual in that some people, in old age, die from different genetic predispositions, i.e., some die of heart disease, some of cancer, etc. (The following explanation is purposely shortened.)

I suggest RSD is the result of prolonged exposure to the adrenal hormone, cortisol. Cortisol is the "stress" hormone and is produced in response to traumatic events, real or perceived. My work suggests that normal growth and development result from effects of the "melatonin-DHEA cycle" on DNA. According to my general theory, cortisol is produced by the adrenal glands during stress to alter the production and effects of DHEA. (DHEA is the major steroid hormone produced by the adrenals, cortisol is second.) In RSD, I suggest cortisol production continues while the melatonin-DHEA cycle is reduced. It is this combination of increased, prolonged cortisol and reduced DHEA that causes the symptoms of RSD.

While it is not always true, RSD often follows injury trauma or surgery (another form of trauma). It is proven that DHEA is reduced by surgery and cortisol increases following stress. In most people, this shuts them down, but they eventually rebound to produce more normal levels of DHEA and cortisol. (This mechanism whereby cortisol shuts down DHEA is the "fight or flight" mechanism. I suggest DHEA stimulates the nervous system, while cortisol shuts it down. Too much stress (cortisol) makes us "run," so we can face another "fight," another day, when our DHEA rebounds.) In the case of RSD, I think cortisol production never stops.

Cortisol is proven to be a nerve toxin, in prolonged exposure. Cortisol will harm other tissues during prolonged exposure. (I checked with Medline and could not find a study of RSD and cortisol, DHEA, or melatonin.) So, since this is my theory, I suggest that RSD often worsens due to prolonged cortisol and reduced DHEA. The cortisol harms tissues, makes the RSD worse, and the reduced DHEA cannot stimulate healing. (My work suggests all tissues need DHEA; if it is reduced, all tissues will reduce function.) This mechanism will follow a continuum in that some will experience RSD for very long periods, while others may heal. It depends on their levels of DHEA and cortisol.

Support for my theory of RSD is circumstantial. In circumstantial arguments, one must consider the evidence. I think DHEA functions along with melatonin as a cycle. While it is anecdotal, many people with RSD report that sleep is deprived. Melatonin is the natural molecule of sleep and DHEA is the natural molecule of alertness. I interpret this to mean that the melatonin-DHEA cycle is disrupted in individuals with RSD. It is also known that RSD is uncommon in children; children are producing a lot of DHEA for growth and development and their melatonin is also high. This would protect children from RSD, due to cortisol. (I am aware that some children do exhibit symptoms of RSD.) My work suggests that cancer uses DHEA at the expense of the body. That is, cancer can reduce the overall availability of DHEA for the body. Therefore, my theory of RSD would suggest that cancer should be able to increase the probability of RSD, because cancer reduces DHEA. (Example, it is proven that breast cancer tumors absorb more DHEA than other tissues.) Consider this quotation: "Spontaneous development of RSD in patients with a history of cancer should alert the physician to the possibility of occult malignancy [in people with RSD]" (Archives of Physical Medicine and Rehabilitation 1996; 77: 7.)

Also, it is also proven that DHEA promotes bone density, and cortisol, in prolonged exposure, can reduce bone density. In my theory of RSD, reduced bone density would be a symptom of RSD, because of the reduced availability of DHEA and increased cortisol. This is supported: "BMD [bone mineral density] and BMC [bone mineral content] were significantly lower in the [RSD] involved side of the patients (28.4 and 45.1% respectively) compared with the contralateral normal limb. Controls [people without RSD] only showed a minimal variation of 2.17% in BMD and 4.38% in BMC between right and left measures. The difference between patients and controls was highly significant." (Journal of Rheumatology 1994; 21: 498. In this case, I suggest the reduced DHEA and increased cortisol greatly increased the normal differences between sides of the body in the RSD patients.

So, in summary, I suggest reflex sympathetic dystrophy results from a prolonged increase in cortisol and a decrease in the melatonin-DHEA cycle. In people who develop RSD, this results in increased pain, etc., due to the toxic effects of prolonged cortisol on nerves and other tissues. Since their DHEA may be reduced, the ability to heal is reduced, so the syndrome is prolonged. It is my suggestion that people with RSD may benefit from melatonin supplements at night and DHEA supplements during the day.