Dear Colleagues:

This month I would like to discuss sequestration of toxic metals (usually mercury) and what this means in the practice of neural therapy. The word sequestration means in chemistry the binding of a chemical element or compound so that it is no longer available for reactions. In pathophysiology, it means binding of an element or compound in a particular location in the body.

It has been known for a long time that toxic substances when introduced to the body do not distribute evenly. Certain organs are more commonly targeted, the kidneys for example. The kidneys therefore "sequester" mercury. However this does not mean that they are more adversely affected than other organs. In fact, the kidneys seem to resist poisoning relatively well. Kidney failure by chronic mercury poisoning is probably rare. (Although I sometimes wonder about the many cases of kidney failure of "unknown cause").

Chemicals deposit in specific areas according to the chemical environment in the area. If a dissolved substance precipitates because of lower pH in a test tube, it will do the same thing in a body tissue. It stands to reason that tissues that are not healthy are therefore more likely to accumulate toxins, especially toxic metals. This becomes a vicious cycle, because the presence of the toxic element worsens the condition of its environment.

Interference fields are by definition areas of disturbed physiology; included in this definition is disturbed chemistry. It should not therefore be a surprise that toxic chemicals can accumulate in interference fields. This has clinical implications.

Experienced neural therapists are aware that neural therapy of an interference field, "opens up" the circulation of the area and helps release toxins. This can be beneficial, as when toxins that have accumulated in the liver (causing an interference field) are released, and liver function improves. Or it can be detrimental, when neural therapy of a tissue containing mercury "opens up" the tissues and releases mercury more quickly than the excretory organs can handle it.

The following case report is an example of the second scenario:

A 51 year old single business woman complained of several years of fatigue. A diagnosis of chronic mercury poisoning was made; her dental amalgam was replaced with composite material and she underwent a detoxification program, including intravenous DMPS chelation. The response to chelation was monitored by regular urinalysis for toxic metals and the chelation was continued to the point that her energy was restored and her urinary excretion of mercury was minimal.

Active treatment was discontinued, but two months later she underwent minor elective oral surgery. She suddenly became fatigued and in fact stated that she felt "exactly as before" her amalgam removal and detoxification. Intravenous DMPS was again administered and a very high mercury level (over 175 micrograms/gm. of creatinine) was measured in the urine in the first 6 hours. Repeat intravenous DMPS injections reduced her mercury excretion to normal and restored her energy level over the ensuing months.

Similar responses may occur with neural therapy of cranial autonomic ganglia, especially the sphenopalatines. Research has shown considerable accumulation of mercury in the soft tissues and bones of the lower face in those with dental amalgam (past or present). Neural therapy of the sphenopalatine ganglion can in certain patients provoke a significant toxic reaction.

Both diagnosis and assessment of the response to treatment of chronic metal toxicity must continue to be matters of clinical judgement. Laboratory tests can be helpful, but sequestration of toxic metals continues to be a confounding factor of which clinicians need to be aware.