Fibromyalgia and Cyanide Sensitivity

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Fibromyalgia and Cyanide Sensitivity written by R. Oesch, MD

In 1982 a microallergist in Houston tested 43 persons (mostly nonsmokers) who

were suspected of or diagnosed with cyanide intoxication resulting from airborne

cyanide pollution. He found that 25 (58%) of these persons tested positive for

immunological sensitivity to cyanide, whereas only one of 200 control patients

tested positive. As the primary physician treating most of these patients, I

came to recognize that the more common symptoms of cyanide intoxication included

such things as fatigue, depression, headache, decreased resistance to

infections, restless sleep, weakness, muscle cramps, forgetfulness, inability to

concentrate, exercise intolerance, muscle aches, and joint pain. Comparatively,

the National Fibromyalgia Research Association listed symptoms occurring in 40%

or more of fibromyalgia patients as muscular pains, fatigue, insomnia, joint

pains, headaches, restless legs, numbness and tingling, impaired memory, leg

cramps, and impaired concentration. Additionally, nervousness was reported to

occur in 32% and major depression in 20% of patients with fibromyalgia.

In testing for sensitivity to cyanide, the microallergist in Houston spun blood

at low to medium speed (1,500 rpm) then collected the buffy layer of serum and

discarded the platelets from the top. He diluted the buffy layer slightly, using

about six parts serum to one part sterile water, to acquire a solution which

contained about 100 white-blood-cells per field using 450X magnification plus a

15X viewing lens. Using meticulously cleaned glassware and equipment, he

prepared antigen jelly slides using Vaseline petroleum jelly as an inert base.

Generally, twenty milligrams of an antigen to be tested were mixed in 20

milliliters of water and allowed to sit overnight. About 2.5 drops of this

antigenic solution were placed on a ring of jelly which was about 1 cm in

diameter. One large drop of WBCs was added to each antigen-jelly slide. On

control slides, the WBCs would not disrupt for about 2 to 3 hours; whereas on

slides where sensitivity was determined to exist, cells would disrupt in about

thirty minutes. The speed and degree of disruption of the white-blood-cells was

observed, and the degree of sensitivity was determined from such observation.

Although some of the persons determined to be suffering from cyanide

intoxication did not show " sensitivity " to cyanide at all (and may have been

suffering due to metabolic inadequacies rather than immunological sensitivity);

other persons, some of whom were notably ill, did show marked sensitivity.

Cyanide is a small molecule which may not be antigenic, but cyanide binds to

several enzymes and other entities within the body, and the resultant molecules

may be antigenic. In addition to binding to cytochrome oxidase, cyanide

reportedly binds to catalase, peroxidase, methemoglobin, hydroxocobalamin,

phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, and succinic

dehydrogenase; and it has been noted that these reactions may contribute to

cyanide's toxicity. [1, 2]. Furthermore, as mentioned in a preceding paragraph,

cyanide is reportedly a carboxylase inhibitor. [3]. Thus, cyanide bound to one

of the aforementioned agents may create an entity which is immunologically

antigenic in some persons; and this may explain the significant degree of aching

muscles and/or joints encountered in fibromyalgia.

I would hypothesize that persons who develop immunological sensitivity to

cyanide may still suffer from cyanide intoxication secondary to impaired ability

to metabolize cyanide (which may, in fact, have greatly contributed toward

developing immunological sensitivity); and that those persons may also suffer

added muscle and joint pain due to immunological reaction to cyanide in the

tissues (which is more likely an immunological response to substances formed by

the combination of cyanide and tissue entities). Such a hypothesis may be

investigated by testing thiocyanate levels during periods of exacerbated

illness, as well as observing response to proper treatment with specific

antidotes to cyanide intoxication. Treatment of patients with cyanide

intoxication who are immunologically sensitive to cyanide may, however, prove

more challenging than treating patients with cyanide intoxication who are not

immunologically sensitive; and such treatment may require very consistent and

thorough maintenance doses of the prescribed remedies. To some extent, avoiding

exposure to cyanide may sometimes be possible, and may help in treatment.

Cyanide, however, may be released into the atmosphere from the burning of

organic or synthetic compounds containing carbon and nitrogen, such as with the

burning of fossil fuels like coal and gasoline. Thus, when mankind began using

fire for cooking and heating, this accomplished the advent of air pollution

containing cyanide---an advent which was appreciably compounded by the invention

of smoking and by various industrial processes. Furthermore, over 2,650 plant

species can produce hydrogen cyanide when eaten, including edible plants such as

almonds, pits from stone fruits, sorghum, cassava, soybeans, spinach, lima

beans, sweet potatoes, maize, millet, sugarcane, and bamboo shoots. [4, 5, 6]

Nonetheless, I believe that increased polluting of the air with cyanide

constitutes the major source of cyanide contributing to cyanide intoxication in

the United States. The half-life of cyanide in the atmosphere is estimated at 1

to 3 years, and perhaps 98% of airborne cyanide remains in the lower atmosphere.

China's atmosphere may reach the west coast of the United States in less than a

week.

References

1.) Ardelt BK, Borowitz JL, Isom GE. Brain lipid peroxidation and antioxidant

protectant mechanisms following acute cyanide intoxication. Toxicology

56:147-154, 1989.

2.) Rieders F. Noxious gases and vapors I: Carbon monoxide, cyanides,

methemoglobin, and sulfhemoglobin. In: DePalma JR, ed. Drill's pharmacology in

medicine, 4th ed. New York, NY: McGraw-Hill Book Company, 1180-1205, 1971.

3.) De Metz M, Soute BAM, Hemker HC, Vermeer C. The inhibition of Vitamin

K-Dependent Carboxylase by Cyanide. FEBS Lett 137(2):253-256, January 1982.

4.) Seigler DS. Cyanide and cyanogenic glycosides. In: G.A. Rosenthal, M.R.

Berenbaum, eds. Herbivores: their interaction with secondary plant metabolites.

Academic Press, New York, N.Y. 35-77, 1991.

5.) Swain E, LI CP, Poulton JE. Development of the potential for cyanogenesis in

maturing black cherry (Prunus serotina Ehrh.) fruits. Plant Physiol (Bethesda)

98(4):1423-1428, 1992.

6.) Fiksel J, C, Eschenroeder A, et al. Exposure and risk assessment for

cyanide. EPA/440/4-85/008. NTIS PB85-220572, 1981.