In any case reports are available where arsenic has accelerated autolytic processes in the liver. However, Hess and Saxl have seen a depression of autolysis from large doses.
ARSENIC EATING AND HABITUATION
Of special pharmacologic interest is the habitual ingestion of arsenic for the maintenance of health and increase of strength and power. The eating of arsenic for increasing strength was mentioned by Avicenna in 1165. The arsenic eaters of Styria are best known. They are very healthy people, usually men with laborious occupations. They begin eating arsenic at 18 but still reach old age, remain healthy, are happy, combative and sexually potent, which must be traced to the eating of arsenic. The disposition is happy and they regard arsenic as a good remedy against shortness of breath. The ingestion increases and diminishes with the moon; with a waning moon they take aloes in increasing doses until diarrhoea occurs. They proceed so far that they may swallow 0.4 g of arsenic without disturbance (maximal single dose is 0.005 g!). The complete well being of these arsenic eaters stands in sharpest contrast to the severe disturbances in chronic industrial arsenic poisoning. This contradiction is explained by experimental investigation in that with the slowly increasing ingestion of arsenic the intestinal epithelial obtains the ability to prevent or only very slowly absorb arsenic.
The amount excreted through the urine may fall to 0.3 Percent of the quantity ingested. Dogs who have tolerated continuous slow increase of arsenic by mouth for months up to many times the fatal dose die from acute arsenic poisoning from the usual dose when it is administered subcutaneously. Moreover a general cell habituation is not present but the habituation may be based upon the altered intestinal conditions. thus a high grade tolerance to dissolved arsenic introduced into the stomach does not exist as for the administration of a powder.
ACTION ON BLOOD
A favorable action of arsenic in anemias has long been observed but the action has not been explained up to the present.
The influence of arsenic on the number of red blood cells and the hemoglobin content in animal experimentation gives extremely variable findings, some investigators reporting an increase in the erythrocytes and of the hemoglobin, particularly in anemic animals, others find no alteration of the blood and still others
a decrease in the erythrocytes and of the hemoglobin. According to many investigators after medicinal doses in the healthy and sick there is usually a decrease of the erythrocytes, more rarely no change in the count. Here also the damages of the red blood cell picture through an organic arsenic compound must be included, as with atoxyl(the sodium salt of aminophenylarsenic acid). It produces a decrease in the number of erythrocytes and the hemoglobin content, moreover, a poikilocytosis and anisocytosis. This picture of intoxication which is similar to pernicious anemia may also support arsenic therapy of this disease in a homoeopathic sense. The conception that peripherally increased destruction of blood caused an increased regeneration of red blood in the bone marrow seemed at first to find some basis in the marked redness of the bone marrow in chronic arsenic poisoning, but exact investigation speak against the conception. There is no increase in the erythroblasts.
There is a distinct reduction of the oxygen utilization of the red blood cells whereby the anemic cells seem to be more sensitive than the normal, even 0.003 of arsenic acts distinctly depressing. English investigators could prove no increase under arsenic medication, but found that the erythrocytes became much more resistant to hemolysis and therein see the favorable action in pernicious anemia. Thiele could not confirm this report. Perhaps some light is thrown in this connection by investigations on the influence of the thyroid on the increased nitrogen excretion with O2 deficiency and the increased blood formation in high altitudes. It shows that after removal of the thyroid, O2 deficiency does not increase nitrogen excretion and that in athyroidetic animals the high altitude not only does not promote new blood formation but even depresses it. From the similarity of arsenic action to that of high altitudes the thought seems likely that the blood action or arsenic occurs through the thyroid, moreover, feeding thyroid can stimulate the formation of blood. Likewise Isaac believes that the thyroid has special significance in the blood regeneration by arsenic.
Certainly the stimulating action of arsenic on the red blood cells is decidedly dependent upon the previous state, the lability, sensitivity and on the dose. But there is also a destructive blood effect. And thus therapeutic use arranges itself immaterially of the school according to the simile rule.
Likewise the reports of the influence of arsenic on the white blood cells are contradictory. By administration of Fowler’s solution up to maximal doses the number of leucocytes diminishes often up to one half. Thereby the neutrophiles are particularly involved. If the lymphocytes are markedly increased, then they fall distinctly. But these alterations are by no means constant; in other cases the number of leucocytes increases. With toxic doses at first a decrease appears which is soon followed by a hyperleucocytosis if the dose has not been lethal.
NERVOUS SYSTEM
That psyche and central and autonomic nervous systems succumb to the action of arsenic is obvious from observations of acute and chronic poisoning.
In his studies Pistorius observed immediately after the injection of arsenic and before the appearance of intestinal irritation, a vomiting which was of central origin in his opinion. Moreover he had the impression in his animals that by gradual poisoning via the subcutaneous route, at first those centers of the brain and medulla which communicate sensory impressions or transmit reflexes from the vessel nerve centers are paralyzed. Perhaps the leucopenia from arsenical medication is obtained through the autonomic nervous system similarly to the leucopenia obtained by intracutaneous wheals.
The respiratory center itself is also involved in arsenic action. Subcutaneous doses at first produce only an increase of respiratory frequency, perhaps a direct excitation of the vagus nerve. The respiratory center is in an “irritated” state so that excitation of the central end of the vagus leads to tetanus of the inspiratory muscles while otherwise only an acceleration of respiration occurs.
Studies by Ringer and Murell on frogs showed that the diminution of reflex excitability is traceable to central paralysis and is not the result of cardiac failure. The excitability of the motor nerves is retained longer, but then is lost and finally the excitability of skeletal muscle. How far the paralytic state in arsenic poisoning is conditioned directly central or from circulatory disturbances is also not as yet determined.
Conduction by peripheral nerves is reduced by arsenic. The paralysis observed in acute arsenic poisoning is probably provoked through a rapidly appearing paralysis of the intramuscular nerve endings. Arsenical neuritis has been observed after therapeutic doses.
HEART AND CIRCULATION
A marked influence of arsenic on the heart and vessels exists beyond any doubt according to the manifestations of poisonings.
Experimentally it has been demonstrated many times that a decrease in the cardiac frequency and finally standstill in diastole is provoked by large doses of arsenic. Very large doses of arsenic can produce an acute paralysis of the heart in which contractions no longer occur after electrical or mechanical stimuli. Loewi concludes from this that a paralysis of the cardiac ganglia as well as the muscle exists. Intravenous injections of large doses in mammals give corresponding slowing of the pulse and falling of the blood pressure, still the action on the blood pressure is not solely dependent upon the heart, but indeed similarly to phosphorus, on the adrenals and on the vascular system, especially on the splanchnics. With small doses of arsenic and subcutaneous injection in warm blooded animals Leeser saw at first an increase in the pulse frequency. We have here also the same conditions as in phosphorus and the phosphites. In the cardiac paralysis after larger doses Leeser found the heart still irritable after some hours, so that according to his experience the heart muscle itself is not paralyzed. According to S.G.Zondek the standstill caused by arsenic can be again removed through calcium ions, while potassium ions increase the action of arsenic.
The capillaries stand under the special influence of arsenic. Arsenic like phosphorus is an outstanding capillary poison. Above all the splanchnic vascular field is prominent arsenic action.
The action involves the capillary wall itself, because, after severe poisoning splanchnic stimuli no longer release any contraction. The intestinal capillary walls are markedly widened and completely filled with blood. There is a high grade stasis oedema with marked exudation which results in a pseudomembranous deposit on the intestinal mucous membrane. The capillaries of the other parts of the body are also involved even if not to the extent of the intestinal vessels. The severe vascular disturbances consist not only in a paralysis but also an increased permeability of the vessel wall. Through this comes the preparation for oedema. In dogs, and in rabbits with an artificial hydremia a marked oedema follows arsenic, an accelerated outpouring of intravenously injected fluid out of the vessels. Transudation occurs also in the pleura, the pericardium and brain ventricles. The peculiar fact that the intestinal wall capillaries succumb to arsenic action so rapidly is not as yet explained. Perhaps it may be associated with the fact that the gastro-intestinal mucous membrane is an important site of excretion for arsenic (even after parenteral introduction). Furthermore it is striking that the organs to which a special capacity for reduction is ascribed, as the intestinal mucosa and the liver also are special points of attack in arsenic poisoning.
Leeser, a Consultant Physician at the Stuttgart Homeopathic Hospital and a member of the German Central Society of Homeopathic Physicians, fled Germany in 1933 after being expelled by the German Medical Association. In England Otto Leeser joined the staff of the Royal London Homeopathic Hospital. He returned to Germany in the 1950s to run the Robert Bosch Homeopathic Hospital in Stuttgart, but died shortly after.
Otto Leeser wrote Textbook of Homeopathic Materia Medica, Leesers Lehrbuch der Homöopathie, Actionsand Medicinal use of Snake Venoms, Solanaceae, The Contribution of Homeopathy to the Development of Medicine, Homeopathy and chemotherapy, and many articles submitted to The British Homeopathic Journal,