The Carbon


General exhaustion with trembling and failure of the legs, chilliness, weak, slow pulse, pale yellow appearance or hectic redness are the expressions of the severe state of disease for which kreosote is suited.

Universal modalities are not known for kreosote. The aggravation from rest, particularly from sitting, refers to the back and sacral pains, but the improvement from lying and the aggravation from movement and walking is observed. One can generalize just as little on the aggravation in the open air and from the cold and the improvement from warmth.



Severe alterations of the blood and tissue. “Decomposition.” Tendency to bleeding, to foul, acrid and corrosive secretions. Putrid inflammations and ulcers. Carcinoma. Diabetic tissue injuries. Cachexia; yellow appearance in chronic deep seated mal- adies.

Chief Trends:

Skin and mucous membranes.

Skin: severe itching, burning; vesicles and pustules. Poorly nourished unhealthy skin, marked bleeding from small wounds, tendency in ulceration and gangrene. Pruritus senilis. Pruritus vulvae. Diabetes! Digestive canal: toothache from caries. Nausea, vomiting of undigested food several hours after eating or regurgitation of sweetish water (organic even malignant alterations or reflexly from other organs).

Old cases of gastric or duodenal ulcer in enfeebled persons.

Gastro-enteritis with nutritional disturbances in children with poor development of teeth.

Female sexual organs: foul, yellow or flesh-like, watery, acrid, corrosive leucorrhoea. Marked inflammatory irritation of the external parts. Putrid ulcers and carcinoma of the portio.

Menses too early, too copious, too prolonged, dark, acrid, offen- sive; intermittent, flow particularly on lying. Intermittent bleeding after coitus. Back and sacral pain with downward pressi- ng in uterine maladies.

Respiratory passages: Copious, purulent sputum. Progressive destructive processes; foetid bronchitis, bronchiectasis, lung gangrene, tuberculosis.


It has been recommended in the D 3 up to the D 30 and higher. I have observed good effects from the D 6.

OTHER TAR PRODUCTS —————— Pix liquida, a product of dry distillation of various conifera, is not proven. Its action on the skin from external application is generally known. The skin inflammations are associated with marked itching and burning, yet on the other side, wood tar through the phenol contained in it, also markedly relieves itching. With prolonged external use there is an inflammation of the hair follicles. Internal use proceeds as the external, in chronic eczema with marked itching, particularly on the backs of the hands, psoriasis and particularly acne.

The internal use for muco-purulent sputum from chronic bronchitis still occurs in many places. As with kreosote the sputum is offensive and here also suggests a destructive process. Moreover rough rales and a pain near the origin of the third rib cartilage on the left side, may be correctly related with the left brochus.

Wood tar also provokes irritative manifestations in the urinary passage and has been employed at times in cystitis. The explanat- ion through a disinfectant effect is not sufficient. The dose is usually in the low potencies.

Ichthyol, a distillation product of bituminous deposits with fossil fish inclusions, is obtained in Tyrol and contains 10 percent sulphur. This tar product is also unproven. Outside of the indications also mentioned for pix liquida there is a connection described bed for rheumatic-gouty affections, which may well be traced to the sulphur fraction.

Naphthalin C10H8 is composed of two benzol rings joined together and is a constituent of bituminous tar. It is also unproven. But its actions are known to some extent from many poisonings when it has been taken in excess for intestinal parasites (hookworm, oxyuris), or when de-mothing tablets are accidentally eaten by children. Also the continual inhalation of the vapor or dust can give occasion for poisoning. Peculiar alterations develop in the eyes by the external or internal influence, particularly chorio- retinitis and turbidity of the lens (naphthalin cataract). Naphthalin has been recommended in cataract, amongst others by Tischner.

In dermatology beta-naphthol, an OH compound of naphthalin, also a phenol, is used in parasitic skin diseases, acne, psoriasis, pruritus and prurigo. Likewise the inhalation of naphthalin can provoke itching and exanthemata, still it is used therapeutically in skin inflammations. The severe toxic manifestations are nephr- itis, hemoglobinuria and methemoglobinuria, icterus, swelling of the spleen, clouding of the mind, loss of consciousness, finally spasms and death. Inflammation of the bladder and the urethra, particularly at the orifice of the urethra are noted. But all these trends of action in homoeopathy have hardly been utilized up to the present. On the other hand asthma, hay fever and whoop- ing cough are the chief indications of the remedy: spasmodic sneezing, spasmodic asthma and dry spasmodic cough in children and old people with emphysema. Usually the lower potencies (1-3 triturations) are recommended but D 12 is suggested by Cartier in bronchitis with spasmodic cough and tenacious sputum.


The simple phenol, C6H5OH, is indeed not an organic acid but like all OH compounds of the aromatic series has a much stronger acid character than the alcohols (OH compounds) of the aliphatic series. Therefore the name carbolic acid is not entirely wrong. Phenol appears in the destruction of living substances. Thus it occurs also in wood tar amongst other homologous phenols. It develops in the animal body as a decomposition product of proteins in the intestine, and after absorption product of proteins in the intestine, and after absorption (particularly after conversion into the polyphenol hydrochinone) is bound to sulphuric acid and glucuronic acid, made harmless, and is excreted in the urine. In general the benzol ring is not split in the organism as the open, aliphatic series.


In contrast to the mixture of phenols and phenol derivatives of kreosote, pure phenol possesses a marked capacity for penetration into the cells. Thereby not the antiseptic property but the corrosive action is increased. And since the resorption occurs rapidly, in phenol there soon appears central nervous system effects. A natural mixture of the less strongly split plant products as kreosote, on the other hand acts more steadily on the receptive organs. But this is an advantage for securing persistent therapeutic actions. We encounter here the same regularity which has such great significance for the relation of the entire plant to its “pure” constituents (alkaloids, glucosides, etc.) in therapeutics.

Even in the corrosive action on the skin, the property of rapid penetration of phenol is revealed in the anesthesia which follows the initial burning pain and proceeds into a dry gangrene as it occurs in the prolonged influence from an application.

After absorption of large amounts of phenol the intoxication soon involves the nervous system with loss of consciousness, sensory and motor paralysis, collapse followed by death. Convulsions may occur. The milder poisoning causes a stupefaction like intoxicat- ion, vertigo, headache, often ear noises, fainting, vomiting. Ga- stro-enteritis, at times icterus, irregular respiration with small pulse may follow. In acute cases the body temperature falls considerably with cyanosis, cold sweat, and collapse, while, on the other side, in prolonged poisonings there is the so-called septic fever, indeed consequent to the cell destruction. The excreted phenol sulphuric acids, in particular the transformation product, hydrochinone sulphate, makes the urine brown-green to black, so- called carboluria. If the pairing with sulphuric acid and the absorbed phenol does not keep pace, then nephritis results.


Intoxications with acidum carbolicum are very numerous. Intentional provings are found:

1. Hoyne: Carbolic acid, Chicago, 1869 (see Journ. of the Hom. Mat. Medorrhinum, vol. 5, p. 329, 1872. Allg. hom. Ztg., Bd. 68, p. 166 ff. 2. Price: Amer. Hom. Observer., Bd. 8, p. 148.

3. Lilienthal: Trans. of N.Y.State Hom. Soc., vol. 8, p. 232,1870.

4. Haeseler: Hahn. Monthly, vol. 5, p. 166, 1869.

5. Danion: Rechrches sur Vacide phenique, Strasbourg, 1869.

6. Mitchell: Amer. Journ. of Hom. Mat. Medorrhinum N.S.vol. 1, p. 354 (use in carious teeth).

7. Hale: New Remedies, 4 Aufl., vol. 1, p. 151, 1875 (1 and 6 are found here).

8. Norton: Public. of Mass. Hom. Soc., vol. 4, p. 285 (of phenol vapors).

9. Williamson: Trans. of Penns. State Hom. Soc., vol. 1, p. 180, 1870 (phenol vapors).

10. Declat: Traite de l’acide phenique, Paris, 1854.

GENERAL ——- Acidum carbolicum stands very near to kresote in its actions. However it acts more acutely, raches the central nervous system more rapidly and seems to condition vasomotor-trophic disturbances more strongly and centrally. But for these reasons the field of action is narrower than that of kreosote. Acidum carbolicum is therefore infrequently employed.

In acidum carbolicum septico-putrid and gangrenous processes on the tissues are also the most frequent substrate, the acrid secretions are corrosive and at the same time offensive; but these processes lead sooner to trembling, sensation of numbness, mental confusion, chills, cold and clammy sweats, and manifestat- ions of collapse.

Pains in the most diverse severe fields, in particular in the right supraorbital, appear and disappear suddenly; numbness, cold less of sensation are the warnings of the trophic disturbances. Disinclination to per-form any mental work proceeds into stupefaction and confusion. Headache as if from a tense elastic band around the head, particularly in the forehead and an acute olfactory sense have some value as special symptoms.

ORGAN SYMPTOMS ————— Outside of paresthesias and anesthesias on the skin there are all stages from itching to vesicles and pustular eruptions to necrosis decubitus and gangrene, as in kreosote, those on a diabetic basis find the most frequent use. From the necrotic processes in the throat comes the clinical recommendation of phenol in malignant scarlet fever and even more in septic diphtheria when the widespread membrane extends to the nose and mouth, there is a strong odor and symptoms of collapse indicate the malignant course. From the stomach and intestine come the same inflammatory, ulcerative and carcinomatous processes as were mentioned under kreosote. Morning vomiting as well as nausea have led to the recommendation in hyperemesis gravidarum and still more, because of the regurgitation, stupefaction and confusion, to the morning vomiting of drunkards. Desire for alcohol and tobacco are cited but they are not found in the provings, and from smoking aggravation as well as improvement is observed. Much is said of the fermentative processes, accumulation of gas in the stomach and intestine. The emissions here too are said to be offensive. Ulcerative processes in the intestine with fever have also given occasion for the use of acidium carbolicum in typhoid and dysentery with a malignant course. In carcinoma of the gastro- intestinal canal and of the uterus phenol, from a practical stand point, is inferior to kreosote. The leucorrhoea is also characterized just as in kreosote. In puerperal fever a foul discharge, vomiting and meteorism should make one think of carbolic acid.

Frequent copious micturition has also been cited as an indication for acidum carbolicum in diabetes. The nephritis which appears in carbolic acid poisoning is scarcely suitable as a therapeutic indication. Inflammatory destructive processes in the urinary passages require considerable doses of acidum carbolicum for effectiveness. Even from this one may conclude that it is less suitable than, for example, the related benzoic acid. And if, from the provings, stiffness and diverse pains in the muscles and joints suggest a certain rheumatic component in carbolic acid effects, then these are far less important than in the benzoic and salicylic acid actions.

SUMMARY ——- Chief Trends:

Septic-gangrenous processes, acrid, corrosive, offensive discharge.

Participation of the central nervous system, particularly the vasomotor-trophic centers.

Paraesthesias, anesthesia; states of confusion; collapse.

Frequent neuralgias, coming and going suddenly.

Headache as from a band around the head. Acute olfaction.

Skin: itching, necrosis, gangrene.

Throat: malignant diphtheria with extensive membranes.

Gastro-intestinal: ulcers (also typhoid and dysentery) carcinoma.

Vomiting of pregnancy. Gastritis of drunkards.

Uterus: Ulcerative processes with foul leucorrhoea. Puerperal fever.


It is given in potencies from D 3 to D 30.


Salicylic acid, o-oxy-benzoic acid with its numerous derived preparations (aspirin, diplosal, salol, salipyrin, etc.) is one of the most commonly used drugs in the world today. Compounds of salicylic acid appear in various plants, for example, types of willows (salix), gaultheria procumbens, spiraea ulmaria. Indeed the very ancient use of such plants, particularly as fever remedies depends upon this constituent; however the chemically simple and synthetically prepared substance should be mentioned here because of its close relation to phenol and benzoic acid the carbon compounds discussed.

Salicylic acid was prepared by Piria in 1838 from the glucoside salicin of the willow (salix alba). Chemical synthesis was obtained by Kolbe and Lautemann 527 and with this was given the basis for the scientific and industrial attempt then instituted to explain salicylic acid (indeed first by Stricker 528 as a specific for acute rheumatic fever. This opinion long remained unconsidered.


It is worthy of note to remark that Ehrlich 529 considered the action of salicylates in rheumatism had an antiseptic basis, were “specific,” that is, “etiotropic.” His there prerequisites for the recognition of chemotherapeutic-etiotropic action: 1, strong depressant or destructive action on the excitor in a test tube; 2, relative harmlessness for the host; 3, antiseptic action in the organism are indeed, even the second (relative harmlessness), not proven for salicylic acid in rheumatism, and even if placed in analogy with the streptococci, at least highly improbable; all findings speak against this conception.

If the non-discovery of the excitor of polyarthritis rheumatica makes direct proof of the etiotropic action impossible, then at least the probability of bacterial depression or destruction should be proven to hold for salicylic acid. But the bactericidal properties of salicylic acid and even if its salts are much less evident outside the organism than of carbolic acid; in weak solutions of salicylic acid, molds develop for example. The percentages for the depression of bacterial growth of solutions of salicylic acid move around 0.1 Percent. (Moreover the greatest concentration of salicylic acid occurs in the blood.) Accordingly the concentration of salicylic acid would never be attained in the organism which has been found necessary for the depression, not to mention the death of the bacteria.

Thereby it is also to be considered that a stronger antiseptic salicylic acid could be liberated at the site of action from its salts. But this is not the case. The oral and in massive doses administered salicylic acid is converted into the sodium salt by the alkali of the intestinal fluids; it is taken up in this form and must circulate as such at the chemical reaction of the blood. Now Binz 531 has presented the theory that in polyarthritis the strong carbon dioxide tension of the blood and other body fluids (joint effusions!) would be in a position to liberate salicylic acid from its salts and has introduced some support for it.

Newer investigations by Hanzlik 532 which considered the H-ion concentration of the blood show the untenability of the CO2 tension theory. The liberation of salicylic acid requires a much higher acidity than that which is obtainable in the living blood. Actually the salicylate containing joint fluid in patients with rheumatic fever shows no free salicylic acid according to Scott, Thoburn and Hanzlik 533.

A way out of the dilemma into which the hypothesis of an etiotro- pic action of salicylic acid in rheumatic fever has been harmed by experimental investigation is opened through the findings of Bondi and Jacoby. 534 They seem to speak for a certain organotrophy of salicylic acid for inflamed joints, because the joints of rabbits which were infected by staphylococci contained more salicylic acid than those of normal rabbits. Such an enrichment of salicylic acid salts in the inflamed tissues would be explained without further trouble from its greater blood supply because according to Bondi and Jacoby the blood has the greatest relative amount of salicylic acid. But now newer investigations 535 have brought definitely opposite results, naturally in arthritis which can be experimentally produced in rabbits by the local application of oil of mustard and croton oil. Finally it is proven by Scott, Thoburn and Hanzlik 536 in patients with rheumatic fever that the salicylate content of the joint fluid is less than in the blood. Thereby the greater affinity of salicylic acid for the inflamed joint cannot be maintained.

MANNER OF ACTION IN RHEUMATISM —————————— In what relation now from a clinical viewpoint does the specificity of salicylic acid stand in acute rheumatic fever? The prompt lowering of the temperature with the outbreak of sweating and the diminution of inflammatory manifestations in the joints, particularly the pains, is so striking with great doses, that indeed one might well think of a specificity. Recently R. Sicard 537 has shown from personal observations as well as those of others that the joint manifestations and the fever are not rarely entirely refractory from the start against the salicylic acid therapy. Moreover it is striking that under the use of salicylic acid in maximal doses, the return of joint symptoms is frequent, and further that cardiac involvement is not avoided nor in any way favorably influenced. 538 But since the cardiac manifestations of the infections disease, polarthritis rheumatica are characteristic, indeed according to many authors an essential part, this must create doubt of the specificity of salicylate salts. Against a specificity in the sense of a one sided selectivity also speaks the fact that other agents which do not contain the salicyl group (particularly atophan with its chinolin group) have the same antipyretic and analgesic action in joint rheumatism, indeed, Hanzlik, Scott and Gauchat 539 have shown that the same or almost equal results can be obtained in rheumatic fever by a combination of analgesic and antipyretics of the type of morphine and quinine, where there is not be least relationship to the salicylate group. But on the other side salicylic acid effect is not limited to acute rheumatism but the analgesic and antipyretic actions are used just as much in many other states of disease. So there is no basis for seeing in salicylic acid more than a pure symptomatic characteristics in this disease. In addition to the antipyresis and analgesia, there is also the lessening of joint swelling. One may designate the action in rheumatism also as a polysymptomatic one so that in this case salicylic acid is a syndrome remedy.

The mechanism of salicylic acid action on the symptoms of joint rheumatism has been explained only to a small extent through numerous studies. In regared to the antipyresis, salicylic acid in the usual small and large doses widens the peripheral vessels, in particular those of the skin, probably through an action on the central nervous system, at the same time with an increase of sweat. Increased heat radiation occurs and in the febrile it is particularly great. While increased heat radiation is hardly evident in the healthy, it is distinctly evident in the labile heat regulation in fever. The production of heat does not seem to be influenced at least by the doses employed clinically. It is established that there is an increase of nitrogen, uric acid, phosphate and sulphate excretion under large doses of salicylic acid.

There is also a lowering of uric acid content of the blood with increased amounts in the urine. 540 After discountinuance of salicylates the uric acid in the blood again increase and the quantity in the urine diminishes. 541

Moreover with doses of salicylic acid under 2 grams, variable output of uric acid in the urine is found. 542

On the other side, very large doses in rats also cause a diminution of nitrogen excretion in consequence to the nephritis which develops.

The influence on water excretion behaves correspondingly. With moderate doses the diuresis is increased; in animals the renal volume increase through widening of the vessels and there is only a transient decrease in the output of urine 543; with doses under 2 grams according to Willy 542 there is no increase in output. With large doses. clinically maximal, of sodium salicylate the amount of urine is decreased and albuminuria appears (and eventu- ally casts) in the urine. 544 In animals nephritis has been found histologically 545 and also in the human at autopsy. 546

The increase of protein conversion under large doses of salicylic acid permits an increase in heat production to be assumed and this is present also according to experiments by Isenschmid. 547 But for the antipyresis, it is decisive that under the conditions of the already febrile increased metabolic, the heat radiation predominates.

Formerly one perceived a close natural connection between the acute rheumatic fever and the uric acid content of the blood and made the increased excretion of uric acid responsible for the favorable influence of salicylic acid. If this hypothesis is not clinically verified in gout, then it is to be doubted in an acute infectious disease as acute rheumatism.

It is exactly the detailed investigations on the N-metabolism under salicylates which have led to the conception that salicylic acid lowers the permeability of the kidney for uric acid and it has often been assumed that the increased permeability of the kidney for other residual products and also the hypothetical toxin of the excitor of joint rheumatism existed. With this there would be in addition to the marked excretion through sweat, a further excretion through the kidney, two ways of canalization, but still no “created” defense of the organism, as one might say.

The actions on the heart and circulation known up to the present cannot contribute much to the explanation of the antipyretic action.

Sensitive persons react to small doses of salicylic acid with acceleration of the pulse and sensations in the cardiac region.

How much the disposition contributes to the action of salicylic acid can be perceived from the existence of a (so-called paradox) increase in temperature which is independent of the dose of the drug. Lewin states 548: “It is evident 1/2-1 hour after the ingestion and is usually introduced by a chilliness which may last over an hour.Following this is a marked sensation of heat and the body temperature itself rises to 41 C. The fever may remain at this height up to two days and then spontaneously diminishes.

Otto Leeser
Otto Leeser 1888 – 1964 MD, PHd was a German Jewish homeopath who had to leave Germany due to Nazi persecution during World War II, and he escaped to England via Holland.
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,