In rickets or avitaminosis D, calcium economy is distinctly disturbed and the manifestations show themselves most distinctly in the depot for calcium salts, the bones. Here an impoverishment of calcium salts appears; there is a cessation f calcification. In the florid state calcium and phosphates are less retained but in the healing stage the retention is considerably greater. In the serum in rickets the amount of phosphates is even lower than the calcium amount in the blood. The low content of the blood in inorganic phosphates depends upon a defective action of the cartilage phosphates. The excretion of phosphates through the kidney continues undisturbed as the renal phosphates is uninfluenced. Probably less calcium is absorbed from the intestine. In rickets the ratio of intestinal calcium excretion to renal calcium excretion is considerably increased in comparison to the normal. The conditions favoring solubility of calcium are less favorable than for deposition in the bones. Because of non-utilization, because of incapacity of the cartilage to deposit, it there is less calcium; in the bones. Calcium cannot be absorbed, further not utilized by the bones, if vitamin D fails. Vitamin D probably alter the colloid state of the cartilage. According to all appearances it acts as a transference catalyzer for ultra- violet radiations and activates the cartilage phosphates. Because, in vitamin D deficiency, the action of phosphates is depressed, it remains unused by the cartilage and will be found in increased amounts there. Phosphate formation which is necessary for the adsorption of complex calcium salts is subnormal and on this account the serum phosphate is low in comparison to normal. Calcium and phosphate metabolism is also inactivated in rickets and can be again activated through vitamin D. it is not the deficiency in Ca and Po4 supply that is in error but the inability to utilize and activate it.
Now it is remarkable that the experimental rat rickets which is brought about by deficiency in vitamin D and phosphates can be healed through increased introduction of phosphates alone which is not true of infantile rickets. Furthermore an experimental rickets can be provoked through excessive introduction of calcium salts gives exactly an experimental basis for the therapeutic use of calcium preparations in the sense of the simile rule. It is not conceived as a substitution therapy but as an excitation of inactivated, wrongly directed, calcium metabolism. The explanation of decalcification, and thereby the frequent ricketic influence of excessive introduction of calcium, can be diverse. First it could be conditioned through defective phosphate resorption. Or the excess flooding with calcium salts could provoke an acidosis, either through the involvement of simultaneously introduced anions or a reduction of cell respiration, so that incompletely burned acid products appear. For the equalization of acidosis the calcium is poured out of the skeleton and acid phosphates are excreted in excess amounts.
That it is impossible for infantile rickets to heal simply through the administration of calcium and phosphates, rests on the impossibility of activating calcium and phosphate metabolism in this way. But this does not deny that an activation could be obtained by calcium salts in another state of form. Concerning the homoeopathic preparations, this can be asserted on the basis of experience. That the activation is obtained easily and rapidly through vitamin D is correct but this does not stand in contradiction. Moreover, vitamin D therapy follows according to the simile rule, even if it is based upon another entirely different train of thought, and is brilliant accomplishment of the analytic method of investigation. While slight (exactly homoeopathic doses) of irradiated ergosterin can lead to a calcium deposition in the bones in rickets and osteomalacia, large doses, in the normal, cause a calcium mobilization out of the bones. Indeed overdoses vitamin D can produce exactly the ricketic osteomalacia picture!
In osteomalacia the process is fundamentally the same as in rickets with the difference that it is not concerned with growing bones. In this instance there is a dependence of calcium economy on the ovaries. This is distinctly apparent in that osteomalacia can be healed by castration, furthermore from the appearance in gravidity, during lactation, in the menopause. The injection of ovarian hormone causes a lowering of the amount of blood-serum calcium and increased excretion of calcium and phosphate (negative calcium balance); castration makes the calcium balance positive.
The most important regulatory organs for calcium metabolism are the parathyroids. Injections of parathormone increase the amount of serum calcium and increase the ejection of calcium and phosphate through the urine (negative calcium and phosphate balance!). Parathormone lessens the fixation of calcium in the tissues or releases it from deposit. Overfunction of the parathyroids seems to play a role in osteitis fibrosa. This loss of bone salts, however, has no similarity to rickets. With loss of the parathyroids the serum calcium falls, the phosphate in the serum increases, and the picture of tetany appears. Potassium and sodium gain a preponderance in contrast of calcium therefore an increase in neuromuscular irritability. The essential is a de-ionization of calcium, a lessened supply of the tissue with active calcium ions.
Outside of parathyroprivic tetany, the respiratory tetany, the phosphate tetany, the alkalosis tetany (or gastric tetany), the bicarbonate tetany are traceable to de-ionization of calcium. With increase of the pH (alkalosis), a de-ionization o f calcium is united. But still other factors play role in tetany. In parathyroprivic an increased adsorption of the complex calcium fraction by the tissues is essential. There is also concerned in tetany an inactivation of calcium ions so that it is not surprising that, with suitable calcium preparations, the calcium metabolism is activated and tetany relieved. Simple introduction of calcium ions into the serum is not lastingly sufficient, because these are just as rapidly excreted, and in any case an activation through an alteration of adsorption rations for calcium is not obtained. The tetanic attacks can be suppressed as well through acidification (NH4Cl, NaH2PO4, CO2, inspiration, milk diet) that is by soluble calcium ions. But for healing, a reversal of calcium metabolism with alteration of the power of adsorption of the colloids for calcium is necessary. Likewise the introduction of magnesium is able to suppress tetany through the detachment and increased excretion of calcium ions.
In infantile tetany the total calcium in the serum is often markedly low but the phosphate is not increased. A de- ionization of the calcium can be used only in part as an explanation. The chief role in infantile tetany is played by increased adsorption of serum calcium onto the colloids. Though this the complex calcium fraction in the serum fails, m and the sudden increased demand of the cells for calcium ions, as with the severe crying of children or other conditions producing alkalosis, cannot be covered: sodium and potassium obtain predominance.
In tetany, peculiar, edematous, but firm swellings appear on the hands and back of the feet. Likewise muscle contraction is strikingly delayed in spite of increased electrical irritability. Both are a sign of impoverishment in. active calcium ions. Activation of calcium metabolism is able to remove the alkaline preponderance and the tissue swelling (puffiness, urticaria, and edema).
Spasmophilia often develops on the basis of a rapidly healing rickets In consequence to the suddenly occurring classification with powerful activation of phosphates influence the calcium salts are excessively absorbed on the cartilage colloids> In consequence there appears the improverishment in active calcium ions> Through parathormone one can release the increased union of serum calcium to proteins. Probably there exists a connection between vitamin D and under-function of the parathyroids.
Other endocrine glands influence the calcium economy, even if not so strikingly as the hormone of the parathyroids. In hyperthyroidoses the calcium and phosphate excretion is increased, on the other hand decreased in comparison with normal in hypothyreosis. The administration of thyroxin releases calcium form the bones and brings it to excretion, the amount of blood calcium in the serum being only slightly increased when it was previously lowered. In the hypothyreoses, particularly in myxedema, the calcium and phosphates are spared and there is a condensation of bone calcium. The action of the thyroid hormone is weakened by calcium (on the contrary increased by phosphates). The picture of disturbed calcium metabolism in many traits recalls the hypothyroid state.
Extracts from the lymphatic tissues thymus, spleen and lymph nodes, seem to act opposite to the parathyroids. If these extracts are injected, their hormones still being unknown, the amount of serum calcium diminishes and a picture like tetany develops. Thereby a connection, perhaps a reciprocal relation, would be given for calcium economy and the formation of lymphocytes, and the possibility opened for influencing disturbances in the lymphatic tissues through an activation of calcium metabolism.
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,