SOME OBSERVATIONS ON RICKETS

Abstract

Dietary deficiency of Ca produces, not rickets, but osteoporosis, and vitamin D is ineffective to ameliorate this condition. Rickets is regarded as due to a deficiency of P relative to the protein content of the diet and the growth potential of the animal, a condition which vitamin D secondarily counteracts by liberation of P2O5 from the body lipins and favoring the absorption of P2O5 from the intestine through the acidosis thereby produced. The administration of CaCOs, instead of being, as frequently averred, a corrective to rickets, favors its appearance. The essence of the rachitic condition is hypertrophy of the osteogenic tissues (without maturation) and not atrophy. The CaO/P2O5 ratio in the diet is of no importance but the percentage of CaO in the diet in relation to its capacity to neutralize the HC1 of the gastric juice is of the utmost consequence. Balancing the P2O5 in the ration with an equivalent amount of CaO results in economic loss from waste of food directly and from the disease that follows. Osteomalacia is essentially a combination of acalcicosis and aphosphorosis due to deficient Ca and P.