Rickets feeding

To define the incidence of fractures and rickets that we were encountering in infants who required prolonged parenteral feeding, we reviewed the roentgenograms of a series of preterm infants who developed necrotizing enterocolitis and who required at least four weeks of total parenteral nutritional support (4). These data are recorded in Table I. 

In 1978, on the basis of a few measurements of urine calcium and phosphate excretion as well as an awareness of the previously mentioned work regarding the amounts of calcium and phosphate normally accreted in utero and postnatally, it became apparent that the demineralization, fractures and rickets we were seeing in our infants were caused by calcium deficiency. Consequently we increased the amount of calcium added to the parenteral alimentation solutions. If more than 12.5 mM of the calcium were added to a liter of hyperalimentation solution, gross precipitation would occur in the feeding solution. If 10 mM of calcium were added per liter, crystalline precipitated began to build up on the inside of our barium-impregnated silicone rubber central venous catheters. This crystalline precipitate resulted in gradual occlusion and functional loss of these lines. After several false starts and six lost catheters, chemical and crystal analysis showed that the precipitate inside these catheters was CaHPO. ... 

Underheating of whole soybean may fail to destroy the trypsin inhibitor and reduce urease and lipase activity, resulting in low protein efficiency for critical feeds. An underheated soybean meal greatly increases the need for vitamin D to prevent rickets in turkey poults. Overheating of whole soybeans tends to inactivate or destroy the essential amino acids lysine, cystine, and methionine and possibly others (31). 

Rickets was once more widespread than it is now. It was thought to be a dietary dehciency disease because it could be prevented in children by feeding them fish liver... 

It is well known that strontium brings about a vitamin D-resistant rickets and markedly reduces intestinal calcium absorption It is now clear that the feeding of strontium represses the renal 25-OH-D3-la-hydroxylase and that the administration of 1,25-(0H)2D3 to strontium-fed animals will restore their ability to absorb calcium Thus at least in part the metabolic basis for strontium-induced rickets has been solved. Recent results suggest that strontium suppresses the 1-hydroxylase by suppressing parathyroid secretion ... 

Vitamin D serves to prevent rickets, and has great importance in animal feed. 

The neonatal form presents as a skeletal disorder with bent bones, soft, undermineralized skull, and respiratory distress because of soft and dysplastic ribs. The infantile form can present unspecifically as poor feeding, failure to thrive, signs of rickets, flail chest and - most importantly - signs of elevated intracranial pressure. Apparently, the mineralization defect results in growth arrest of the cranial sutures ( functional craniosynostosis). In adults, mild hypophosphatasia may present as recurrent stress fractures and so-called pseudofractures (looser zones). In both children and adults, premature loss of teeth may be a sign of hypophosphatasia. 

Lipid-soluble phosphorus. Phospholipids are present in both ceUs and plasma, giving a concentration of 10-12 mg of lipid-soIuble P per 100 ml of whole blood. The phosphorus content of blood, unlike that of calcium, varies with the dietary intake. A low intake is associated with a low plasma P level and it is relatively easy to induce rickets in rats by feeding them a diet low in phosphorus. 

By the late 1920s, it had been established that rickets could t)e prevented and cured by exposure to direct sunlight (ever since, vitamin D has been popularly called the sunshine vitamin), by irradiation with ultraviolet light, by feeding irradiated food, or by feeding cod-liver oil. Eater, the natural vitamin D offish liver oils was identified as the same suE)stance that is produced in the skin by irradiation. 

Food and feed samples, which contain vitamin D in very low concentrations, are not usually assayed by chemical methods. For these substances, bioassays are the only means available for the eissessment of vitamin D activity. Rats and chicks are used fis test animals rats respond equally well to 2 and D3, whereeis chicks respond only to D3. The assays measure the alleviation (curative test) or the development (prophylactic test) of vitamin D deficiency in terms of the degree of rickets produced. 

The increase in rickets in the US is occurring primarily in African-American and Hispanic children who have gone off breast-feeding and are not getting sufficient calcium and vitamin D in their diets. This problem has been more common in the southern US despite greater availability of sunlight. In large part, rickets is an educational issue that requires input from both medical and public health professionals. 

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