Three experiments were conducted to investigate the effect of zeolites on laying hens (Experiments 1 and 2) and broiler chickens (Experiment 3). Each experiment used corn and soybean meal-based practical diets. Experiment 1 was a 90-day trial and used 200 40-wk-old laying hens. The basal diet contained 2.75% calcium and .7% total phosphorus. The dietary treatments were the basal diet and the basal diet plus 1.5% synthetic zeolite (SZ; Ethacal). Experiment 2 was a 56-day trial and used 360 36-wk-old laying hens. The dietary treatments were .12, .22, .32, and .42% nonphytin phosphorus with and without 1.0% SZ and 1.0% natural zeolite (NZ; Zar-Min). All diets contained 3.5% calcium. Experiment 3 utilized 240 broiler cockerels from 1 to 16 days. The dietary treatments were two calcium levels (.65 and 1.0%) with and without 1.0% supplementary SZ and NZ. In Experiment 1, egg specific gravity was significantly increased with SZ supplementation. Egg weight and egg production were unaffected. Phytin phosphorus retention and plasma dialyzable phosphorus were significantly reduced by SZ. In Experiment 2, egg specific gravity was not affected by SZ or NZ. Egg weight, egg production, plasma dialyzable phosphorus, and the retention of phosphorus and phytin phosphorus were significantly reduced by SZ with the effect on egg weight and egg production being the most severe at the lower levels of dietary nonphytin phosphorus. Natural zeolite had no effect on egg weight, egg production, plasma calcium, plasma phosphorus, or on the retention of calcium, phosphorus, and phytin phosphorus. In Experiment 3, weight gain and percentage tibia bone ash were significantly reduced by SZ. The SZ had no effect on the incidence and severity of tibial dyschondroplasia. Weight gain, feed efficiency, and the incidence and severity of tibial dyschondroplasia were significantly reduced and the percentage bone ash significantly increased by 1.0% calcium. Natural zeolite significantly improved feed efficiency and had no effect on any other parameter measured.

Two experiments were designed to determine the effect of dietary boron on broiler cockerels and four experiments were conducted to determine whether an interaction exists among dietary boron, cholecalciferol, and calcium. The parameters measured were weight gain, feed efficiency, tibia bone ash, rickets, tibial dyschondroplasia, and plasma minerals. All experiments were conducted with tibial dyschondroplasia-inducing basal diets fed to broiler cockerels from 1 to 16 days of age. Experiments 1 and 2 had four levels of dietary boron (0, 20, 40, and 80 mg/kg (Experiment 1) and 0, 5, 10, and 20 mg/kg (Experiment 2). Boron had no effect on weight gain, feed efficiency, or plasma minerals in either experiment. In Experiment 2, increasing levels of boron had no influence on tibial dyschondroplasia but did exert a quadratic effect on bone ash with 5 and 10 mg/kg boron increasing bone ash. In Experiment 1, bone ash and the incidence of tibial dyschondroplasia were unaffected, but the severity of tibial dyschondroplasia linearly increased by increasing boron levels. Experiments 3 to 6 had a 2 x 2 x 2 factorial arrangement of treatments with calcium at .65 and .90%, cholecalciferol at 110 and 1,100 ICU/kg, and boron at 0 and 40 mg/kg (Experiments 3 to 5) or 0 and 3 mg/kg (Experiment 6). The higher levels of calcium and cholecalciferol improved weight gain, decreased the incidence of rickets, and decreased the incidence and severity of tibial dyschondroplasia. Feeding cholecalciferol at 1,100 ICU/kg increased plasma calcium and plasma dialyzable phosphorus and decreased plasma magnesium. Calcium at .90% had no effect on plasma magnesium or plasma dialyzable phosphorus and increased plasma calcium only in Experiment 4. The only response to boron in Experiments 3 to 6 was a boron effect and a boron by cholecalciferol interaction on bone ash in Experiment 3, in which boron reduced bone ash at .65% calcium and 110 ICU/kg cholecalciferol. From these experiments, there is no indication that an interaction among boron, cholecalciferol, and calcium exists in broiler cockerels.

Experiments were conducted to determine whether dietary silicon will reduce the toxic effects of dietary aluminum on broiler chickens. The parameters measured were weight gain, feed efficiency, percentage bone ash, tibial dyschondroplasia, and the retention of calcium, phosphorus, and phytin phosphorus. Experiments 1 and 2 were conducted with casein and gelatin-based purified diets and Experiments 3 and 4 with corn and soybean meal-based practical diets. All experiments used day-old broiler cockerels and lasted 16 days. Aluminum significantly reduced weight gain, feed efficiency, and percentage bone ash in all four experiments. Aluminum supplementation reduced the incidence and severity of tibial dyschondroplasia, but this effect was associated with a reduction in weight gain. Increasing dietary aluminum reduced the retention of phosphorus and phytin phosphorus. Silicon did not alleviate the effects of aluminum toxicity on any of the parameters measured but did independently increase growth rate in Experiments 1 and 2, Supplementary dietary silicon does not appear to reduce aluminum toxicity in broiler chickens. Aluminum appears to exert its toxic effect on chickens by reducing the retention of phosphorus and phytin phosphorus.

Studies were conducted to determine the basic requirement of the bird for cholecalciferol in the absence of ultraviolet light by utilizing filter sleeves on fluorescent lights in the room and brooder. In Experiment 1, some pens were fitted with filter tubes and some lights were turned off. All the birds received a cholecalciferol-deficient diet. Birds with ultraviolet light excluded grew slowly, developed rickets (95%), had low plasma calcium, and low bone ash (27%); whereas birds exposed to the fluorescent light had normal growth and plasma calcium, slightly low bone ash (38%), and some rickets (12%). Experiments 2 and 3 were conducted to determine the amount of cholecalciferol that must be added to the diet under conditions in which ultraviolet light was excluded. In Experiment 2, the highest level of cholecalciferol fed was 400 ICU/kg. This level was not sufficient to permit the chickens to have weight gain or bone ash equal to the birds receiving the ultraviolet light. The birds receiving 400 ICU/kg of diet also had a 77% incidence of rickets compared with 20% for the birds receiving ultraviolet lights. In Experiment 3, when birds received 800 or 1,600 ICU/kg of cholecalciferol in the diet, they grew and were comparable to those receiving ultraviolet light for the criteria measured.

A series of experiments was conducted to investigate interactions of dietary calcium levels with ultraviolet light, cholecalciferol (D3), 1,25-dihydroxycholecalciferol [1,25-(OH)2D3], dietary protein, and a synthetic zeolite on the development of tibial dyschondroplasia in broilers. A basal diet low in calcium, high in phosphorus and chloride, and known to promote a high incidence of tibial dyschondroplasia was used. The chicks received ultraviolet radiation from fluorescent lights in addition to 1,100 ICU/kg (27.5 micrograms/kg) of D3 in the basal diet when these were not experimental variables. Regardless of whether the calcium level was low (.65%) or adequate (.95%), the incidence of tibial dyschondroplasia was significantly lower in chicks receiving ultraviolet radiation or dietary vitamin D3 levels well above the required amounts. The addition of 10 micrograms/kg of 1,25-(OH)2D3 to the diet when calcium levels varied from .45 to .95% resulted in a reduction in the incidence of tibial dyschondroplasia and increased tibial bone ash when dietary protein levels were 18 or 22%. The addition of 1% synthetic zeolite to the diet did not influence the incidence of tibial dyschondroplasia when the diet contained widely varying dietary calcium levels (.65 to 1.81%) and .73% phosphorus.