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Article

Negative Impact of a Disproportionally Elevated Level of Dietary 25-Hydroxycholecalciferol on the Performance and Meat Yield of Ross 708 Broilers †

by
Seyed Abolghasem Fatemi
* and
Edgar David Peebles
Department of Poultry Science, Mississippi State University, Starkville, MS 39762, USA
*
Author to whom correspondence should be addressed.
†
This publication is a contribution of the Mississippi Agriculture and Forestry Experiment Station. This material is based upon work that is supported by the National Institute of Food and Agriculture, U.S. Department of Agriculture, Hatch project under accession number 1011797. Use of trade names in this publication does not imply endorsement by Mississippi Agricultural and Forestry Experiment Station of these products, nor similar ones not mentioned.
Poultry 2025, 4(3), 37; https://doi.org/10.3390/poultry4030037
Submission received: 19 June 2025 / Revised: 4 August 2025 / Accepted: 12 August 2025 / Published: 14 August 2025
(This article belongs to the Collection Poultry Nutrition)
Browse Figure
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Abstract

Optimal commercial conditions have been shown to improve the performance and meat yield of broilers. Also, dietary 25-hydroxycholecalciferol (25OHD3; crystalline form) has not shown a negative impact on chicken health when it was fed at 10 times (10×) higher than 69 μg/kg. The objectives of this study were to determine the effects of up to 8 times (8×) higher than the commercial level (69 μg/kg of feed) of dietary 25OHD3 on the performance, breast meat yield, and serum 25OHD3 concentration of broilers. Eighteen male chicks were randomly assigned to each of 20 pens within each of the two dietary treatments. Treatments were commercial diets containing 250 IU/kg of vitamin D3 (control) for the starter [(0 to 14 days post-hatch (poh), grower (15 to 28 poh), and finisher (29 to 42 poh) dietary phases; or diets containing Hy-D (water-soluble source of 25OHD3) that consisted of 552 (8×) μg/kg of 25OHD3 for the starter, 276 (4×) μg/kg of 25OHD3 for the grower, and 34.5 (0.5×) μg/kg of 25OHD3 for the finisher dietary phases. Live performance variables as well as serum 25OHD3 concentrations were measured in each dietary phase. At 14, 28, and 39 poh, breast meat yield that included pectoralis major (P. major) and pectoralis minor (P. minor) muscle weights was determined in ten replications per dietary treatment. Breast yield was also calculated by adding the values of the P. major and P. minor muscles. From 14 to 42 poh, the Hy-D diets decreased (p < 0.0001) broiler body weight (BW) and BW gain and increased (p < 0.0001) total mortality and feed conversion ratio in comparison to control treatment groups. In addition, birds fed Hy-D diets had significantly (p < 0.0001) lower P. major and breast meat yields from 14 to 39 poh as compared to those birds fed the control diet. Serum 25OHD3 concentration was significantly (p < 0.0001) higher (10×) in birds that belonged to the Hy-D diet treatment than those in the control diet treatment group. These results indicate that the disproportionally high (8×) level of dietary 25OHD3 resulted in detrimental effects on the performance and meat yield of broilers. A reduction in both performance and meat yield of broilers in response to the elevated level of dietary 25OHD3 may have been due to vitamin D3 toxicity, which can result in an association with the overproduction of the active form of the vitamin in response to elevated serum concentrations of 25OHD3.

1. Introduction

Cholecalciferol or vitamin D3 (VitD3) is an essential nutrient due to its function in the direct absorption of calcium (Ca) and phosphorus (P) in mammals and chickens [1]. The functionality of VitD3 in poultry is not only limited to Ca and P absorption, but it also extends to its activity as an agent in immunomodulation [2,3,4,5,6,7,8,9,10,11,12,13], bone development [13,14,15,16], and neonatal and prenatal muscle growth [17,18,19,20,21,22,23]. Vitamin D can be absorbed via the conversion of 7-dehydrocholesterol to VitD3 in the skin by the action of ultra-violet light, or it can be supplemented in the diet [1]. Birds have limited access to sunlight in modern poultry product systems, which would require the provision of a dietary source of VitD3. In order for VitD3 to become biologically active, it has to undergo two hydroxylation steps. First, it is converted to 25-hydroxycholecalciferol (25OHD3) by the action of 25-hydroxylase in the liver, and then 25OHD3 is converted to its active form [1,25-dihydroxycholecalciferol (1,25 (OH)2 D3)] through 1 α-hydroxylase activity in renal cells [24,25]. The second hydroxylation is tightly regulated by several factors, including vitamin D receptor (VDR) distribution and concentration, and circulating levels of Ca, P, parathyroid hormone (PTH), and 1,25 (OH)2 D3 [1,25]. Furthermore, under normal circumstances, when 25OHD3 concentrations are high, 25OHD3 is converted to the inactive form of vitamin D [24,25-dihydroxycholecalciferol (24,25 (OH)2 D3)] by 24 α-hydroxylase. This inactive form is also known as the excretory form of vitamin D [1]. The aforementioned vitamin D metabolic conversions not only occur in hepatic and renal cells but also take place at smaller levels in the breast and thigh muscles, small intestine, bone tissue, and immune cells [25,26]. Impaired live performance [15], egg production [27], immune responses [28], and high embryonic mortality rates [29] have been reported when vitamin D sources were supplemented below 250 IU/kg, which is equivalent to 6.25 µg/kg feed. On the other hand, the elevated intake of vitamin D sources can lead to vitamin D toxicity (or hypervitaminosis D).
As compared to vitamin D deficiency, vitamin D3 toxicity is less common but can cause severe damage to interior organs, the subsequent impairment of growth, and an increase in the mortality rates of broilers [30] and layers [31]. Hypervitaminosis D as a result of the supply of elevated levels of vitamin D sources has been shown to cause microscopic renal lesions and increased renal Ca and inorganic P concentrations in chicks exhibiting normal serum Ca concentrations [30]. The active form of vitamin D also makes birds more susceptible to hypervitaminosis D. For example, dietary levels that are three times greater than the 200 IU/kg of feed (5 µg/kg of feed) level that is recommended by the NRC can result in hypervitaminosis D in modern broiler chickens [32]. This may be the basis for the banning of the active form of VitD3 [1,25 (OH)2 D3] in the diets of commercial broilers. In addition, a 100-fold increase in VitD3 and a 10-fold increase in 25OHD3 in the diets of broilers [30] and layers [30] throughout the growing period have been shown to result in hypervitaminosis D. Nevertheless, because VitD3 and 25OHD3 have been shown to significantly increase the intestinal absorption of Ca and P in broilers and layers, the tolerance levels of chickens to the dietary supplemental use of these vitamin D sources may require revisiting. As compared to VitD3 at the same level of dietary inclusion (2560 IU/kg or 69 µg/kg feed), 25OHD3 is twice as active in Ca and P absorption [33], and subsequently enhances bird performance [13,14,16,18,20,21,22,23,34,35], breast meat yield [18,20,21,22], bone formation and development [13,14,15,16,17], and adaptive and innate immune responses in birds raised under commercial conditions or when subjected to a coccidiosis infection [2,3,4,5,6,7,8,9,10,11,12,16,17]. Therefore, 25OHD3 is the preferred form, as it boosts the health and production of broilers and layers. It is also worth mentioning that in the blood stream, the half-life of 25OHD3 is approximately 15 days [36,37], but that of VitD3 is only 15 h [36,38]. However, both sources can be stored in adipose tissue for longer periods of time, and can be stored in other tissues in different proportions, such as breast and thigh muscle [39]. Therefore, 25OHD3 is known for being a safe and effective source of vitamin D for use in commercial poultry production [1]. It is well-established that intensive genetic selection has resulted in an increase in the growth efficiency and internal organ development of poultry [40]. In addition, Ca and P requirements for broiler production have been shown to decrease by approximately 20% [41], indicating that a ten-fold increase in the use of supplemental 25OHD3 may not be safe in new generation broilers. It should also be noted that this study was funded by the United States Department of Agriculture, which mandates that trials be terminated when a 20% mortality rate is reached. Therefore, the objectives in this study were to test the effects of a disproportionally elevated [up to eight times (8×) higher than the recommended commercial level] water-soluble form of dietary 25OHD3 (69 μg/kg of feed) on the performance, breast meat yield, and serum 25OHD3 concentrations of Ross 708 broilers.

2. Materials and Methods

2.1. Experimental Design and Treatment Layout

A total of 1200 eggs were collected from 35-week-old broiler breeder hens belonging to local commercial broiler operation (Peco Farms, Walnut Grove, MS, USA), in which commercial procedures and vaccinations were used. Eggs were later incubated and hatched in the hatchery of the Mississippi State University Poultry Research Facility following commercial procedures as described by Fatemi et al. [42]. After hatching, 18 male Ross 308 broiler chicks, selected by feather-sexing, were randomly placed in each of 10 replicate floor pens in each of the 2 treatment groups (360 total birds). Treatments were commercial diets containing 6.25 μg/kg (250 IU/kg) of vitamin D3 (control) for the starter [(0 to 14 days of age (doa) post-hatch (poh)], grower (15 to 28 doa poh), and finisher (29 to 42 doa poh); or Hy-D diets that consisted of 552 (8×) μg/kg of 25OHD3 (water-soluble source) for the starter, 276 (4×) μg/kg of 25OHD3 for the grower, and 34.5 (0.5×) μg/kg of 25OHD3 for the finisher dietary phases. ROVIMIX® Hy-D® 1.25% (DSM Nutritional Products Inc., Parsippany, NJ, USA) was the source of 25OHD3 and all diets were formulated according to Ross 708 commercial guidelines [42,43]. Floor pens contained used litter top-dressed with fresh wood shavings and were 1.22 m × 0.914 m (1.12 m2) in dimension, which allowed for a 0.062 m2/bird stocking density. Birds had ad libitum access to water and feed and were brooded according to the Ross 708 guidelines throughout the 42 doa grow-out period [43]. The feed compositions for each dietary treatment in each of the dietary phases are provided in Table 1. The calculated and actual levels of the dietary VitD3 and 25OHD3 in the starter, grower, and finisher dietary phases are presented in Table 2.

2.2. Performance, Meat Yield, and Serum 25OHD3 Concentration

The bird performance variables that were examined included body weight (BW), BW gain (BWG), average daily BW gain (ADG), feed intake (FI), average daily feed intake (ADFI), and feed conversion ratio (FCR; g FI/g BWG). At the end of each dietary phase, the following determinations were made: the batch weight of all birds in a pen for the calculation of average BW, total bird mortality, and the calculation of the FCR that was adjusted for bird mortality. At 14, 28, and 39 doa, one bird from each of the ten replicate pens per dietary treatment were randomly selected (20 total birds), and were bled by venipuncture of the wing brachial artery. After collection, blood samples were allowed to clot and were then centrifuged. An approximate 1 mL volume of serum was subsequently extracted for determination of 25OHD3 concentration according to an RIA assay procedure described by Hollis et al. [43]. Later, the same sample of birds were individually weighed and euthanized by CO2 for meat yield determinations that included the percentage pectoralis major (P. major), and pectoralis minor (P. minor) weights. Total breast yield percentage was also calculated by adding the values of the P. major and P. minor muscles. At 14, 28, and 39 doa, one bird from each of the ten replicate pens per dietary treatment were randomly selected (20 total birds) and were bled by venipuncture of the wing brachial artery. An approximate 1 mL volume of serum was subsequently extracted for the determination of the 25OHD3 concentration according to an RIA assay procedure described by Hollis et al. [44].

2.3. Statistical Analysis

A randomized complete block experimental design was used in the analysis of the effects of treatment on performance, meat yield, and serum 25OHD3 concentration, while the floor pen was considered as the blocking factor and a unit of treatment replication. All data were tested for normality by PROC UNIVARIATE using the Shapiro–Wilk test at α = 0.05, and all were subsequently normally distributed. One-way analysis of variance was used to analyze all data separately within each time period using the procedure for linear mixed models (PROC GLIMMIX) of SAS©, version 9.4 [45]. Treatment differences were deemed to be significant at a p-value equal to or lower than 0.05, and for the determination of mean separations, Fisher’s protected least significant difference was performed [46]. The following model was performed for the analysis of all data:
Yij = μ + Bi+ Dj + Eij
where μ was the population mean; Bi was the block factor (i = 1 or 10); Di was the effect of each dietary injection treatment (j = 1 to 2); and Eij was the residual error.

3. Results

For D3-containing diets, the actual values for VitD3 in all dietary phases ranged between 80 and 120% of formulated values. Also, for 25OHD3-containing diets, actual 25OHD3 levels in the same dietary phases ranged between 95 and 102% of the formulated values. From 0 to 42 doa poh, BW, BWG, ADG, FI, and ADFI were significantly (p < 0.0001) higher for control-fed birds in comparison to those fed the Hy-D diets. Additionally, a significantly (p < 0.0001) lower FCR was observed for birds fed the control diet in comparison to those in the Hy-D dietary treatment group during the same period of time. In comparison to the control diet, the Hy-D diet significantly increased bird mortality between 15 and 28 doa poh (p = 0.031) and between 29 and 42 doa poh (p < 0.0001) (Table 3). Furthermore, P. major, P, minor, and breast meat yield were significantly (p < 0.0001) lower in birds fed Hy-D diets than in those fed control diets at both 14 and 39 doa poh (Table 4). In comparison to birds fed the control diet, serum 25OHD3 concentration was significantly higher in HyD-fed birds by approximately five-fold, three-fold, and two-fold at 14 (p = 0.003), 28 (p < 0.0001), and 39 (p < 0.0001) doa poh, respectively (Figure 1).

4. Discussion

The observed results provided relevant information to achieve the objectives in this study, which were to test for the effects of a disproportionally elevated level (8× higher than the recommended level) of dietary 25OHD3 on the performance and meat yield of modern broilers. It has been shown that broiler hatchlings aged up to 14 doa poh can tolerate VitD3 levels as high as 50,000 IU per kg with minimal effects on bone formation and growth [47]. In contrast to that of VitD3, renal calcification was observed in broilers when dietary 25OHD3 was supplemented at levels that were 5 to 10 times greater than the recommended level [34]. In general, hypervitaminosis D is mainly associated with renal tubular mineralization in both chickens and turkeys [48], whereas mineralization in the skin, breast, thigh, and lower level of the liver is classified as a more severe case [31]. Additionally, hypervitaminosis D can result in a decrease in eggshell quality, egg weight, and egg production, as well as increases in the risk of renal tubular calcification, anorexia, and muscular atrophy and emaciation [49]. The damaging effects of hypervitaminosis D are associated with high levels of serum 25OHD3 that can result in the production of the more active form of VitD3 that mostly occurs in the renal cells, and in bone and muscle tissue [1]. In chickens, elevated serum Ca levels are highly associated with increases in serum 25OHD3 concentrations in response to dietary 25OHD3 that is above the recommended level [1,12,30]. In addition, 25OHD3 is conserved in the blood stream for approximately 2 weeks, which increases its chances of being stored in many organs. This along with continual supplementation of elevated levels can cause circulating concentrations to become toxic [30]. It is well observed that renal calcification is initiated when dietary levels reach 100 µg/kg, and that renal Ca retention increases five-fold when dietary 25OHD3 is supplemented at 1000 µg/kg (40,000 IU/kg) [30]. In addition, an excessive production of the active form of vitamin D (1,25 (OH)2 D3), in response to high levels of serum 25OHD3 has been shown to result in an increase in the incidence of kidney calcification in mice [50]. Renal calcification in birds has also been observed when they are supplemented with 5× the recommended level of 25OHD3 [20], which is associated with renal tubular, and less commonly, arterial mineralization [48,51] in response to elevated serum 25OHD3 concentration [20]. In humans, severe occurrences of hypervitaminosis D were observed when serum 25OHD3 levels reached between 88 [52] and 150 [53] ng/mL. Conversely, serum 25OHD3 concentrations at significantly lower levels have been associated with hypervitaminosis D in chickens [20]. An increase in serum 25OHD3 is directly linked to an increase in Ca serum levels or hypercalcemia [1,51,52,53,54]. An elevated level of circulating Ca is damaging, leading to alterations in cell membrane permeability linked to changes in Ca pump activity that can ultimately lead to cellular necrosis [55,56]. With increasing toxicity levels of 25OHD3, cardiac arrhythmias and death in response to both renal and cardiac failure have been reported [57]. It is well observed that normal 25OHD3 serum concentrations result when birds are supplemented with between 10 and 20 ng/mL of the water-soluble form of 25OHD3 [20,53,54]. In this study, 8×, 4×, and 1/2× levels of dietary 25OHD3 resulted, respectively, in serum 25OHD3 concentrations of 115, 50, and 37 ng/mL, indicating that not only was the 8× level damaging, but also that birds were still subject to some level of damage when doses were gradually lowered. In addition, hatchling chicks are more susceptible to toxic supplementation due to their immature digestive and immune systems [58]. Moreover, any significant damage that may be incurred in the internal organs of a bird can be unrecoverable as they develop. Our findings showed that chicks fed 8× the recommended level of 25OHD3 failed to recover from the negative effects that hypervitaminosis D caused on their meat yield and performance despite the gradual reduction in supplementation throughout the growing phase.
Among vitamin D sources, both VitD3 and 25OHD3 have been approved for being safely used as dietary sources in poultry production, although 25OHD3 is a more potent enhancer of broiler growth and health, while VitD3 is less toxic [1,20]. A dietary VitD3 concentration of 2.5 mg/kg (100,000 IU/kg), which is 36 times greater than the recommended level, has been shown to negatively affect the bone quality and growth of broilers through 28 doa poh. Clinical symptoms of the negative effects of those toxic levels have included watery faces, polydipsia, polyuria, and severe dehydration. In addition, diffused heterophilic cell infiltration, pulmonary hemorrhaging, and necrosis and metastatic calcification of their renal tubular epithelia were observed [58]. Moreover, a dietary VitD3 concentration of 550 mg/kg (22,000,000 IU/kg) has been shown to have similar damaging effects on the bone, liver, kidney, lung, and brain tissue of broilers [59,60]. However, studies in the late 1970s and 1990s attributed signs of 25OHD3 toxicity in 42 doa broilers, in response to a 25OHD3 dietary concentration of 1 mg/kg (40,000 IU/kg), to decreases in BW and FI without negatively affecting mortality rate. Conversely, when also compared to recommended levels, a designation of toxicity was not assigned to a dietary concentration of 0.5 mg/kg (20,000 IU/kg) of 25OHD3 [30]. Similar conclusions for the same doses of 25OHD3 were also reported for layer pullets between 0 and 122, and 123 and 225 doa [31]. The results of the current study revealed that the dietary inclusion of 552 µg/kg (22,080 IU/kg) of 25OHD3 in the starter phase adversely affected bird growth and meat yield, and that these conditions worsened along with an increase in mortality rate while 25OHD3 doses in the grower and finisher phases decreased. Nevertheless, it is worth mentioning that no symptom of pathogenic infection was observed in the dead birds that were necropsied. In chickens, elevated serum Ca levels are highly associated with increases in serum 25OHD3 concentrations in response to dietary 25OHD3 that is above the recommended level [1,30]. In addition, 25OHD3 is conserved in the blood stream for approximately 2 weeks, which increases its chances of being stored in many organs. This along with continual supplementation of elevated levels can cause circulating concentrations to become toxic [30]. A partial reason for the susceptibility of modern broilers to elevated Ca levels may be linked to their lower requirement for Ca as a result of an improvement in its absorption in the intestine. Zuidhof et al. [40] reported that when compared to past generations, modern broilers exhibit an increase in growth of 400% and a decrease in FCR of 50% within 42 doa poh. In addition, a 20% reduction in the recommended requirement levels of dietary Ca has been shown to have no negative effects on broiler health and performance [35].
In addition to differences in the elevated levels of serum 25OHD3 reported by Morrissey et al. [30] and Terry et al. [31] and the current study, the source of 25OHD3 was also different between the studies. The form of 25OHD3 used in the previous studies conducted concerning 25OHD3 toxicity in broilers and layers was suspended in ethanol, whereas the form in this study was water-soluble. Although the water-soluble form of 25OHD3 may have been a more active form, the current results also showed that modern broilers are more susceptible to disproportionally high doses of 25OHD3. In addition to VitD3 being a safer dietary form than 25OHD3, the effects of VitD3 reported in this study were consistent with those of other studies in which the effects of dietary 25OHD3 were tested. Because both types of tests consistently revealed that modern broilers have become more susceptible to high doses of both kinds of vitamin D sources, further research is required to determine the precise margin of dose safety that is required for the use of both vitamin D sources that will promote bird growth and production while having minimal negative physiological effects. This would be particularly important during the early poh period when chicks are most sensitive to hypervitaminosis D.

5. Conclusions

In conclusion, increases in dietary 25OHD3 levels in the starter phase that were up to 8 times greater than those that are recommended had detrimental effects on all the modern broiler performance variables examined, including meat yield. Furthermore, its negative effects remained throughout the grow-out period, even when its dose levels were reduced to those that were 4 times and 1/2 times greater than the recommended levels in the grower and finisher dietary phases, respectively. It is suggested that the bases for these effects are associated with an increase in serum 25OHD3 that can lead to elevated Ca levels in the blood stream and in various vital organs such as the kidney and liver. Elevated levels in these vital organs can subsequently cause tissue cell damage.
Further research is needed to determine serum 25OHD3 concentrations in conjunction with histopathological changes in the organs of broilers using the same doses of VitD3 in the three dietary phases employed in this study. Also, determinations as to the precise doses of VitD3 and 25OHD3 that are safe in the diets of both broilers and layers during their early stages of poh growth are required in order to promote their growth and productivity while minimizing any possible negative physiological effects that hypervitaminosis D could cause.

Author Contributions

Conceptualization, S.A.F. and E.D.P.; methodology, S.A.F.; software, S.A.F.; validation, S.A.F. and E.D.P.; formal analysis, S.A.F.; investigation, S.A.F.; resources, E.D.P.; data curation, S.A.F.; writing—original draft preparation, S.A.F.; writing—review and editing, S.A.F. and E.D.P.; visualization, S.A.F. and E.D.P.; supervision, S.A.F.; project administration, S.A.F.; funding acquisition, E.D.P. All authors have read and agreed to the published version of the manuscript.

Funding

This research was supported through agreement no. 58-6064-9-016 with the United States Department of Agriculture (USDA).

Institutional Review Board Statement

This research was conducted upon approval by the Mississippi State University Institutional Animal Care and Use Committee (protocol # IACUC-20-248), approved on 18 June 2020.

Informed Consent Statement

Not applicable.

Data Availability Statement

The contributions that are presented are included in this article. Further inquiries may be transmitted to the corresponding author.

Acknowledgments

The authors appreciate the assistance that Eric Nixon, Rodney Johnson, and a Zoetis research team provided. Also, our appreciation is extended to DSM Nutritional Products for their assistance in the measurement of the serum 25OHD3 concentrations and in providing the vitamin D sources.

Conflicts of Interest

The authors indicate that there are no conflicts of interest. The funder was not involved in the design, collection, analysis, and interpretation of the study results, nor with the writing of this article or the decision made to submit it for publication.

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Poultry 04 00037 g001
Figure 1. Serum 25OHD3 concentrations of birds fed control and Hy-D diets at 14, 28, and 39 days of age (doa) post-hatch (poh). Treatment means within the same variable column within types of treatment with presence of asterisk are significantly different (p < 0.05).
Figure 1. Serum 25OHD3 concentrations of birds fed control and Hy-D diets at 14, 28, and 39 days of age (doa) post-hatch (poh). Treatment means within the same variable column within types of treatment with presence of asterisk are significantly different (p < 0.05).
Poultry 04 00037 g001
Table 1. Feed composition of the experimental diets from 0 to 42 days of age (doa) post-hatch (poh).
Table 1. Feed composition of the experimental diets from 0 to 42 days of age (doa) post-hatch (poh).
Commercial DietHy-D diet
Starter (0 to 14 doa poh)
Item
Ingredient (%)PctPct
Yellow corn53.2353.23
Soybean meal38.2338.23
Animal fat2.62.6
Dicalcium phosphate2.232.23
Limestone1.271.27
Salt0.340.34
Choline chloride 60%0.100.10
Lysine0.280.28
DL-Methionine0.370.37
L-Threonine0.150.15
Premix 10.250.25
Coccidiostat 20.050.05
BMD 30.050.05
25-hydroxycholecalciferol (25OHD3; ng/mL) 40552
Total100100
Calculated nutrients
Crude protein 2323
Calcium0.960.96
Available phosphorus0.480.48
Apparent metabolizable energy (AME; Kcal/kg)30003000
Digestible Methionine0.510.51
Digestible Lysine1.281.28
Digestible Threonine0.860.86
Digestible total sulfur amino acid (TSAA)0.950.95
Sodium0.160.16
Choline0.160.16
Grower (15 to 28 doa poh)
Item
Ingredient (%)PctPct
Yellow corn57.1357.13
Soybean meal34.834.8
Animal fat3.53.5
Dicalcium phosphate22
Limestone1.171.17
Salt0.340.34
Choline chloride 60%0.100.10
Lysine0.210.21
DL-Methionine0.320.32
L-Threonine0.160.16
Premix0.250.25
Coccidiostat0.050.05
BMD0.050.05
25OHD3 (ng/mL) 50276
Total100100
Calculated nutrients
Crude protein 21.521.5
Calcium0.870.87
Available phosphorus 0.4350.435
AME (Kcal/kg)31003100
Digestible Methionine0.470.47
Digestible Lysine1.151.15
Digestible Threonine0.770.77
Digestible TSAA0.870.87
Sodium0.160.16
Choline0.160.16
Finisher (29 to 42 doa poh)
Item
Ingredient (%)PctPct
Yellow corn54.2354.23
Soybean meal38.2338.23
Animal fat2.52.5
Dicalcium phosphate2.232.23
Limestone1.271.27
Salt0.340.34
Choline chloride 60%0.100.10
Lysine0.280.28
DL-Methionine0.370.37
L-Threonine0.150.15
Premix0.250.25
Coccidiostat0.050.05
BMD0.050.05
25OHD3 (ng/mL) 6034.5
Total100100
Calculated nutrients
Crude protein 19.519.5
Calcium0.780.78
Available phosphorus 0.390.39
AME (Kcal/kg)32003200
Digestible Methionine0.430.43
Digestible Lysine1.021.02
Digestible Threonine0.680.68
Digestible TSAA0.80.8
Sodium0.160.16
Choline0.160.16
1 The broiler premix provided per kilogram of diet: vitamin A (retinyl acetate), 10,000 IU; cholecalciferol, 4000 IU; vitamin E (DL-α-tocopheryl acetate), 50 IU; vitamin K, 4.0 mg; thiamine mononitrate (B1), 4.0 mg; riboflavin (B2), 10 mg; pyridoxine HCL (B6), 5.0 mg; vitamin B12 (cobalamin), 0.02 mg; D-pantothenic acid, 15 mg; folic acid, 0.2 mg; niacin, 65 mg; biotin, 1.65 mg; iodine (ethylene diamine dihydroiodide), 1.65 mg; Mn (MnSO4H2O), 120 mg; Cu, 20 mg; Zn, 100 mg; Se, 0.3 mg; Fe (FeSO4.7H2O), 800 mg. 2 Decocx® (Zoetis, Parsippany, NJ, USA). 3 Bacitracin methylene disalicylate (BMD 110; Zoetis, Parsippany, NJ, USA) containing 55 mg of BMD per kg. 4 Hy-D®, 22,080 IU/kg (DSM Nutritional Products Inc., Parsippany, NJ, USA). 5 Hy-D®, 11,040IU/kg (DSM Nutritional Products Inc., Parsippany, NJ, USA). 6 Hy-D®, 1380IU/kg (DSM Nutritional Products Inc., Parsippany, NJ, USA).
Table 2. Actual and calculated values of vitamin D3 (VitD3) and 25-hydroxycholecalciferol (25OHD3) in the starter, grower, and finisher diets.
Table 2. Actual and calculated values of vitamin D3 (VitD3) and 25-hydroxycholecalciferol (25OHD3) in the starter, grower, and finisher diets.
VitD3 CalculatedVitD3 Actual25OHD3 Calculated25OHD3 Actual
-------------------------------IU/kg------------------------------
Starter
Control 12502610ND 2
Hy-D 325028122,08022,520
Grower
Control2502900ND
Hy-D 425031111,04010,520
Finisher
Control 12502760ND
Hy-D 525029413801320
1 D3 was formulated at 250 IU/kg feed and 25-hydroxycholecalciferol (25OHD3) was not supplemented. 2 Not detected; the detection limit was 2 μg/kg (equivalent to 80 IU/kg). 3 A diet supplemented with 552 μg/kg 25OHD3 and 250 IU/kg feed of D3 from 0 to 14 days of age (doa) post-hatch (poh). 4 A diet supplemented with 276 μg/kg 25OHD3 and 250 IU/kg feed of D3 from 15 to 28 doa poh. 5 A diet supplemented with 34.5 μg/kg 25OHD3 and 250 IU/kg feed of D3 from 29 to 39 doa poh.
Table 3. Effects of control and Hy-D diets on live performance variables from 0 to 42 days post-hatch (poh).
Table 3. Effects of control and Hy-D diets on live performance variables from 0 to 42 days post-hatch (poh).
TreatmentBW0 1 (g)BW 1 (g)FI 1 (g)ADFI 1 (g)BWG 1 (g)ADG 1 (g)FCR 1 (g/g)Mortality 1 (%)
-------------------------------------------------------Days 0 to 14----------------------------------------------------------
Control42.80447 a501 a35.7 a405 a28.9 a1.23 b1.7
HyD (×8) 242.75225 b263 b18.5 b183 b13.1 b1.42 a3.1
Pooled SEM0.4215.560.314.80.340.0181.5
p-Value0.923<0.0001<0.0001<0.0001<0.0001<0.0001<0.00010.185
-------------------------------------------Days 15 to 28---------------------------------------------------------
Control 1537 a1562 a111 a1133 a80.9 a1.36 b1.1 b
HyD (×4) 3 513 b537 b38 b331 b23.6 b1.64 a4.0 a
Pooled SEM 20.520.91.418.21.30.0321.82
p-Value <0.0001<0.0001<0.0001<0.0001<0.0001<0.00010.031
-----------------------------------------Days 29 to 39------------------------------------------------------
Control 3059 a2525 a210 a1519 a109 a1.95 b0.9 b
HyD (1/2) 4 931 b1114 b93 b416 b30 b3.35 a11.6 a
Pooled SEM 40.257.74.842.430.2320.08
p-Value <0.0001<0.0001<0.0001<0.0001<0.0001<0.0001<0.0001
a,b Treatment means within the same variable column within types of treatment with no common superscripts are significantly different (p < 0.05). 1 BW, BW gain (BWG), average daily gain (ADG), feed intake (FI), average daily feed intake (ADFI), feed conversion ratio (FCR), and mortality rate. 2 A diet supplemented with 552 μg/kg 25OHD3 from 0 to 14 days of age (doa) post-hatch (poh). 3 A diet supplemented with 276 μg/kg 25OHD3 from 15 to 28 doa poh. 4 A diet supplemented with 34.5 μg/kg 25OHD3 from 29 to 39 doa poh.
Table 4. Effects of control and Hy-D diets on various meat yield variables expressed as percentages of live body weight (BW) from 14 to 39 days post-hatch (poh).
Table 4. Effects of control and Hy-D diets on various meat yield variables expressed as percentages of live body weight (BW) from 14 to 39 days post-hatch (poh).
TreatmentBW (g)P-Major (%)P-Minor (%)Breast (%)
--------------------Day 14---------------------
Control454.7 a13.3 a2.85 a16.1 a
HyD (×8) 1261.4 b10.3 b2.35b 12.6 b
Pooled SEM14.60.470.1140.58
p-Value<0.0001<0.0001<0.0001<0.0001
--------------------Day 39---------------------
Control2882 a21.1 a3.95 a25 a
HyD (1/2) 21134 b13.6 b3.14 b16.7 b
Pooled SEM97.70.520.140.57
p-Value<0.0001<0.0001<0.0001<0.0001
a,b Treatment means within the same variable column within types of treatment with no common superscripts are significantly different (p < 0.05). 1 A diet supplemented with 552 μg/kg 25OHD3 from 0 to 14 days of age (doa) post-hatch (poh). 2 A diet supplemented with 34.5 μg/kg 25OHD3 from 29 to 39 doa poh.
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Fatemi, S.A.; Peebles, E.D. Negative Impact of a Disproportionally Elevated Level of Dietary 25-Hydroxycholecalciferol on the Performance and Meat Yield of Ross 708 Broilers. Poultry 2025, 4, 37. https://doi.org/10.3390/poultry4030037

AMA Style

Fatemi SA, Peebles ED. Negative Impact of a Disproportionally Elevated Level of Dietary 25-Hydroxycholecalciferol on the Performance and Meat Yield of Ross 708 Broilers. Poultry. 2025; 4(3):37. https://doi.org/10.3390/poultry4030037

Chicago/Turabian Style

Fatemi, Seyed Abolghasem, and Edgar David Peebles. 2025. "Negative Impact of a Disproportionally Elevated Level of Dietary 25-Hydroxycholecalciferol on the Performance and Meat Yield of Ross 708 Broilers" Poultry 4, no. 3: 37. https://doi.org/10.3390/poultry4030037

APA Style

Fatemi, S. A., & Peebles, E. D. (2025). Negative Impact of a Disproportionally Elevated Level of Dietary 25-Hydroxycholecalciferol on the Performance and Meat Yield of Ross 708 Broilers. Poultry, 4(3), 37. https://doi.org/10.3390/poultry4030037

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