Impact of Vitamin E Supplementation on Newly Received Calves: A Review and Meta-Analysis

By Elam, N A

ABSTRACT Seven different studies comprising 1,481 lightweight steers and heifers provided with 10 different vitamin E amounts (0 to 2000 IU/animal daily) were compiled for a meta-analysis of the relationships between supplemental vitamin E and stressed receiving calf performance. The statistics of interest were estimated relationships between vitamin E supplementation and DMI, ADG, G:F, and percent morbidity. For the slope coefficients estimated, a whole unit change in the independent variable (X) represented a 100-IU change in vitamin E intake per day. Based on the data used to generate the estimates for these analyses, no predictive relationship exists for vitamin E supplementation and DMI, ADG, or G:F (P >/= 0.45). However, for percent morbidity the predictive model suggests that for every 100 IU increase in vitamin E intake per day, a 0.35% decrease (P = 0.08) in morbidity would be expected. The data discussed herein provides evidentiary support for vitamin E supplementation to newly received calves at high risk of morbidity. However, because the entire data set is bounded between 0 and 2,000 IU/d of vitamin E intake, predictions regarding the linearity beyond 2,000 IU should be avoided.

Key words: high-risk calves, nutrition, receiving health, vitamin

INTRODUCTION

Vitamin E is recognized as an important nutrient for numerous functional purposes. McDowell (2000) cited literature demonstrating the essential role of vitamin E for the integrity and optimum function of the reproductive, muscular, circulatory, nervous, and immune systems. The ability of supplemental vitamin E to enhance growth during disease episodes or periods of stress has been variable; however, a general trend associated with vitamin E supplementation is the ability to reduce morbidity. Stress-related disease episodes for newly received calves can be attributed to numerous causative agents, including weaning stress, poor immunization prior to weaning, receiving management and nutrition, and numerous other factors. Duff and Galyean (2007) compiled a thorough review of the literature comprising highly stressed, newly received feedlot cattle and the most costly disease complex to the US beef industry, bovine respiratory disease. As such, it seems reasonable that for stressed receiving cattle the principal objective for supplementing vitamin E would be to support immune functions.

REVIEW AND DISCUSSION

Animal Growth Performance

The vitamin E concentration in diets for nonstressed calves is suggested by the National Research Council (NRC, 1996) to range between 15 and 60 IU/kg of dry feed. Pehrson et al. (1991) obtained Swedish dairy calves ranging between 3 and 7 wk of age and demonstrated that providing 600 mg of DL-alpha-to-copheryl acetate increased ADG relative to control subjects during the last 4 mo of a 9-mo study. Similarly, Velasquez-Pereira et al. (1999) used Holstein bull calves to demonstrate that supplementing either 700 or 1,400 IU of vitamin E/kg of feed resulted in increased ADG compared with calves receiving a diet supplemented with only 30 IU of vitamin E/ kg of diet. In both these studies, results were obtained on nonstressed calves during feeding periods subsequent to initial milk replacer trials. As such, applying responses to stressed beef calves should be done cautiously.

Based on the work of Hutcheson and Cole (1986), which demonstrated a decrease in DMI by immune-compromised calves, the NRC (1996) recommended that the concentration range of vitamin E be 75 to 100 IU/ kg of dry feed to ensure adequate nutrient intake in cattle received under stress conditions. However, research conducted on the effects of increased supplemental vitamin E on stressed receiving cattle has generated variable results. Early reports involving vitamin E supplementation often resulted in optimistic conclusions for economically important measures of animal performance. secrist et al. (1997) reviewed the early literature and reported overall improvements in animal performance when stressed receiving calves were provided supplemental vitamin E. Weighted means from the 5 reported studies demonstrated a 15% increase (P = 0.14) in ADG and a 27.5% improvement (P = 0.10) in feed efficiency for supplemented vs. control receiving calves. Furthermore, apparent general trends existed for decreases in morbidity when vitamin E was supplemented. In contrast, more recent research has not indicated a strong relationship between vitamin E supplementation and animal performance beyond effects of potential improvements in health.

Rivera et al. (2002) evaluated the effects of 100-fold increases in supplemental vitamin E ranging between 285 and 1,140 lU/animal daily for stressed, newly received steers and heifers. In both experiments, animal performance measured via ADG and feed efficiency were not statistically improved as vitamin E supplementation increased. Numerically, the steers showed a slight decrease in ADG, whereas the heifers had slightly increased ADG and somewhat surprisingly, morbidity (both first treatments and retreatment percent) was not improved in either experiment as vitamin E supplementation increased. Recognizing that studies involving increasing levels of supplemental vitamin E had been explored, Carter et al. (2005) investigated the effects of supplying a relatively high dose (2,000 IU of vitamin E/animal daily) for varying time periods during the receiving period (7, 14, or 28 d). Once again, ADG and feed efficiency were not improved with increased days of vitamin E supplementation; however, medical cost ($/calf medicated) tended to decrease (P = 0.08), and the percent morbidity did not differ (P = 0.22) as days of supplemental vitamin E increased. Regarding the medical costs, it should be noted that it is unclear whether BW at the time of therapeutic treatment were similar among treatment groups, which could affect total monetary medical expenditures for any group of animals because dose amounts are usually based on BW. Cusack et al. (2005) further tested the ability of increased supplemental vitamin E to improve immunity in an experimentally induced disease challenge model using bovine herpesvirus-1 (BHV1) as an infectious agent. Heifers received diets containing either 15 or 185 IU/ kg of dry diet at a rate of 2.7% of BW for 4 wk before the disease challenge. As noted above for other experiments, ADG and feed efficiency were both unaffected by increasing the dietary concentration of supplemental vitamin E.

It is unclear why results vary, but cattle source and origin are plausible explanations, as well as the possibility that supplementation with antioxidants during bouts of stress and dis ease affect or result in, or both, the repartitioning of nutrients and energy from tissue growth toward immune function. Furthermore, it should be noted that the studies reviewed by Secrist et al. (1997) with the most noted differences in performance involved calves that were offered ad libitum access to hay and supplemented with 0.91 kg (d 0 to 21) or 0.45 kg (d 22 to 28) of a pelleted feed that carried the vitamin E, compared with the more recent receiving studies where calves were offered a total mixed diet fortified with vitamin E and only supplemented with hay for a brief period of time early in the receiving period.

Animal Health

Humoral and Cell Mediated Immunity. The ability of cytokines to affect growth both indirectly via manipulation of the somatotropic axis and directly through catabolic functions on lipid and protein tissues has been reviewed by Spurlock (1997). Han and Meydani (2000) compiled numerous studies demonstrating the immunostimulatory ability of antioxidants to modulate the production of cytokines. Most important to this discussion were the studies that demonstrated the ability of increased supplemental vitamin E to increase the production of interleukin (IL)-2 and interferon-gamma (INF-gamma) and decrease the production of IL-1 and tumor necrosis factor-a. Furthermore, Han et al. (2000) experimentally infected mice with influenza and demonstrated the ability of supplemental vitamin E to increase the production of IL-2 and IFN-gamma, which were associated with lower viral titers. The authors further demonstrated that increased supplemental vitamin E resulted in a decrease in prostaglandin E^sub 2^ (PGE^sub 2^), which likely explains their previous results because PGE^sub 2^ is a known modulator of T- helper-1 cytokines. Betz and Fox (1991) demonstrated that T-cell responses to PGE^sub 2^ vary, but noted that both IL-2 and INF- gamma were decreased, IL-4 was unaffected, and IL-5 production was upregulated when PGE^sub 2^ concentrations are increased in vivo. Rivera et al. (2002) challenged steers previously adapted to their environment for 21 d with an injection of ovalbumin and noted a tendency (P

Swick (1984) discussed the energetically unfavorable hepatic use of oxygen for cytochrome P-450-dependent mixed function oxidase activity to detoxify the body when xenobiotics such as aflatoxins or pyrrolizidine alkaloids are consumed. Zanzalari et al. (1989) demonstrated that consumption of endophyte-infected fescue hay resulted in increased hepatic antipyrine uptake, which is an indirect measure of mixed function oxidase activity. Even more interesting was the research completed by Takayanagi et al. (1986) that demonstrated hydroxylases specific to cytochrome P-450 are vulnerable to ROM damage. Using a vitamin E-depleted human adrenal microsome model, the authors were able to demonstrate that as the vitamin E concentration in adrenal microsomes decreased below 1 [mu]g/mg protein, MDA formation increased exponentially. Furthermore, lipid peroxidation resulted in decreased 17a- hydroxylase and 17,20-lyase, both critically vital enzymes to the synthesis of androgens, estrogens, and cortisol (Miller et al., 1993).

The previous discussion provides a possible explanation as to why certain sources of cattle might respond more favorably to vitamin E supplementation. Moreover, it is evident, at least in non-bovine models, that vitamin E is actually an immunomodulator and has the potential to direct nutrient utilization toward the synthesis of proteins responsible for immune functions.

Meta-Analysis

Data from the studies reviewed by Secrist et al. (1997) as well as Rivera et al. (2002), Carter et al. (2005), and Cusack et al. (2005) were compiled and analyzed under a SAS mixed model analysis (SAS Institute Inc., Cary, NC) designed to account for the fixed and random effects of each individual study (St-Pierre, 2001). Seven different studies were included, comprising 1,481 lightweight steers and heifers with 10 different vitamin E amounts providing 0 to 2,000 IU/d. The statistics of interest were estimated relationships between vitamin E supplementation and DMI, ADG, G:F, and percent morbidity. For the slope coefficients a whole unit change in the independent variable (X) equals a 100-IU change in vitamin E intake per day.

Table 1. Meta-analyses estimated regression coefficients for the effect of supplemental vitamin E on the performance of newly received beef calves1

Based on the data used to generate the estimates for these analyses, no predictive relationship exists for vitamin E supplementation and DMI, ADG, or G:F (Table 1). For percent morbidity, however, the predictive model suggests that for every 100 IU increase in vitamin E intake per day a 0.35% decrease in morbidity would be expected. Because percent morbidity was significant, a quadratic model was tested for vitamin E supplementation, but no significant relationship existed beyond the original linear equation. The estimated slope coefficient for percent reduction in morbidity fits well with the data reported by Carter et al. (2005) when calves were supplemented with 2,000 IU of vitamin E/d for either 14 or 28 d. Because the entire data set is bounded between 0 and 2,000 IU/d of vitamin E intake, predictions regarding the linearity beyond 2,000 IU should be avoided. As with every biological system, the law of diminishing returns exists for increased vitamin E supplementation, but insufficient data are available to provide an estimate of where such an inflection point might occur.

IMPLICATIONS

The previous discussion provides ample evidence for the health benefit of supplemental vitamin E in stressed receiving calves. The predictive estimate derived from the meta-analysis of existing literature suggests the percentage of morbidity can be decreased 0.35% for every 100 IU increase in daily vitamin E intake. Until further data are available, this estimate is limited to a range in vitamin E supplementation up to 2,000 IU/d.

LITERATURE CITED

Betz, M., and B. S. Fox. 1991. Prostaglandin E2 inhibits production of Thl lymphokines but not of Th2 lymphokines. J. Immunol. 146:108.

Carter, J. N., D. R. Gill, C. R. Krehbiel, A. W. Confer, R. A. Smith, D. L. Lalman, P. L. claypool, and L. R. McDowell. 2005. Vitamin E supplementation of newly arrived feedlot calves. J. Anim. Sci. 83:1924.

Cusack, P. M. V., N. P. McMeniman, and I. J. Lean. 2005. The physiological and production effects of increased dietary intake of vitamins E and C in feedlot cattle challenged with bovine herpesvirus 1. J. Anim. Sci. 83:2423.

Duff, G. C., and M. L. Galyean. 2007. Boardinvited review: Recent advances in management of highly stressed, newly received feedlot cattle. J. Anim. Sci. 85:823.

Han, S. N., and S. N. Meydani. 2000. Antioxidants, cytokines, and influenza infection in aged mice and elderly humans. J. Infect. Dis. 182(Suppl 1):S74.

Han, S. N., D. Wu, W. K. Ha, A. Beharka, D. E. Smith, B. S. Bender, and S. N. Meydani. 2000. Vitamin E supplementation increases T helper 1 cytokine production in old mice infected with influenza virus. Immunology 100:487.

Hutcheson, D. P., and N. A. Cole. 1986. Management of transit- stress syndrome in cattle: Nutritional and environmental effects. J. Anim. Sci. 62:555.

McDowell, L. R. 2000. Vitamins in animal and human nutrition. 2nd ed. Iowa State University Press, Ames.

Miller, J. K., E. Brzezinska-Slebodzinska, and F. C. Madsen. 1993. Oxidative stress, antioxidants, and animal function. J. Dairy Sci. 76:2812.

NRC. 1996. Nutrient requirements of beef cattle. 7th ed. Natl. Acad.Press, Washington, DC.

Pehrson, B., J. Hakkarainen, M. Tornquist, K. Edfors, and C. Possum. 1991. Effect of Vitamin E supplementation on weight gain, immune competence, and disease incidence in barley-fed beef cattle. J. Dairy Sci. 74:1054.

Rivera, J. D., G. C. Duff, M. L. Galyean, D. A. Walker, and G. A. Nunnery. 2002. Effects of supplemental vitamin E on performance, health, and humoral immune response of beef cattle. J. Anim. Sci. 80:933.

Secrist, D. S., F. N. Owens, and D. R. Gill. 1997. Effects of Vitamin E on performance of feedlot cattle: A Review. Prof. Anim. Sci. 13:47-54.

Spurlock, M. E. 1997. Regulation of metabolism and growth during immune challenge: an overview of cytokine function. J. Anim. Sci. 75:1773.

St-Pierre, N. R. 2001. Invited review: Integrating quantitative findings from multiple studies using mixed model methodology. J. Dairy Sci. 84:741.

Swick, R. A. 1984. Hepatic metabolism and bioactivation of mycotoxins and plant toxins. J. Anim. Sci. 58:1017.

Takayanagi, R., K. Kato, and H. Ibayashi. 1986. Relative inactivation of steroidogenic enzyme activities of in vitro vitamin E-depleted human adrenal microsomes by lipid peroxidation. Endocrinology 119:464.

Toepfer-Berg, T. L, J. Escobar, W. G. Van Alstine, D. H. Baker, J. Salak-Johnson, and R. W. Johnson. 2004. Vitamin E supplementation does not mitigate the acute morbidity effects of porcine reproductive and respiratory syndrome virus in nursery pigs. J. Anim. Sci. 82:1942.

Velasquez-Pereira, J., C. A. Risco, L. R. McDowell, C. R. Staples, D. Prichard, P. J. Chenoweth, F. G. Martin, S. N. Williams, L. X. Rojas, M. C. Calhoun, and N. S. Wilkinson. 1999. Long-term effects of feeding gossypol and vitamin e to dairy calves. J. Dairy Sci. 82:1240.

Zanzalari, K. P., R. N. Heitmann, J. B. McLaren, and H. A. Fribourg. 1989. Effects of endophyte-infected fescue and cimetidine on respiration rates, rectal temperatures and hepatic mixed function oxidase activity as measured by hepatic antipyrine metabolism in sheep. J. Anim. Sci. 67:3370.

N. A. Elam1

Clayton Livestock Research Center, New Mexico State University, Clayton 88415

1 Corresponding author: nelam@nmsu.edu

Copyright American Registry of Professional Animal Scientists Oct 2007

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