Joseph H. Harrison1
and Dale Hancock2
1Department of Animal Sciences
Washington State University
Puyallup Research and Extension Center
Puyallup, WA 98371-4998
2Field Diseases Investigation
Unit
Washington State University
Pullman, WA 99164
Historically, postpartum reproductive diseases, such as retained placenta (RP), endometritis (MET) and cystic ovaries (CO), have been considered to be distinct entities. During the past decade, however, it has become increasingly evident that, rather than being independent, these disorders are among a constellation of intercorrelated syndromes of a postpartum disease complex (Stevenson and Call, 1988; Grohn et al., 1990; Correa et al., 1993; Lewis, 1997). The dependent relationships are evident when considering associations in large databases of farm treatment records. For example, in one large study a cow with RP was at 4.4 times the risk of developing MET than a cow without RP; and a cow with MET was, in turn, at 1.5 times the risk of developing CO compared to a cow without MET (Grohn et al., 1990). Notably, this web of intercorrelated postpartum syndromes is not limited to reproductive disorders but includes a number of metabolic diseases and other conditions long considered to be under the control of nutritional management (Grohn et al., 1990; Correa et al., 1993). Thus, a body of evidence has developed that postpartum reproductive disease is largely a reflection of nutritional deficiencies and imbalances, especially in the dry period (Studer, 1998; Ferguson, 1996). Among the deficiencies that have been linked to reproductive disorders are those of selenium and vitamin E.
The primary purpose of this paper is to summarize the studies giving evidence for or against the proposition that selenium and vitamin E deficiencies play a role in postpartum reproductive disease and herd fertility. Although reproductive syndromes are discussed as individual entities, it should be kept in mind that they are sufficiently intercorrelated so that evidence for a role of selenium/vitamin E nutrition in one is, to some degree, evidence for involvement in the spectrum of postpartum reproductive disease. A second purpose of this paper is to briefly review studies that shed light on possible pathogenic mechanisms by which selenium and vitamin E deficiency are involved in postpartum reproductive disease.
Retained placenta (RP) was first shown to be a Se-vitamin E responsive condition by Trinder et al. (1969). Although RP can be the result of insufficient Se-vitamin E, numerous other factors also have been associated with RP and include season of the year, abortions, milk fever, dystocia, multiple births, gestation length, parity and nutrition (Muller and Owens, 1974). Since the report of Trinder et al. (1969), there have been at least l9 peer-reviewed papers published evaluating the effect of Se, vitamin E or the combination of Se-vitamin E on retained placenta and reproduction of the dairy cow. The publications represent studies from around the world, including Mexico, Italy, United Kingdom, Israel, Canada, Portugal and Korea. Thirteen of the 19 citations report positive responses in prevention of RP with Se-vitamin E supplementation. A great deal of diversity existed in the level, duration and mode of supplementation of Se, as well as the basal Se status of those herds utilized for experimentation. Experimental group sizes ranged from l to 275 cows. The range of Se supplementation was from a single injection of 2.3 mg to 50 mg, and vitamin E of 70 IU to 3,000 mg as a single injection, mostly at approximately 21 days prepartum (Table 1). The incidence of RP in control groups ranged from 7 to 77% (Table 1), while treated groups ranged from 0 to 51%. In addition to the diversity of Se-vitamin E treatment regimens, the timing also varied, with most supplementation only occurring during the dry period; however, at least one study only supplemented cows with Se-vitamin E while cows were lactating (Stowe et al., 1988).
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Table 1. Effect of Se, vitamin E, or Se-vitamin E in combination on the incidence of retained placentas in dairy cows. Trials showing positive effect of treatment in reducing retained placenta. |
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|---|---|---|---|---|---|---|
| Percent response* | ||||||
| Control | Se | Vitamin E | Se-vitamin E | Comments | Citation | Location |
| 47(7/15)* | 12(2/17) | 4(1/25) |
15 mg Se/680 IU Vit E injection 28 days prepartum |
Trinder et al., 1973 | UK | |
| 41(16/39) | 11 (6/53) | 15 mg Se 28 days prepartum | ||||
| 52 (12/23) | 10 (4/37) | 50 mg SE/680 IU Vit E injection 40 + 20 days or 20 days prepartum |
Julien et al., 1976a | Ohio | ||
| 77 (7/9) | 0 (0/14) | |||||
| 66 (6/9) | 0 (0/9) | |||||
| 50 (4/8) | 0 (0/2) |
12.5 mg Se daily then weekly and 8% CP diet |
Julien et al., 1976b | Ohio | ||
| 50 (4/8) | 0 (0/3) |
12.5 mg Se daily then weekly and 8% CP diet |
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| 20 (1/5) | 0 (0/3) | 12.5 mg Se daily then weekly and 15% CP diet |
||||
| 20 (1/5) | 0 (0/3) | 12.5 mg Se daily then weekly and 15% CP diet |
||||
| 50 (4/8) | 0 (0/2) |
50 mg sodium selenite + 680 IU Vit E injected 20 days prepartum and 8% CP diet |
Julien et al., 1976b | Ohio | ||
| 50 (4/8) | 0 (0/3) | 50 mg sodium selenite + 680 IU Vit E injected 10 days prepartum and 8% CP diet |
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| 20 (1/5) | 0 (0/1) | 50 mg sodium selenite + 680 IU Vit E injected 20 days prepartum and 16% CP diet |
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| 20 (1/5) | 0 (0/1) | 50 mg sodium selenite + 680 IU Vit E injected 20 days prepartum and 16% CP diet |
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| 38 (72/191) | 20 (17/84) | IM injection of 50 mg Se and 680 IU Vit E 15 to 40 days prepartum |
Shigemoto et al., 1980 | Hawaii | ||
| 31 (82/275) |
51 (18/35) |
32 (25/79) | IM injection of 50 mg Se and 680 IU Vit E 15 to 40 days prepartum. Vit E-treated cows received 700 IU of Vit E IM 15 to 40 days prepartum |
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| 16 (3/19) | 17 (3/18) | 20 (4/20) | 0 (0/21) | IM Se of 50 mg 21 days prepartum, .74 g Vit E/day orally |
Harrison et al., 1984 | Ohio |
| 29 (21/73) | 11 (7/65) | 2.3 mg Se IM 21 days prepartum | Eger et al., 1985 | Israel | ||
| 21 (27/128) | 7 (8/112) | 4.6 mg Se IM
+ 140 IU Vit E 21 days prepartum |
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| 35 (25/72) | 12 (8/67) | 9.2 mg Se IM + 280 IU Vit E 21 days prepartum |
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| 16 (20/122) | 12 (12/98) | 2.3 mg Se IM + 700 IU Vit E 21 days prepartum |
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| 28 (26/92) |
9 (8/90) |
2.3 mg Se IM + 70 IU Vit E 21 days prepartum |
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| 28 (26/92) | 15 (14/94) | 4.6 mg Se IM + 70 IU Vit E 21 days prepartum |
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| 28 (26/92) | 22 (19/88) | 9.2 mg Se IM + 280 IU Vit E 21 days prepartum |
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| 30 (7/22) | 15 (5/31) | 38 (10/27) | 29 (9/31) | 500 IU Vit E/day, 2 mg Se/day orally during lactation only |
Stowe et al., 1988 | Michigan |
| 37 (6/16) | 27 (4/15) | 25 (4/16) | 19 (3/16) | - 1,000 IU Vit E, 3 mg Se orally for 6 wk prepartum |
Brzezinska- Slebodzinska, et al., 1994 |
Tennessee |
| 10 (10/99) | 3 (3/99) | - 50 mg Se IM + 680 IU Vit E 21 days prepartum |
Arechiga et al., 1994 | Mexico | ||
| 33 (4/12) | 8 (1/13) | - 5 mg Se + 25 IU Vit E IM/100 kg BW 3 and 1.5 wk prepartum |
Lacetera et al., 1996 | Italy | ||
| 12 (27/204) | 6 (13/204) | - Single IM injection of 3,000 mg Vit E 8 to 14 days before expected parturition |
Erskine et al., 1997 | Michigan | ||
| 30 (9/39) | 20 (6/30) | 27 (8/30) | 13 (4/30) | - 40 mg Se, 500 IU Vit E IM 20 days prepartum |
Kim et al., 1997 | Korea |
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* Number in parentheses = number of cows. |
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Although the diversity of the experimental designs made it difficult to discern absolute trends from data, in Table 1, we took the statistical liberty to average the incidence of RP by treatment category. This exercise showed the following observations: Control, 32% with 32 observations; Se, 10% with 10 observations; vitamin E, 28% with 6 observations; and Se-vitamin E, 11% with 26 observations. At first glance it appeared that Se alone would possibly be as effective as a combination of Se-vitamin E in prevention of RP. In five experiments (Table 1) where Se and Se-vitamin E were experimental treatments, the average incidence of RP was l8% for Se-treated cows and 13% for Se-vitamin E-treated cows, suggesting a synergistic effect in prevention of RP.
Table 2 summarizes data from six citations where no benefit was observed for Se-vitamin E supplementation for prevention of RP. In most of these citations, there was limited or no information available about dietary levels of Se or vitamin E. Three citations noted that animals were already adequate in Se status (Ishak et al., 1983; Kappel et al., l984; Hidiroglou et al., 1987), and one showed low vitamin E status (Campbell and Miller, l998). Incidence of RP in these studies was generally low (~10%) except for Ishak et al. (1983) and Hidiroglou et al. (1987) where it ranged from 21 to 32%.
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Table 2. Trials showing no response of treatment in reducing retained placenta. |
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|---|---|---|---|---|---|---|
| Percent response* | ||||||
| Control | Se | Vitamin E | Se-vitamin E |
Comments | Citation | Location |
| 10 (19/190) | 13 (21/160) |
21.9 mg sodium selenite + 500 mg Vit E 28 to 30 days prepartum |
Gwazdauskus et al., 1979 | Virginia | ||
| 27 (8/29) | 32 (9/28) |
50 mg Se + 680 IU Vit E IM 3 to 4 wk prepartum |
Ishak et al., 1983 | Nebraska | ||
| 10 (6/62) | 12 (7/60) |
50 mg sodium selenite and 680 IU Vit E IM 20 days prepartum or 40 days and 20 days prepartum |
Tahira et al., 1983 | Portugal | ||
| 10 (6/62) | 13 (8/61) | |||||
| 0 (0/65) | 1 (1/74) | 50 mg Se and 680 IU Vit E IM 21 days prepartum |
Kappal et al., 1984 | Louisiana | ||
| 21 (46/217) | 25 (47/190) |
45 mg Se and 2,040 IU Vit E 21 ays prepartum, 30 g Se intraruminal pellets 2 mo prior to calving |
Hidiroglou et al., 1987 | Canada | ||
| 21 (46/217) | 26 (57/220) | |||||
| 17 (3/18) | 16 (3/18) |
- 1,000 IU Vit E orally for 42 days prepartum |
Canada | |||
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* Number in parentheses |
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In comparison to RP, MET is a much less reliable dependent variable for a study examining effects of nutrition on reproductive disease. No consistently agreed-upon criteria exist for defining MET (Gilbert, 1992). Furthermore, gross findings, which necessarily constitute the basis for diagnosis in large studies, are only modestly (though significantly) correlated to endometrial biopsy scores (Studer and Morrow, 1978), and even histopathologic assessments made from endometrial biopsies are subject to reliability and interpretation problems (Bonnett et al., 1991). Nevertheless, at least three research groups have attempted to examine the effect of selenium and vitamin E supplementation on the incidence of MET. These are shown in Table 3. Harrison et al. (1984) reported a significant effect of selenium supplementation on MET but found no evidence of an effect of vitamin E or of an interaction between vitamin E and selenium. A more detailed analysis of data from this study examined decreases in uterine size with days postpartum (involution). In this analysis, it was found that, among cows with metritis, selenium-supplemented groups had a significantly more rapid involution (Harrison et al., 1986). No effect of vitamin E supplementation was found. Erskine et al. (1997), in contrast, reported a significant effect of prepartum vitamin E injections on the incidence of MET. Stowe et al. (1988) did not find a significant effect of either selenium and vitamin E on MET. An additional study evaluated average "uterine infection scores" and found no effect (Ishak et al., 1983).
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Table 3. Trials examining effects of Se, vitamin E or Se-vitamin E supplementation on metritis and cystic ovaries. |
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|---|---|---|---|---|---|
| Control | Se | Vitamin E | Se-vitamin E | Comments | Citation |
|
Metritis, incidence, %* |
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| 83.0a | 65.0b | 84.0a | 57.0b |
IM Se of 50 mg 21 days prepartum, .74 g Vit E/day orally |
Harrison et al., 1984 |
| 30.0a |
10.0 a |
21.0a | 33.0a |
500 IU Vit E/day, 2 mg Se/day orally during lactation only |
Stowe et al., 1988 |
| 9.0a | 4.0b |
Single I.M. injection of 3,000 mg Vit E 8 to 14 days before expected parturition |
Erskine et al., 1997 | ||
|
Average uterus infection score** |
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| .7a | .6a | .7a | .8a | 50 mg Se + 680 IU Vit E IM 3 to 4 wk prepartum |
Harrison et al., 1984 |
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Cystic ovaries, incidence, % |
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| 50.0a | 19.0b | 44.0a | 19.0b |
IM Se of 50 mg 21 days prepartum, .74 g Vit E/day orally |
Harrison et al., 1984 |
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* Incidences in the same line which do not share a superscript are significantly different (P < .05). ** 0 = none, 1 = mild, 2 = severe. |
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The diagnosis of CO is also somewhat less tangible than that of RP. Ultrasonography studies have shown that CO does not always conform to the traditional diagnostic criteria, and that diagnosis by rectal palpation is subject to a modest error rate (Farin and Estill, 1993). We know of only one study that examined the effect of selenium and vitamin E supplementation on CO. As shown in Table 3, Harrison et al. (1984) found that selenium-supplemented cows had a significantly lower incidence of CO compared to control cows and to cows supplemented only with vitamin E. Two observational studies have failed to find evidence of a beneficial effect of blood selenium on CO (Jukola et al., 1996; Mohammed et al., 1991). However, it is worth noting that neither of these studies were examining effects of supplementation, but arguably, the deviation of blood selenium levels in individual cows (CO-affected and not) around a herd mean (as estimated in unaffected control cows) produced by a supplementation level that was not under direct experimental control. In such a study, it is difficult to discriminate genetic from environmental effects (i.e., indirect from direct associations), and even the effects of competing environmental influences on both CO and blood selenium levels are very difficult to separate in an observational study (i.e., confounding bias).
While RP, MET and CO are multicausal conditions, with selenium and vitamin E nutrition being only two possible causes among many, the reproductive statistics such as those in Table 4 have an even greater number of factors influencing them. For example, while Harrison et al. (1984) noted significant differences on RP, MET and CO, a significant effect on days to first breeding was not noted. Although one would fully expect reductions in RP, MET and CO to result in decreased days to first service, one must also recognize that factors other than these three reproductive diseases influence days to first service, notably, voluntary waiting period and heat detection. Much larger sample sizes under a variety of management conditions would thus be necessary to directly quantify the impact of selenium and vitamin E on statistics, such as average days open. However, herd performance statistics, such as average days open, are directly linked to profitability. Although precise estimates of impact cannot be stated for selenium and vitamin deficiencies, large multi-herd studies showing an impact of RP, MET and CO on herd reproductive efficiency statistics (Eicker et al., 1996) lead one to conclude that some impact exists and that it might be substantial. The data in Table 4 seems consistent with this conclusion.
| Table 4. Studies examining effects of Se, vitamin E, or Se-vitamin E supplementation on reproductive statistics. | |||||
|---|---|---|---|---|---|
| Control | Se | Vitamin E | Se-vitamin E | Comments | Citation |
| Days to 1st estrus/ovulation* | |||||
| 22.0a | 27.0a | 27.0a | 21.0a | 50 mg Se+680 IU Vit E IM 3 to 4 wk prepartum | Ishak et al., 1983 |
| 19.0a | 17.0a | 19.0a |
45 mg Se and 2,040 IU Vit E 21 days prepartum, 30 g Se intraruminal pellets 2 mo prior to calving |
Hidiroglou et al., 1987 | |
|
Days to 1st observed estrus |
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| 70.0 a | 96.0b | 66.0a | 66.0a | IM Se of 50 mg 21 days prepartum, .74 g Vit E/day orally | Harrison et al., 1984 |
|
Days to 1st breeding |
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| 98.0a | 106.0a | 88.0a | 96.0a | IM of 50 mg Se 21 days prepartum, .74 g Vit E/day orally | Harrison et al., 1984 |
| 103.0a | 78.0b | 81.0b | 59.0c | 40 mg Se, 500 IU Vit E IM 20 days prepartum | Kim et al., 1997 |
|
67.0a |
67.0a | 50 mg Se IM + 680 IU Vit E 21 days prepartum | Arechiga et al., 1994 | ||
| 62.0a | 64.0a | 60.0a |
45 mg Se and 2,040 IU Vit E 21 days prepartum, 30 g Se intraruminal pellets 2 mo prior to calving |
Hidiroglou et al., 1987 | |
|
Days to conception/days open |
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| 110.0a | 108.0a | 21.9 mg sodium selenite + 500 mg Vit E 28 to 30 days prepartum | Gwazdauskus et al., 1979 | ||
| 136.0ab | 175.0c | 161.0c | 118.0a | IM of 50 mg Se at 21 days prepartum, .74 g Vit E/d orally | Harrison et al., 1984 |
| 141.0a | 121.0b | 50 mg Se IM + 680 IU Vit E 21 days prepartum | Arechiga et al., 1994 | ||
| 122.0a | 122.0a | 129.0a | 115.0a | 50 mg Se + 680 IU Vit E IM 3 to 4 wk prepartum | Ishak et al., 1983 |
| 86.0a | 89.0a | 92.0a | 45 mg Se and 2,040 IU Vit E 21 days prepartum, 30 g Se intraruminal pellets 2 mo prior to calving | Hidiroglou et al., 1987 | |
| 102.0a | 102.0a | 93.0a | 88.0a | 500 IU Vit E/day, 2 mg Se/day orally during lactation only | Stowe et al., 1988 |
|
Services per conception |
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| 2.1a | 1.9a | 21.9 mg sodium selenite + 500 mg Vit E 28 to 30 days prepartum | Gwazdauskus et al., 1979 | ||
| 2.1a | 2.6a | 2.7a | 2.1a | IM of 50 mg Se 21 days prepartum, .74 g Vit E/day orally | Harrison et al., 1984 |
| 1.7a | 1.2a | 1.6a | 1.4a | 40 mg Se, 500 IU Vit E IM 20 days prepartum | Kim et al., 1997 |
| 2.4a | 2.2a | 2.4a | 1.8a | 500 IU Vit E, 2 mg Se/day orally during lactation only | Stowe et al., 1988 |
| 2.8a | 2.3b | 50 mg Se IM + 680 IU Vit E 21 days prepartum | Arechiga et al., 1994 | ||
| 1.6a | 1.6a | 1.8a | 45 mg Se and 2,040 IU Vit E 21 days prepartum, 30 g Se intraruminal pellets 2 mo prior to calving | Hidiroglou et al., 1987 | |
|
Pregnant at 1st service, % |
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| 25.0a | 41.0b | 50 mg Se IM + 680 IU Vit E 21 days prepartum | Arechiga et al., 1994 | ||
|
Conception rate, % |
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| 71.0a | 80.0a | 71.0a | 83.0a | 40 mg Se, 500 IU Vit E IM 20 days prepartum | Kim et al., 1997 |
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* Means or proportions in the same line which do not share a superscript are significantly different (P < .05). |
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The postpartum uterus is normally contaminated by environmental bacteria, and the placenta is also a foreign substance that must be removed. The epidemiology of MET (sometimes called uterine infection) is not consistent with that of a communicable infectious disease, and attempts to correlate it with farm hygiene have been unsuccessful (Noakes et al., 1991). Whether or not a cow develops MET, a syndrome that is associated with failure to clear opportunistic bacteria, is at least partly due to the functionality of lymphocytes and neutrophils (Cai et al., 1994; Sato et al., 1995; McEvoy and Pollack, 1994). Retained placenta also has been found to be strongly associated with reduced chemotaxis of leukocytes (Gunnink et al., 1984). More broadly, the reduced functionality of leukocytes could partly explain the observed intercorrelation of reproductive syndromes with other postpartum diseases. For example, it has been proposed that the observed correlation between RP and postpartum mastitis (estimated relative risk = 3) is due to the impact that reduced functionality of peripheral leukocytes has on both conditions (Schukken, 1989). Selenium and vitamin E have been reported to play an important role in lymphocyte (Pollock et al., 1994) and neutrophil (Boyne and Arthur, 1979; Boyne and Arthur, 1981; Smith et al., 1997) function. On a theoretical basis, therefore, one would expect selenium and vitamin E deficiencies to increase rates of RP and MET.
Selenium and vitamin E have been reported to have an effect on uterine motility, and this effect has been posited to play a role in the pathogenesis of RP in deficient animals (Segerson et al., 1980). Oxidative stress due to production and slow clearance of reactive hydoxy radicals has also been proposed as a mechanism that could be involved in RP and by which a beneficial impact of selenium and vitamin E would be expected (Brzezinska-Slebodzinska et al., 1994; Campbell and Miller, 1998).
Evidence of hormonal effects of selenium deficiency also has been reported. Kamada and Hodate (1998) reported that otherwise deficient cows supplemented with selenium had significantly increased plasma progesterone. Progesterone concentration was typically lower after the first postpartum cycle, and return to higher levels appeared to be an important part of the involutionary process (Kamimura et al., 1993). Blood progesterone concentration fills a key link in the feedback loop with the hypothalamus-pituitary axis in the release of gonaotropic hormones and the pre-ovulatory LH surge (Farin and Estill, 1993). Thus, it is conceivable that an impact of selenium deficiency on CO could be mediated, at least partly, through the reduced progresterone levels noted by Kamada and Hodate (1998). Endometrial disease also can impact ovulation and luteanization and hence the ovarian-hypothalamus-pituitary feedback loop (Farin and Estill, 1993). Thus, selenium and vitamin E nutrition could potentially influence the incidence of CO through MET, a hypothesis that is consistent with the aforementioned correlation, which has been observed between these disorders (Grohn et al., 1990).
Although the weight of the evidence makes a strong case that selenium and vitamin E deficiencies negatively impact reproductive health and performance and that supplementation can redress these losses, several key issues remain to be clarified. First, the mode of supplementation needs to be better clarified. With the wide use of oral Se and vitamin E supplementation in today's dairy herds, it would be worthy of further investigation to know if Se-vitamin E injections are required when oral levels of supplementation are providing for adequate blood levels of Se and vitamin E during the dry period. From a practical standpoint, eliminating one injection of the cow each year would save time for the herd manager to attend to other management details, and would result in financial savings if the injections were determined to be unnecessary. Any study on this point must include the spectrum of conditions linked to selenium/vitamin E deficiency (e.g., mastitis, colostrum yield). Dosage is another key issue to be addressed. We clearly need to titrate the level of Se and vitamin E needed for overall health and productive function of the dairy cow, not just prevention of RP. Exploration of nutritional interactions, which could impact required dosage, adds an additional dimension to these studies. Finally, better knowledge of the pathogenesis of reproductive diseases would allow more focused studies that are better designed to examine aspects of selenium and vitamin E nutrition than have been possible in the past.
In the words of Eger et al. (1985), "...dosage, timing, mechanism, and interactions of selenium with other factors in prevention of RP remain poorly understood and need further clarification." Though progress has been made since Eger wrote these words in 1985, the same basic issues remain before us.
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