Manipulating Dietary Anions and Cations for Prepartum Dairy Cows to Reduce Incidence of Milk Fever

Manipulating Dietary Anions and Cations for Prepartum Dairy Cows to Reduce Incidence of Milk Fever 1

ABSTRACT

Twenty preparturient dairy cows were in a 2-yr switchover design to test effects of dietary ions on incidence of milk fever. In yr 1, cows were blocked and assigned randomly 45 days preparmm to one of two diets; one diet contained an excess of anions, and the second diet contained an excess of cations. In yr 2, cows were changed to the opposite diet. Both diets were equivalent for crude protein (11%), calcium (.65%), phosphorus (.25%), and energy on a dry basis but differed for quantities of chlorine, sulfur, and sodium. Both diets were chopped alfalfa hay, corn silage, high moisture corn, and vitamin- mineral mix. Diets were available ad libitum as complete rations.

There were no differences in dry matter intake of the diets. Cows consuming the anionic diet had no milk fever, but cows consuming the canionic diet had 47.4% incidence. Samples of blood plasma showed that cows consuming the anionic diet maintained calcium and phosphorus through parturit ion, whereas cows consuming the cationic diet decreased in these minerals around calving. Hydroxy- proline was higher for cows consuming the anionic diet during the peripartal period compared to cows consuming the cationic diet. Milk produced in the lac- tat ion subsequent to prepartum treatment was 6.8% less for cows offered the cationic diet. When milk product ion of paretic and nonparetic cows offered the cationic diet was compared, milk was reduced 14% with milk fever.

Received October 12, 1983. 1 This research was supported entirely by the Con-

sell des Recherches et Services Agricoles du Qu6bec, Ministere de l'Agrieulture, des Pecheries et de l'Ali- mentation.

ELLIOT BLOCK Department of Animal Science

Macdonald College of McGill Univer'sity Ste-Anne de Bellevue, Quebec, Canada H9X 1C0

INTRODUCTION

Research has elucidated various measures for prevention of hypocalcemic parturient paresis (milk fever). These measures include manipulating amounts and ratios of calcium (Ca) and phosphorus (P) in the prepartum diet of cows (4, 6, 7, 15, 16, 19, 25, 27, 30, 38), feeding prepartum cows diets containing high or low alkalinity (10, 13, 14), and oral or parenteral administration of vitamin D or its metaboli tes at specific times prepartum (17, 18, 20, 21, 22, 23, 26, 31, 34, 35, 36).

Problems exist with implementat ion of the various preventive measures. In some areas of Quebec it is difficult to reduce amounts of Ca or ratio of Ca to P fed to cows for several reasons: inabili ty to grow sufficient quantities of feeds, such as corn silage, for the entire herd; suitability of land for legume crops, which are high in Ca; and inabili ty to add sufficient P to lower the ratio of Ca to P due to palatabil i ty when quantities of P are added to a ration. Although treatment with vitamin D and its metaboli tes is effective for preventing milk fever, timing of t reatment in relation to actual calving date appears critical to efficacy of treatment. Retreatments with vitamin D and its metaboli tes are necessary if the calving date is mispredicted; however, vitamin D toxic i ty has been reported (28). Acidification of the diet is efficacious in promoting bone mobilization in rats (2, 3, 33); however, mineral acids can present danger to the user.

A possibility exists to prevent milk fever by increasing the quant i ty of acidogenic minerals in prepartum diets in relation to the alkalogenic minerals. Proposed was that alkali-alkalinity (anion-cation balance) of diets fed to cows prepartum could be important for determining Ca availability (11, 14, 29). Milk fever was precipitated in 9 of 14 calvings from five Nor- wegian Red and White cows by diets in the prepartum period that contained acids or that contained excess anionic minerals in relation to cationic minerals (11). However, diets offered

1984 J Dairy Sei 67:2939--2948 2939

2940 BLOCK

to these cows contained ingredients that are atypical of North American dairy rations (i.e., beets, formic acid treated silage, herring meal). Others (29) showed that excess anions in diets for prepartum cows influence Ca absorption only when these diets maintain a positive Ca balance in the cow.

Use of various combinations of ions in diets for poultry has affected ions in blood as well as acid-base balance of blood (9, 24, 37). Ions examined in most of the experiments were Na, K, C1, S, Mg, and P with emphasis on Na and C1.

My objective was to ascertain if diets com- monly fed in North America that are high in ratio of Ca to P can be fed to prepartum cows without precipitating milk fever if the diets contain sufficient quantities of anions in relation to cations. Because anions are considered acidogenic and cations alkalogenic, the hypothesized mode of action is that an excess of acid-forming elements at times of Ca stress will increase concentrations in blood either via increased intestinal absorption or bone mobilization.

MATERIALS AND METHODS

Twenty mature cows (12 Holstein and 8 Ayrshire) with at least three previous records of milk production and at least one record of high milk production (>7,500 kg) were in a 2-yr switchover design to test if dietary anions and cations influence incidence of hypocalcemic parturient paresis (milk fever). Cows were assigned to 10 blocks of two cows each. Block- ing was according to expected date of calving, breed, and milk production in the previous lactation.

In the 1st yr of the trial, cows within each block were assigned to one of two dietary treatments for the prepartum period: a diet containing an excess of cations relative to anions (designated the cation diet), or a diet containing an excess of anions relative to cations (designated the anion diet). The cation diet contained (dry basis) 39% chopped alfalfa hay, 57% corn silage, 2.5% high moisture ear corn, and 1.5% of mineral premix formulated to provide an excess of Na and K relative to C1 and S. The anion diet contained identical quantities of chopped alfalfa and corn silage as the cation diet plus (dry basis) 1.7% high moisture ear corn, .23% CaC12, .86% AI2

(SO4)3, .74% MgSO4, and .5% of mineral premix formulated to provide an excess of C1 and S relative to Na and K. Mineral premixes were formulated to meet nutrient requirements in the diets and to deliver excess cations or anions. Ingredients in these premixes were NaC1, COC12, MnSO4, ZnO, FeSO4, KI, CaCO3, NaHCO3, NaCO3, CuSO4, ZnC12, Ca(IO3)2, and CaCI. The anion-cation balance of the diets was calculated and determined by using and manipulating quantities of Na, K, C1, and S in the rations. The equation for calculating anion- cation balance was milliequivalents [(Na + K) -- (C1 + S)]. Diets were formulated to meet requirements of dry pregnant cows (32) except for Na, K, C1, S, Ca, and P; these minerals met or exceeded requirements of dry pregnant cows dependent upon the anion-cation balance of the ration and maintenance of a ratio of Ca to P of 2.5 in both diets.

Cows assigned to each dietary treatment received their respective rations beginning 45 days prepartum and continuing through parturition. Dietary components were mixed and offered as a complete ration once daily at 1000 h. Animals were allowed ad libitum consump- tion to assure feed refusals were 10% of the original quantity of feed offered. Feed refusals were obtained daily at 0900 h. After parturition cows entered the normal feeding and management program at the Macdonald College Farm Centre of McGill University. The ration for cows in early lactation consisted of corn silage, legume-grass haylage, alfalfa hay, grain mix, and supplements containing (dry basis) 17% crude protein, 1.63 Mcal/kg NE L (net energy for lactation), .9% Ca, .6% P, and .7% NaHCO3.

In the 2nd yr of the trial the same cows and diets were used; however, cows were offered the dietary treatment opposite that offered in yr 1.

Rations were sampled weekly, composited into monthly samples, and frozen. Composite samples were analyzed for dry matter (DM) in a vacuum oven at 60°C for 24 h; the oven-dried samples then were analyzed for Kjeldahl nitrogen and Ca, P, Na, C1, and S by atomic absorption spectrophotometry. Blood samples were obtained from the jugular vein of each c o w on days 30 ± 7, 20 -+ 7, 5, 4, 3, 2, and 1 prepartum, at parturition, and on days 1

Journal of Dairy Science Vol. 67, No. 12, 1984

DIETARY ANIONS AND CATIONS AND MILK FEVER 2941

through 5 postpartum. Pre- and postpartum blood samples were obtained at approximately 1100 h. Blood samples were divided and placed into two test tubes. One test tube contained potassium oxalate as the anticoagulant; this sample was centrifuged with the plasma, then withdrawn and frozen for subsequent analysis of Ca, P, and Na by atomic absorption spectrophotometry and for hydroxyproline (39) to indicate bone mobilization (5, 12). The second test tube contained lithium heparin as the anticoagulant; this sample was centrifuged with the plasma, withdrawn, and then frozen for subsequent analysis of K and C1 by atomic absorption spectrophotometry.

Body weights were obtained weekly by averages of weighings twice daily at 1100 and 1600 h on 2 consecutive days. Milk production for the lactation subsequent to prepartum dietary treatment was obtained from the Qu6bec Dairy Herd Analysis Service (DHAS) and reported as 4% fat-corrected milk (FCM) for a 305-day lactation. Cows were diagnosed with milk fever only if they exhibited two or more of the typical symptoms of the disease (i.e., typical recumbant position, lowered temperature of extremities, inability to rise, grinding of teeth, inappetance). Cows diagnosed with milk fever were treated intravenously with

a calcium borogluconate solution; blood samples required were taken immediately before treatment.

Statistical analyses were at the McGill Computing Centre by the Statistical Analysis System (1). Data were analyzed as a switchover design with randomized blocking of animals. In addition to the overall analysis, the 2 individual yr of the trial were analyzed as two separate random block experimental designs. Animals offered the cation diet over both years were grouped into paretic and nonparetic cows and analyzed in a complete random design. Signifi- cant differences were claimed at 5%.

R ESU LTS

Chemical analyses for the two diets are in Table 1. Ratios of Ca to P of both diets were able to cause milk fever and were similar at 2.63 and 2.89 for cation and anion diets. Average intakes of Ca and P for the 2-yr trial were 85.5 and 33.9 g/day for cows offered the cation diet and 92.5 and 32.2 g/day for cows offered the anion diet. Major differences between diets were contents of Na, C1, and S that were .53, .42, and .15% of the total DM for the cation diet and .16, .57, and .56% of the total DM for the anion diet. Average intakes of Na, K, el, and S for the 2-yr trial were 71.9,

TABLE 1. Nutrient composition of diets (dry basis) containing an excess of cations and anions that were offered to cows beginning 45 days prepartum, a

Nutrient Cation Anion

SE X, SE Crude protein, % 11.1 .15 11.0 .17 Net energy lactation, Mcal/kg b 1.37 1.33 Calcium, % .63 .02 .69 .03 Phosphorus, % .25 .03 .24 .03 Sodium, % .53 .03 .16 .02 Potassium, % 1.22 .09 1.22 .06 Chlorine, % .42 .01 .57 .02 Sulfur, % .15 .01 .56 .01 Anion-cation balance per kg

dry matter c +33.05 -12.85

acomposition based on 24 monthly composites of each ration are reported as averages except net energy, calcium-phosphorus ratio, and anion-cation balance.

bNet energy calculated from tabular data (32). Ccalculated as miUiequivalents [(Na + K) - (CI + S)] from nutrient analysis assuming the molecular weights

of 22.9, 39.1, 35.45, and 32.07 for Na, K, el, and S, respectively.


2942 BLOCK

165.6, 57, and 20.4 g/day for cows offered the cation diet and 21.5, 163.6, 76.5, and 75.1 g/day for cows offered the anion diet. Potas- sium was constant in both diets at 1.22% of the total DM. Anion-cation balances per kilogram DM were calculated from mineral analyses (Table 1) and were +33.05 and -12 .85 for cation and anion diets.

Table 2 contains results of the trial. The average age of cows in the trial was 7.2 yr. One cow died each year in the positive group; these deaths were attributable to milk fever. There- fore, in yr 2, the remaining nine cows per treatment were used for analysis. Table 3 shows results for each year (analyzed for each year as randomized block design), overall results (analyzed as a switchover design), and for cows fed the cation ration analyzed for paretic vs. nonparetic cows. Dietary treatments caused the same results each year. Treatments had no effect on DM intake in any of the analyses. However, because diets had different anion-

cation balances (Table 1), averages of daily anion-cation balance of cows between treatments within each year and in the overall analysis were different, i.e., highly positive for cows offered the cationic diet and highly negative for cows offered the anionic diet.

Incidence of milk fever for cows offered the cation diet was 5 of 10 (50%) in yr 1, 4 of 9 (44.1%) in yr 2, and an overall incidence of 47.4% in the switchover analysis (Table 2). Incidence of milk fever for cows offered the anion diet was nil. Milk fever occurred only in Holstein cows. Both diets had ratios of Ca to P conducive to milk fever. Lactation records subsequent to the prepartum dietary treatments for yr i were lower (P<.05) for cows offered the cation diet (high incidence of miIk fever) than for cows offered the anion diet (no milk fever) (Table 2). Although the trend was the same fo ry r 2, the difference was not significant. In the overall trial cows offered the cation diet produced 6.8% less milk (P<.05) than cows

TABLE 2. Daily dry matter intake (DMI) as a percentage of body weight (% BW) and daily anion-cation balance for the prepartum period, incidence of milk fever at parturition, and subsequent milk production (4% fat- corrected) for cows offered diets prepartum with an excess of cations and anions.

Milk DMI Anion-cation Incidence of production

No. cows Ration % BW balance a milk fever (%) (kg/305 days)

Year 1 10 Cation 1.87 +450.1 50 6585 b 10 Anion 1.78 --168.7 0 7203 c SE .067 47.8

Year 2 9 Cation 1.83 +446.9 44.1 6735 9 Anion 1.85 --176.4 0 7075

SE .061 69.9

Summary -- Overall Trial Analysis 19 Cation 1.85 +448.6 47.4 6656 b 19 Anion 1.81 -172.3 0 7142 c SE .073 52.9

Summary of Cation Group 10 Cation 1.92 +473.3 0 7128 b 9 Anion 1.77 +421.4 100 6132 c

SE .068 46.4

acalculated as (milliequivalents [(Na + K) -- (C1 + S)]) (daily DMI). b'CMeans in the same column with different superscripts differ (P<.05).

Journal of Dairy Science Vol. 67, No. ! 2, 1984


offered the anion diet. When cows in the cation group were separated and analyzed as paretic vs. nonparetic, milk product ion was reduced 14% for paretic cows (P<.05).

Blood plasma was analyzed for Ca, P, Na, C1, K, and hydroxyprol ine (OHPRO). Resuhs for blood composit ion represent the combined data for the entire trial for cows offered the cation and anion diets.

Figure 1 shows the blood plasma analyses for Ca, P, Na, C1, K, and OHPRO for cows fed cation and anion diets. Table 3 shows similar data only for cows offered the cation diet but separated into paretic and nonparetic cows. Plasma Ca and P concentrations (Figure 1) were lower (P<.05) for cows offered the cation diet at and around parturit ion. Cows offered the cation diet that became paretic had a more dramatic drop of plasma Ca and P at calving (P<.05) than cows offered the cation diet that were not paretic (Table 3). Plasma Na tended toward greater concentration for cows offered the cation diet (Figure 1) with significant differences (P<.05) on day 4 prepartum. For cows offered the cation diet (Table 3), those that were paretic had higher Na in plasma (P<.05) on days 4, 3, and 1 prepartum than cows that were not paretic. Plasma C1 concentrations were higher (P<.01) for cows offered the anion diet from day 20 prepartum through parturi t ion (Figure 1) compared with cows offered the cation diet. Plasma C1 tended lower for all cows offered the cation diet (Table 3) regardless of disease status at parturi t ion with cows that were paretic having lower (P<.05) plasma C1 on day 2 prepartum, at parturit ion, and on day 1 postpar tum than cows fed the cation diet that were not paretic. Plasma K was consistently lower (P<.05) for cows offered the cation diet from d a y . 2 0 prepartum through, and including, day 1 postpar tum (Figure 1). Cows offered the cation diet that were paretic tended to have lower plasma K with lower (P<.05) plasma K on day 4 prepartum compared with cows that were not paretic (Table 3). Plasma OHPRO was consistently lower (P<.05) for cows offered the cation diet (Figure 1) from day 5 prepartum through day 2 postpar tum compared with cows offered the anion diet. Moreover, OHPRO increased for cows fed the anion diet, whereas OHPRO of cows fed the cation diet remained unchanged until day 2 postpar tum (Figure 1). Concentra-

tion of OHPRO showed the same differences between cows offered the cation diet that were and were not paretic (Table 3) as cows offered cation and anion diets (Figure 1); cows offered the cation diet that were paretic had lower (P<.05) OHPRO than cows fed the cation diet that were not paretic from day 5 prepartum through day 2 postpartum. Concentrations of Ca, P, and OHPRO in nonparetic cows offered the cation diet were higher, on specific days, than paretic cows offered the cation diet (Table 3) and tended to be lower than for cows offered the negative diet (Figures 1).

DISCUSSION

Results confuse current thoughts on the etiology of milk fever in that prepartum cows consuming diets with a high ratio of Ca to P did not become paretic if the diet contained an excess of anions relative to cations. These results suppor t (11, 13, 14). The reason cows did not become, paretic was that Ca and P were maintained during Ca stress. However, the physiological response is unclear. This does not suggest that the feeding of diets with a low ratio of Ca to P or low quantities of Ca to prepartum cows is undesirable; this method still is considered the choice in most cases. How- ever, in cases where feeding low ratios of Ca to P is not possible, manipulating the anion-cation balance of prepartum diets does have advantages over treating cows with vitamin D or its me- tabolites. Use of vitamin D products (17, 18, 20, 22, 26, 31, 34, 36)requires careful moni- toring for dosage, timing of t reatment relative to parturit ion, number of retreatments, and risks of toxic i ty (28). Once a formulation is derived, anion-cation balance for preventing milk fever is accomplished simply by mixing the minerals with other dietary ingredients.

Although for my trial the equation meq [(Na + K) -- (C1 + S)] worked well, the cation diet did not cause milk fever in all cases. In another trial (11) the same equation showed that diets with an anion-cation balance of - 2 5 5 prevented milk fever in most cases but allowed milk fever to develop in one case; however, some cows consuming diets with highly positive anion-cation balances did not become paretic or became only slightly paretic while other cows consuming diets with the same anion-cation balances became paretic.


~7 4 TABLE 3. Blood plasma components for cows offered the cation diet that were diagnosed with milk fever (MF) versus healthy (H) cows f rom day-5 prepartum to day-5 postpartum, a

to xo 4 ~

¢~ ,¢

Plasma Disease Days prepartum Days postpar tum component status 5 4 3 2 1 0 1 2 3 4 5

O

G', .q

Z 9

4~

Calcium, mg/lO0 ml MF 8.87 8.29 8.02 b 7.75 b 7.22 b 4.83 b 5.69 b 6.79 b 7.43 8.12 8.33

H 8.66 8.19 8.24 c 8.40 c 8.43 e 7.75 c 8.52 c 8.75 c 8.95 c 8.78 8.38 SE .24 .29 .26 .14 .37 .23 .24 .20 .44 .25 ,32

Phosphorus mg/lO0 ml MF 4.60 4.52 4.68 4.28 3.07 b 2.43 b 2.76 b 3.32 b 4.03 4.07 3.96

H 4.30 4.52 4.50 4.32 4.22 c 3.33 c 3.67 c 4.02 c 4.23 3.97 4.12 SE .25 .21 .19 .14 .33 .18 .21 .25 .11 .19 .11

Sodium, meq/liter

Chlorine, meq/liter

Potassium, meq/liter

Hydroxyproline, /~g/ml

MF 144.6 157.6 b 149.0 b 139.4 142.6 b 138.2 136.2 133.2 129.3 127.3 132.8 H 142.0 148.0 c 137.4 c 134.8 132.0 c 132.8 138 .4 137.8 133.6 139.6 126.6 ~) SE 33.2 17.1 12.9 30.4 18.4 20.7 25.4 24.6 28.7 36.1 31.2 C3

MF 103.8 104.8 103.6 103.6 b 102.6 lO0.Ob 103.2 b 107.2 108.0 109.5 106.5 H 104.8 105.4 105.0 106.0 c 104.6 105.4 c 109.2 c 112.0 112.4 109.0 111.2 SE .49 .71 1.17 1.36 .89 .80 1.98 .94 .93 1.49 1.75

MF 3.83 3.56 b 3.83 4.20 4.22 4.06 3.92 3.74 4.26 3.85 3.57 H 3.97 4.17 c 3.89 4.26 4.35 4.10 4.04 4.19 3.77 3.68 4.30 SE .28 .134 .06 .26 .23 .26 .33 .21 .25 .20 .181

MF 1.90 b 1.82 b 1.84 b 1.84 b 1.78 b 1.64 b 1.66 b 1.82 b 2.25 2.48 2.95 H 2 . 2 2 c 2 .08 c 2 .06 c 2 .08 c 2.14 c 2.14 c 2.30 c 2.98 e 3.10 3.02 3.00 SE .04 .05 .04 .04 .03 .07 .09 .27 .15 .1 .06

an = Nine cows diagnosed paretic and 10 healthy cows.

b'CMeans in the same column within each blood component with different superscripts differ (P<.05).


PHOSPHORUS

.~ .~ .~S .n .m .Or .~.~ J0 .~S .0~ ~ .~0 .0~

M 4 , G

3 . M L

[ 1 / i

P R E P A ~ T U M P O ~ T P A R T O ~

CALCIUM .~ .11 .]2 .~S ,~ .0~ .~ .0P .0Z ~ .Cq .~ .O8 .~

8"

PREPARTUM POSTPARTUM

POTASSIU 8 1,~ .OZ .g .~b .~ .~ ,~ .~ ,~ .~ .47 .~ .~

I16"


H~ROXYPROLINE .o6 .o, .c~ .o? .o~ .o~ ,oi b .~ .~ .~? .o~ .o~ .os

5 '

2:.

[ I , ," I '1 3 o 5k½~ I;12½~;


M 1 1 ~ " Q / 1[ 1 0 8 " T E R 1 0 4 "

U 2. G / M L

1 .

SODIUM 8.28 8.08 16.6 8.55 ~ 6.45 15.2 9.2 /0.35 ]2.7 12.3 14.35 18.05 15.6

1 6 0 -

M 158- Q / IL 140" T E R 130"

1 2 : O I


CHLORIDE

4~5"

M 4 - E Q

IL 3 . 5 - T E R 3-

2 . 5 I I / : t : : : I I


Figure 1. Calcium, phosphorus, sodium, potassium, chloride, and hydroxyproline in blood plasma of cows offered the cation (D) and anion (o) diets prepartum on days 30, 20, and 5 through 1, at parturition, and on days 1 through 5 postpartum. Numbers at top of each graph are standard errors for the sampling date. a) Cows fed cation and anion diets differ (P<.05). b) Cows fed cation and anion diets differ (P<.O1).

There is uncertainty of which ions to include and which equation to use in calculation of anion-cation balance. Although (11) used meq [(Na + K) - (El + S)], (29) examined daily intake of [(Na + K) -- (El + S)], [(Na + K) -- (C1 + S + P)], (C1 + S), (CL + S + P), and (Na + K) in relation to digestible Ca, and (14) examined meq [(Na + K) -- (C1 + S)]and meq [(Ca + Mg + K + Na) -- (P + S + C1)]. In (29) was suggested that the inclusion of P in the calculation improves the relation between dietary ions and Ca digestibility. A further confusing point is that other equations have

• been used with poultry. Ionic equations such as dietary Na/C1 (24), (Na + K)/C1 (8), (Na + K -

C1), and C1/(Na + K) (37) have been used to describe effects of ions on eggshell forma- tion, blood ionic constitutents, and acid-base balance in poultry.

Suggestions have been made (11, 14, 29) that diets containing acid forming ions cause greater Ca absorption by cows via decreasing intestinal pH. My trial indicates that blood of cows responds fo anion cation-balanced diets as shown by the response of plasma OHPRO (Figure 1) by cows offered the anion diet and lack of response by cows offered the cation diet. It appears that the anion (acidogenic) diet altowed for easier bone-mobilization during Ca-stress even though diets contained a high


2946 BLOCK

ratio of Ca to P. Therefore, in addition to intestinal effects of a diet balanced for excess anions, as shown by (14, 19), there must be a systemic response by cows to this diet. This systemic response may be as simple as a slight decrease of blood pH and as complex as affecting liver and kidney function, which subsequently affects vitamin D metabolism. Because the kidney plays a major role in blood acid-base balance and in regulating blood ionic composition, these suggested effects of dietary ions are worth investigating.

The intestinal response of acidogenic diets in increasing Ca absorption only occurs when Ca balance is positive (29), precluding the use of acidogenic diets to increase blood Ca when cows are in early lactation or when the prepartum diet has low Ca or low ratio of Ca to P. However, the reason for increased Ca absorption is unknown. The suggestion is that acid- forming elements in the intestine allow for greater Ca solubility and easier absorption (11, 13, 14, 29). If the passive absorptions of Ca is increased by excess anions via reduction in intestinal pH, then active absorption of Ca should decrease through the parathyroid hormone (PTH) and 1 hydroxylase systems. As these systems become inactive, bone resorption should decrease and plasma OHPRO should remain low. In this study OHPRO increased in the anion group as parturition approached (Figure 1), indicating that bone was responsive. In the cation group lower plasma Ca should have stimulated the PTH and 1 hydroxylase systems to increase intestinal absorption of Ca and bone resorption; however, the bone was un- responsive as shown by plasma OHPRO concentration (Figure 1), and the gut was apparently not ready to meet Ca demands of lactation.

Possible effects of the dietary A1 have not been considered in this article or by (11). In my trial cows fed anion diet were consuming 18.4 g A1 per day as AI2(SOa)s. This is equivalent to 1358.8 ppm AI in diet. Research has shown that 2000 ppm in rations for lambs (40) caused feed refusal, decreased concentrations of Mg and P in plasma, and no change of plasma Ca. These researchers proposed that excess dietary A1 reduced intestinal absorption of P. The possibility exists that in my trial dietary A1 decreased P absorption, thus stimulating 1 hydroxylase system. However, this is unlikely because feed intake (Table 2) and plasma P

(Figure 1) were not different between anion and cation groups in the prepartum period.

Another possible explanation for my results is that anion diet turns off absorption of Ca from the intestine and mimics a low Ca diet even in the presence of high quantities of dietary Ca. If this were the case, then bone would re- spond through hormonaLly-mediated Ca homeo- static mechanisms. Other mechanisms of action are possible, such as increased binding sites for the active absorption o f Ca or an effect of the ions on intestinal cells subsequently affecting action of the hormone, 1,25-dihydroxychole- calciferol. These possibilities as well as intestinal pH have yet to be explored.

Blood plasma C1 responded in accordance with dietary treatment; the higher dietary C1 elevated plasma C1; this also was shown in poultry (8). The response of plasma Na and K in cows is more obscure. Plasma Na tended to be higher for cows consuming more Na but was only significantly higher for 1 day of blood sampling. Alternatively, dietary K was equivalent in both diets, yet plasma K was depressed for cows consuming the anion diet. These results may be explained by an interaction between K and Na, especially when the diet is low in C1 as shown by (8).

Results show a 14% reduction of milk produced for an entire lactation by paretic cows (Table 2, summary of cation group). From the switchover design, it appears that this loss was not permanent between years. How- ever, because milk fever is more common in cows with previous occurrences of milk fever, and if the cow's productive life is shortened by the disease, then there is a significant loss of milk for the lifetime of a cow that becomes paretic.

As mentioned earlier, diets for prepartum cows containing low ratios of Ca to P or low quantities of Ca reduce the risk of milk fever and should be used where possible. However, it appears that the high Ca fed prepartum may not be the direct cause of milk fever per se. The positive Ca balance created by a diet with a high ratio of Ca to P coupled with excesses in Na and K intake may be the cause of milk fever, whereas effects of Na and K are over- ridden with a negative Ca balance created by a diet with a lower ratio of Ca to P by the inter- vention of the active absorption and homeo- static mechanisms for Ca. For example, the

Journal o f Dairy Science VoL 67, No. 12, 1984


n u t r i e n t c o m p o s i t i o n of alfalfa h a y (32) shows a h igh Ca con t en t . This shou ld cause mi lk fever in cows fed alfalfa p r e p a r t u m . However , alfalfa has small a m o u n t s of C1 and large a m o u n t s of K and Na; coupl ing this wi th t he posi t ive Ca ba lance c rea ted b y feeding alfalfa leads to occu r r ence o f mi lk fever. I t appears t h a t the bes t m e t h o d s for r educ ing inc idence o f mi lk fever are to feed low Ca die ts p r e p a r t u m (4, 6, 7, 27, 30) or to feed d ie ts t h a t are acid or acidogenic .

ACKNOWLEDGMENTS

The a u t h o r t h a n k s G. Beaul ieu and W. C h a b o t o f t he M a c d o n a l d College F a r m Cen t re for t he care and m a n a g e m e n t o f the animals , D. Mar t in for feed ing and sampl ing animals , B. J a c k s o n and W. M c D o n a l d for da ta handl ing , B. R. D o w n e y for a m b u l a t o r y and ve te r ina ry services, J. F. Hayes for assisting w i t h s ta t i s t ica l analyses, and t he C r a m p t o n N u t r i t i o n Labora- t o ry o f M a c d o n a l d College for chemica l anal: yses.

REFERENCES

1 Barr, A. J., J. H. Goodnight, J. P. Sail, and J. T. Helwig. 1976. In A user's guide to SAS 76. SAS Inst., Inc., Raleigh, NC.

2 Barzel, U. S. 1969. The effect of excessive acid feeding on bone. Calcif. Tiss. Res. 4:94.

3 Barzel, U. S. 1975. Studies in osteoporosis: The long-term effect of oophorectomy and of am- monium chloride ingestion on the bone of mature rats~ Endocrinology 96:1304.

4 Beitz, D. C., D. J. Burkhart, and N. L. Jacobson. 1974. Effects of calcium to phosphorus ratio in the diet of dairy Rows on incidence of parturient paresis. J. Dairy Sci. 57:49.

5 Black, H. E., and C. C. Capen. 1971. Urinary and plasma hydroxyproline during pregnancy, parturition and lactation in cows with parturient hypocalcemia. Metabolism 20: 337.

6 Boda, J. M. 1956. Further studies on the influence of dietary calcium and phosphorus on the incidence of milk fever. J. Dairy Sci. 39:66.

7 Boda, J. M., and H. H. Cole. 1954. The influence of dietary calcium and phosphorus on the incidence of milk fever. J. Dairy Sci. 37:360.

8 Cohen, I., and S. Hurwitz. 1974. The response of bood ionic constitutents and acid-base balance to dietary sodium, potassium and chloride in laying fowls. Poultry Sci. 53:378.

9 Cohen, I., S. Hurwitz, and A. Bar. 1972. Acid-base balance and sodium-to-chloride ratio in diets of laying hens. J. Nutr. 102:1.

10 Dishington, I. W. 1974. The role of age on the induction of hypocalcemic paresis puerperalis in dairy cows. Nord. Veterinaermed. 26:205.

11 Dishington, I. W. 1975. Prevention of milk fever

(hypocalcemic paresis puerperalis) by dietary salt supplementation. Acta Vet. Scand. 16:503.

12 Dull, T. A., and P. H. Henneman. 1963. Urinary hydroxyproline as an index of collagen turnover in bone. N. Engl. J. Med. 268:132.

13 Ender, F., and I. W. Dishington. 1970. Etiology and prevention of paresis puerperalis in dairy cows. Page 71 in Parturient hypocalcemia. J.J.B. Ander- son, ed. Academic Press, New York and London.

14 Ender, F., I. W. Dishington, and A. Helgebostad. 1971. Calcium balance studies in dairy cows under experimental induction and prevention of hypocal- caemic paresis puerperalis. Z. Tierphysiol. Tierer- n~ihr., Futtermittelkd. 28:233.

15 Fish, P. A. 1929. Recent progress in our knowledge of milk fever. J. Am. Vet. Med. Assoc. 75:695.

16 Gardner, R. W. 1970. Avoiding milk fever. Anita. Nutr. Health 25:6.

17 Gnat, D. R., R. L. Horst, N. A. Jorgensen, and H. F. Deluca. 1979. Potential use of 1,25-dihydroxy- cholecalciferal for prevention of parturient paresis. J. Dairy Sci. 62:1009.

18 Gnat, D. R., J. P. Marquardt, N. A. Jorgensen, and H. F. Deluca. 1977. Efficacy and safety of 1- hydroxyvitamin D 3 for prevention of parturient paresis. J. Dairy Sci. 60:1910.

19 Goings, R. L., N. L. Jacobson, D. C. Beitz, E. T. Littledike, and K. D. Wiggers. 1974. Prevention of parturient paresis by a prepartum calcium deficient diet. J. Dairy Sci. 57:1184.

20 Gregorovic, F., F. Skusek, F. Kesuar, and L. Beks. 1967. Crystalline vitamin D 3 for the prevention of milk fever in cattle. Vet. Rec. 79:161.

21 Hibbs, J. W., and H. R. Conrad. 1960. Studies of milk fever in dairy cows. VI. Effect of three prepartai dosage levels of vitamin D on milk fever incidence. J. Dairy Sci. 43:1124.

22 Hibbs, J. W., and H. R. Conrad. 1966. Calcium, phosphorus, and vitamin D. J. Dairy Sci. 49:243.

23 Hibbs J. W., and W. D. Pounden. 1955. Studies on milk fever in dairy cows. IV. Prevention by short- time, prepartum feeding of massive doses of vitamin D. J. Dairy Sei. 38:65.

24 Hurwitz, S., I. Cohen, A. Bar, and S. Bornstein. 1973. Sodium and chloride requirements of the chick: Relationship to acid-base balance. Poultry Sci. 52:903.

25 Jorgensen, N. A. 1974. Combating milk fever. J. Dairy Sci. 57:933.

26 Julien, W. E., H. R. Conrad, J. W. Hibbs, and W. L. Crist. 1977. Milk fever in dairy cows. VIII. Effect of injected vitamin D 3 and calcium and phosphorus intake on incidence. J. Dairy Sci. 60:431.

27 Little, W. L., and N. C. Wright. 1925. The aeti- ology of milk fever in cattle. Br. J. Exp. Pathol. 6:129.

28 Littledike, E. T., and R. L. Horst. 1982. Vitamin D~ toxicity in dairy cows. J. Dairy Sci. 65:749.

29 Lomba, F., G. Chauvaux, E. Teller, L. Lengels, and V. Bienfet. 1978. Calcium digestibility in cows as influenced by the excess of alkaline ions over stable acid ions in their diets. Br. J. Nutr. 39:425.

30 Manston, R. 1967. The influence of dietary cai- cium and phosphorus concentration on their absorption in the cow. J. Agric. Sci. 68:263.


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31 Manston, R., and J. M. Payne. 1964. Mineral imbalance in pregnant "milk-fever-prone" cows and the value and possible toxic effects of treatment with vitamin D 3 and dihydrotachysterol. Br. Vet. J. 120:167.

32 National Research Council. 1978. Nutrient requirements of dairy cattle. No. 3. Nutrient requirements of domestic animals. Nail. Acad. Sci., Washington, DC.

33 Newell, G. K., and R. E. Beauchene. 1975. Effect of dietary calcium level, acid stress, and age on renal, serum, and bone responses of rats. J. Nutr. 105:1039.

34 Olson, W. H., N. A. Jorgensen, A. N. Bringe, L. H. Schultz, and H. F. Deluca. 1974. 25-Hydroxy- cholecalciferal (25-OHD~). I. Treatment for parturient paresis. J. Dairy Sci. 56:885.

35 Payne, J. M. 1964. Recent advances in our knowl-

edge of milk fever. Vet. Rec. 76:1275. 36 Payne, J. M., and R. Manston. 1967. The safety of

massive doses of vitamin D~ in the prevention of milk fever. Vet. Rec. 79:215.

37 Sauveur, B., and P. Mongin. 1978. Interrelationships between dietary concentrations of sodium, potassium and chloride in laying hens. Br. Poult. Sci. 19:475.

38 Scott, C. H. 1968. Dietary influence on the incidence of parturient paresis. Fed. Proc. 27:156.

39 Tepper, T., and L. DeVos. 1975. An automated determination of free plasma h);droxyproline. Clin. Chim. Acta 59:373.

40 Valdivia, R., C. B. Ammerman, P. R. Henry, J. P. Feaster, and C. J. Wilcox. 1982. Effects of dietary aluminum and phosphorus on performance, phosphorus utilization and tissue mineral composition in sheep. J. Anita. Sci. 55:402.


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Manipulating Dietary Anions and Cations for Prepartum Dairy Cows to Reduce Incidence of Milk Fever

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