Dietary Cation-Anion Balance in Dairy Cow Nutrition

Elliot Block

Dept. of Animal Science Macdonald Campus, McGill University,
Ste. Anne de Bellevue, QC, H9X 3V0, Canada

Dietary cation-anion difference (DCAD) is a relatively new topic in dairy cattle nutrition and is making its way into many ration formulations as another specification, just as degradable protein has. The value of DCAD is easy to calculate as only two cations (sodium Na+ and potassium, K+) and two anions (chloride, Cl - and sulfate, SO4- are used. The equation is milliequivalents (Na+ and K+) - (Cl-+ SO4=) per kilogram of dry matter. For those who like a more simplified equation and forgot how to calculate milliequivalents (like myself), the following equation will take care of all decimal places and includes the atomic weights of the minerals:

DCAD meq/kg = 10,000 × + - + ×2.

Therefore, one can calculate a DCAD for any feed ingredient, concentrate, supplement, or total ration by knowing the percentages of the four minerals used in the equation.

Why do we bother to calculate DCAD and what does it mean to the animal? The direct answer is apparently quite simple. These four minerals are intricately involved in the acid base status of the animal; not rumen acids and bases, but systemic (blood) acids and bases. Sodium and K+ are thought to be alkalogenic in that their metabolism and excretion leads to an elevation of blood buffering capacity via bicarbonate retention (HCO3-) and an increase of blood pH (acid). Metabolism of Cl-and S= lead to a decrease of blood buffering capacity (lower HCO3-) and a reduced blood pH; therefore, Cl-and S= are considered to be acidogenic. A high DCAD would, therefore, indicate that a feed or diet will promote a high blood buffering capacity and a low DCAD would promote a reduced blood buffering capacity. In the extreme case of a negative DCAD (Na + K) is less that (Cl + S=) a mild acidosis can occur in the blood. The specific effects of DCAD on organs such as kidney, liver and bone and on enzyme and hormone functions appear to all be related back to this effect on acid-base status.

How can we use DCAD to manipulate or control the acid-base status of cows to improve production performance and health status? Erdman et al. (7) demonstrated that the indices of acid-base status in cows tend toward alkalinity with increasing time postpartum. Blood pH, HC03, and partial pressure of CO2 (pCO2) increase with days in milk. This indicates that cows in early lactation or high producers tend to be acidotic and require a high DCAD. However, the literature is devoid of any associations between whole animal acid-base status and productivity.

Figure 1. The Na+ - K+ ATP-dependent pump mechanism in the entry of glucose to cells.

Erdman (6), in a review of buffer requirements of dairy cows, made a good case for alterations in blood pH, HCO3, and pCO2 caused by environmental temperature. However, changes in these parameters caused by diet have not been investigated. Erdman (6) also pointed out that, although NaHCO3 tends to increase blood pH, HCO3-, and pCO2 when these values are depressed by high environmental temperatures (heat stress), whether the response is due to NaHCO3 or to Na+ alone is uncertain. Schneider et al. (29) suggested that production and intake responses to NaHCO3when cows are heat-stressed are due to increased dietary Na+ and not due to a need for HCO3-. In the same review, Erdman (6) cited literature showing that responses of cows appear to be more consistent with added dietary Na+ in the form of NaHCO3 that as NaCl leading the reader to assume that the added HCO3- from NaHCO3 has some specific role. Using the previous discussion on DCAD, however, one cannot yet conclude a specific role for HC03- as implied by Erdman (6). When calculating DCAD, added NaHCO3 would lead to a more positive number than would NaCl because HCO3- is not in the equation. Therefore, NaHCO3 would be more alkalogenic that would NaCl ever at equivalent inclusion rates of Na+ from both sources.

This theory is further illustrated from literature data when NaHCO3 was included in diets and DCAD was calculated. It is well documented (23) that NaHCO3 added to rations for dairy cows with low concentrations of fat in their milk will partially correct milk fat levels when the low concentration of milk fat is due to low forage-to-concentrate ratios in the diet. The response in this case probably is due to a specific buffering effect by NaHCO3 in the rumen and replacing NaHCO3 lost because of low salivary flow rates. The effects of added NaHCO3 to rations that do not create a depression in milk fat is less clear, and the reason for the lack of clarity may be in the DCAD of the ration. For example, Kilmer et al. (19) added NaHCO3 to rations that did not depress milk fat and found little or no response of cows over the duration of the trial. However, the control and buffered rations contained an equivalent DCAD (220 and 270 meq kg-1 of ration DM, respectively) when calculated as milliequivalents (Na+ + K+ - Cl-). The equivalent DCAD were because the Na+ of NaHCO3 replaced the Na+ from NaCl in the buffered ration. Conversely, St. Laurent and Block (30) found more responses to NaHCO3 when NaHCO3 was added in addition to the basal level of NaCl in the control ration, thus increasing the DCAD in the buffered ration.

Unfortunately, few other cases are reported for which any recommendations can be made on optimal DCAD for lactating dairy cows because of inadequate data. It appears logical, however, to keep the DCAD highly positive (cationic) for lactating cows because these cows have a high metabolic rate and because the cellular environment tends to be acidotic. Keeping the balance highly positive would necessitate higher dietary Na+ and K+ relative to Cl-, thus counteracting the acidotic condition with the alkalogenic effects of Na+ and K+. Support for this hypothesis was given by Tucker et al. (34). Those authors used cows from 3 to 8 mo. postpartum and demonstrated that cows fed a positive DCAD of +200 meq kg-1 (calculated as meq Na + K-Cl) produced more milk that cows fed a DCAD of -100 meq kg-1. Additionally, blood pH and HCO3and urinary pH increased linearly with DCAD. Similar results were reported by West et al. (37). The ideal DCAD for lactating cows would, however, change as lactation progresses and milk production decreases (i.e., metabolic activity declines). Theoretically, the DCAD should be high at the beginning of lactation and decrease progressively throughout the lactation, which may explain why buffers such as NaHCO3 have little effect on cows that are beyond 100 DIM when receiving a ration that does not depress milk fat (23). Support for this hypothesis what shown by Delaquis and Block (3). Cows in early and mid-lactation responded to a positive DCAD with higher milk yield but not cows in late lactation. Cows fed the positive DCAD also excreted more HCO-3 in urine at all stages of lactation.

The theory above explains much about some of the anecdotal and scientific information related to NaHCO3. Not always, but most of the time, cows fed rations based on legume forages do not respond to added NaHCO3 while cows fed rations containing grasses or corn silage do respond to NaHCO3. The reason might be that legume forages have a high DCAD (Table 1) due to their high Na and K content while grasses and corn silage have lower DCAD's ; the extra Na+ from NaHCO3 helps high producing cows fight acidosis when fed grasses or corn silage.

Table 1. Calculated dietary cation-anion balance (DCAD) of individual feedstuffs.1
% of DM
Feed Na + K+ Cl- S= DCAD2
Alfalfa hay (late vegetative) .15 2.56 .34 .31 +431.1
Timothy hay (late vegetative) .09 1.6 .37 .18 +232.0
Corn silage .01 .96 -- .15 +156.4
Corn grain .03 .37 .05 .12 +18.8
Oats .08 .44 .11 .23 -26.95
Barley .03 .47 .18 .17 -23.4
Distillers' grain .10 .18 .08 .46 -219.38
Soybean meal .03 1.98 .08 .37 +266.37
Fish meal .85 .91 .55 .84 -75.6

1 From NRC (24) for Na+, K+, Cl- and S=.

2 Calculated as milliequivalents of (Na+ + K+) - (Cl- + S=) kg -1 of DM.

West et al. (36) demonstrated that increasing DCAD increased dry matter intake in heat-stressed cows. They hypothesized that the increase in blood buffering capacity with higher DCAD was responsible for the increase in dry matter intake. The increases in blood buffering capacity and dry matter have also been reported for cows that were not heat-stressed (2, 37). Although elevated blood buffering may be part of the reason for increased dry matter intake with increased DCAD, water intake also must increase with increases in dry matter intake, milk production, or both. Delaquis (2) showed that there were increases in water intake, water absorption, and urine volume with elevated DCAD and no significant alterations to glomerular filtration rate or effective renal plasma flow.

Figure 2. Role of Na+ in mobilization of H+ in proximal tubules (a), secretion of H+ in distal tubules (b), and ammonia production in distal tubules (c) (c.a. = carbonic anhydrase).

Figure 3. Reaction of erythrocyte in tissue and lung, and plasma changes in respiration, in relation to Na+, K+, Cl; and the chloride shift.

More work has been generated on the role of DCAD for prepartum cows for the prevention of milk fever. Basically, milk fever occurs at the initiation of lactation when Ca2+ is drained from blood for colostrum synthesis and is not replaced rapidly enough from intestinal absorption, bone mobilization (resorption), and reabsorption in the kidney, resulting in paresis tentany of muscles and, if untreated, death of the animal.

Prevention of Milk Fever

Prevention is the most desirable means of reducing the economic losses occurring from milk fever. These losses include loss of milk, veterinary costs, labor costs, and possible loss of the cow (1). Because of the importance of Ca metabolism in the etiology of milk fever, preventive approaches have been focussed in this direction. Dietary manipulations and injections of vitamin D3 and it metabolites have been reported as possible methods for reducing the incidence of the disease.

Oral and intramuscular doses of vitamin D3 have prevented milk fever successfully (11, 16, 17). However, repeated treatments necessitated by inaccurate prediction of date of parturition may lead to toxicity (22). The metabolites of vitamin D3 (hormones) are more active in metabolism of Ca and have been used successfully to prevent the disease (8, 27, 28). However, the active metabolite, 1,25 dihydroxyvitamin D (1,25(OH)2D3) was reported to be higher in the blood of cows with milk fever (12 ,14, 18). Therefore, Horst and Reinhardt (13) hypothesized that cows with milk fever have a reduced sensitivity (via interference or low receptors for the hormone) to 1,25(OH)2D3.

Parathyroid hormone (PTH) is involved in Ca homeostasis, however, PTH also is higher in blood of cows with milk fever (12). Therefore, the direct cause of milk fever does not lie in hormone production, but somehow in the activity of the hormones on their target issues (bone, intestine, and kidney) to keep Ca constant in the blood at calving. Might the activity of hormones be affected by the acid-base status within the target cells?

Manipulation of DCAD has also been shown to prevent milk fever in dairy cows. Dishington (4) successfully prevented milk fever in 92% of cases when prepartum dairy cows were fed rations with a negative DCAD (calculated as milliequivalents (Na+ + K+)- (Cl- + S-)] and a high Ca content. A better response to the diet occurred when dietary concentration of Ca was high (5). Block (1) showed a 47% incidence of milk fever when prepartum cows were fed a ration with DCAD [calculated as milliequivalents (Na+ + K+) - (Cl- + S-)] of +330.5 meq kg-1 DM. Oetzel et al. (26) also showed a reduction in the incidence of milk fever, regardless of dietary Ca, when a DCAD of -75 meq kg-1 of DM was fed compared to a DCAD of +189 meq kg-1 of DM in prepartum diets. Sulfur was included by these workers because of the acidifying effect of SO4 in biological fluids as demonstrated by (38).

Block (1) and Goff et al. (10) found that the concentration of plasma Ca was higher in cows fed the negative DCAD during the periparturient period, and Oetzel et al. (26) found that plasma ionized Ca was higher at calving when DCAD was negative. This result was also reported in a kinetic study with sheep (33). Digestibility of Ca was not determined in the trial by Block (1). However, he found that the maintenance of blood Ca in cows fed the negative DCAD was partly a result of an increase in bone mobilization, as indicated by hydroxyproline.

Leclerc and Block (20) fed four different rations to prepartum cows with DCAD [milliequivalents (Na+ + K+) - (Cl- + S=)] of 400, 200, 100 and 50 meq kg-1 of DM and found that the correlation between DCAD and concentration of plasma Ca was -.51 from d 2 prepartum to d 1 postpartum (Table 2). In other words, as DCAD was reduced, concentration of plasma Ca increased regardless of paresis. The reason for the higher blood Ca in the trial by Leclerc and Block (20) was a result of higher bone mobilization, indicated by hydroxyproline, as dietary DCAD was reduced.

Table 2. Correlation between the concentration of plasma calcium and dietary anion-cation difference during the periparturient period of dairy cows (n=20).1
Time (h) Coefficient of correlation P > F
48 -.471 .048
36 -.379 .121
24 -.334 .162
12 -.463 .046
Parturition -.548 .015
Post partum
12 -.590 .013
24 -.287 .248
36 -.455 .058

1 Leclerc and Block (36).

In feeding trials with sheep, Takagi and Block (31) showed that, as DCAD was reduced, apparent digestibility of Ca did not change, but retention of Ca was reduced by an increase in urinary excretion. In a subsequent trial, those researchers fed rations to sheep with progressively lower DCAD and infused EDTA to deplete Ca from blood (32). The results indicated that sheep fed the lower DCAD were more resistant to depletion of blood Ca. Although not measured, we hypothesized that at the lower DCAD the bone was in a state of mobilization, thereby preventing a sharp decline in plasma Ca upon infusion of EDTA.

Gaynor et al. (9) found results similar to those of Block (1). They (9) fed Jersey cows diets containing high Ca concentrations prepartum (>1.0% Ca) with three different DCAD, calculated as milliequivalents (Na+ + K+) - (Cl-), at 22.0 (anionic), 59.9 (intermediate) and 125.8 (cationic) meq 100g-1 of DM. It is interesting to note that these DCAD are equivalent to those of Block (1) if SO2-4 , were removed from the equation (22.1 and 50 meq 100 g-1 of DM for the anionic and cationic diets of Block (1), respectively). Gaynor et al. (9) found that their anionic diet produced the fewest cases of milk fever and produced higher urinary excretions of Ca and Mg. Those workers also measured 1,25 (OH)2D3 in blood and found that cows fed the anionic diet had elevated concentrations of the vitamin at three days prepartum. As an explanation, they cited research using rats and dogs showing that tissues are refractory to PTH during metabolic alkalosis (i.e., cationic DCAD), thereby reducing 1,25 (OH)2D3 production. Goff et al. (10) showed that a reduction in DCAD increased the production of 1,25(OH2)D3 per unit of PTH and thus reversed tissue resistance to PTH that develops at the end of pregnancy and onset of lactation.

Therefore, negative DCAD in rations for prepartum cows prevents a decline in blood Ca at the initiation of lactation by one or more of the following mechanisms: increasing the rate of bone mobilization of Ca directly; increasing the rate of bone mobilization of Da indirectly via increased excretion (reduced retention) of Ca; or increasing intestinal absorption of Ca. Regardless of how this occurs, excretion of endogenous Ca must follow because plasma concentration of Ca is maintained within the range of 10 + 2 mg dl-1 unless a disorder such as milk fever occurs. The question that arises is whether a metabolic basis exists for the described mechanisms to increase the entry of Ca to the blood by altering DCAD.

It is important to emphasize that for the trials in which negative DCAD aided in prevention of milk fever (1, 9, 10, 26), dietary concentrations of Ca were high (1.5% Ca). Negative DCAD increases urinary excretion of Ca (2,32, 33, 35), therefore, if dietary Ca were low with a negative DCAD, hypocalcemia may occur, regardless of and separately from milk fever. Conversely, high dietary Ca with low DCAD may be necessary for this method to be successful. However, the optimal dietary Ca content has not been established.

Dietary Cation-Anion Balances of Feeds and Its


As stated, DCAD is usually positive or highly cationic. Table 1 was developed using standard North American values (24). The table demonstrates that all typical forage sources are cationic and that alfalfa hay is the most cationic, which almost precludes the use of alfalfa as a prepartum feed because the cationic nature of the feed predisposes cows to milk fever. The amounts of Cl - or SO42 salts, devoid of Na+ or K+, to decrease DCAD of alfalfa becomes impractical because of the low palatability of anionic salts (25). Obviously, timothy forage is a more likely choice for these prepartum cows. The possibility exists, therefore, that grasses fed prepartum will decrease the incidence of milk fever because of their lower DCAD and not because of their lower Ca content compared with legumes.

From Table 1, we can conclude that DCAD for typical grains (corn, barley, oats) is approximately zero for practical purposes (range of -27 to +19 meq kg-1 of DM). The protein sources in Table 1 indicate that DCAD is negative except for soybean meal, primarily because of the S content of these feedstuffs. Interestingly, fish meal has a less negative DCAD than other protein sources in spite of its high concentration of S, because of its equally high content of Na.

For high producing cows in early lactation, it is difficult to presume an ideal DCAD. Assuming that most grains have a DCAD around 0 meq kg-1 of DM, a ration of 50% alfalfa, 50% grain would have a DCAD of approximately 200 to 300 meq kg-1 of DM (possibly lower, depending on protein supplementation). For lower producing cows in mid-lactation, the diet probably would contain more grass forage and less legume for a DCAD of 100 to 200 meq kg-1 of DM. Considering that some cows fed alfalfa-corn diets that do not depress milk fat show a response to NaHCO3 in early but not late lactation, we must presume that DCAD should be > 200 meq kg-1of DM at high milk production and can be <200 at lower production. Furthermore, during the dry period, DCAD should be negative, and probably a minimum negativity of -75 meq kg-1 is necessary.

Creating more positive DCAD is no problem with the plethora of Na and K salts in the form of carbonates. Theoretically, Na and K should be equal on an equivalent basis, but this has yet to be proven. Creating more negative DCAD with Cl or SO4 salts (without Na or K) has been tested by Oetzel et al. (25). Six anionic salts [MgCl2, MgSO4, CaCl2, CaSO4, NH4Cl, (NH4)2SO4], when included in diets to obtain the same negative DCAD, produced the same effects (compensated metabolic acidosis, decreased blood HCO3, urinary pH and urinary base excess, and increased fractional excretion of urinary Ca) (25). Therefore, DCAD seems more important than the specific salt used. Those authors (25) caution that mixtures of salts would be best to avoid toxicity or induced deficiencies of minerals (Mg and NH4 being of greatest concern).


Much more research is needed before specific recommendations can be made regarding optimal DCAD in rations for dairy cows. Based on the discussion, if some biological functions can be manipulated by altering ion balance, then certainly others can follow suit. However, optimal DCAD will not be the same for all productive functions.

Indications exist in the literature for a relationship of cationic DCAD and calf performance (15) and for anionic DCAD and prevention of udder edema (21) and alleviation of heat stress (36). Other production diseases that are associated with acid-base balance or buffering capacity of blood include laminitis and ketoacidosis. Investigations should be directed toward the relationship of these diseases with DCAD.

Some biological functions will respond better when the balance is positive, but others will do so when the balance is negative. The combined efforts of researchers in basic and applied sciences in more fully describing rations fed to animals in experimental trails with regard to mineral content will increase our knowledge in this obscure are of nutrition.


  1. Block, E. 1984. Manipulating dietary anions and cations for prepartum cows to reduce incidence of milk fever. J. Dairy Sci 67:2939.
  2. Delaquis, A.M. 1992. The effects of dietary cation-anion balance, stage of lactation and ration ingredients on acid base metabolism and productivity of dairy cows. Ph.D. Diss. Fac. Graduate Stud. Res., McGill Univ., Montreal, PQ, Canada.
  3. Delaquis, A. and E. Block. 1991. Cation-anion balance, milk production, and acid base status in dairy cows. J. Dairy Sci. 74(1):310.(Abstr.)
  4. Dishington, I.W. 1975. Prevention of milk fever by dietary salt supplements. Acta Vet. Scand. 16:503.
  5. Ender, F., I.W. Dishington, and A. Helgebostad. 1971. Calcium balance studies in dairy cows under experimental induction and prevention of hypocalcaemic paresis puerperalis. A. Tierphysiol. Tierernahr., Futtermittelkd. 28:233.
  6. Erdman, R.A. 1988. Dietary buffering requirements of the lactating dairy cow: a review. J. Dairy Sci. 71:3246.
  7. Erdman, R.A., R.W. Hemken and L.S. Bull. 1982. Dietary sodium bicarbonate and magnesium oxide for early postpartum lactating dairy cows: effects on production, acid-base metabolism and digestion. J. Dairy Sciu. 65:712.
  8. Gast, D.R., J.P. Marquardt, N.A. Jorgensen and H.F. DeLuca. 1979. Potential use of 1,25 dihydroxycholecalciferol for prevention of parturient paresis. J. Dairy Sci. 62:1009.
  9. Gaynor, P.J., F.J. Mueller, J.K. Miller, N. Ramsey, J.P. Goff and R.L. Horst. 1989. Parturient hypocalcemia in Jersey cows fed alfalfa haylage-based diets with different cation to anion rations. J. Dairy Sci. 72:2525
  10. Goff, J.P., R.L. Horst, F.J. Mueller, J.K. Miller, G.A. Kiess and H.H. Dowlen. 1991. Addition of chloride to prepartal diets high in cations increases 1,25-dihydrozy vitamin D. Response to hypocalcemia preventing milk fever. J. Dairy Sci. 74:3863.
  11. Hibbs, J.W. and H.R. Conrad. 1960. Studies of milk fever in dairy cows. VI. Effect of three prepartal dosage levels of vitamin D on milk fever incidence. J. Dairy Sci. 43:1124.
  12. Horst, R.L., N.A. Jorgensen and H.F. DeLuca. 1978. Plasma 1,25-dihydroxyvitamin D. And parathyroid hormone levels in paretic dairy cows. Am. J. Physiol. 235:E634.
  13. Horst, R.L. and T.A. Reinhardt. 1983. Vitamin D. Metabolism in runinants and its relevance to the periparturient cow. J. Dairy Sci. 66:661.
  14. Horst, R.L., R.M. Shepard, N.A. Jorgensen, and H.F. DeLuca. 1979. The determination of vitamin D. Metabolites on a single plasma sample: changes during parturition of dairy cows. Arch. Biochem. Biophys. 192:512.
  15. Jackson, J.A., D.M. Hopkins, Z. Xin and R.W. Hemken. 1992. Influence of cation-anion balance on feed intake, body weight gain, and humoral responses of dairy calves. J. Dairy Sci. 75:1281.
  16. Jorgensen, N.A. 1974. Combatting milk fever. J. Dairy Sci. 57:933.
  17. Julien, W.E., H.R. Conrad, J.W. Hibbs and W.L. Crist. 1976. Milk fever in dairy cows. VIII. Effect of injected vitamin D3 and calciumand phosphorus intake on incidence. J. Dairy Sci. 60:431.
  18. Kichura, T.S., R.L. Horst, D.C. Beitz and E.T. Littledike. 1982. Relationships between prepartal dietary calcium and phosphorus, vitamin D. Metabolism, and parturient paresis in diary cows. J. Nutr. 112:480.
  19. Kilmer, L.H. L.D. Muller and T.J. Snyder. 1981. Addition of sodium bicarbonate to rations of postpartum dairy cows: physiological and metabolic effects. J. Dairy Sci. 64:2357.
  20. Leclerc, H. and E. Block. 1989. Effects of reducing dietary cation-anion balance for prepartum dairy cows with specific reference to hypocalcemic parturient paresis. Can. J. Anim. Sci. 69:411.
  21. Lema, M., W.B. Tucker, M. Aslam, I.S. Shim, P. LeRuvet and G.D. Adams. 1992. Influence of calcium chloride fed prepartum on severity of edema and lactational performance of dairy heifers. J. Dairy Sci. 75:2388.
  22. Littledike, E.T. and R.L. Horst. 1982. Vitamin D3 toxicity in diary cows. J. Dairy Sci. 65:748.
  23. Muller, L.D. and L.H. Kilmer. 1979. Page 35 in Sodium Bicarbonate in Dairy Nutrition. Natl. Feed Ingred. Assoc. West Des Moines, IA>
  24. National Research Council. 1988. Nutrient Requirements of Dairy Cattle. 6th rev. ed, Nat. Acad. Press, Washington, D.C.
  25. Oetzel, G.R., M.J. Fettman, D.W. Hamar and J.D. Olson. 1991. Screening of anionic salts for palatability, effects on acid-base status, and urinary calcium excretion in dairy cows. J. Dairy Sci. 74:965.
  26. Oetzel, G.R., J.D. Olson, C.R. Curtis and M.J. Fettman. 1988. Ammonium chloride and annomium sulfate for prevention of parturient paresis in dairy cows. J. Dairy Sci. 71:3302.
  27. Olson, W.H., N.A. Jorgenson, A.N. Bringe, L.H. Schultz and H.F. DeLuca. 1974. 25-Hydroxycholecalciferol 25-OHD3. I. Treatment for parturient paresis. J. Dairy Sci. 56:885.
  28. Reinhardt, T.A. and H.R. Conrad. 1980. Mode of action of pharmacological doses of cholecalciferol during parturient hypocalcemia in diary cows. J. Nutr. 110:589.
  29. Schneider, P.L., D.K. Beede and C.J. Wilcox. 1986. Response of lactating cows to dietary sodium source and quantity and potassium quantity during heat stress. J. Dairy Sci. 69:99.
  30. St. Laurent, A.M. and E. Block. 1985. Effects of sodium bicarbonate additions to conventional diets for lactating dairy cows. Res. Rep. 10-16. Dep. Anim. Sci., Macdonald College of McGill Univ., Ste. Anne de Bellevue, PQ, Canada
  31. Takagi H. and E. Block. 1991. Effects of manipulating dietary cation-anion balances in sheep. J. Dairy Sci. 74:4202
  32. Takagi, H. and E. Block. 1991. Effects of various dietary cation-anion balances on response to experimentally induced hypocalcemia in sheep. J. Dairy Sci. 74:4215.
  33. Takagi, H. and E. Block. 1991. Effects of reducing dietary cation-anion balance on calcium kinetics in sheep. J. Dairy Sci. 74:4225.
  34. Tucker, W.B., G.A. Harrison and R.W. Hemken. 1988. Influence of dietary cation-anion balance on milk, blood, urine and rumen fluid in lacttion dairy cows. J. Dairy Sci. 71:346.
  35. Wang, C. and D.K. Beede. 1992 Effects of ammonium chloride and sulfate on acid-base status and calcium metabolism of dry Jersey cows. J. Dairy Sci. 75:820.
  36. West, J.W., K.D. Haydon, B.G. Mullinix and T.G. Sandifer. 1992. Dietary cation-anion balance and cation source effects on production and acid-base status of heat-stressed cows. J. Dairy Sci. 75:2776.
  37. West, J.W., B.G. Mullinix and T.G. Sandifer. 1991. Changing dietary electrolyte balance for dairy cows in cool and hot environments. J. Dairy Sci. 74:1662.
  38. Whiting, S.J. and H.H. Draper. 1981. Effection of chronic acid load as sulfate or sulfur amino acids on bone metabolism in adult rats. J. Nutr. 111:1721.