The dietary cation-anion difference (DCAD) of a feed can be used to characterize large animal diets. DCAD (also known as DCAB or dietary cation-anion balance) of the diet is a major determinant of blood SID as the strong ions enter the blood from the digestive tract (Riond 2000). DCAD is the difference between the strong base cations and strong acid anions:
DCAD = (Na+ + K+ + Ca2+ + Mg2+) – (Cl–+ SO42- + H2PO4-) mEq/kg DM
(Kronfeld 2001, Graham-Thiers et al. 1999)
DCAD affects systemic acid-base balance because it defines the overall net cation to anion content of the feed. The chemical components of the diet affecting acid-base status include the amount of protein, Cl-, P-, Na+, K+, Ca2+, and Mg2+. The ions present in diet only alter [SID]p if they are absorbed into the blood. Kronfeld (2001) allows for an assumption of a 100% absorption rate for monovalent ions and 50% for divalent ions. A common equation currently used is:
DCAD = (Na+ + K+) – Cl- mEq/
This DCAD equation takes into account the most readily absorbed ions with the greatest metabolic impact on acid-base balance (Baker 1991, 1998). It includes only monovalent dietary electrolytes, except for sulfur, and ions with a higher valence are ignored. Some studies include SO42- in the equation (Baker et al. 1998; Cooper et al 1998; Popplewell et al. 1993), however the contents of Ca2+, Mg2+ and SO42- in feed act to neutralize each other and have a variable and incomplete intestinal absorption (Spears et al. 1985). Baker and colleagues (1998) found that if SO42- was to be included in the DCAD equation it would need a modifying coefficient as it is not as acidogenic as Cl-. They also confirmed that Na+ and K+ have similar alkalogenic properties. H2PO4- is also left out of the equation, as it is a weak acid and exists in feed in low concentrations.
A neutral DCAD, which doesn’t result in changes in acid-base status, can be between 250-300 mEq/kg of feed dry matter (DM) (Lindinger 2003). A DCAD of greater than 300 mEq/kg may result in an increased cation content of extracellular fluids, creating a systemic alkalosis, which increases the plasma pH and the concentrations of plasma Na+, HCO3-, PCO2 and Ca2+ balance, and decreases the [Cl-] (Baker 1993; Popplewell 1993). A DCAD of less than 250 mEq/kg may result in a metabolic acidosis, decreasing plasma pH, and the concentrations of plasma Na+, K+, Mg2+, HCO3-, PCO2 and increasing Cl-; as well as increasing the urinary excretion of K+, Na+ Cl- and Ca2+ (Topliff 1989, Baker et al. 1992, 1993, 1998; Mueller 1999, McKenzie 2002, 2003, Topliff 1989). Plasma pH and [HCO3-], and urine pH have been shown to increase in proportion to DCAD over a range of 0 to 407 mEq/Kg (Baker et al. 1992, 1998; Topliff et al. 1989).
When a high DCAD feed is consumed the high cationic and low anionic components result in increased cation content of extracellular fluids through absorption in the small intestine. With the continuation of a high DCAD diet the cations are accompanied by HCO3- and Cl-, which can produce a mild systemic alkalosis (Lindinger 2003). Depending on diet composition, the blood bicarbonate level can be regulated in the intestine by increasing or decreasing the amount of alkali from pancreatic secretion. The liver and other metabolically active tissues then use the products of pancreatic secretion as substrates for generating acids or alkalis. Excess cations are excreted from the kidneys. Some H+ are also lost in feces.
McKenzie (2002, 2003) found that a high DCAD diet resulted in higher [Pi]p and lower [K+]p compared to a neutral diet, but that [Na+]p, [ Cl-]p and [Mg2+]p did not differ between horses consuming the neutral and high DCAD diets. Popplewell et al (1993) found that horses on a high DCAD diet had faster times in a standard anaerobic test (1.64 km) compared to those on a lower DCAD diet. Graham-Thiers et al. (2001) also found that horses on the higher DCAD diets were faster than those on a low DCAD diet (20 mEq/kg DM) and found no difference between the medium and high DCAD diets (125 – 350 mEq/kg). Although there is no consensus on whether a high DCAD diet will enhance performance in horses, the expectation is that it will help to offset or delay the acidic component of fatigue (Graham-Thiers et al. 2001).
A low DCAD diet produces a systemic acidosis which may lead to a negative calcium balance from increased Ca2+ loss through the urine due to and an overall weakening of the skeletal system (Wall et al.1992, Fressetto et al. 2001, Sebastian et al.1994, Baker et al.1998). However, Cooper and colleagues (2000) found that weanling horses consuming highly anionic diets were able to make up for an increased urinary excretion of Ca2+, and growth performance was not affected by DCAD. More research is needed to look into the effect of DCAD and Ca2+ with respect to growth and performance specifically to horses.
Grains have low cation content (Na+ + K+ + Ca2+) and high anion content (Cl-), which results in a low DCAD, while forages generally have higher levels of cations with an increased DCAD. The NRC (1989) rated corn with a DCAD at about 58 mEq/kg dry matter (DM) and oats at 73 mEq/kg DM, as compared to alfalfa at 323 mEq/kg DM and Bermuda grass hay at 427 mEq/kg DM. Dietary protein and fat have also been found to affect acid-base status, however, with fat, a change is exhibited only during exercise.
Originally it was thought that the metabolic acidosis following ingestion of a high grain meal was due to lactic acid production from the digestion of starch (Ralston 1993). DCAD was not considered. The current thinking, however, is that the acidosis is due to the low levels of cations typically found in cereal grains contributing to a low DCAD (1999 Mueller). Mueller (1999) found no significant differences in plasma pH between both starch sources and starch intake.
When grains are fed in high concentration they tend to cause a metabolic acidosis (Roby et al. 1987; Abu Damir et al. 1990; Ralston 1994). Many foals and performance horses are fed a high grain ration, which contains a low DCAD (<100 mEq/L), consisting of equal to or greater than 50% of their total intake. A chronic metabolic acidosis may increase the incidence of developmental orthopedic diseases, including stress fractures in athletic horses from a decreased bone mineral content. For example, Jones (1989) found that 58.1% of 2-yr old racehorses experienced an injury. Similarly, Fressetto et al. (2001) found that a high DCAD diet, often with a deficiency of K+, caused growth retardation in children and decreased muscle and bone mass in adults. In these cases, it may be the DCAD and not the actual food source that is responsible for acid-base changes. Hence a systemic acidosis could be corrected by increasing the DCAD in a high starch diet (Mueller 2001).
A diet consisting of only forage ration seems to have a lesser immediate effect on acid-base balance when compared to eating grain rations. Ralston (1993) fed hay only and found its digestion had minimal effects on plasma pH during the first hour of feeding. However, they did not extend the testing time out to when more effects from feeding hay would have been seen. Kerr and Snow (1992) found no change in PCV, [PP] or [K+] after a morning feed of 1.8 kg of a commercial cube diet (composed of high fiber, low starch, no cereal grain). It was not until following a second feed of the same diet at noon and during a feeding of 2.7 kg cubes with 5.5 kg of hay at 1700 hr that there was an increase in both the PCV and [PP] and a decrease in [K+]p.
Stutz and colleagues (1992) fed a ratio of 60% concentrate: 40% Bermuda grass hay with four diets of different DCAD measurements and took hourly jugular venous blood samples for 17h. Horses were fed at t=0 h and 12h. All diets exhibited a maximal decrease in pH and increased PCO2 at 1h post feed, with a return to baseline values over the following 12h. The plasma [HCO3-] decreased for the first 3-h following feeding and then also returned to baseline values over the next 5-9 h.
Ralston (1993) compared two meals of differing grain: forage ratios that were controlled for DCAD, protein and caloric content. The first was at 60% grain: 40% forage, and the second was with 10% grain: 90% forage. A decrease in pH was seen consistently at 30-60 min after a meal of grain. However, the drop was fairly minimal, and though statistically significant it was perhaps not physiologically significant. pH remained depressed for up to 2-3 h if no other feed was available and was reflected in a decrease in urine pH 3-4 hours later. Fecal pH was lower in horses fed 50% grain versus those fed hay only. Their conclusion was that the amount of starch in the diet, and not the DCAD, which caused the different acid-base responses following ingestion.
However, to illustrate that the DCAD does cause acid-base changes, Mueller and colleagues (1999) used 3 high DCAD and 3 low DCAD diets, with starch comprising 45-49% of each diet. They found that high starch diets had no effect on plasma acid-base balance, regardless of source (corn, oats or alfalfa). They concluded that the acidogenic effects of a high starch source were overcome by increasing the DCAD of that feed source.
Ralston and colleagues (1997) manipulated the feed DCAD with the addition of 1% NaHCO3 to a 50:50 ratio grain and alfalfa diet. This reduced the decrease in the resultant post-feeding plasma pH and increased blood HCO3-. Baker et al. (1998) also found that feeding additional strong cations in bicarbonate or citrate form to increase the diet DCAD, increased urine and plasma pH and blood bicarbonate levels. Fressetto et al. (2001) also found that using small amounts of exogenous base, potassium bicarbonate (KHCO3), to neutralize the diet improved Ca2+ and K+ balances, reduced bone absorption rates and improved the nitrogen balance. Furthermore, Sebastian (1994) neutralized blood acid-base composition with KHCO3 added to the diet, and found significant improvements in health.
These studies show that although the amount of starch has an affect on acid-base balance through the DCAD of the feed, it is possible to minimize that effect by manipulating the DCAD. Although horses seem to be able to compensate for a high anionic diet, it is thought that a higher DCAD diet is more beneficial to the overall health of a horse.
The control of DCAD in feed, specifically to maintain high DCAD levels, is important to have the most advantageous diet for horses to allow horses to perform at their highest capabilities.
Some studies have found that dietary protein has an effect on plasma acid-base status of horses. Protein is acidogenic as it contains sulfur and phosphorus that oxidize to sulfate (SO42-) and phosphate (Pi), which become elevated in plasma. Graham-Thiers et al (1999, 2001) found that plasma SID and pH were higher and PCO2 was lower in horses that were fed less protein. However, the effects on acid-base balance may be due to the low DCAD of the high protein diet. Greppi et al (1996) found no differences in plasma biochemistry between feeding 3 different levels of protein over 27 days at 713g crude protein (CP) (7.4% of diet), 824g CP (8.2%), and 962g CP (9.8%). Graham-Thiers et al (1999, 2001) also used diets at 7.5% CP and 14.5% CP so perhaps Greppi et al (1996) did not sufficiently vary the amount of CP or it is the overall percentage of the CP in the diet that elicits a response. Although these studies suggest that a low protein diet may have an alkalizing acid-base response, those effects are so small that they are of questionable physiological significance.
There appears to be no influence of fat supplementation on acid-base status at rest (Graham-Thiers et al. 2001, Kronfeld 2001). However, with exercise it may spare protein during energy demanding states, for example, fat adaptation influenced acid-base responses to repeated sprints (Graham-Thiers et al. 2001). This effect is thought to be largely due to limiting the increase in PCO2 in venous blood (Kronfeld et al. 1998). With high fat diet supplementation (10% of diet intake), high intensity exercise fat adaptation increased plasma [Lac-] and decreased acidosis (Custalow et al. 1993; Taylor et al. 1993; Ferrante et al. 1994).
This article is an excerpt from A Summary of the Effects of Feeding and Daily Variation on Acid-Base Status in Resting Horses. The complete article is available for download and this portion is provided here to attempt to explain DCAB, which I think is important for all competitive riders to understand. Below is the reference list. If you have any updated information I would love you to send it to me!
(1989). NRC: Nutrient Requirements of Horses., 5 ed. National Academy Press, Washington, DC.
(2000). Effect of dietary cation-anion difference on mineral balance, serum osteocalcin concentration and growth in weanling horses. J Equine Vet Sci 20.
Abu Damir (1990). Anim Prod 51, 547.
Baker LA, Topliff DR, Freeman DW, & Breazile JE (1992). Effect of dietary cation-anion balance on acid-base status in horses. J.Equine Vet Sci 12, 160-163.
Baker LA, Wall DL, & Topliff DW (1993). Effect of dietary cation-anion balance on mineral balance in anaerobically exercised and sedentary horses. J Equine Vet Sci 13, 557-561.
Baker LA, Wall DL, Topliff DR, Freeman DW, Teeter RG, Breazile JE, & Wagner DG (1993). Effect of dietary cation-anion balance on mineral balance in anaerobically exercised and sedentary horses. Equine Nutrition and Physiology Society, 13th Symposium 13, 557-561.
Baker LA, Topliff DR, Freeman DW, Teeter RG, & Stoecker B (1997). The comparison of two forms of sodium and potassium and chloride versus sulfur in the dietary cation-anion difference equation: effects on acid-base status and mineral balance in sedentary horses. Equine Nutr and Physiol Society Annual Symposium 18, 389-395.
Baker LA, Topliff DR, & Freeman RG (1998). The comparison of two forms of sodium and potassium, and chloride versus sulfur in the dietary cation-anion difference equation: Effects on acid-base staus and mineral balance in sedentary horses. J Equine Vet Sci 18, 389-396.
Block, E. (1993). Manipulation of Dietary Cation-Anion Difference on Nutritionally Related Production Diseases, Productivity, and Metabolic Responses of Dairy Cows. J Dairy Sci 77, 1437-1450.
Cooper SR, Kline KH, Foreman JH, & Frey LP (1998). Effects of dietary cation-anion balance on pH, electrolytes, and lactate in Standardbred horses. J Equine Vet Sci 18, 662-666.
Custalow SE, Ferrante PL, Taylor LE, Moll HD, Meacham TN, Kronfeld DS, & Tiegs W (1993). Lactate and glucose responses to exercise in the horse are affected by training and dietary fat. 13th Equine Nutrition and Physiology Symposium Proceedings, U.Florida.
Dunnett, M., Harris, R. C., Dunnett, C. E., & Harris, P. A. (2002). Plasma carnosine concentration: diurnal variation and effects of age, exercise and muscle damage. Equine Vet J Suppl 283-287.
Ferrante PL, Kronfeld DS, Taylor LE, & Meacham TN (1994). Plasam [H+] responses to exercise in horses fed a high-fat diet and given sodium bicarbonate. J Nutr 124, 2736s-2737s.
Frassetto L, RC Morris Jr., DE Sellmeyer, K Todd, & A Sebastian (2001). Diet, evolution and aging. Eur J Nutr 40, 200-213.
Graham-Thiers PM, Kronfeld DS, & Kline KA. (1999). Dietary protein influences acid-base responses to repeated sprints. Equine Exercise Physiology 5. Equine Vet J Suppl 30, 463-467.
Graham-Thiers PM, Kronfeld DS, Kline KA, & Sklan DJ (2001). Dietary protein restriction and fat supplementation diminish the acidogenic effect of exercise during repeated sprints in horses. J Nutr 131, 1959-1964.
Greppi GF, Casini L, Gatta D, Orlandi M, & Pasquini M (1996). Daily fluctuations of haematology and blood chemistry in horses fed varying levels of protein. Equine Vet J 28, 350-353.
Jansson, A. & Dahlborn, K. (1999). Effects of feeding frequency and voluntary salt intake on fluid and electrolyte regulation in athletic horses. J Appl.Physiol 86, 1610-1616.
Jansson, A., Lindholm A, Lindberg JE, & Dahlborn, K. (1999). Effects of potassium intake on potassium, sodium and fluid balance in exercising horses. Equine Vet J Suppl 30, 412-417.
Jones WE (1989). Racetrack breakdown epidemiology. Equine Vet.Data 10, 190-191.
Kerr MG & Snow DH (1982). Alterations in haematocrit, plasma proteins and electrolytes in horses following the feeding of hay. Vetrinary Record 110, 538-540.
Kronfeld DS, Custalow SE, Ferrante PL, Taylor LE, Wilson JA, & Tiegs W (1998). Acid-base responses of fat adapted horses: relavence to hard work in the heat. Appl Anim Behav Sci 59, 61-72.
Kronfeld DS (2001). Body fluids and exercise: influences of nutrition and feeding management. Veterinary Review 21, 417-428.
Lindinger MI. Acid-Base physiology during exercise and in response to training. Equine Sports Medicine and Surgery. 2003 (In Press)
McKenzie, E. C., Valberg, S. J., Godden, S. M., Pagan, J. D., Carlson, G. P., MacLeay, J. M., & DeLaCorte, F. D. (2002). Plasma and urine electrolyte and mineral concentrations in Thoroughbred horses with recurrent exertional rhabdomyolysis after consumption of diets varying in cation-anion balance. Am.J Vet Res. 63, 1053-1060.
Mongin P (1981). Recent advances in dietary cation-anion balance: applications in poultry. Proc Nutr Soc 40, 285-294.
Mueller, R. K., Topliff DR, Freeman DW, MacAllister C, Carter SD, & Cooper SR. Effect of varying DCAD on the acid-base status of mature sedentary horses with varying starch source and level of intake. Animal Science Research Report. 1999. Oklahoma State University, USA. Ref Type: Report
Mueller, R. K., S.R.Cooper, D.R.Topliff, D.W.Freeman, C.MacAllister, & S.D.Carter (2001). Effect of dietary cation-anion difference on acid-base status and energy digestibility in sedentary horses fed varying levels and types of starch. Journal of Equine Veterinary Science 21, 498-502.
Popplewell JC, Topliff DR, Freeman DW, & Breazile JE (1993). Effects of dietary cation-anion balance on acid-base balance and blood parameters in anaerobically exercised horses. Proc 13th Equine Nutr and Physiol Symp Gainesville, Fl. 13, 191.
Ralston SL (1994). Equine Practice 16, 10.
Ralston SL (1997). Bicarbonate supplementation of young horses fed high grain rations. Proc fourteenth Equine Nutr Physiol Symp Ontario CA. 4.
Remer T (2001). Influence of nutrition on acid-base balance – metabolic aspects. Eur J Nutr 40.
Riond, J. L. (2001). Animal nutrition and acid-base balance. Eur.J Nutr. 40, 245-254.
Roby KA (1987). Am J Vet Res 48, 1012.
Sebastian, A., Harris, S. T., Ottaway, J. H., Todd, K. M., & Morris, R. C., Jr. (1994). Improved mineral balance and skeletal metabolism in postmenopausal women treated with potassium bicarbonate. N.Engl.J Med. 330, 1776-1781.
Stutz WA, Toppliff DR, Freeman DW, Tucker WB, Breazile JE, & Wall DL (1992). Effect of dietary cation-anion balance on acid-base status on blood parameters in exercising horses. J Equine Vet Sci 12, 164.
Taylor LE, Ferrante PL, Meacham TN, Kronfeld DS, & Tiegs W (1993). Acid-base responses to exercise in horses trained on a diet containing added fat. 13th Equine Nutrition and Physiology Symposium Proceedings, U.Florida.
Topliff DR, Kennerly MA, & Freeman DW (1989). Changes in urinary and serum calcium and chloride concentrations in exercising horses fed varying cation-anion balances. Proc 11th Equine Nutr Phsiol Symp 1-4.
Wall DL, Topliff DR, Freeman DW, Wagner DG, & Breazile JE (1991). Effects of dietary cation-anion balance on urinary mineral excretion in exercised horses. J Equine Vet Sci 12, 168.
Yashiki K, Kusunose R, & Takagi S (1995). Diurnal variations of blood constituents in young thoroughbred horses. J Equine Sci 6, 91-97.