10 Macro and trace elements in equine nutrition

Overview

The elements discussed in this chapter (Table 10-1) are essential for animals as well as for most plants. The differentiation between macro- and trace elements is not linked to their chemical structure but simply reflects their essentiality and average required dietary concentration: ≥100 ppm = macro, <100 ppm = trace element. This approach is very helpful in practice and is linked to content of these elements in animal tissue.

Table 10-1 Macro- and Trace Elements with Nutritional Relevance

*Merian et al 2004, Anke 2004; **Hohenheim 1976.

1 Indication of the likelihood of toxicity to occur/ how serious or life-threatening such toxicity may be; likelihood: + very rare, experimentally has been produced, ++ may happen, +++ frequently seen; life-threatening if toxic doses are ingested:+ no, ++ possible +++ in most cases; note that the given range for the elements in typical horse feeds are far below toxic levels (see Table 10-4)

2 per kg dry matter

3 for the EU; legally defined upper limits for a complete diet and daily ration, respectively, referring to 88% dry matter.

The differences in the required amounts of macro vs. trace elements and the potential to induce negative effects in the animal when provided in excess form the foundation for the differing legislation which covers the various elements. In most countries, more detailed legal restrictions exist regarding the trace elements in comparison to the macro elements.

Inadequate intake is still a common event and can be associated with visible clinical signs. However, such occurrences are not typically due to a lack of available knowledge either with respect to requirements or the availability from mineral carriers but are usually due to poor application of this information or even lack of understanding. In addition, it is important to recognize that there is limited tolerance for high mineral intakes. Common reasons for over-supplementation, in particular with trace elements, include the selection of inappropriate mineral supplements or the unthinking usage of such supplements. The potential for adverse consequences to develop when mineral intake exceeds the upper safe margins is commonly underestimated; this practice does pose a high risk for negative effects on health and performance.

The adverse effects of mineral deficiencies or excesses on horse health are an important veterinary issue and can be divided into acute and chronic responses.

Acute responses: For some elements, effects may be seen within a relatively short time scale when the available amounts do not cover tissue requirements; hypocalcemia is a prominent example. In these circumstances, effects are typically linked to disturbances in the internal balance and distribution of an element even when the intake is not particularly low. Acute responses can also occur if the intake increases to toxic levels (e.g., Se toxicosis), in which cases the high intakes are typically mirrored by abnormal tissue concentrations.

Chronic derangements in mineral intake induce adaptations in the animal; however, even these adaptations can be overridden by critically low or high intakes that may induce nonspecific effects such as growth retardation. Certain tissues become depleted or enriched depending on the intake. The value of ration evaluation to support the development of a clinical diagnosis is commonly underestimated. There might be some difficulties in quantifying feed intake precisely but use of estimates for intake and typical mineral concentrations in the feeds can yield at least sufficient basic information to judge whether one needs further, potentially costly, ration analysis and evaluation or not.

Factors determining requirements

In theory, zero mineral intake, a situation that can occur under experimental conditions, results in a negative mineral balance due to continual mineral excretion, mainly via the feces, urine and skin. The required intake to compensate for these unavoidable losses, defined as endogenous losses, represents the maintenance requirement. Such data, with respect to horses, are available for all of the macrominerals apart from sulfur (S). Data analysis for the balance between intake and retention, based on a broad range of intakes, ideally yields a linear relationship: y = a + bx. The principle is presented in Fig. 10.1. The value for “a” represents the endogenous losses and “b” gives the rate of utilization; both parameters are specific for the individual elements.

Figure 10.1 Principle of mineral balance trials with very low and high intake.

The value of “a” ‘(endogenous loss) is influenced by the

1. physiological role of the element

2. dry matter intake (see below)

3. concentration of the mineral in various secretions as part of its role within tissues, e.g., bile secretion

4. capability of an organ to activate conservation mechanisms (e.g. renal reabsorption of sodium).

Dry matter intake (DMI) may impact mineral requirements by inducing an increase in mucosal cell apoptosis and cell regrowth. Additionally, most secretions in the gastrointestinal tract (GIT) are related to DMI (e.g., saliva).

The utilization of the element b, visualized by the slope of the regression line, is affected by the:

1. type/ chemical nature of the naturally occurring compound (e.g. CaCO₂ vs. Ca-phosphate )

2. digestibility of the feedstuff or supplement containing the element

3. distribution in tissues

4. physiological uptake by tissues.

When considering the requirements for gestation, lactation, growth and exercise, mineral accretion in the respective “products” must be considered, i.e., in the pregnant uterus, in postnatal weight gain, milk, and sweat. As energy and mineral requirements do not change in parallel to the increase in these products, it is not possible to give a certain mineral : energy ratio as a guideline for feeding in practice. Commonly, recommendations are given in g or mg per kg body weight (BW), kg metabolic BW (BW^0.75) or per kg feed on a DM basis. However, the accuracy of latter as a target value for rations is low, due to the wide variability in possible DM-intakes (range of 15–>40 g DM/kg BW; see Chapter 3).

Trace element balance studies are very challenging and despite the high quality of some of the existing knowledge, requirements are less precisely defined than for the macroelements. Most data are based on dose–response studies in which the required intake for ensuring adequate tissue levels (blood or organ, e.g., muscle) is evaluated. Although it is not recommended to use the factorial approach to determine intake requirements for trace elements, it is possible to use their known concentrations in products such as milk to determine rough estimates based on such a factorial approach. This enables evaluation of the plausibility of requirement data.

In theory, there is no tissue that acts as a designated mineral sink (an exception is the liver for Cu) or a strategic reservoir when intake exceeds requirements. This is in contrast to the capacity of the body to store energy in adipose tissue. Even bone is not adapted to store Ca above that required for the optimal level of bone strength. However, bone can act as a buffer in case of a temporary shortage in exogenous Ca supply. Consequently, simple strategies are required for the organism to manage naturally occurring high intakes:

• limiting absorption (e.g., Fe) and increasing fecal excretion

• enforced renal excretion (e.g., Na)

• enforced excretion via milk (e.g., iodine).

Key Points

• Overconsumption of minerals induces an abnormal load in certain tissues and increases the risk of cell damage. This is the case in particular for I and Se.

• When comparing the risk of over-supplementation with Ca or Fe vs. Se or I, it is logical that for rare elements like Se the evolutionary need to establish an “overconsumption management strategy” was quite low (in contrast to Ca or Fe) and therefore the risk of toxicity of such elements through over-supplementation will be higher.

Minerals as essential nutrients

Mineral intake through the ingestion of plants or plant products does not guarantee adequate intake; additional supplementation is often required. The approach to macro vs. trace mineral supplementation is quite different. Macro elements are used fairly freely, provided as oxides, chlorides or sulphates. Some (e.g., CaCl₂) can induce mucosal damage and require either high dilution or specific coating to avoid adverse effects. A selection of commonly used mineral compounds is presented in Table 10-2.

Table 10-2 Commonly used Mineral Compounds as Source for Macroelements ¹

1 Beside the provision of an individual element by the compounds shown above, it is common to use a mineral supplement which combines different elements. A mineral supplement is defined in some countries by the crude ash (CA) content, e.g., Germany min. 400 g CA/kg, and requires specific labeling

Use of feed grade quality compounds helps to ensure safety with respect to contamination by elements that may interfere with utilization (e.g., high Fe) or the uptake of undesirable elements and substances (e.g., Pb and dioxins). The trace elements, partly due to their toxic potential, are regulated by law within the EU and, for certain trace elements (e.g., Se) also in the USA. The EU legal restrictions include the definition of permitted trace element carriers (Table 10-3) as well as the maximum concentration in the diet. Adverse effects are a substantial risk in the case of over-dosage, including negative interaction with the availability of other minerals, tissue accumulation, and the impairment of cellular functions. These factors are considered in defining a safe upper limit (SUL). Current data on SULs are summarized in Table 10-4 (Anke 2004, NRC 2005, Poppenga, 2001).

Table 10-3 Example Compounds Permitted as Carriers for Trace Elements (i.e., Registered for the Provision of Trace Elements which are in Turn Classified as Additives in EU Legislation)

Element	Compound	Content of element (%)
Fe	FeCl₂ + 4 H₂O	28
	FeSO₄ + 7 H₂O	20
	Fe_II-fumarate	32
Iodine	KJ	76
	NaJ	68
	Ca(JO₃) + 6 H₂O	51
Co	CoCl₂ + 6 H₂O	25
	CoSO₄ + 7 H₂O	21
Cu	CuCl₂ + 2 H₂O	37
	CuSO₄ + 5 H₂O	25
	CuCO₃	58
	CuO	80
	Cu(H₂H₃O₂)₂ + H₂O	32
Mn	MnCl₂ + 4 H₂O	28
	MnSO₄	36
	MnSO₄ + 4 H₂O	25
	KMnO₄	35
Se	Na₂SeO₃	46
	Na₂SeO₄	42
Zn	ZnCl₂	48
	ZnSO₄ + 7 H₂O	23
	ZnO	80
	ZnCO₃	52
	Zn(C₂H₃O₂)₂ +2 H₂O	30

Table 10-4 Minimal Requirement Data and Maximum Tolerable Dietary Minerals (data from NRC 2005, Poppenga, 2001, GfE 2013)

1 ND = not determined.

2 >500 mg/kg BW/day may increase water intake and cause diuresis.

Calcium (Ca)

Ca in the pure elemental form is a hard metal (density 1.55 g/cm³); combined with organic or inorganic anions Ca is the most abundant macroelement in the mammalian body. The Ca-content of a newborn foal is close to 20 g/kg BW and decreases to ~15 g/kg BW in adults (Grace et al 1999b, Meyer & Ahlswede 1976). About 99% of total body Ca is found deposited in bone. The biochemistry of Ca in bone ensures two functions: (a) the formation of a tissue with high mechanical load capacity, and (b) buffering of changes in Ca-homeostasis. This fact ensures a high flexibility in Ca turnover via the “feeding” of the mobile Ca pool in blood or muscle by the mobilization of Ca from bone. The import and export of Ca into and out of bone is regulated by calcitonin and parathyroid hormone, respectively.

Major functions

Distribution over tissues

Total body Ca is close to 15 g/kg; the bulk is found in bone. Bone ash (metacarpus, tarsus) contains 385 g Ca (Table 10-5) and 177 g P/kg with no effect of gender or age (Vervuert et al 2010). The fetus has slightly higher Ca content related to the prioritization of bone formation during gestation. Ca accretion is described by an exponential model which reflects that the most intensive bone growth occurs during the last 4 months of gestation.

Ca in bone

As Ca-hydroxyapatite (Ca₅(PO₄)₃(OH)), calcium is an essential contributor to the physical nature of bone and teeth. The high apatite formation and inclusion of Ca in enamel (~38% Ca (Kodaka et al 1991)) produces the highest known mechanical resistant material in the equine body, able to cope with the enormous masticatory forces of >300 N (Huthmann et al 2009). With respect to the radius and tibia, the cortical hydroxyapatite density (commonly taken as bone mineral density, BMD) is 1175 mg/cm³ (Fürst et al 2008). This corresponds to ~470 mg Ca and 87 mg P/cm³. Although there is a strong positive age effect on mechanical strength, at least in metacarpal and metatarsal bones (Glade et al 1986), it seems that the BMD is less sensitive to age (Fürst et al 2008). Bone is formed by collagen fibers (type I, 90% of total protein) and non-collagenous proteins. Spindle- or plate shaped crystals of hydroxyapatite (Ca₁₀[PO₄]₆[OH]₂) are found on the collagen fibers and in the ground substance. The mechanisms of mineralization are not fully understood. The ground substance is composed of glycoproteins plus proteoglycans. These highly anionic complexes have a high ion-binding capacity and are thought to play an important role in the calcification process and in the fixation of hydroxyapatite crystals to the collagen fibers. Osteocalcin, a non-collagenous protein which is synthesized by the osteoblasts, is thought to affect the growth or maturation of Ca²⁺-phosphate incorporating structures. However, Mg also plays an important role in mineralization as it has been shown to bind to the surface of hydroxyapatite crystals and seems to compete with Ca for the same absorption site (Rude et al 2003, 2009). In addition, studies in laboratory animals have shown negative effects of excessive Mg intake on crystal size and structure as well. In summary, low and high Mg intake in horses has the potential to interact with Ca in the “building of proper hydroxyapatite crystals”.

As a consequence of the biology of bone, Ca and P constitute a mobile component as they can be mobilized from bone on demand in case of a mismatch between intake and the need to maintain homeostasis. This means that the physical properties of bones essentially change during gestation and lactation (Glade 1993, Gruber & Stover 1994). Regardless of Ca intake, a major impact on equine bone quality and bone mineral content is caused by exercise. Stabling horses induces a reduction in BMD whereas natural exercise on pasture as well as short term training bouts induce an increase in BMD, which should result in a corresponding response in bone Ca (Bell et al 2001, Hiney et al 2004, Porr et al 1998). It is evident that the positive impact of natural exercise is underestimated in practice.

Key Points

• ~99% of Ca is deposited in bone and is key in supporting the mechanical property of bone

• Ca in bone can be rapidly mobilized to maintain blood Ca²⁺ concentrations

• There is no benefit on the mechanical properties of bone when the Ca supply in the diet exceeds requirements

• Immobility/stabling of a horse results in a loss of minerals from the bone – regardless of being provided an adequate Ca intake – and such tissue responses cannot be fully overcome by increasing the mineral supply. The stimulus of physical activity (load bearing exercise) is also required

Other functions

In addition to its contribution to ossification, Ca is involved in blood clotting, muscle contraction, enzyme activities related to energy metabolism, and digestive processes as well as the transmission of nerve signals ((Wijnberg et al 2002a, b, c).

The second highest ranked tissue for Ca content is muscle where the Ca²⁺ is essentially linked to the contractility of muscle fiber. Inside the muscle cell, Ca shows the lowest concentration, in comparison to other ions, being in the range of 4–19 mmol (160–462 mg)/kg dry matter (DM) (Gottlieb-Vedi et al 1996). Release of Ca from the sarcoplasm and reuptake drive muscle contraction and relaxation (with an impressive exchange rate of ~200 nmol/g muscle). The energy used for maintaining the Ca²⁺ gradient accounts for ~30–50% of total heat production within the muscle (Hasselbach & Oetliker 1983, Kobayashi & Sugi 1980). The Ca²⁺-ATPase plays an important role in this aspect of muscle function (Hasselbach 1998); the Ca²⁺-ATPase varies between 20–29 nmol/kg wet weight in gluteus medius and semitendinosus muscles. There is no influence of age but concentrations are higher in pastured animals in comparison to exercised or stabled horses (Suwannachot et al 2003). The fact that the concentration of ATPase in masseter muscle is only ~20% of the above level may indicate that there is a variable distribution of Ca²⁺ , accompanied with differences in ATPase activity, according to muscle fiber type.

Ca requirements

Using the traditional factorial approach the sum of all endogenous losses plus the amount of Ca deposited or excreted in any product divided by the rate of utilization will give the minimum requirement.

Maintenance

The maintenance requirement (see Table 10-5) is related to body weight. In contrast to ruminants there is no effect of DM intake on endogenous losses and thereby on requirements.

Growth

It is evident that any type of growth results in a remarkable increase in requirement.

The Ca concentration in the conceptus increases over time because intrauterine growth shows a preference for connective tissue development in the last 4 months of gestation in order to make the newborn ready for standing and flight-fright responses. The postnatal growth curve (see Chapter 12) determines the development of Ca requirements in the growing foal. Postnatally, in relation to bone, there is a preferred growth of soft tissue and therefore the proportion of Ca in the mature body mass is lower than in a newborn. Therefore, the product “postnatal daily gain” has a lower Ca content vs. preterm gain.

Lactation

On average, Ca in mare’s milk is ~1740 mg/kg but there is a continuous decrease in concentration throughout lactation. The Ca excretion via milk therefore varies according to the day of lactation and milk yield. In fact, the most demanding performance with respect to Ca requirements is milk production (see Fig. 10.2). Although milk yield in mares is difficult to define, a current model based on measured milk volumes and energy requirements of the foal suggests that the maximum mineral excretion via milk occurs within the first 40 days of lactation. Taking into consideration the time dependent drop in mineral concentrations (Ca, P, Mg) in mares’ milk, this results in a nonlinear description of lactogenic Ca export (Fig. 10.2).

Figure 10.2 Model of milk yield in horses as well as Ca and P excretion via milk. (milk volume, g kg BW^0.82 d⁻¹ = 66d^0.1727e^−0.00539d; Ca-secretion, g kg BW^0.82 d⁻¹ = 0.1161d^0.00757e^−0.00599d; P-secretion, g kg BW^0.82 d⁻¹ = 0.0700d^−0.02276e^−0.00649d; Coenen et al 2010)

Exercise

Weak data and conflicting recommendations exist with respect to the Ca requirements of exercising horses. Long-lasting effects of exercise on Ca are associated with an adaptation of bone; a likely temporary shift of bone formation towards resorption results in a loss of BMD which can be overridden by an elevated Ca intake. However, neither the persistence of this tissue sensitivity nor the beneficial effects of extra Ca is sufficiently defined. Short-term exercise induces changes in Ca homeostasis which are associated with PTH secretion in part to compensate for the trapping of Ca²⁺ by lactate. This temporary shrinkage in the Ca²⁺ pool indicates an extra requirement in response to exercise but it is likely that this small increase, coupled with the small increase in Ca loss via the sweat will only elevate Ca requirements for exercising animals by a small amount. Practically, it can be stated that 1.5-fold of maintenance requirements is sufficient for horses in exercise work.

Ca balance

Ca intake

The Ca-concentrations in feeds typically varies between 0.5 and 15 g/kgDM. A guide to the ranking according to content (g/kgDM) is:

The contribution of roughage to total Ca intake is closely linked to the botanical composition of the ration. Alfalfa, clover or herbs like dandelion contain the highest Ca concentrations. Where such plants contribute to the plant community on a pasture, overall content will be >6 g Ca/kg DM. This provides Ca above the requirements for maintenance or exercise if the daily intake of such a pasture is ~20 g DM/kg BW. Typical grass hay provides on average around 4–5 g Ca/kg DM, but it is important to recognize that there is a wide variation in the Ca content of grass and conserved forages; a high percentage of grass forages are below this average value (Fig. 10.3) especially in the UK. This is particularly relevant to the management of Ca nutrition in lactating and growing animals. Cereals in particular are low in Ca (oats > rye & barley & wheat > corn) (Table 10-6). By-products vary between 2 (wheat bran) and >15 g Ca/kg DM (citrus pulp). Cereal straw contains ~1.8 g Ca/kg DM without major differences depending on the source. At DMIs of 80 and 130 g kg^0.75 BW for maintenance and lactation, respectively, a Ca intake concentration of 5 g/kg DM results in a Ca supply which would provide ~2 fold and ~1.1-fold of recommended requirements.

Figure 10.3 Distribution of Ca and P in grass, grass silages and hay (581 samples, northern Germany; means: Ca 4.6, P 3.7 g/kg DM).

Table 10-6 Ca (g/kg DM) in Different Grains (Total Plant in Early Stage) and Several Products

The use of mineral supplements is very common in practice, although in most circumstances the feeding of a Ca-containing supplement in addition to average pasture or hay will create a Ca intake that exceeds the requirement (Fig. 10.4).

Figure 10.4 Supply of energy and minerals to a 500 kg horse through typical preserved grass forage relative to requirements (=1).

¹For each life stage/activity level the > number represents the DM intake, kg/100 kg BW used for the calculations. The number behind each parameter on the y-axis is the corresponding concentration per kg hay DM in MJ, g (macroelements) and mg (trace elements) used for developing this figure.

Key Points

• The presence of significant amount of legumes or certain herbal species (e.g., dandelion) in pasture or hay typically results in >6 g Ca/kg DM. This level of intake covers Ca needs in most circumstances providing that DMI is in the normal physiological range

• High grain rations are likely to provide a low intake of Ca (but high P) if not supplemented

• Typically grass or preserved grass forages may be low in overall Ca content and will require specific countermeasures, such as supplementation, especially for pregnant and lactating mares as well as growing animals

Ca secretion and absorption

Ca needs to be dissociated for transmenbrane transport; the nature of Ca in animal and plant tissue corresponds to this situation, Ca-oxalate being the exception. This Ca complex is a special form of Ca storage in some plants.

Secretion

Saliva (see Table 10-9) contains 157 g/l Ca (Coenen 1985a); assuming 6 liters of saliva production per kg DM of roughage (Meyer et al 1986); this would result in Ca secretion of about 9.4 g/day for a horse consuming 10 kg DM of hay. There is only negligible Ca secretion in the stomach (see Table 10-7). However, the acidic environment may have an important role with respect to Ca availability. The Ca compounds that are of nutritive value (not Ca-oxalates) either from plant tissue or from added minerals are readily soluble in acids. As in other animals, the acidic gastric environment leads to dissociation of Ca, forming Ca²⁺ ions. This gastric process has two functions: (a) optimizing the solubility of Ca and thereby its absorption, and (b) modulation of gastric acid secretion via the interaction of Ca²⁺ with Ca-sensing receptors (Ca-sR) and consequent increase in gastrin secretion and gastric acid output. There is some absorption of Ca from the stomach but the majority is absorbed in the small intestine (Schryver et al 1970a, b).

Table 10-7 Estimated Volumes and Mineral Concentrations in Equine Gastrointestinal Secretions (Meyer & Coenen 2002)

The chronic administration of acid-suppressor drugs like omeprazole has been proposed to decrease Ca absorption in humans (Insogna 2009). Although there are no equine data about this interaction it should be taken as a valid hypothesis that the intensive use of antiacidic drugs will have an impact on Ca absorption. In addition, with respect to the Ca-CasR-gastrin axis, careful evaluation prior to the use of Ca containing mineral supplements is required in order to avoid requirement exceeding intake and vice versa (Shulkes et al 2006).

Ca is secreted in pancreatic juice and bile; the volumes and mineral concentrations are summarized in Table 10-7. Pancreatic Ca secretion is independent of Ca intake but is linked to DM intake (Zebrowska et al 1983). Calcium plays a role in fluid and electrolyte transfer during bile formation. The sensitivity of this function to variations in Ca intake is not known. Cholelithiasis occurs in horses but currently there are no data showing an impact of Ca intake or Ca turnover on this condition.

Absorption

Calcium absorption in the small intestine is driven by a Ca²⁺ concentration gradient in the lumen and occurs by both trans- and paracellular routes. Foals have higher capacity for Ca absorption but there is no further effect of aging on absorptive capacity. As in other species, binding of Ca²⁺ to a Ca-binding protein (Calbindin) is the first step in transport (Fullmer & Wassermann 1972). The expression of this protein has been identified in equine placenta, kidney and the intestinal tract, with highest expression in the duodenum (Rourke et al 2010, Wooding et al 2000). Calbindin expression is probably not regulated by vitamin D as Ca uptake in the horse is thought to be independent of vitamin D (Rourke et al 2010). However, recently published studies showed vitamin D receptors throughout the equine gut and an active transmucosal Ca-transport (Sprekeler et al 2011).

Prececal Ca absorption averages ~60–67% of intake (Meyer et al 1982) whereas total tract absorption varies from -5% to 50%, a lower and wider range when compared to small intestinal absorption. This is because the secretion of Ca into the hindgut is related to the amount of fiber in the diet, which obviously varies between 10–40 mg/kg BW/day (Meyer et al 1982, Schryver et al 1970b).

In contrast to ruminants, there is only a weak adaptation in Ca absorption rate in response to dietary intake. A literature survey (Kienzle & Burger 2012 in press) defined a linear relationship between Ca intake (x) and fecal excretion (y) by the following equation: y = 32.11 + 0.54x; r = 0.79, n = 103; intake and excretion in mg/kg BW^0.75. From these data, it can be concluded that true digestibility of Ca is ~46%. The Ca : P ratio has no impact on Ca absorption but other factors may reduce Ca absorption. For example, assisted enteral (tube) feeding decreases Ca absorption by ~50% perhaps due to increase rate of intestinal transit (Coenen 1986). Excessive Ca intake (>4-fold of requirement) also reduces the absorption rate (Kienzle & Burger 2012). Feeding fat to horses may negatively affect Ca availability via the formation of Ca salts from unsaturated fatty acids; however, no negative effect of oil feeding on preileal Ca absorption was observed in fistulated animals (Meyer et al 1997). Ca-oxalate is the only naturally occurring Ca compound in feedstuffs that has markedly reduced digestibility. Oxalic acid at >1 % of dietary DM depresses Ca absorption to <10% of intake (Walthall & McKenzie 1976, Swartzman et al 1978, Blaney et al 1981, Hintz et al 1984, Cymbaluk & Christensen 1986, Teleb 1984). Phytic acid, a member of the phosphoinositol family, also forms Ca complexes and limits absorption. Cereals like barley and oats contain up to ~8 g phytate and ~11 g total inositol phosphates per kg DM; these form complexes with P, Ca, Fe, and Zn (Brooks & Lampi 2001). The addition of phytase to the diet improves Ca absorption (van Doorn et al 2004). However, although cereals are high in phytate in typical rations they provide only a minor contribution to total Ca supply. However, the contribution of Ca from the cereal component of the diet can be assumed to be ~10% of the original Ca content. There is no routinely used analytical method for assessment of phytate content.

Ca-excretion

Fecal Ca excretion is linearly related to intake (Fig. 10.5) indicating that absorptive processes do not adapt to differences in Ca intake. Aging also does not appear to affect net absorption (Elzinga, Geor & Harris, personal communication 2011; net absorption, % of intake in mature vs. aged horses, 44 vs. 47). As there is no intestinal adaptation to counteract high Ca intake, the renal route becomes very important with respect to the elimination of Ca when the absorbed amount exceeds requirements and cannot be stored. As such, the kidney acts as a safety relief valve. Effectively, the Ca concentration in urine reflects intake (although sedimentation within the bladder can influence the content in voided sample) and can increase to levels which can provoke precipitation or even stone formation. Urolithiasis in the equine is mostly associated with the formation of insoluble Ca-compounds (Diaz-Espineira et al 1997, Duesterdieck-Zellmer 2007, Laverty et al 1992) as in other hindgut fermenters like manatees and rabbits (Kamphues 1991, Keller et al 2008). See Chapter 36 for more detail on urolithiasis.

Figure 10.5 A summary of selected literature data on calcium balance in horses.

A further veterinary aspect is the effect of glucocorticoid treatment in horses. In a dose dependent manner, horses develop negative Ca balance within few days of glucocorticoid treatment due to elevated fecal and renal losses (Glade et al 1982). Glucocorticoids have also been suggested to reduce the activity of the Ca-binding protein in intestinal mucosa (Glade et al 1982).

Key Points

• The small intestine is the major site for Ca absorption

• Ca absorption is not substantially modified by the level of intake

• Absorbed but not utilized Ca is excreted by the kidney

Regulation of Ca homeostasis

Blood Ca content represents the bound and ionized (Ca²⁺) fractions. There is no distinct postprandial change in either total Ca or Ca²⁺ concentration despite the rapid flow of Ca into the extracellular fluid due to highly effective homeostatic mechanisms. In response to an increase in circulatory Ca concentrations, the hormone calcitonin (CT) is immediately secreted (Rourke et al 2009) and subsequently interacts with receptors in the gut, kidney and bone, tissues that can act as a Ca sink (Johnston et al 1989, Rourke et al 2009). The CT response is rapid but brief (Johnston et al 1989, Rourke et al 2009). A decrease in circulating Ca stimulates secretion of parathyroid hormone (PTH); the Ca²⁺ set point (the Ca²⁺ concentration at which PTH reaches 50% of its maximum concentration in response to hypocalcemia) for horses is 1.37 mmol/l (Toribio et al 2003) and is higher in comparison to other species. This indicates that feed back signals, mediated by increasing Ca²⁺ have a delayed response with respect to the reduction of PTH secretion in comparison to other species. The action of PTH on bone as well as the fractionation of Ca in blood (47.4% bound to protein, 48.5% ionized, 4.1% complexed Ca; Lopez et al 2006) restricts our ability to understand Ca homeostasis simply through analysis of blood total Ca concentrations.

Vitamin D supplementation can induce an increase in blood Ca, which suggests that there is a link between 1,25 dihydroxycalciferol and Ca homeostasis. The exclusion of vitamin D from the diet coupled with depression of sunlight-dependent activation of this vitamin resulted in bone abnormalities in horses (El Shorafa et al 1979). On the other hand, vitamin D precursors and vitamin D activity itself are very low in horses (Breidenbach et al 1998, Harmeyer & Schlumbohm 2004). Under physiological conditions, vitamin D intake has minimal effect on Ca homeostasis.

Consequences of failures in calcium intake or deranged homeostasis

There is no significant effect of Ca intake on Ca homeostasis (total vs. ionized Ca) in horses in exercise training (Vervuert et al 2002). Reference values for Ca²⁺ are lower for lactating mares and foals in comparison to adults at maintenance (Berlin & Aroch 2009). At low Ca-intakes, PTH mobilizes Ca from bone in order to maintain circulating Ca²⁺ concentration within a narrow range.

A low Ca intake may predispose to tetany, although this condition is rare in horses when compared to dairy cows (Baird 1971, Meijer 1982). Calcium absorption can be impaired by oxalic acid which complexes Ca within the GIT and reduces absorption (Laan et al 2000, Swartzman et al 1978, James & Butcher 1972). A diet providing 1% oxalic acid induced negative Ca balance (Swartzman et al 1978). Rumex species (Rumex obtusifolius, R. crispius) can contain up to ~10% DM oxalic acid (Panciera et al 1990) and this may be a relevant factor in horses on poorly managed pastures.

Under practical conditions, an imbalanced mineral intake is more likely to have an impact on Ca homeostasis than overt deficiency. A relative Ca deficiency can result from high P intake or a low Ca : P ratio. Primary and secondary hyperparathyroidism are the result of a persistent catabolic stimulus of the Ca-sensing system affecting bone. Even the very early reports of these conditions draw attention to the compensatory enlargement of bones (Brevard 1824, Hornbrook 1826). “Big head disease” or Millers disease still occurs even though we have the knowledge on Ca requirements that should prevent this condition (Luthersson et al 2005, Stewart et al 2010).

Defects in Ca-homeostasis are important for some conditions. A short-term shortage in mobile Ca²⁺ in body fluids can be the result of increased Ca export through milk. Tetanic dysfunction of the muscle in lactating mares can occur towards the peak of lactation (Montgomerie et al 1929, Richardson et al 1991). In the first weeks of lactation, milk Ca is ~1 g/l and is responsible for high losses of Ca from the mare (see Fig. 10.4). The above conditions can be treated or prevented by appropriately adjusting Ca (and P) intake to the increased requirements.

An internal shift in Ca balance via trapping of Ca²⁺ can influence Ca homeostasis. Hypocalcemia (low Ca²⁺) occurs during exercise due to the binding of Ca²⁺ to protein and/or lactate (Vervuert et al 2002). This can result in conditions such as synchronous diaphragmatic flutter (Carlson & Mansmann 1974, Mansmann et al 1974). The exercise induced drop in Ca²⁺ occurs despite an increase in PTH during physical activity. A two- or threefold increase in Ca intake in comparison to recommendations mitigates the Ca²⁺ nadir during exercise but cannot maintain normocalcemia (Vervuert et al 2006). Decreased ionized Ca has been observed in horses with severe systemic illness (e.g., colic, endotoxemia, sepsis; Garcia-Lopez et al 2001, Delesalle et al 2005, Toribio et al 2001, 2005, 2007, Hurcombe et al 2009). Moreover, persistence of low ionized Ca was associated with poor outcome during treatment of critically ill horses (Delesalle et al 2005, Hurcombe et al 2009). In other species, some inflammatory cytokines have been shown to decrease PTH secretion, and it is possible that a similar mechanism accounts for low Ca²⁺ during inflammatory events in horses.

Key Points

• Blood Ca concentration is not useful for assessment of calcium nutrition

• Exercise results in very little change in Ca requirements

• In case of some disease PTH may not efficiently ensure Ca⁺⁺-homeostasis but hypocalcaemia is a critical factor for survival

Phosphorus (P)

The total body P content is around 8.6 g/kg (Table 10-8). Similar to Ca, the bulk of body P is in bone (80.8%). Bone ash is about 150–200 g P per kg (Vervuert et al 2010). The P content of bone is age insensitive. Age-related differences in bone composition mostly result from differences in the fat content. Muscle tissue is the second highest ranked tissue with respect to P partitioning in the body but has similar content per gram of tissue to the liver.