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2
Overview of Calcium

INTRODUCTION

Calcium as a nutrient is most commonly associated with the formation and metabolism of bone. Over 99 percent of total body calcium is found as calcium hydroxyapatite (Ca10[PO4]6[OH]2) in bones and teeth, where it provides hard tissue with its strength. Calcium in the circulatory system, extracellular fluid, muscle, and other tissues is critical for mediating vascular contraction and vasodilatation, muscle function, nerve transmission, intracellular signaling, and hormonal secretion. Bone tissue serves as a reservoir for and source of calcium for these critical metabolic needs through the process of bone remodeling.

Calcium metabolism is regulated in large part by the parathyroid hormone (PTH)–vitamin D endocrine system, which is characterized by a series of homeostatic feedback loops. The rapid release of mineral from the bone is essential to maintain adequate levels of ionized calcium in serum. During vitamin D deficiency states, bone metabolism is significantly affected as a result of reduced active calcium absorption. This leads to increased PTH secretion as the calcium sensing receptor in the parathyroid gland senses changes in circulating ionic calcium. Increased PTH levels induce enzyme activity (1α-hydroxylase) in the kidney, which converts vitamin D to its active hormonal form, calcitriol. In turn, calcitriol stimulates enhanced calcium absorption from the gut. Not surprisingly, the interplay between the dynamics of calcium and vitamin D often complicates the interpretation of data relative to calcium requirements, deficiency states, and excess intake.



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2 Overview of Calcium INTRODUCTION Calcium as a nutrient is most commonly associated with the formation and metabolism of bone. Over 99 percent of total body calcium is found as calcium hydroxyapatite (Ca10[PO4]6[OH]2) in bones and teeth, where it provides hard tissue with its strength. Calcium in the circulatory system, extracellular fluid, muscle, and other tissues is critical for mediating vas- cular contraction and vasodilatation, muscle function, nerve transmission, intracellular signaling, and hormonal secretion. Bone tissue serves as a res- ervoir for and source of calcium for these critical metabolic needs through the process of bone remodeling. Calcium metabolism is regulated in large part by the parathyroid hor- mone (PTH)–vitamin D endocrine system, which is characterized by a series of homeostatic feedback loops. The rapid release of mineral from the bone is essential to maintain adequate levels of ionized calcium in se- rum. During vitamin D deficiency states, bone metabolism is significantly affected as a result of reduced active calcium absorption. This leads to in- creased PTH secretion as the calcium sensing receptor in the parathyroid gland senses changes in circulating ionic calcium. Increased PTH levels induce enzyme activity (1α-hydroxylase) in the kidney, which converts vi- tamin D to its active hormonal form, calcitriol. In turn, calcitriol stimulates enhanced calcium absorption from the gut. Not surprisingly, the interplay between the dynamics of calcium and vitamin D often complicates the interpretation of data relative to calcium requirements, deficiency states, and excess intake. 35

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36 DIETARY REFERENCE INTAKES FOR CALCIUM AND VITAMIN D SOURCES OF CALCIUM Ingested calcium comes from food sources and dietary supplements. In this report dietary calcium refers to both food sources and supple- ments combined (although some researchers reserve the term dietary calcium to mean only food sources) and is most often referred to as total calcium intake for clarity. With more than one-half of the U.S. population (Bailey et al., 2010)—and between 24 and 60 percent of Canadians (2004 Canadian Community Health Survey, personal communication, D. Brulé, Health Canada, April 29, 2010)—reporting use of dietary supplements of some type, dietary supplements must be taken into account when consider- ing the sources of calcium in the diet and, in turn, estimating total calcium intake. Current estimates from 2003 to 2006 indicate that the median total intake of calcium from all sources for persons > 1 year of age ranges from 918 to 1,296 mg/day, depending upon life stage (Bailey et al., 2010). Only small amounts of calcium are contributed by water, depending upon geo- graphic location. Chapter 7 of this report contains an assessment of quanti- tative calcium intake in the U.S. and Canadian populations. Food Calcium is classically associated with dairy products; milk, yogurt, and cheese are rich sources of calcium, providing the major share of calcium from foods in the general diet in the United States and Canada. In the United States, an estimated 72 percent of calcium comes from milk, cheese and yogurt and from foods to which dairy products have been added (e.g., pizza, lasagna, dairy desserts). The remaining calcium comes from vegeta- bles (7 percent); grains (5 percent); legumes (4 percent); fruit (3 percent); meat, poultry, and fish (3 percent); eggs (2 percent); and miscellaneous foods (3 percent).1 Similar data from Canada are not currently available. Fortification with calcium for a number of foods that do not naturally contribute calcium—such as orange juice, other beverages, and ready-to- eat cereals—is becoming commonplace in the United States (Calvo et al., 2004; Rafferty et al., 2007; Poliquin et al., 2009). These practices challenge the ability of national food composition databases, such as those main- tained by U.S. Department of Agriculture (USDA), to keep abreast of these newer products and may result in some underestimation of actual calcium intake from food sources. However, for those persons who choose such foods, total calcium intake is increased. 1U.S. Department of Agriculture/Economic Research Service Nutrient Availability Data (2009). Available online at http://www.ers.usda.gov/Data/FoodConsumption/Nutrient AvailIndex.htm. Accessed October 19, 2010.

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37 OVERVIEW OF CALCIUM Dietary Supplements Among the U.S. population, about 43 percent of all persons—but almost 70 percent of older women—reported calcium intake from supple- ments, based on a national survey conducted between 2003 and 2006 (Bailey et al., 2010). When calcium from supplement use is taken into account based on these survey data, the average intake increases by about 7 percent for males and 14 percent for females. However, this is not a meaningful snapshot of the effect of supplement use, because non-users of supplements are averaged with users, meaning that the effect is much more skewed than can be reflected by a mean estimate. Similar data are not avail- able for Canada, but the frequency of use data show that 48 to 82 percent of Canadians reported taking a calcium supplement within the previous 30 days (2004 Canadian Community Health Survey, personal communication, D. Brulé, Health Canada, April 29, 2010). The most common forms of supplemental calcium are calcium carbon- ate and calcium citrate.2 The bioavailability of the calcium in these forms is discussed below in the section titled “Other Factors Related to Calcium Nutriture.” Generally fewer tablets of calcium carbonate are required to achieve given dose of elemental calcium because calcium carbonate gen- erally provides 40 percent elemental calcium, compared with 21 percent for calcium citrate. Thus, costs tend to be lower with calcium carbonate (Heaney et al., 2001; Keller et al., 2002) than with calcium citrate, and com- pliance may be higher among patients who do not want to take (or have difficulty swallowing) multiple pills. Chewable calcium carbonate supple- ments are also available. However, compared with calcium citrate, calcium carbonate is more often associated with gastrointestinal side effects, includ- ing constipation, flatulence, and bloating (Straub, 2007). Calcium citrate is less dependent than calcium carbonate on stomach acid for absorption (Hunt and Johnson, 1983; Recker, 1985; Straub, 2007) and thus can be taken without food. It is useful for individuals with achlorhydria, inflamma- tory bowel disease, or absorption disorders or who are taking histamine-2 receptor blockers or proton pump inhibitors; for residents of long-term care facilities where calcium supplements are not given with meals; and for others whose schedules preclude taking supplements with food (Bo- Linn et al., 1984; Carr and Shangraw, 1987; Straub, 2007). Calcium can compete or interfere with the absorption of iron, zinc, and magnesium. For this reason, persons with known deficiencies of these other minerals who require calcium supplementation usually take calcium supplements between meals (Straub, 2007). 2Other forms of calcium dietary supplements include lactate, gluconate, glucoheptonate, and hydroxyapatite; their relevance for life stage groups may vary.

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38 DIETARY REFERENCE INTAKES FOR CALCIUM AND VITAMIN D METABOLISM OF CALCIUM Absorption Calcium is absorbed by active transport (transcellularly) and by passive diffusion (paracellularly) across the intestinal mucosa. Active transport of calcium is dependent on the action of calcitriol and the intestinal vitamin D receptor (VDR). This transcellular mechanism is activated by calcitriol and accounts for most of the absorption of calcium at low and moderate intake levels. Transcellular transport occurs primarily in the duodenum where the VDR is expressed in the highest concentration, and is dependent on up-regulation of the responsive genes including the calcium transport protein called transient receptor potential cation channel, vanilloid fam- ily member 6 or TRPV6 (Li et al., 1993; Xue and Fleet, 2009). These features—up-regulation of VDR and TRPV6—are most obvious during states in which a high efficiency of calcium absorption is required. Passive diffusion or paracellular uptake involves the movement of cal- cium between mucosal cells and is dependent on luminal:serosal electro- chemical gradients. Passive diffusion occurs more readily during higher calcium intakes (i.e., when luminal concentrations are high) and can oc- cur throughout the length of the intestine (Ireland and Fordtran, 1973). However, the permeability of each intestinal segment determines passive diffusion rates. The highest diffusion of calcium occurs in the duodenum, jejunum, and ileum (Weaver and Heaney, 2006b). From a recent series of controlled metabolic studies undertaken by the USDA, mean calcium absorption (also referred to as “fractional calcium absorption,” which is the percentage of a given dose of calcium that is absorbed) in men and non-pregnant women—across a wide age range— has been demonstrated to be approximately 25 percent of calcium intake (Hunt and Johnson, 2007). Mean urinary loss averages 22 percent and fecal loss 75 percent of total calcium intake, with minor losses from sweat, skin, hair, etc. In general, mean calcium absorption and calcium intake are directly related (Heaney et al., 1975; Gallagher et al., 1980; Hunt and Johnson, 2007). However, fractional calcium absorption varies inversely with calcium intake when the intake is very low (Malm, 1958; Spencer et al., 1969; Ireland and Fordtran, 1973). For example, when calcium intake was lowered from 2,000 to 300 mg, healthy women increased their fractional whole body retention of ingested calcium, an index of calcium absorp- tion, from 27 percent to about 37 percent (Dawson-Hughes et al., 1993). This type of adaptation occurs within 1 to 2 weeks and is accompanied by a decline in serum calcium concentration and a rise in serum PTH and calcitriol concentrations (see section below titled “Homeostatic Regulation of Calcium”). The fraction of calcium absorbed rises adaptively as intake

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39 OVERVIEW OF CALCIUM is lowered. However, this rise is not sufficient to offset the loss in absorbed calcium that occurs as a result of the lower intake of calcium—however modest that decrease may be—and thus net calcium absorption is reduced. Fractional calcium absorption varies during critical periods of life. In infancy, it is high at approximately 60 percent, although the range is large (Fomon and Nelson, 1993; Abrams et al., 1997). Calcium absorption in newborns is largely passive and facilitated by the lactose content of breast milk (Kocian et al., 1973; Kobayashi et al., 1975). As the neonate ages, pas- sive absorption declines and calcitriol-stimulated active intestinal calcium absorption becomes more important (Ghishan et al., 1980; Halloran and DeLuca, 1980; Ghishan et al., 1984). A recent preliminary report on breast-fed infants in the first 2 months of life (Hicks et al., 2010) reported calcium absorption of approximately 33.7 ± 2.0 mg/100 kcal. In an earlier study using stable isotopes (Abrams et al., 1997), calcium absorption was measured in 14 breast milk–fed in- fants who were 5 through 7 months of age at the time of the study. Mean absorption was 61 ± 23 percent of intake when approximately 80 percent of the calcium intake was from human milk (IOM, 1997). There was no significant relationship between calcium intake from solid foods and the fractional calcium absorption from human milk. This finding suggests that calcium from solid foods does not negatively affect the bioavailability of calcium from human milk (IOM, 1997). Using measured urinary calcium and estimates of endogenous excretion, net retention of calcium was cal- culated to be 68 ± 38 mg/day for those infants. Abrams (2010) concluded that in infancy, based on calcium intakes that vary from as low as 200 mg/ day in exclusively breast-fed infants in the early months of life to 900 mg/ day in older formula-fed infants receiving some solids, calcium absorption depends primarily on the level of intake. The author reported that the absorption fraction can range from somewhat above 60 percent with lower intakes to about 30 percent with higher intakes. As the infant transitions into childhood, fractional calcium absorption declines, only to rise again in early puberty, a time when modeling of the skeleton is maximal. Abrams and Stuff (1994) found fractional absorption in white girls with a mean cal- cium intake of about 931 mg/day to average 28 percent before puberty, 34 percent during early puberty (the age of the growth spurt), and 25 percent 2 years after early puberty. Fractional absorption remains about 25 percent in young adults. In 155 healthy men and women between 20 and 75 years of age, mean calcium absorption was 24.9 ± 12.4 percent of total intake (Hunt and Johnson, 2007). During pregnancy, calcium absorption doubles (Kovacs and Kronenberg, 1997; Kovacs, 2001). Metabolic status also influ- ences calcium absorption such that severe obesity is associated with higher calcium absorption and dieting reduces the fractional calcium absorption by 5 percent (Cifuentes et al., 2002; Riedt et al., 2006).

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40 DIETARY REFERENCE INTAKES FOR CALCIUM AND VITAMIN D With aging and after menopause, fractional calcium absorption has been reported to decline on average by 0.21 percent per year after 40 years of age (Heaney et al., 1989). Nordin et al. (2004) and Aloia et al. (2010) also reported decreased absorption with age. There are early reports of an inverse correlation between age and calcium absorption in women (Avioli et al., 1965), and several studies have indicated that despite an increase in circulating levels of calcitriol in older women, which would be anticipated to increase calcium uptake, fractional calcium absorption was unaffected (Bullamore et al., 1970; Alevizaki et al., 1973; Gallagher et al., 1979; Tsai et al., 1984; Eastell et al., 1991; Ebeling et al., 1992). Thus, although cal- cium absorption (active calcium transport) has been reported to decrease with age, it is challenging to take this factor into consideration given that calcium intake must be very high to have a significant effect on calcium uptake via the passive absorption. Homeostatic Regulation of Calcium Maintaining the level of circulating ionized calcium within a narrow physiological range is critical for the body to function normally, and con- trol of serum calcium levels is maintained through an endocrine system—a system of glands that secrete hormones and is characterized by controlling factors and feedback mechanisms—that includes a major role for vitamin D metabolites, principally calcitriol, and PTH. Calcium balance within the body is closely linked to the hormonal actions of calcitriol. The vitamin D- related endocrine system that maintains serum calcium levels is discussed in Chapter 3 but is also summarized below and illustrated in Figure 2-1. The vitamin D metabolic system forms the basis of the calcium ho- meostatic mechanism in mammals. Total calcium concentration in serum is tightly regulated to remain between 8.5 and 10.5 mg/dL (2.12 and 2.62 mmol/L). If this level deviates slightly, the calcium sensing receptor of the parathyroid gland signals the secretion of PTH, which functions as a calcium sensor. PTH then stimulates the kidney to produce calcitriol, the hormonal form of vitamin D, as well as to activate bone resorption, which will increase extracellular calcium levels. Calcitriol acts in an endocrine manner on the intestine, bone, and kidney to raise serum calcium lev- els; it also acts on the intestine and, to some extent, the kidneys to raise serum phosphorus levels. As the serum calcium level rises, the feedback mechanism causes the calcium sensing receptor to be turned off and PTH secretion to drop. If there is an overshoot in serum calcium levels, the “C” cells (parafollicular) cells of the thyroid gland secrete calcitonin, which can block bone calcium resorption, helping to keep serum calcium levels in the normal range. Calcitriol, through its receptor, also provides feedback rela- tive to suppressing the production and release of PTH, commonly referred

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41 OVERVIEW OF CALCIUM Total Serum Calcium Calcitriol FIGURE 2-1 Endocrine feedback system that maintains serum calcium levels: In- volvement of vitamin D and parathyroid hormone (PTH). NOTE: CT = calcitonin; PTG = parathyroid gland. fig 2-1.eps SOURCE: Reprinted with permission from Hector DeLuca. bitmap with 2 vector labels to as PTH suppression. Not shown in the figure is that calcitriol is also di- rectly controlled by the serum phosphorus level; a high serum phosphorus level suppresses the formation of calcitriol, whereas a low level stimulates it. Excretion Calcium leaves the body mainly in urine and feces, but also in other body tissues and fluids, such as sweat. Calcium excretion in the urine is a function of the balance between the calcium load filtered by the kidneys and the efficiency of reabsorption from the renal tubules. Nearly 98 per- cent of filtered calcium (i.e., glomerular filtrate) is reabsorbed by either passive or active processes occurring at four sites in the kidney, each con- tributing to maintaining neutral calcium balance. Seventy percent of the filtered calcium is reabsorbed passively in the proximal tubule. Active cal- cium transport is regulated by the calcium sensing receptor located in the ascending loop of Henle, where, in response to high calcium levels in the extracellular fluid, active reabsorption in the loop is blocked through ac- tions of the calcium sensing receptor. In contrast, when the filtered calcium load is low, the calcium sensing receptor is activated, and a greater fraction of the filtered calcium is reabsorbed. In the distal tubule, the ion chan-

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42 DIETARY REFERENCE INTAKES FOR CALCIUM AND VITAMIN D nels known as transient receptor potential cation channel, vanilloid family member 5 or TRPV5 control active calcium transport and this process is regulated by calcitriol and estradiol (Hoenderop et al., 2000). Finally, the collecting duct also can participate in passive calcium transport, although the relative percentage of total calcium reabsorption in the collecting duct is low. Overall, a typical daily calcium loss for a healthy adult man or woman via renal excretion is 5 mmol/day (Weaver and Heaney, 2006a). Calcium is excreted through the feces as unabsorbed intestinal cal- cium and is shed in mucosal cells and secretions including saliva, gastric juices, pancreatic juice, and bile. Endogenous fecal calcium losses are approximately 2.1 mg/kg per day in adults and about 1.4 mg/kg per day in children (Abrams et al., 1991). These intestinal losses as well as minor losses in sweat are referred to collectively as endogenous calcium excretion. Endogenous calcium excretion, in contrast to urinary excretion, does not change appreciably with aging (Heaney and Recker, 1994). PTH can be a major determinant of urinary calcium excretion; during states of low calcium intake, secondary increases in PTH levels result in reduced urinary calcium excretion. Impaired renal function due to aging paradoxically reduces calcium loss due to impaired filtration, but there is also a secondary increase in PTH levels due to reduced phosphate clear- ance. However, renal 1α-hydroxylase activity declines with impaired renal function, so the net result is calcium loss from the kidney, but also reduced active transport of calcium from the intestine. Excess Intake Although excess intake of calcium is almost never due to calcium in- take from foods, the use of calcium supplements (including the voluntary fortification of a range of foods that are not naturally sources of calcium) has increased (Ricci et al., 1998; Riedt et al., 2005), and excess calcium intake may occur as a result of high intake from calcium supplements. Excess calcium intake can result in adverse effects. Calcium plays a major role in the metabolism of virtually every cell in the body and interacts with a large number of other nutrients, and as a result, disturbances of calcium metabolism may give rise to a variety of adverse effects (IOM, 1997). A review of the considerations related to adverse effects from excess calcium ingestion can be found in Chapter 6, which focuses on the establishment of Tolerable Upper Intake Levels (ULs). FUNCTIONS AND PHYSIOLOGICAL ACTIONS OF CALCIUM Calcium is an integral component of the skeleton, and the skeleton provides a reservoir of calcium for other essential calcium-dependent func- tions throughout the body. The skeleton serves at least three main func-

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43 OVERVIEW OF CALCIUM tions. First, calcium, as part of the mineral hydroxyapatite, deposited into the organic matrix of the skeleton, is critical for its structure and is neces- sary for tissue rigidity, strength, and elasticity. This function allows for nor- mal movement and exercise. Second, the skeleton functions as a source of minerals and alkali and therefore is critical for overall mineral homeostasis. The skeleton is the principal depot for calcium, containing 98 percent of total body calcium. It can be called on repeatedly, through the processes of bone formation and resorption (referred to as remodeling, as discussed below), to maintain circulating levels of calcium at a constant level. While the same qualitative processes apply to skeletal calcium metabolism across the life cycle, there are quantitative differences by age and hormonal sta- tus. These life cycle differences for skeletal growth and remodeling are discussed in a section below. Excessive calcium resorption can compromise the integrity and strength of the skeletal tissues. Third, the marrow cavity of bone serves as a major site for the development of hematopoietic cells and as a major compartment of the immune system. Several of the cell types involved in bone remodeling originate in the bone marrow compart- ment. Stromal or connective tissue cells are found in the bone marrow; at one time, these were thought to be inert, but they are now considered multi-potent stem cells that can become either fat or bone cells under the influence of specific differentiation factors (Muruganandan et al., 2009). A principal physiological function of calcium apart from its role in maintaining the skeleton, is as an essential intracellular messenger in cells and tissues throughout the body. Although this pool of calcium is quanti- tatively small, the ionized calcium present in the circulatory system, extra- cellular fluid, muscle, and other tissues, is critical for mediating vascular contraction and vasodilatation, muscle function, nerve transmission, and hormonal secretion. Ionized calcium is the most common signal transduc- tion element in biology, owing to its ability to reversibly bind to proteins and to complex with anions such as citrate and bicarbonate (Weaver and Heaney, 2006b). Bone Formation and Remodeling Bone is composed of a mineral compartment, predominantly calcium hydroxyapatite and an organic matrix, osteoid, composed principally of collagen and non-collagenous proteins and growth factors. The relative contributions of the mineralized and organic compartments depend on the age of the individual; in general, 50 to 70 percent of bone is mineral, 20 to 40 percent is organic matrix, and the rest is water and lipid. The or- ganic matrix is critical for both the structural and functional components of the skeleton, providing elasticity and contributing to regenerative and remodeling properties. Much of the organic matrix is composed of type I collagen fibrils that are organized in such a manner that strength and

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44 DIETARY REFERENCE INTAKES FOR CALCIUM AND VITAMIN D elasticity are combined. Numerous non-collagenous proteins are also pres- ent in the organic matrix. Some of them, such as osteocalcin and matrix GLA protein, contain γ-carboxyglutamate, an amino acid with high affin- ity for calcium that is required for proper mineralization of the matrix (see below). The role of phosphate in bone development should not be overlooked. As described below, first phosphorus is laid down during the mineralization process, and then calcium binds to it. Calcitriol stimulates the uptake of both calcium and phosphorus from the intestine. Development The skeleton develops through a process of either intramembranous or endochondral bone formation, depending on location and function. Intramembranous bone formation is the predominant process in the skull, whereas endochondral bone formation occurs in long bone and the axial skeleton. Intramembranous bone is formed by direct differentiation of mesenchymal precursors into osteoblasts, cells of the fibroblast–stromal lineage that produce bone matrix proteins and synthesize a lattice for subsequent mineralization. In contrast, during endochondral bone forma- tion chondrocytic differentiation occurs first, leading to a soft cartilaginous infrastructure. The cartilage then becomes calcified, and the provisional calcified cartilage is subsequently replaced by bone. This occurs by vascular invasion, which allows entry of hematopoietic precursors and osteoclasts, macrophage-like cells that originate from the monocyte–macrophage lin- eage, which remove apoptotic chondrocytes and cartilage (Provot and Schipani, 2007). New bone is formed by osteoblasts. Osteoblastogenesis follows chondrogenesis after release of growth factors from terminally dif- ferentiated chondrocytes. The first bone formed is woven and relatively un- organized. However, through osteoclastic modeling that bone is replaced by lamellar bone, which is highly organized and provides the strength necessary to support soft tissue (Yang and Yang, 2008). Endochondral bone formation allows for linear development of the growth plate as well as periosteal expansion, which ultimately results in a longer and thicker bone. Mineralization is the final stage in terminal differ- entiation of the osteoblast and occurs through a complex process whereby ion deposition is followed by crystal formation between the collagen fibrils. This occurs because of undersaturation of calcium hydroxyapatite in the extracellular fluid and the binding of calcium to non-collagenous proteins in the matrix (Favus, 2008). Initially, phosphate drives the mineralization by being laid down in bone as hydroxyapatite; the negative charge of hy- droxyapatite then causes calcium to avidly bind to it. In states of phospho- rus deficiency, unmineralized osteoid persists despite adequate calcium intake. Bone mechanical properties are then influenced by the distribu-

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45 OVERVIEW OF CALCIUM BOX 2-1 Bone Remodeling Terms and Definitions • Cortical bone: One of two types of bone; makes up the outer part of all skeletal structures (nearly 80 percent of the skeleton); is dense and compact with a slow turnover rate and is highly resistant to bending and torsion. • Trabecular bone: Second of the two bone types; found inside of long bones, vertebrae, pelvis, and other large flat bones; is less dense than cortical bone and has a higher turnover rate. • Osteoblast: A type of bone cell that is responsible for the production of bone and bone formation. • Osteoclast: A type of bone cell that resorbs bone using acid and enzymes. • Bone remodeling: Process that occurs throughout the lifetime that results from the pairing action of osteoclasts (breaking down) and osteoblasts (building up), which replaces damaged bone with new material. • Bone modeling: A similar process to remodeling, except that new bone is formed at a location different from the site of resorption, such as during times of growth. SOURCE: Hadjidakis and Androulakis, 2006. tion, size, and density of the apatite crystals. Too much or too little mineral can lead to impaired bone strength; the former makes the bone too brittle, whereas the latter makes the bone too ductile and weak. Remodeling Calcium balance is preserved within the non-bone tissues of the body, because adult bone constantly undergoes remodeling through bone re- sorption, mainly by osteoclasts and bone formation mainly by osteoblasts.3 Terminology associated with remodeling is shown in Box 2-1. In adults, vir- tually all of the human skeleton is remodeled over a 10-year cycle, although trabecular bone turns over more readily. In contrast, bone formation incor- porates calcium into the matrix, and this process requires significant time 3Not all calcium enters the skeleton through bone formation or leaves the skeleton through bone resorption, as discussed by Parfitt (2003). Moreover, during lactation and in response to other acute demands for calcium, osteocytes have been shown to resorb the matrix surround- ing them and then to restore it after the stress is over (Teti and Zallone, 2009).

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64 DIETARY REFERENCE INTAKES FOR CALCIUM AND VITAMIN D Foods and Food Components Sodium and potassium in the diet may also affect calcium nutriture. High intakes of sodium increase urinary calcium excretion. In contrast, adding more potassium to a high-sodium diet might help decrease calcium excretion, particularly in postmenopausal women (Sellmeyer et al., 2002; IOM, 2005). Alcohol intake can affect calcium nutriture by reducing calcium ab- sorption (Hirsch and Peng, 1996), although the amount of alcohol re- quired to cause an effect and whether moderate alcohol consumption is helpful or harmful to bone are unknown. Caffeine from coffee and tea modestly increases calcium excretion and reduces absorption (Heaney and Recker, 1982; Bergman et al., 1990). Two studies have indicated that caffeine intake (two to three or more cups of coffee per day) will result in bone loss, but only in individuals with low milk or low total calcium intake (Barrett-Connor et al., 1994; Harris and Dawson-Hughes, 1994). Phosphate is also of interest. Food phosphate is a mixture of inorganic and organic forms, and there is no evidence that its absorption efficiency varies with dietary intake. A portion of phosphorus absorption is due to saturable, active transport facilitated by calcitriol. However, fractional phosphorus absorption is virtually constant across a broad range of intakes suggesting that absorption occurs primarily by a passive, concentration- dependent process. Several observational studies have suggested that the consumption of carbonated soft drinks with high levels of phosphate is associated with reduced bone mass and increased fracture risk, but it is likely that the effect is due to replacing milk with soda, rather than to phosphorus itself (Calvo, 1993; Heaney and Rafferty, 2001). REFERENCES Aaron, J. E., J. C. Gallagher, J. Anderson, L. Stasiak, E. B. Longton, B. E. Nordin and M. Nicholson. 1974. Frequency of osteomalacia and osteoporosis in fractures of the proxi- mal femur. Lancet 1(7851): 229-33. Abrams, S. A., J. B. Sidbury, J. Muenzer, N. V. Esteban, N. E. Vieira and A. L. Yergey. 1991. Stable isotopic measurement of endogenous fecal calcium excretion in children. Journal of Pediatric Gastroenterology and Nutrition 12(4): 469-73. Abrams, S. A., N. V. Esteban, N. E. Vieira, J. B. Sidbury, B. L. Specker and A. L. Yergey. 1992. Developmental changes in calcium kinetics in children assessed using stable isotopes. Journal of Bone and Mineral Research 7(3): 287-93. Abrams, S. A. and J. E. Stuff. 1994. Calcium metabolism in girls: current dietary intakes lead to low rates of calcium absorption and retention during puberty. American Journal of Clinical Nutrition 60(5): 739-43. Abrams, S. A., J. Wen and J. E. Stuff. 1997. Absorption of calcium, zinc, and iron from breast milk by five- to seven-month-old infants. Pediatric Research 41(3): 384-90.

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