Dietary Reference Intakes for Calcium and Vitamin D (2011) / Chapter Skim
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2 Overview of Calcium
2 Overview of Calcium
Pages 35-74
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From page 35... ...
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)
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Brulé, Health Canada, April 29, 2010) -- reporting use of dietary supplements of some type, dietary supplements must be taken into account when considering the sources of calcium in the diet and, in turn, estimating total calcium intake.
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For this reason, persons with known deficiencies of these other minerals who require calcium supplementation usually take calcium supplements between meals (Straub, 2007)
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. 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)
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. There was no significant relationship between calcium intake from solid foods and the fractional calcium absorption from human milk.
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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 control 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.
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From page 41... ...
Active calcium 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 actions 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.
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From page 42... ...
. 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.
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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)
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In states of phosphorus deficiency, unmineralized osteoid persists despite adequate calcium intake. Bone mechanical properties are then influenced by the distribu
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Remodeling Calcium balance is preserved within the non-bone tissues of the body, because adult bone constantly undergoes remodeling through bone resorption, mainly by osteoclasts and bone formation mainly by osteoblasts.3 Terminology associated with remodeling is shown in Box 2-1. In adults, virtually all of the human skeleton is remodeled over a 10-year cycle, although trabecular bone turns over more readily.
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From page 46... ...
is associated with a profound uncoupling of remodeling, such that bone resorption is dramatically increased, whereas bone formation is suppressed. These changes cause rapid bone loss and are a major problem for long-term spaceflight.
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This study found significant increases in bone accretion for total bone density, distal and proximal radius, and metacarpal indexes after 4 years of supplementation; by 7 years, however, only the proximal radius and metacarpal indexes still showed significantly increased bone accretion over non-supplemented controls. These findings corroborate a role for calcium intake and skeletal size; however, they also suggest that bone accretion diminishes during skeletal consolidation in late adolescence, and attainment of a peak bone mass was transient for some skeletal sites, even though the study subjects continued calcium supplementation through year 7.
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The bone loss associated with menopause results from uncoupling in the bone remodeling units, such that resorption of bone is greater than formation of new bone. Over time, such changes lead to skeletal fragility and decreased bone mass.
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Poor calcium intake is associated with secondary increases in PTH in an attempt to compensate for low serum calcium levels. The secondary hyperparathyroidism of calcium deficiency states is associated with increased bone resorption and suppression of bone formation.
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This clinical scenario can be related to both nutrient insufficiency and the coincidental progression of age-related bone loss. Osteoporosis and Fractures Osteoporosis is a skeletal disorder associated with aging and characterized by compromised bone strength due to reduced bone mass and reduced bone quality.
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FIGURE 2-2 Bone mineral density (BMD) , osteoporotic fracture rate, and number of women with fractures.
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The major physiological activities include bone accretion during skeletal growth and maintenance of bone mass after growth is completed. Later in adult life, net calcium is lost from the body when bone formation no longer keeps up with bone resorption.
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Childhood and Adolescence Calcium deposition into bone is an ongoing process throughout childhood and into adolescence, reaching maximal accretion during the pubertal growth spurt. Measures of bone density in adolescent girls indicate that about 37 percent of total skeletal bone mass is achieved between pubertal stages 2 (mean age 11 years)
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. These effects disappear during or after cessation of increased calcium intake; final bone mass, measured in randomized trials of calcium supplementation during this period, did not differ between controls and calciumsupplemented individuals (Matkovic et al., 2005)
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. Later in menopause -- and in men over 70 years of age -- if reduced calcium intake occurs, it contributes to a secondary form of hyperparathyroidism, which serves as a compensatory mechanism to maintain extracellular calcium balance.
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Lactation Breast milk calcium content is homeostatically regulated, and maternal calcium intake does not appear to alter the breast milk calcium content (Kalkwarf et al., 1997; Jarjou et al., 2006)
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Balance studies embody a metabolic approach to examining the relationship between calcium intake and calcium retention and are based on the assumption that the body retains the amount of calcium that is needed. As such, measures of calcium balance (or of "calcium retention")
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In the 1997 IOM report that focused on calcium DRIs (IOM, 1997) , metabolic studies of calcium balance were used to obtain data on the relationship between calcium intakes and retention, from which a non-linear regression model was developed; from this was derived an intake of calcium that would be adequate to attain a predetermined desirable calcium retention.4 The approach used in 1997 was a refinement of an earlier approach suggested to determine the point at which additional calcium does not significantly increase calcium retention, called the plateau intake (Spencer et al., 1984; Matkovic and Heaney, 1992)
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, the non-linear regression model describing the relationship between calcium intake and retention was solved to obtain a predetermined desirable calcium retention that was specific for each age group. According to the report, the major limitation of the data available was that bone mineral accretion during growth had not yet been studied over a wide range of calcium intakes.
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From page 60... ...
The method combines estimates of losses of calcium via its main routes in apparently healthy individuals and then assumes that these losses represent the degree to which calcium intake, as corrected by estimated absorption, is required to balance these losses. The weakness in this method is that it is unusual for all of the necessary measurements to be obtained within a single study.
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gAbsorption is 38% for mean age 13 years on calcium intakes of 1,330 mg/day (Wastney et al., 1996)
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Indeed, bone remodeling is not directly regulated by calcium, although it can suppress PTH-induced increases in bone resorption under certain conditions. Circumstances that enhance bone resorption, such as estrogen deficiency, or glucocorticoid use, alter the organic matrix and reduce the thickness and density of trabeculae, independent of calcium intake.
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. In contrast, some epidemiological studies suggest that high protein diets reduce bone mass; this has been attributed to a higher acid load, leading to a buffering response by the skeleton and greater urinary calcium excretion.
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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)
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1994. Peak bone mass.
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1988. Effect of lowering dietary calcium intake on fractional whole body calcium retention.
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2007. Childhood bone mass acquisition and peak bone mass may not be important determinants of bone mass in late adulthood.
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1989. Calcium absorption in women: relationships to calcium intake, estrogen status, and age.
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1997. Calcium retention in relation to calcium intake and postmenarcheal age in adolescent females.
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1991. Calcium metabolism and calcium requirements during skeletal modeling and consolidation of bone mass.
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1995. Calcium requirements of lactating Gambian mothers: effects of a calcium supplement on breast-milk calcium concentration, maternal bone mineral content, and urinary calcium excretion.
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1985. Correlates of forearm bone mass among women during maximal bone mineralization.
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1994. Calcium kinetics in lactating women with low and high calcium intakes.
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Point. American Journal of Clinical Nutrition 89(5)
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