Calcium, vitamin D, and your bones: MedlinePlus Medical Encyclopedia
Calcium is a nutrient needed for strong bones, but your body cannot absorb it properly without the help of vitamin D. The combination of calcium and vitamin D . Getting enough calcium and vitamin D in your diet can help maintain bone strength and lessen your risk of developing osteoporosis. The Bottom Line: Recommendations for Calcium Intake and Bone Health; References Calcium supplements often contain vitamin D; taking calcium paired with . they still found no association between calcium intake and fracture risk.
It is often added to orange juice, soy milk, tofu, ready-to-eat cereals, and breads. Check the labels on these foods for added calcium. Other Sources of Calcium Green leafy vegetables, such as broccoli, collards, kale, mustard greens, turnip greens, and bok choy Chinese cabbageare good sources of calcium.
Other good food sources of calcium are: Salmon and sardines that are canned with their bones you can eat these soft bones Almonds, Brazil nuts, sunflower seeds, tahini sesame pasteand dried beans Blackstrap molasses Other tips to make sure your body can use the calcium in your diet: Cook high-calcium vegetables in a small amount of water for the shortest possible time. Be careful about what you eat with calcium-rich foods. Certain fibers, such as wheat bran and foods with oxalic acid spinach and rhubarbcan prevent your body from absorbing calcium.
Your doctor may recommend a calcium or vitamin D supplement for the calcium and vitamin D you need. An earlier study followed pre-pubertal males and females mean age 8. In a longer-term randomized clinical trial, Matkovic et al. 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.
Vitamin D and Bone Health; Potential Mechanisms
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.
When considered together, these studies support an increase in skeletal size and mineralization that occurs with calcium supplementation, but fail to show consistently that BMC is retained over the long term, particularly after supplementation is withdrawn.Mayo Clinic Minute: Bone Up on Calcium
Effect of Menopause Studies of bone histomorphometry Recker et al. The span of 5 to 10 years surrounding menopause is characterized by a decrease in estrogen production and an increase in resorption of calcium from bone Stevenson et al.
For example, Ebeling et al. The bone loss is most rapid in the early years of menopause, and then approximately 6 to 7 years postmenopause the loss continues at a slower rate Pouilles et al.
Over time, such changes lead to skeletal fragility and decreased bone mass. Some cohort studies demonstrate that accelerated bone loss is an independent risk factor for fracture, such that the combination of low bone mass and high rates of bone turnover markedly increase the potential for a future fracture Garnero et al.
Bone remodeling in postmenopausal osteoporosis includes changes in osteoid thickness, surface area, and volume. Considerable variability exists among women regarding the effects of menopause on bone loss, and such effects vary according to body mass index and ethnicity Finkelstein et al. However, the use of such therapy has declined as a result of recent reports of adverse non-skeletal effects.
Because rapid bone loss occurs after estrogen treatment is discontinued Gallagher et al. Skeletal Disorders Rickets and Osteomalacia Rickets is the term for the end-stage condition in infants and children that begins with suboptimal bone mineralization at the growth plate and progresses with associated physiological perturbations that include secondary hyperparathyroidism, hypocalcemia, and hypophosphatemia leading to irreversible changes in skeletal structure.
The disease is a disorder of the growth apparatus of bone in which growth cartilage fails to mature and mineralize normally. Because the bone is undermineralized it is also soft and ductile, and this leads to bowing of the limbs, widening and compression of the ends of the long bones, etc.
The similar condition of osteomalacia defective mineralization of bone and softening of bone also occurs, and is seen in adults as well as children. Although these conditions are commonly associated with inadequate vitamin D exposure, each can also result from calcium or phosphorus deficiency. Rickets and osteomalacia due to a lack of calcium in the diet cannot be corrected by increasing levels of calcitriol i.
Rickets In rickets, during prolonged deficiency of calcium and phosphatethe body increases PTH to prevent hypocalcemia by causing osteoclastic absorption of the bone. This, in turn, causes the bone to become progressively weaker, resulting in rapid osteoblastic activity.
The osteoblasts produce large amounts of organic bone matrix, osteoid, which does not become calcified Guyton and Hall, Consequently, the newly formed, uncalcified osteoid gradually takes the place of other bone that is being reabsorbed. During the later stages of rickets, the serum calcium level falls precipitously, and tetany neuromuscular spasm develops. In infants and young children, a long-standing calcium intake deficiency, in association with suboptimal vitamin D exposure, can produce rickets.
Indeed, in experimental animals and in humans with extremely low vitamin D levels, genetic absence of calcitriol vitamin D—dependent rickets [ VDDR ] type Ior genetic absence of the vitamin D receptor VDDR type IIthe use of increased calcium supplementation or calcium infusions will prevent and treat rickets.
These observations indicate that the primary cause of rickets is inadequate delivery of calcium to the bone surface, not a defect in osteoblast function. In other words, the primary role for vitamin D and calcitriol in regulating skeletal homeostasis is indirectly accomplished by stimulating the intestinal absorption of calcium and phosphorus.
The clinical symptoms of rickets include stunted growth and bowing of the extremities. Osteomalacia In osteomalacia, as seen in adults, the newly deposited bone matrix fails to mineralize adequately. 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.
As a result, older adults who have calcium-poor diets and very low vitamin D levels may develop not only osteoporosis, as described below i. Osteomalacia is actually the clinical syndrome of undermineralization of bone associated with muscle weakness, bone pain, and fractures.
The characteristic histological feature of osteomalacia is unmineralized matrix, which is often represented experimentally as the ratio of osteoid volume to bone volume.
Ultimately, reductions in mineralization lead to impaired bone strength and significant softening of the skeleton. The calcium levels in the blood of patients with osteomalacia are often normal despite the undermineralization of bone, underscoring the importance of maintaining the blood calcium level over maintaining the mineralization of the skeleton.
However, serum phosphorus levels are frequently low, PTH concentrations are 5 to 10 times the normal levels, and there is an increased level of alkaline phosphatase together with increased markers of bone turnover. Bone scans often indicate dramatically increased skeletal uptake by resident osteoblasts.
As recognized by Parfitt et al. During the earliest stages preosteomalaciathere exists a calcium-deficient state, even though the osteoid thickness, mineralization lag time, and osteoid volume are still normal. Subsequently, more dramatic changes occur including a greater increase in osteoid thickness, and impaired mineralization.
Osteomalacia is estimated to be present in about 4 to 5 percent of general medical and geriatric patients Anderson, ; Stacey and Daly, ; Campbell et al.
However, the clinical syndrome of bone pain, muscle weakness, and impaired bone mineralization is much less frequently recognized. In the face of severe osteoporosis, the diagnosis of osteomalacia can only be made by bone biopsy, usually using the method of double tetracycline labeling, demonstrating impaired mineralization of the skeleton Villareal et al.
In fact, osteomalacia is noted histologically in the bones of 20 to 40 percent of first-time hip fracture patients Jenkins et al. These results suggest that these individuals may be presenting with a mixture of osteoporosis and osteomalacia.
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. Reduced bone mass—as measured by low BMD —increases bone fragility and, in turn, predisposes a person to an increased risk of fracture, notably at the vertebrae, hip, and forearm NIH Consensus Development Panel on Osteoporosis Prevention, Diagnosis, and Therapy, As shown in Figurethe relationship between BMD measures and the incidence of fractures is notable.
Overall, osteoporosis-related morbidity and mortality, as well as health care costs, are a significant public health concern NIH Consensus Development Panel on Osteoporosis Prevention, Diagnosis, and Therapy, Osteoporosis is most commonly associated with women, but the condition also occurs in men.
Archives of Internal Medicine Menopause can initiate osteoporosis through elevated bone remodeling, which occurs characteristically in postmenopausal women. Remodeling activity, although designed to repair weakened bone, actually makes it temporarily weaker when remodeling is excessive. It can lead to enhanced skeletal fragility Heaney, Although it is unclear to what extent calcium intake can mitigate such bone loss, inadequate calcium intake can exacerbate the situation.
Men experience age-related bone loss as well, although not due to menopause.
This, in turn, can result in osteoporosis. However, the incidence of fracture risk increases some 5 to 10 years later in men than it does in women Tuck and Datta, 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. For all life stages highlighted below, specific studies and conclusions are detailed in Chapter 4. Infancy At full-term birth, the human infant has accrued about 26 to 30 g of calcium, most of which is in the skeleton.
When calcium transfer from the placenta ceases at birth, the newborn infant is dependent on dietary calcium. Calcium deposition into bone occurs at a proportionately higher rate during the first year of life than during other periods.
Breast-fed infants absorb about 55 to 60 percent of the calcium in human milk Abrams et al. Formula-fed infants receive more calcium than breast-fed infants because formula contains nearly double the calcium of breast milk. However, fractional calcium absorption is lower in formula-fed infants, averaging about 40 percent among different formula types Abrams et al.
Studies to establish the level of calcium provided by human milk are long-standing in nature, and little information has emerged to change the conclusions of earlier analyses.
This estimate is based on the average concentrations found in several studies from the United States and the United Kingdom, as summarized in Atkinson et al. Variations in milk calcium content have been found between population groups.
- Calcium and bones
- Calcium, vitamin D, and your bones
- Relationship Between Vitamin D & Calcium
Relative to the average amount of milk consumed by infants, there are three key studies based on weighing full-term infants before and after feeding Butte et al. While it has been noted that the volume of intake is somewhat lower during the first month of life than in subsequent months Widdowson, ; Southgate et al.
Childhood and Adolescence Calcium deposition into bone is an ongoing process throughout childhood and into adolescence, reaching maximal accretion during the pubertal growth spurt. For growing children, bone modeling i.
Modeling requires mineralization; hence, calcium requirements are increased, particularly during neonatal and pubertal growth spurts. Approximately 40 percent of total skeletal bone mass is acquired within a relatively short window of 3 to 5 years, when gonadal steroids and growth hormone secretion are maximal Weaver and Heaney, b. During this time, bone formation far outpaces resorption and longitudinal growth, and consolidation of bone occurs.
During this developmental period, calcium absorption is maximal and variation in calcium intake accounts for 12 to 15 percent of the variance in calcium retention for both boys and girls.
Increases in total calcium transiently enhance bone mass Lee et al. 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 calcium-supplemented individuals Matkovic et al. However, this period of bone accretion determines adult bone mass, which, in turn, is a significant predictor of fracture risk late in life.
Young Adults After puberty and throughout most of adulthood, bone formation and resorption are balanced. During this period, bone mass is consolidated, and calcium requirements are relatively stable. Peak bone mass, the maximum amount of bone that can be accumulated, is reached in early adulthood Bonjour et al. The ability to attain peak bone mass is affected by genetic background and by lifestyle factors such as physical activity and total calcium intake. Specific skeletal sites have been found to reach peak bone mass at different ages, and bone mineral accretion has been reported to continue slowly into the third decade of life Recker et al.
Bone is a dynamic tissue, and a number of clinical studies suggest that increasing bone mass early in life has a transient effect, but does not confer protection against later bone loss and osteoporosis Gafni and Baron, The calcium content of bone at maturity is approximately 1, g in women and 1, g in men Ilich and Kerstetter, ; Anderson, In men, this level remains relatively constant until the onset of age-related bone loss later in life.
In women, the level remains relatively constant until the onset of menopause. Although bone mass generally remains at a plateau during reproductive years, some studies have suggested that mean bone mass gradually reaches a plateau and then declines slowly with age.
Older Adults Age-related bone loss, in both men and women, results when bone remodeling becomes uncoupled and bone resorption exceeds bone formation. However, the pathogenesis of bone loss is a multi-faceted process. The roles and interactions of various hormonal, genetic, and other factors in bone loss and risk for decreased bone health are not yet clear. Moreover, the ability of increased calcium intake to overcome the effects of bone loss related to menopause or normal aging continues to be debated.
In postmenopausal women, estrogen loss increases the rate of bone remodeling, characterized by an imbalance between osteoclast and osteoblast activity, resulting in irreversible bone loss Riggs et al.
Estrogen loss can further accelerate bone loss through its effect on decreased absorption of calcium and increased urinary loss of calcium Nordin et al. Evidence suggests that remodeling in women becomes imbalanced just prior to, during, and immediately after menopause, when the rate of bone loss becomes more rapid. However, the rate of bone loss as a result of menopause varies greatly depending upon a number of factors, including genetics, body composition, other hormonal changes and endogenous production of estradiol.
The effects of lower estrogen levels on calcium balance continue to be debated. However, the principal effect of estrogen deficiency on the skeleton is increased bone resorption.
The range of bone loss in the 7 to 10 years around the onset of menopause can range from 3 to 7 percent annually Kenny and Prestwood, In women over age 65, the rate of bone loss slows again to 0.
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. This compensation results in accelerated bone resorption, leading to a net loss of bone mass under these conditions. For men over 65 years of age, the loss of bone is about 1 to 2 percent per year Orwoll et al.
Additionally, reduced glomerular filtration rate is another factor associated with aging that affects renal conservation of calcium in both men and women Goldschmied et al. This is underscored by patients with renal disease who have renal osteodystrophy, now referred to as chronic kidney disease—mineral disorder Demer and Tintut, ; Peacock, Pregnancy and Lactation Pregnancy The fetal need for calcium is met by maternal physiological changes, primarily through increased calcium absorption.
There is currently debate about whether calcium is also mobilized from maternal skeleton, as discussed in Chapter 4. In any case, calcium is actively transported across the placenta from mother to fetus, an essential activity to mineralizing the fetal skeleton. Intestinal calcium absorption of the mother doubles beginning early in pregnancy—even though there is little calcium transfer to the embryo at this stage Heaney and Skillman, ; Kovacs and Kronenberg, —and continues through late pregnancy Kent et al.
Overall, relatively few studies have examined the effect of calcium supplementation on either fetal or maternal outcomes. Maternal serum calcium falls during pregnancy Pedersen et al.
Reports indicate that the concentration of ionized calcium remains normal during pregnancy Frolich et al.
Vitamin D and Bone Health; Potential Mechanisms
Within the developing human fetus, calcium metabolism is regulated differently from that of its mother.
Few vitamin D fortified foods, aside from margarine, are available within Western Europe possibly owing to early adverse advent incidents of infantile hypercalcaemia attributed to over-fortification of dried milk with vitamin D [ 16 ]. Other countries, including the USA fortify foods; however, surveys have suggested significant differences between the actual and reported levels of fortification [ 1718 ]. Vitamin D absorption occurs in the ileum and jejunum.
Excess non-hydroxylated vitamin D is stored in the liver, adipose tissue and muscle [ 24 ]. The kidney however, is not the only source of CYP27B1: Once the hormone has been metabolized it is converted to calcitroic acid and excreted. The primary effect of vitamin D is enhanced calcium absorption in the small intestine [ 232425 ]. The hormone interacts with the vitamin D receptor [VDR] in intestinal cells and complexes with the retinoic acid x receptor [RXR] in the nucleus [ 2324 ].
This complex binds to the vitamin-D-responsive element [VDRE] of the calcium channel [TRPV6] which increases uptake of calcium into the cells and increases the absorption of calcium [ 2425 ]. This conversion releases chemicals such as hydrochloric acid to metabolise calcium stores from the bones into circulation to maintain the optimal physiological range [ 25 ]. Figure 1 Summary diagram of vitamin D metabolism and function. Vitamin D Intake and Status Until recently, it was generally assumed that enough vitamin D was synthesized from sun exposure to meet requirements and no recommendations for dietary intakes for adults aged yrs were set.
However, research highlighting the effects of low vitamin D status [ 2627 ] has indicated the importance of vitamin D in the diet. The difficulty in assigning a RNI for vitamin D intake is exacerbated by the current lack of agreement on optimal vitamin D status.
Over extended periods of time, insufficiency has been associated with increased bone loss and secondary hyperparathyroidism leading to increased fracture risk [ 36 ]. Sufficiency has been regarded as the point at which further intakes will have no additional beneficial effects on PTH and calcium metabolism in regard to bone health.
The relationship between Calcium and Vitamin D | Kauvery Hospital
However, the cut-off values for sufficiency are still under debate. As mentioned earlier, the dietary intake of vitamin D required to prevent vitamin D deficiency and ensure optimal vitamin D status will vary depending on sun exposure preferences.
However, the authors also calculated that a dietary intake of Such intakes are considerably higher than estimated vitamin D intakes in Ireland [3. Vitamin D toxicity is rare [ 45 ]. The symptoms include vomiting, nausea, constipation, weight loss, weakness and kidney stones with subsequent hypercalcaemia and ectopic calcification of soft tissue [ 46 ]. However, as discussed earlier, the formation of vitamin D from sunlight is a self-limiting reaction; thus preventing toxicity from sun exposure.
Vitamin D and Bone Health Peak bone mass is attained by the third decade of life [ 50 ] with genetics, physical activity, nutrition and lifestyle factors [ 5152 ] playing key roles in the accumulation and maintenance of bone.
Age related bone loss occurs around the fourth decade [ 53 ], resulting in a gradual decline of BMD though this process is accelerated in females during and up to 10 years post-menopause owing to possible oestrogen deficiency derived bone loss [ 54 ]. The development of bone disease in later life is related to the attainment of maximum peak bone mass and the maintenance of bone mass in adulthood [ 55 ]. In relation to vitamin D, research has shown that inadequate vitamin D intakes over long periods of time can lead to bone demineralization [ 56 ].