Osteoporosis micronutrient role

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Hi All,

See the references available from the HTML below paper outlining micronutrient

factors in osteoporosis.

Nieves JW.

Osteoporosis: the role of micronutrients.

Am J Clin Nutr. 2005 May;81(5):1232S-9S.

PMID: 15883457

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstra\

ct & list_uids=15883457

INTRODUCTION

The most recent definition of osteoporosis is a disease characterized by loss of

bone mass, accompanied by microarchitectural deterioration of bone tissue, which

leads to an unacceptable increase in the risk of skeletal failure (fracture).

Osteoporosis and low bone mass are currently estimated to be a major public

health

threat for almost 44 million US men and women aged 50 and older, or 55% of the

population in that age range (1). In fact, 1 in 2 women and 1 in 4 men over the

age

of 50 will fracture at some point in their lifetime. The costs to the healthcare

system associated with osteoporotic fracture are 17 billion dollars annually

(2),

with each hip fracture having total medical costs of $40 000.

Adequate nutrition plays a major role in the prevention and treatment of

osteoporosis; the nutrients of greatest importance are calcium and vitamin D.

Numerous studies have shown that higher calcium intake at various ages are

associated with higher bone mineral density compared with the bone mass of those

with lower calcium intakes (3). In older postmenopausal women, the benefits of

vitamin D and calcium supplementation in preventing bone loss, decreasing bone

turnover, and decreasing nonvertebral fractures are clear (4).

An inadequate intake of either calcium, vitamin D, or both will influence

calcium-regulating hormones. A deficiency of either calcium or vitamin D will

result

in reduced calcium absorption and a lower concentration of circulating ionized

calcium. When this occurs, parathyroid hormone (PTH) secretion is stimulated and

there is a resulting increase in PTH levels. The cumulative effect of higher PTH

levels, secondary to poor calcium and vitamin D nutrition (secondary

hyperparathyroidism), is an increase in bone remodeling leading to significant

loss

of bone and an increased fracture risk. Vitamin D supplementation, often in

combination with calcium, appears to reduce the degree of secondary

hyperparathyroidism associated with poor nutrition.

The recommended calcium intake changes with age and the current recommended

intakes

are listed in Table 1 (5). One of the highest daily intakes is required after

age

50. Important dietary sources of calcium are dairy products (milk, yogurt,

cheese),

dark green vegetables; canned fish with bones (but not fish fillets); nuts; and

more

recently, fortified foods (including juices, waffles, cereals, crackers, and

snack

foods). The average US diet contains only 600 mg calcium a day and thus falls

far

below the recommended intakes (6). If an adequate calcium intake is not possible

in

the diet, a calcium supplement may be required and should optimally be taken in

doses < 500 mg at a time to maximize absorption, because absorption decreases

with

greater calcium loads. The preferred time to take most supplements is with

meals,

because calcium is better absorbed with food. Calcium carbonate has more calcium

per

tablet (40%) than some of the other forms of calcium such as calcium citrate

(23%).

In most healthy individuals calcium intakes up to 2500 mg/d are safe (5).

TABLE 1 Food and Nutrition Board Dietary Reference Intakes (Recommended Average

Intakes for Calcium and Vitamin D)1

Age (y) Calcium (mg) Vitamin D (IU)

---------------------------------------

3–8 800 200

9–17 1300 200

18–50 1000 400

51–70 1200 400

>70 1200 600

----------------------------------

1 Institute of Medicine: " Dietary Reference Intakes for calcium, magnesium,

phosphorus, vitamin D and Fluoride. " Food and Nutrition Board, Institute of

Medicine. Washington, DC: National Academy Press, 1997.

In younger individuals, vitamin D synthesis in the skin is the primary

determinant

of serum 25(OH)D levels; however, the cutaneous synthesis is reduced in the

elderly.

Elevations in serum PTH and greater bone loss are often associated with lower

levels

of 25(OH) D. Vitamin D insufficiency is believed to play a strong role in

osteoporosis. The current US recommendation for vitamin D intake in people age

51 to

70 y is 10 µg/d (400 IU/d) and over age 70 y is 15ug/d (600 IU/d; see Table 1

(5)).

However, higher doses of vitamin D (800–1000 IU/d) in the elderly (age 65 y)

may

actually be required for optimal bone health, because these vitamin D doses have

been shown to reduce fracture risk in this population (3, 4). Rich sources of

vitamin D include fatty fish, fish-liver oils (cod liver oil), and liver.

Several

foods are also fortified with vitamin D including milk, margarine, orange juice,

and

cereals. There is general agreement that the serum levels of 25(OH)D are the

best

indication of adequate and inadequate vitamin D levels (7, 8).

In the United States, in the cohort 65 y and older in national health and

nutrition

examination survey (NHANES) III, 32% of whites, 64% of blacks and 53% of

Hispanics

had levels of 25(OH)D < 54 nmol/L, the median for the entire NHANES cohort (9).

In a

recent consensus conference, it was suggested that adequate 25(OH)D levels may

be 80

nmol/L or 32 ng/mL, and that intakes of vitamin D of over 1000 IU per day are

needed

to achieve these serum levels (7). Vitamin D adequacy is often defined in older

adults as the level of 25(OH)D needed to maximally suppress PTH levels. Serum

25(OH)D was the most significant (negative) determinant of serum PTH in a study

of

almost 1000 postmenopausal women (10). The rise in serum PTH appeared to start

when

serum 25(OH)D fell < 80 nmol/L. These data further suggest that the optimal

level of

serum 25(OH)D in postmenopausal women may be at least 80 nmol/L.

Suboptimal serum Vitamin D levels are widespread and should be evaluated,

particularly in the elderly. However, the following populations are at

particularly

high risk of vitamin D deficiency: patients with malabsorption syndromes;

patients

with liver or kidney diseases; patients taking certain medications that

interfere

with vitamin D metabolism including steroids, dilantin, and phenobarbitol.

CALCIUM AND BONE MASS

Considerable epidemiologic data have been accumulated seeking to evaluate the

relation between calcium intake and bone density. Peak bone mass, that is

attained

during adolescence/young adulthood, can be maximized by raising calcium intake

to

the adequate intake levels recommended by the 1997 Food and Nutrition Board (see

Table 1). Higher calcium intakes have been related to higher bone mass in

children,

young adults, and postmenopausal women in 64 out of 86 observational

epidemiologic

studies (11).

Clinical trials with calcium supplements in children and adolescents have been

short

term (1 to 3 y) and have shown an overall positive effect of calcium on bone

mass

accrual between 1 and 6% per year in the total body and between 1% and 10% at

each

skeletal region compared with placebo (3, 12). In children, results are often

dependent on pubertal stage. For example, in one recent study, postmenarcheal

adolescent girls (<15.5 y of age) with baseline low calcium intakes (<800 mg/d).

Those who were given calcium supplementation (1000 mg per day) had enhanced bone

mineral acquisition compared with girls given placebo, especially in girls > 2 y

past the onset of menarche (13). A meta-analysis of calcium intake in slightly

older

premenopausal women concluded that calcium supplementation led to an average

increase in bone density at the spine and forearm of 1.1% per year compared with

women receiving placebo (14). However, in most studies, the benefit of added

calcium

on bone mass disappears when supplementation is halted (15, 16), although one

trial

showed a persistent benefit persisting after 3–4 y (17). These data suggest that

adequate calcium intake needs to be maintained throughout childhood,

adolescence,

and young adulthood to have a lasting impact on peak bone mass.

Considerable epidemiologic data have been accumulated seeking to evaluate the

relation between calcium intake and bone density. In postmenopausal women,

reviews

of over 20 studies have concluded that calcium supplementation can decrease bone

loss by 1% per year (18). In a meta-analysis of 13 trials, calcium induced

significant mean gains (or slowed loss) of 0.6% at the forearm, 3% at the spine

and

2.6% at the femoral neck (19). A more recent meta-analysis found that in 15

trials,

calcium changes were 1.66% at the lumbar spine and 1.64% at the hip (20).

Therefore,

calcium supplementation has been shown to be effective in retarding bone loss in

postmenopausal women. The beneficial effect of calcium intake on bone mass in

postmenopausal women may be modified by factors including age, number of years

since

menopause, baseline calcium intake before supplementation, and possibly physical

activity level. In addition, the effect of calcium may be greater at the sites

with

more cortical bone (21–22), in elderly and late postmenopausal women, and in

women

with low baseline calcium intakes. In large enough doses calcium can reduce the

higher PTH levels and lower the rate of bone remodeling (23). Calcium

supplementation appears to improve the efficacy of antiresorptive therapy, such

as

with hormone replacement therapy (HRT), on bone mass (24).

VITAMIN D AND BONE MASS

There have been several studies of vitamin D supplementation, typically in

combination with calcium (500 to 1200 mg/d). The % difference between treatment

with

vitamin D and placebo resulted in average differences of 1.0%, 1.2%, and 0.2%

respectively for the spine, femoral neck, and forearm (25–28). The prevalence of

serum 25(OH)D deficiency and peak bone mass has been recently investigated. In

this

Finnish study, the median levels of serum 25(OH)D were 44, 24, and 41 nmol/L in

July, winter, and again in July. These data indicate a fair number of young men

aged

18–20 have low serum 25(OH)D. The authors found a positive correlation between

serum

25(OH)D and bone mineral content at all sites (29). This study points to the

potential need for intervention studies on the effects of vitamin D

supplementation

on the attainment of peak bone mass.

A French study reported that supplementation with 500 mg calcium and 400 IU of

vitamin D given to women with serum 25(OH)D < 12 ng/mL, compared with placebo

significantly decreased PTH and markers of bone turnover and improved bone

mineral

density (BMD). In this study, short-term changes in bone resorption markers can

predict long term variations in bone density in elderly women with vitamin D

insufficiency receiving vitamin D and calcium (30).

In another study of younger women (1 to 10 y postmenopausal), who had normal

25(OH)D

levels (mean 82 nmol/L), the addition of 10 000 IU vitamin D per week to calcium

supplementation at 1000 mg per day did not confer any benefits on BMD beyond

that

which was achieved with calcium supplementation alone (31). Although the elderly

clearly require supplementation, in younger populations, there may be less

benefit

of vitamin D supplementation if serum 25(OH)D levels are normal.

IMPACT OF CALCIUM AND VITAMIN D ON FALLS IN THE ELDERLY

Falls are often the cause of hip fracture, which may result in death, morbidity,

and

admission to a nursing home. Clearly muscle strength, in particular lower

extremity,

should be one of the factors assessed and treated in older persons at risk for

falls

(32). In a recent analysis of NHANES data, in both active and inactive

ambulatory

elderly subjects, there was a strong improvement in lower extremity function

based

on walking speed and sit-to-stand speed, in serum 25(OH)D levels between 5 and

40

nmol/L, with continued but less significant improvement up to 90 nmol/L (9).

Clearly

vitamin D supplementation should be an important part of fall prevention, which

in

turn may reduce osteoporotic fractures. Adults with vitamin D deficiency have

muscle

weakness and are more likely to fall (33). In a meta-analysis (34), vitamin D

supplementation appeared to reduce falls by 20%, and furthermore if 15 patients

were

treated with vitamin D, 1 fall could be prevented.

PREVENTION OF FRACTURE WITH CALCIUM AND VITAMIN D

A review of 16 observational studies assessing hip fracture and calcium intake

found

that an increase in usual calcium intake of 1 g a day was associated with a 24%

reduction in the risk of hip fracture (35). A recent prospective cohort study

did

not show an association between dietary calcium and vitamin D intake and

fracture in

a cohort of Swedish women aged 50–85 y(36). In a follow-up of the cohort from

the

Nurses Health Study (37), an adequate vitamin D intake was associated with a

lower

risk of hip fracture, although neither milk intake nor a high calcium diet were

associated with hip fracture reduction. A meta-analysis of observational studies

relating calcium intake to fracture risk (38) also failed to show any

association

between calcium and hip fracture, although there was a suggestion that

individuals

with extremely low calcium intake may be at increased fracture risk.

However, data from randomized trials are much less prone to bias than the

previously

discussed observational studies. Two randomized clinical trials, which evaluated

calcium supplementation found vertebral fractures to be reduced by 28% and

symptomatic fractures to be reduced by 70% in the calcium supplemented group

(39–40). Significant reductions in fracture (26 to 54% reduction in hip and

non-spine fracture rates) have also been seen in those randomized clinical

trials

where calcium was given in conjunction with vitamin D (25–27, 41–42). In the

studies

where fractures were not reduced, the participants had higher baseline serum

25(OH)D

levels, were not given additional calcium, or were given a lower dose of vitamin

D

(400 IU; 28; 43). One important study, published this year, was a randomized

double

blind controlled trial of 100 000 IU oral vitamin D3 (cholecalciferol)

supplementation or matching placebo every 4 mo over 5 y in 2037 men and 649

women

aged 65–85 y. The supplements were provided by mail every 4 mo. After 5 y, 268

men

and women had incident fractures, of which 147 had fractures in common

osteoporotic

sites (hip, wrist, or forearm, or vertebrae). Relative risks in the vitamin D

group

compared with the placebo group were 0.78 (95% CI 0.61 to 0.99, P = 0.04) for

any

first fracture and 0.67 (0.48 to 0.93, P = 0.02) for first hip, wrist or

forearm, or

vertebral fracture. This study demonstrated that a widespread public health

effort

could be successful at preventing fractures without adverse effects in men and

women

living in the general community (44). Another important public health study of

9605

community dwelling Danish residents reported that 400 IU vitamin D and 1000 mg

of

calcium supplements significantly reduced fracture by 16% in this Northern

European

region that is known to be deficient in vitamin D (45).

A meta-analysis found that vitamin D decreased vertebral fractures and may

decrease

nonvertebral fractures (46).

To sustain the benefits of increased calcium and vitamin D the higher intake of

these nutrients must be maintained. In a 2-year follow-up of participants in the

Dawson- trial, the bone density gains were lost and bone turnover markers

increased (47).

PHOSPHORUS

Phosphorus intake does not seem to influence skeletal homeostasis within normal

ranges of intake (RDA 700 mg/d), although excessive intakes particularly when

combined with low calcium intake may be deleterious (48). Alternatively,

adequate

phosphorus intake is essential for bone building during growth and low serum

phosphate will limit bone formation and mineralization (49). Foods that are high

in

phosphorus are milk, milk products, poultry, fish, meat, eggs, grains and

legumes,

and sodas, with only milk (and milk products) also having high amounts of

calcium.

High phosphorus intakes in the face of low calcium intake may lead to secondary

hyperparathyroidism and bone loss. A diet adequate in calcium, with moderate

protein

and sufficient phosphorus was related to higher bone density (50). Phosphorus

deficiency may be a marker of general nutritional inadequacy, similar to protein

deficiency seen in the elderly, and in that regard could lead to an increased

risk

of fracture. These low phosphorus intakes or negative phosphorus balance due to

food

phosphorus being bound to supplemental calcium may create a relative phosphorus

deficiency, which could limit osteoblast function and enhance osteoclastic bone

resorption (51). At any age, the ratio of phosphorus to calcium is probably more

important than the intake of phosphorus alone (51–52).

SALT

Sodium causes an increase in renal calcium excretion. The mean urinary calcium

loss

is 1 mmol per 100 mmol sodium (53). If absorbed calcium is less than the amount

needed to offset these obligatory calcium losses that are related to sodium

intake,

then bone mass will be negatively impacted. In observational studies, higher

salt

intake leads to higher levels of PTH and greater rates of bone resorption in

postmenopausal women and men (54, 55). Furthermore, those with low calcium and

high

salt diets have lower BMD (55–58). The optimal intake of sodium for calcium

conservation and to meet the American Heart Association (AHA) guideline is 2400

mg

per day. An adequate intake of calcium allows a more liberal use of sodium in

the

diet. Recently, the Dietary Approaches to Stop Hypertension (DASH) diet was

shown to

reduce bone turnover (59). Increased sodium intake leads to increased renal

calcium

excretion. However, if AHA guidelines are followed (2400 mg sodium/d) there will

be

no negative impact on bone health. Markers of bone resorption do relate to

sodium

intake but generally BMD does not relate to sodium intake. The anion is

important

with sodium chloride increasing urinary calcium more than other salts such as

sodium

bicarbonate or sodium acetate (60). Sodium intake will not be a problem in the

face

of adequate calcium intake (61) or potassium (55).

POTASSIUM

The main importance of potassium is based on the influence of potassium on

calcium

homeostasis, particularly the urinary conservation and excretion of calcium. Low

potassium diets increase urinary calcium losses and high potassium diets reduce

it.

Potassium is found in several vegetables, fruits, legumes, and milk and tends to

have alkaline ash characteristics. There have been some studies relating the Net

Endogenous Acid Production (NEAP) to potassium intake and bone density (62–63).

Furthermore, increased intake of potassium citrate was able to ameliorate the

higher

bone resorption seen with high salt diets (55). Higher potassium intake,

primarily

from fruits and vegetables, was associated with higher baseline BMD and less

bone

loss (64). The need to ensure adequate potassium intake from fruits and

vegetables

is a strong rationale for the " 5 to 10 servings per day recommendation " (65).

VITAMIN K

Vitamin K is a fat-soluble vitamin that functions as a cofactor in enzymes

involved

in the synthesis of blood coagulation factors and may be required for bone

metabolism, to facilitate carboxylation of proteins such as osteocalcin

(involved in

bone formation) and to reduce urinary calcium excretion (66–67). Vitamin K is

present in dark green leafy vegetables, fruits, and vegetable oils with small

amounts in dairy products and grains. Vitamin K2 is found in fermented dairy and

soy

products, fish, meat, liver, and egg. The current adequate intake (AI) for

vitamin K

is set at 120 µg for men and 90 µg for women.

Observational studies indicate that vitamin K intake and serum levels are

positively

related to bone density (68–71) and patients who sustain fractures have been

reported to have lower serum vitamin K levels. Epidemiologic studies have also

found

that higher vitamin K intake is related to lower fracture incidence (72–75).

Furthermore, a high percentage of undercarboxylated serum osteocalcin as seen

with

low serum vitamin K may be a predictor of fracture risk (66, 76–78), although

many

of these studies are confounded by overall poor nutrition. However, in healthy

girls

with a typical US diet, better vitamin K status was associated with decreased

bone

turnover (79).

Deficiency or antagonism of vitamin K (coumarin derivatives) can result in the

undercarboxylation of specific proteins involved in bone metabolism including

osteocalcin. In cohort studies, warfarin use for more than 1 year was an

independent

predictor of spine and hip fracture (80) but this was not confirmed in a

separate

study (81), perhaps because of the small number of women on warfarin.

Several small controlled vitamin K supplementation studies have found reductions

in

calcium excretion, bone resorption, and the undercarboxylated fraction of

osteocalcin. A compound derived from vitamin K (MK4) had a positive effect on

BMD in

large doses when given to women with osteoporosis (82) and strokes (83). High,

pharmacologic doses of vitamin K2 (45 mg) were also related to lower rates of

bone

loss and a lower incidence of fractures (84–85).

Based on the current evidence of observational studies, studies on intermediate

endpoints, and small studies with bone density and limited fracture data, there

are

insufficient data to recommend the required level of vitamin K supplementation

for

optimal bone health. One trial with a 3-y supplementation of phylloquinone (1

mg/d)

with calcium and vitamin D reduced hip bone loss (86). A healthy diet, high in

fruits and vegetables, ensures that vitamin K intake is adequate for most of the

population.

VITAMIN C

Vitamin C is an essential cofactor for collagen formation and synthesis of

hydroxyproline and hydroxylysine. Rich dietary sources of vitamin C include

citrus

fruit and juices, peppers, broccoli, and tomato products and green leafy

vegetables.

The dietary reference intakes (DRIs) for vitamin C are 75 mg/d for adult women

and

90 mg/d for adult men. Epidemiologic studies show a positive association between

vitamin C and bone mass; low intakes of vitamin C are associated with a faster

rate

of BMD loss, and one study found that higher vitamin C was associated with fewer

fractures; however, there are no randomized clinical trials (87–94). Recommended

intakes of 5 or more servings of fruits and vegetables should supply enough

vitamin

C for bone health.

VITAMIN A

Recommended dietary allowance of vitamin A is 800 µg/d retinol equivalent (RE)

for

females and 1000 µg/d RE for males. Vitamin A is a fat-soluble vitamin required

for

vision, growth, fighting infection, and for bone remodeling. There are different

types of vitamin A in the diet and in supplements: retinol and ß-carotene (and

other

carotenoids). Excess vitamin A may be detrimental to bone health with intakes of

higher than 1500 µg of RE related to a 2-fold increased risk of hip fracture in

the

United States and Sweden but not in Iceland or in another US study (95–98).

These

population studies show excess vitamin A intake from retinol appeared to

increase

the risk of hip fracture.

There is no evidence of any association between ß-carotene intake and

osteoporosis

or related fracture. Vitamin A from fruits and vegetables (carotenoids) does not

negatively affect bone health.

MAGNESIUM

Magnesium, complexed with adenosine triphosphate (ATP) takes part in many enzyme

reactions including synthesis of proteins and nucleic acid. The intake

recommended

for healthy adult males is 420 mg/d and for women is 320 mg/d. Because magnesium

is

present in most foods—particularly legumes, vegetables, nuts, seeds, fruits,

grains,

fish and dairy—severe magnesium deficiency is rarely seen in healthy people.

However, many intakes in the United States fall below this recommended level.

Furthermore, a magnesium supplement may be required in frail elderly with poor

diets

(99) or persons with intestinal disease (100), alcoholics, or persons on

treatment

with diuretics or chemotherapy that depletes magnesium. In addition, as calcium

supplements sometimes result in constipation, a supplement with magnesium might

be

useful to keep bowel habits regular.

Magnesium deficiency is easily detected with biochemical symptoms (eg, low serum

magnesium, low serum calcium, resistance to vitamin D) or clinical symptoms (eg,

muscle twitching, muscle cramps, high blood pressure, irregular heartbeat).

Lastly,

magnesium deficiency is easily treated.

Several small epidemiologic studies have found that higher magnesium intakes are

associated with higher BMD in elderly men and women (101). There have been only

small controlled clinical trials of magnesium supplementation (102–103) that

were

primarily effective in magnesium-depleted subjects. There is little evidence

that

magnesium is needed to prevent osteoporosis in the general population. Overall,

observational and clinical trial data concerning magnesium and bone density or

fractures are inconclusive and, in fact, one recent study from the WHI reported

that

higher intakes of magnesium were associated with a higher risk of wrist fracture

(104).

FLUORIDE

Fluoride is an essential trace element that is required for skeletal and dental

development. The adequate daily adult intake is 4 mg for males and 3 mg for

females.

The concentration of fluoride in the soil, water, and many foods varies by

geographic region. Major dietary sources include drinking water, tea, coffee,

rice,

soybeans, spinach, onions, and lettuce. There is no need to add fluoride

supplements

to an adult diet for skeletal health. The lower doses of fluoride typically

found in

drinking water have no effect on bone density or on fractures (105–107);

however, in

some endemic high fluoride areas, higher hip fracture rates have been seen.

Excess

fluoride ingestion causes fluorosis, a painful condition associated with

extra-osseous calcification and brittle bones. High doses of fluoride can

stimulate

osteoblasts; however, the quality of bone that is formed may be abnormal and the

effect on fracture rates is unclear (108).

OTHER NUTRIENTS

The effects of trace metals on bone remain unknown. Three studies have shown

that a

combination of several minerals (zinc, manganese and copper) with calcium was

able

to reduce spinal bone loss in postmenopausal women (109–110).

Boron is not an essential nutrient so there are no recommended intakes. Although

studies have found that 3 mg daily of boron may have a positive effect on bone

(102,

111), controlled trials are needed. Boron is present in several foods such as

fruits, vegetable, nuts, eggs, wine, and dried foods. Copper is an essential

element

required by many enzymes including lysyl oxidase, which is required for cross

linking of collagen. Severe deficiency does have profound effects on bone. There

have only been a few intervention trials with variable results on bone turnover

and

bone density (112–114), or a mixture of trace elements has been studied (109).

Profound zinc deficiency leads to reduced bone growth and maturation. However,

there

is little evidence that zinc has an effect on bone mass or osteoporotic

fractures.

Dietary silicon intake was reported to correlate with BMD at the hip in a cohort

of

men and premenopausal women (115). These results will require further follow-up.

In 2 recent studies, poor vitamin B12 status was associated with low BMD in men

and

women, and osteoporosis in elderly women but not men (116,117). It is unclear

whether associations such as this are really an indication of overall poor

nutrition

and frailty. Similarly, in another study increased dietary iron intake was

associated with greater bone mineral density at all sites (118).

RECOMMENDATIONS

The nutritional needs for optimizing bone health can be easily met by a healthy

diet

with adequate calcium and vitamin D intakes through dairy or calcium fortified

foods. Foods are a preferred source to maintain calcium balance because there

are

other essential nutrients that are found in high calcium foods. For those

individuals where there is inadequate calcium intake from diet, supplemental

calcium

can be used. Supplemental or dietary calcium should be spread out throughout the

day

with 500 mg or less being consumed at each meal to optimize absorption.

In all individuals over the age of 70, vitamin D intakes of at least 600 IU per

day

(ideally 800-1000 IU/d) are recommended, in addition to the calcium requirement

of

1200 mg/d. Vitamin D from foods, supplements, and/or multivitamins can be used

to

meet the vitamin D requirement. Recent evidence suggests that the optimal level

of

serum 25(OH)D may be close to 80 nmol/L (7, 8). Severe vitamin D deficiency can

be

easily treated by giving the patient an oral dose of 50 000 IU of vitamin D once

a

week for 8 wk or by giving 50 000 IU of vitamin D daily for 10 days (119–120).

The

fortification of food products is becoming frequently used as a method to

improve

calcium intake and may also be a reasonable method to increase the vitamin D

intake

of the population and reduce the prevalence of hypovitaminosis D. The use of

calcium

and vitamin D supplements in an elderly population has been shown to be

cost-effective for hip fracture prevention (121–122). Medical professionals need

to

be aware of the importance of ensuring adequate calcium and vitamin D intakes

for

patients on osteoporosis therapy (123).

The effects of calcium and vitamin D on bone cannot be considered in isolation

from

the other components of the diet (124). The other micronutrient needs for

optimizing

bone health can be easily met by a healthy diet that is high in fruits and

vegetables (5 servings per day) for magnesium, potassium, vitamin C, vitamin K

and

other potentially important nutrients (125–126).

Al Pater, PhD; email: old542000@...

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