Bone, vitamin intake

Antioxidants in fruits and vegetables including vitamin C and (3-carotene reduce oxidative stress on bone mineral density, in addition to the potential role of some nutrients such as vitamin C and vitamin K that can promote bone cell and structural formation (Lanham-New 2006). Many fruits and vegetables are rich in potassium citrate and generate basic metabolites to help buffer acids and thereby may offset the need for bone dissolution and potentially preserve bone. Potassium intake was significantly and linearly associated with markers of bone turnover and femoral bone mineral density (Macdonald and others 2005). 

The physiological role of vitamin K is in blood clotting and is essential for the synthesis of at least four of the proteins (including prothrombin) involved in this process. Vitamin K also plays a role in the synthesis of a protein (osteocalcin) in bone. Vitamin K deficiency is rare but can result from impaired absorption of fat. Vitamin K levels in the body are also reduced if the intestinal flora is killed (e.g. by antibiotics). Vitamin K toxicity is rare but can be caused by excessive intake of vitamin K supplements. Symptoms include erythrocyte haemolysis, jaundice, brain damage and reduced effectiveness of anticoagulants. 

Oral calcium has long been used for the treatment of osteoporosis, both in the form of dietary and pharmacological supplements. In patients with calcium deficiency, oral calcium at doses of 1000-1500 mg/day corrects a negative calcium balance and suppresses PTH secretion. Sufficient calcium intake is most important for the acciual of peak bone mass in the young, but is also considered the basis of most anti-osteoporotic regimens. In the elderly, supplementation with oral calcium and vitamin D reduces the risk of hip fracture by about 30 4-0%. 

Osteoporosis Oral calcium supplementation (1000-5000 mg/day) Oral vitamin D Calcifediol (1000 lU/day) Calcitriol (0.5 mcg/day) Hormone-replacement therapy Calcitonin or oral bisphosphonates If daily intake less than 1000 mg elemental calcium Documented deficiency If kidney functioning If kidney not functioning Post-menopausal women without contraindications Documented loss in bone mineral density greater than 3% Data lacking for bisphosphonates in patients with Rl... 

Some osteoporosis risk factors (see Table 53-1) are non-modifiable, including family history, age, ethnicity, sex, and concomitant disease states. However, certain risk factors for bone loss may be minimized or prevented by early intervention, including smoking, low calcium intake, poor nutrition, inactivity, heavy alcohol use, and vitamin D deficiency. 

Although most fragility fractures in women occur after age 50, certain groups of premenopausal women are at high risk for osteoporosis. The NOF recommends measuring bone mineral density in premenopausal women with risk factors in addition to sex and race, in whom treatment would be considered.1 Premenopausal women at risk for osteoporosis should follow all nonpharmacologic recommendations for exercise and adequate calcium and vitamin D intake. Currently, no good data... 

Factors that can predispose patients to developing metabolic bone disease include deficiencies of phosphorus, calcium, and vitamin D vitamin D and/or aluminum toxicity amino acids and hypertonic dextrose infusions chronic metabolic acidosis corticosteroid therapy and lack of mobility.35,39 Calcium deficiency (due to decreased intake or increased urinary excretion) is one of the major causes of metabolic bone disease in patients receiving PN. Provide adequate calcium and phosphate with PN to improve bone mineralization and help to prevent metabolic bone disease. Administration of amino acids and chronic metabolic acidosis also appear to play an important role. Provide adequate amounts of acetate in PN admixtures to maintain acid-base balance. 

Finally, Yano et al.18 reported a significant negative association between forearm bone mineral content and current caffeine intake among a group of elderly Japanese-American women living in Flawaii, after controlling for intake of milk, calcium, and vitamin D. 

However, results obtained by Koo et al. (1991) indicate that low to moderate lead exposure (average lifetime PbB level range of 4.9-23.6 pg/dL, geometric mean of 9.8 pg/dL, n=105) in young children with adequate nutritional status, particularly with respect to calcium, phosphorus, and vitamin D, has no effect on vitamin D metabolism, calcium and phosphorus homeostasis, or bone mineral content. The authors attribute the difference in results from those other studies to the fact that the children in their study had lower PbB levels (only 5 children had PbB levels >60 pg/dL and all 105 children had average lifetime PbB levels <45 pg/dL at the time of assessment) and had adequate dietary intakes of calcium, phosphorus, and vitamin D. They concluded that the effects of lead on vitamin D metabolism observed in previous studies may, therefore, only be apparent in children with chronic nutritional deficiency and chronically elevated PbB levels. Similar conclusions were reached by IPCS (1995) after review of the epidemiological data. 

Milk is an excellent source of calcium, phosphorus, riboflavin (vitamin B2), thiamine (vitamin Bl) and vitamin B12, and a valuable source of folate, niacin, magnesium and zinc (Food Standards Agency, 2002). In particular, dairy products are an important source of calcium, which is vital for maintaining optimal bone health in humans (Prentice, 2004). The vitamins and minerals it provides are all bioavailable (i.e. available for absorption and use by the body) and thus milk consumption in humans increases the chances of achieving nutritional recommendations for daily vitamins and mineral intake (Bellew et al., 2000). 

Calcium is essential for bones, teeth, metabolic signaling and regulation, and other bodily functions. Adults require an intake of around lg per day only about 10% of the calcium ingested is absorbed into the body - less from a low-protein diet, more from a high-protein diet. Vitamin D facilitates absorption, as does... 

Age, calcium intake, hormonal status, exercise and vitamin status have all been implicated in the development of osteoporosis. Estrogen levels represent an important factor in skeletal calcium retention and homeostasis. In therapeutic trials in which post-menopausal women were given daily doses of estrogens, such therapy has been demonstrated to be partially effective in reducing the rate of bone resorption. However, this therapy has the concomitant hazard of endometrial cancer (10). Vitamin D and its hormones have been given considerable attention in the more recent studies. Without adequate dietary and tissue levels of such vitamins, calcium absorption and bone status will be impaired. 

In summary, the results of this life-long experiment on female mice indicated that low or high Ca intake early in life did not have any significant effect on the skeletal Ca in adulthood, but the continued high Ca intake reduced the turnover rate in old age. Consequently the strengh of the bone was better preserved than that in the mice fed the low Ca diet. This supports the use of Ca supplements even in old patients suffering from osteoporosis, provided their vitamin D status is adequate. Dietary fluoride... 

A number of nutrients affect bone integrity early in life. While the role of certain minerals and vitamins bearing on skeletal integrity is well established, that of protein remains controversial, especially when consumed in excessive amounts. Protein-included calciuric effect as observed in adult man and animals may also occur early in life and thus conceivably affect peak bone mass adversely, particularly when calcium intakes may be marginal. In studies reported here (test model young female rats), it was found that a diet approaching adequacy in protein and based equally on plant and animal sources would favor some parameters which bear on skeletal mass at maturity more than other combinations of protein consumed. 

Vitamin D hormone is derived from vitamin D (cholecalciferol). Vitamin D can also be produced in the body it is formed in the skin from dehydrocholesterol during irradiation with UV light. When there is lack of solar radiation, dietary intake becomes essential, cod liver oil being a rich source. Metaboli-cally active vitamin D hormone results from two successive hydroxylations in the liver at position 25 ( calcifediol) and in the kidney at position 1 ( calci-triol = vit. D hormone). 1-Hydroxylation depends on the level of calcium homeostasis and is stimulated by parathormone and a fall in plasma levels of Ca or phosphate. Vit D hormone promotes enteral absorption and renal reabsorption of Ca and phosphate. As a result of the increased Ca + and phosphate concentration in blood, there is an increased tendency for these ions to be deposited in bone in the form of hydroxyapatite crystals. In vit D deficiency, bone mineralization is inadequate (rickets, osteomalacia). Therapeutic Liillmann, Color Atlas of Pharmacology... 

Martini and Wood (2002) tested the bioavailability of 3 different sources of Ca in 12 healthy elderly subjects (9 women and 3 men of mean SEM age 70 3 and 76 6 years, respectively) in a 6-week crossover trial conducted in a Human Study Unit. Each Ca source supplied 1000 mg Ca/day and was ingested for 1 week with meals (as 500 mg Ca 2x/day), thus contributing to a high-Ca intake (1300 mg Ca/day). A low-Ca intake (300 mg Ca/day strictly from the basal diet) was adhered to for 1 week in-between each treatment. The Ca sources included skim milk, CCM-fortified OJ, and a dietary supplement of CaCOa. Assessment parameters were indirect measures predicted to reflect the relative bioavailability of Ca postprandially via an acute PTH suppression test (hourly for 4h). Longer-term responses to Ca supplementation were assessed via a number of urinary and serum hormone, mineral, and bone resorption biomarkers (i.e., vitamin D, Ca, phosphorus, and collagen t) e 1 N-telopeptide cross-links). 

Vitamin D is converted in the liver and kidneys to 1,25-dihydroxyvitamin D, which is the hormone-active compounds. The principal physiological function is to maintain the serum calcium and phosphorus concentrations in a range that support cellular processes, neuromuscular function, and bone ossihcation [417], Only a few foods contain vitamin D in quantities that have an impact on the dietary intake hsh liver, hsh liver oils, fatty fish, and egg yolks. Thus, some countries practice fortihcation of certain foods with vitamin D, most often milk, margarine, and/or butter. 

Vitamin A deficiency can result from insufficient dietary intake, from malabsorption and it has been recognized that also malfunction of RAR-receptors can lead to symptoms of vitamin A deficiency. These symptoms include skin lesions, night blindness, corneal ulcerations and conjunctivitis and poor bone remodeling. Vitamin A deficiency associated with malnutrition is wide spread in large parts of the world and may be fatal in infants and young children suffering from kwashiorkor or marasmus. 

High daily doses of retinoids can lead to hyper-vitaminosis A manifesting itself as dermal toxicity such as erythematous dermatitis, bone pains, neurological symptoms and hepatosplenomegaly. A recent study shows a correlation between low bone mineral density and too high intake of vitamin A. 

The role of estrogens in the prevention and treatment of osteoporosis has been carefully studied (see Chapter 42). The amount of bone present in the body is maximal in the young active adult in the third decade of life and begins to decline more rapidly in middle age in both men and women. The development of osteoporosis also depends on the amount of bone present at the start of this process, on vitamin D and calcium intake, and on the degree of physical activity. The risk of osteoporosis is highest in smokers who are thin, Caucasian, and inactive and have a low calcium intake and a strong family history of osteoporosis. Depression also is a major risk factor for development of osteoporosis in women. 

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