Calcium & Disease Prevention - Part 1

Colorectal Cancer

Colorectal cancer is the most common gastrointestinal cancer and the second leading cause of cancer deaths in the U.S. Colorectal cancer is caused by a combination of genetic and environmental factors, but the degree to which these two factors influence the risk of colon cancer in individuals varies widely. In individuals with familial adenomatous polyposis, the cause of colon cancer is thought to be almost entirely genetic, while dietary factors appear to influence the risk of colon cancer in others. Animal studies are strongly supportive of a protective role for calcium in preventing intestinal cancers. In humans, controlled clinical trials have found modest decreases in the recurrence of colorectal adenomas (precancerous polyps) with calcium supplementation of 1,200-2,000 mg/day. However, most large prospective studies have found increased calcium intake to be only weakly associated with a decreased risk of colorectal cancer. These weak associations might be explained by the presence of groups within the population that differ in their response to calcium. A recent case-control study of 511 men found that increased calcium intake was more strongly associated with decreased colorectal cancer risk in those men with higher circulating levels of a growth factor known as IGF-1 . There is some evidence that individuals with increased circulating levels of IGF-1 are at increased risk of colorectal cancer, and increased calcium intake may benefit this subgroup more than others. Before conclusions can be drawn, more research is needed to clarify whether specific subgroups in the larger population have different calcium requirements with respect to decreasing the risk of colorectal cancer.

Osteoporosis

Osteoporosis is a skeletal disorder in which bone strength is compromised, resulting in an increased risk of fracture. Sustaining a hip fracture is one of the most serious consequences of osteoporosis. Nearly one third of those who sustain osteoporotic hip fractures enter nursing homes within the year following the fracture, and one person in five dies within one year of sustaining an osteoporotic hip fracture. Although osteoporosis is most commonly diagnosed in white postmenopausal women, women of other racial groups and ages, men, and children may also develop osteoporosis.

Osteoporosis is a multifactorial disorder, and nutrition is only one factor contributing to its development and progression. Other factors that increase the risk of developing osteoporosis include, but are not limited to, increased age, female gender, estrogen deficiency, smoking, metabolic disease (e.g., hyperthyroidism), and the use of certain medications (e.g., corticosteroids and anticonvulsants). A predisposition to osteoporotic fracture is related to one's peak bone mass and to the rate of bone loss, after peak bone mass has been attained. After adult height has been reached, the skeleton continues to accumulate bone until the third decade of life. Genetic factors exert a strong influence on peak bone mass, but life style factors can also play a significant role. Strategies for reducing the risk of osteoporotic fracture include the attainment of maximal peak bone mass and the reduction of bone loss later in life. Although, calcium is the nutrient consistently found to be most important for attaining peak bone mass and preventing osteoporosis, adequate vitamin D intake is also required for optimal calcium absorption.

Physical exercise is another lifestyle factor of benefit in the prevention of osteoporosis and osteoporotic fracture. There is evidence to suggest that physical activity early in life contributes to the attainment of higher peak bone mass. Exercise in the presence of adequate calcium and vitamin D intake probably has a modest effect on slowing the rate of bone loss later in life. One compilation of published calcium trials indicated that the beneficial skeletal effect of increased physical activity was achievable only at calcium intakes above 1,000 mg/day. High impact exercise and resistance exercise (weights) are likely the most beneficial for reducing bone loss. Lower impact exercise like walking, swimming, and cycling have beneficial effects on other aspects of health and function, but their effects on bone loss have been minimal. However, exercise later in life, even beyond 90 years of age, can still increase strength and reduce the likelihood of a fall, another important risk factor for hip fracture. Supplemental calcium alone cannot usually restore lost bone in individuals with osteoporosis. However, optimal treatment of osteoporosis with any drug therapy also requires adequate intake of calcium (1,200 mg/day) and vitamin D (600 IU/day). For more information about osteoporosis, visit the National Osteoporosis Foundation Web site.

Kidney stones

Approximately 12% of the U.S. population will have a kidney stone at some time. Most kidney stones are composed of calcium oxalate or calcium phosphate. Although their cause is usually unknown, abnormally elevated urinary calcium (hypercalciuria) increases the risk of developing calcium stones. Increasing dietary calcium increases urinary calcium slightly, and the rise is more pronounced in those with hypercalciuria. However, other dietary factors such as sodium and protein are also known to increase urinary calcium. A large prospective study that followed men over a period of twelve years found the incidence of symptomatic kidney stones to be 44% lower in men in the highest quintile (1/5) of calcium intake, averaging 1,326 mg/day, compared with men in the lowest quintile of calcium intake, averaging 516 mg/day . Similar results were observed in a large prospective study of women over four years. The authors of the two studies suggested that increased dietary calcium might inhibit the absorption of dietary oxalate and reduce urinary oxalate, a risk factor for calcium oxalate stones. Support for this idea comes from a study in which people ingested oxalate with or without supplemental calcium. Providing 200 mg of elemental calcium along with the oxalate significantly reduced its absorption and urinary oxalate excretion.

Although calcium stone formers have been advised to restrict calcium intake in the past, a cross-sectional study of 282 patients with calcium oxalate stones found that dietary salt, as measured by urinary sodium excretion, was the dietary factor most strongly associated with urinary calcium excretion (23). A study of 85 calcium stone forming patients found that those with low bone mineral density were significantly more likely to have higher salt intake and higher urinary sodium excretion, leading the authors to suggest that reduced salt intake should be recommended for calcium stone forming patients. Findings that calcium stone forming patients with lower calcium intakes are more likely to have decreased bone mineral density also call into question the therapeutic use of dietary calcium restriction. At present, the only dietary change proven effective in reducing kidney stone recurrence is increasing fluid intake, although no controlled clinical trials of calcium supplementation or restriction have been reported in the literature.

See Also: