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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #37441
Title: VITAMIN D RECEPTOR ALLELES AND RATES OF BONE LOSS: INFLUENCES OF YEARS SINCE MENOPAUSE AND CALCIUM INTAKE

Author
item KRALL ELIZABETH - TUFTS-HNRCA
item PARRY PAULINE - SEQUANA LABS
item LICHTER JAY B - SEQUANA LABS
item DAWSON-HUGHES BE - TUFTS-HNRCA

Submitted to: Journal of Bone and Mineral Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/24/1995
Publication Date: N/A
Citation: N/A

Interpretive Summary: It is well known that osteoporosis has an inherited component. Recently the gene regulating the vitamin D receptor (VDR) was linked to bone mineral density in adults. Vitamin D and its intestinal receptor are important in the process of calcium absorption, particularly in those on low-calcium diets. This study was conducted to determine whether genetic VDR status is related to rates of bone loss in postmenopausal women and, if so, whether calcium intake influences the association. Genetic VDR status was determined in 229 women who had participated in an earlier two-year calcium supplement trial. Those with the reportedly undesirable VDR status lost bone mineral more rapidly from the hip, spine, and whole body. At the hip, this genetic influence was present only in women with calcium intakes under 650 mg per day (average 400 mg per day). We conclude that genetic VDR status influences rates of bone loss in postmenopausal women and that individuals with the undesirable status can offset this hereditary effect by raising their calcium intake.

Technical Abstract: A genetic marker for the 1,25-dihydroxyvitamin D receptor (VDR) is reported to account for much of the heritable component of bone density. It is not known whether VDR genotype influences bone accretion or loss or how it is related to calcium metabolism. VDR genotype was determined in 229 healthy postmenopausal women who previously participated in a calcium trial. VDR alleles were designated according to presence (b) or absence (B) of recognition of the BsmI restriction enzyme. There were 83 bb, 102 Bb and 44 BB. Two-thirds took a 500 mg calcium supplement (high calcium category, mean intake=892 mg/d) and one-third a placebo (low calcium, mean=376 mg/d). Bone density at the femoral neck, spine and radius were measured by dual- and single-photon absorptiometry at baseline and after two years. Bone loss at the femoral neck was greater in BB than in bb (BB,-0.98+/-0.5 percent per year; bb, +0.40+/-0.42 percent; p=0.043) but loss in BB was modified by calcium intake (+0.01+/-0.61 percent in the high calcium and -1.97+/-0.75 percent in the low calcium consumers, p=0.035). Rates of change at the radius and spine were also greater in the BB group than bb. The influence of calcium at these sites was similar in direction to the femoral neck but not statistically significant. These results indicate that postmenopausal bone loss has a genetic component and that an adverse effect at the hip of the susceptible allele can be reduced by raising calcium intake.