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      Caffeine intake increases the rate of bone loss in elderly women and interacts with vitamin D receptor genotypes

      1 , 1 , 1 , 1
      The American Journal of Clinical Nutrition
      Oxford University Press (OUP)

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          Abstract

          The role of caffeine as a risk factor for bone loss is controversial. Our goals were 1) to compare in both a cross-sectional study and a 3-y longitudinal study the bone mineral density (BMD) of postmenopausal women consuming high or low amounts of caffeine and 2) to study the interaction between caffeine intake, vitamin D receptor (VDR) polymorphism, and BMD in the longitudinal study. The results are derived from cross-sectional measurements of BMD in 489 elderly women (aged 65-77 y) and from longitudinal measurements made in 96 of these women who were treated with a placebo for 3 y. Changes in BMD were adjusted for confounding factors and were compared between groups with either low (< or =300 mg/d) or high (>300 mg/d) caffeine intakes and between the VDR genotype subgroups of the low- and high-caffeine groups. Women with high caffeine intakes had significantly higher rates of bone loss at the spine than did those with low intakes (-1.90 +/- 0.97% compared with 1.19 +/- 1.08%; P = 0.038). When the data were analyzed according to VDR genotype and caffeine intake, women with the tt genotype had significantly (P = 0.054) higher rates of bone loss at the spine (-8.14 +/- 2.62%) than did women with the TT genotype (-0.34 +/- 1.42%) when their caffeine intake was >300 mg/d. Intakes of caffeine in amounts >300 mg/d ( approximately 514 g, or 18 oz, brewed coffee) accelerate bone loss at the spine in elderly postmenopausal women. Furthermore, women with the tt genetic variant of VDR appear to be at a greater risk for this deleterious effect of caffeine on bone.

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          Most cited references32

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          Competitive protein-binding radioassay for 25-hydroxycholecalciferol.

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            Caffeine, urinary calcium, calcium metabolism and bone.

            Oral doses of caffeine increase the urinary excretion of calcium, magnesium, sodium and chloride for at least 3 h after consumption. The hypercalciuric effect can be blocked by adenosine receptor agonists. The effect is proportional to dose per lean body mass and no adaptation to the urinary losses occurs with continuing consumption of caffeine. Uncompensated losses of calcium would be a risk factor for development of osteoporosis. Risks of osteoporosis due to caffeine consumption are reviewed. Comparison of data from epidemiological surveys and animal and human studies suggests that for younger adult women consuming adequate calcium, moderate caffeine intakes may have little or no deleterious effects. Increased urinary and intestinal losses may be compensated for by increased intestinal calcium absorption. However older women do not seem to compensate adequately to maintain their former calcium balance, especially when calcium intakes are below recommendations.
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              Caffeine, moderate alcohol intake, and risk of fractures of the hip and forearm in middle-aged women.

              In 1980, 84,484 US women aged 34-59 y completed an independently validated dietary questionnaire. During the ensuing 6 y, 593 forearm and 65 hip fractures occurred in association with mild to moderate trauma. We observed a positive relation between caffeine intake and risk of hip but not forearm fracture. After potential risk factors were controlled for the relative risk (RR) of hip fracture for women in the top quintile of caffeine consumption was 2.95 (95% CI = 1.18-7.38, P, trend = 0.003). Alcohol intake was independently associated with increased risk of both hip and forearm fractures and with a dose-response relation. Compared with nondrinkers, women consuming greater than or equal to 25 g alcohol/d had an RR of 2.33 (95% CI = 1.18-4.57) for hip fractures and an RR of 1.38 (95% CI = 1.09-1.74) for forearm fractures. These prospective data suggest that caffeine and alcohol consumption both increase the risk of osteoporotic fractures in middle-aged women.
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                Author and article information

                Journal
                The American Journal of Clinical Nutrition
                Oxford University Press (OUP)
                0002-9165
                1938-3207
                November 2001
                November 01 2001
                November 2001
                November 01 2001
                : 74
                : 5
                : 694-700
                Affiliations
                [1 ]From the Bone Metabolism Unit, Creighton University, School of Medicine, Omaha; the National Institute of Environmental Health Sciences, Laboratory of Reproductive and Developmental Toxicology, Research Triangle Park, NC; and Ryschon Health and Technology Services, Valentine, NE.
                Article
                10.1093/ajcn/74.5.694
                11684540
                2e81ac49-ff1c-4dd8-910b-c2cc540ccca7
                © 2001
                History

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