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Abstract
Introduction: Investigations in rodents as well as in vitro experiments have suggested
an anabolic influence of specific collagen peptides (SCP) on bone formation and bone
mineral density (BMD). The goal of the study was to investigate the effect of 12-month
daily oral administration of 5 g SCP vs. placebo (CG: control group) on BMD in postmenopausal
women with primary, age-related reduction in BMD. Methods: 131 women were enrolled
in this randomized, placebo-controlled double-blinded investigation. The primary endpoint
was the change in BMD of the femoral neck and the spine after 12 months. In addition,
plasma levels of bone markers—amino-terminal propeptide of type I collagen (P1NP)
and C-telopeptide of type I collagen (CTX 1)—were analysed. Results: A total of 102
women completed the study, but all subjects were included in the intention-to-treat
(ITT) analysis (age 64.3 ± 7.2 years; Body Mass Index, BMI 23.6 ± 3.6 kg/m2; T-score
spine −2.4 ± 0.6; T-score femoral neck −1.4 ± 0.5). In the SCP group (n = 66), BMD
of the spine and of the femoral neck increased significantly compared to the control
group (n = 65) (T-score spine: SCP +0.1 ± 0.26; CG −0.03 ± 0.18; ANCOVA p = 0.030;
T-score femoral neck: SCP +0.09 ± 0.24; CG −0.01 ± 0.19; ANCOVA p = 0.003). P1NP increased
significantly in the SCP group (p = 0.007), whereas CTX 1 increased significantly
in the control group (p = 0.011). Conclusions: These data demonstrate that the intake
of SCP increased BMD in postmenopausal women with primary, age-related reduction of
BMD. In addition, SCP supplementation was associated with a favorable shift in bone
markers, indicating increased bone formation and reduced bone degradation.
Postmenopausal osteoporosis is a serious health problem, and additional treatments are needed. We studied the effects of oral alendronate, an aminobisphosphonate, on bone mineral density and the incidence of fractures and height loss in 994 women with postmenopausal osteoporosis. The women were treated with placebo or alendronate (5 or 10 mg daily for three years, or 20 mg for two years followed by 5 mg for one year); all the women received 500 mg of calcium daily. Bone mineral density was measured by dual-energy x-ray absorptiometry. The occurrence of new vertebral fractures and the progression of vertebral deformities were determined by an analysis of digitized radiographs, and loss of height was determined by sequential height measurements. The women receiving alendronate had significant, progressive increases in bone mineral density at all skeletal sites, whereas those receiving placebo had decreases in bone mineral density. At three years, the mean (+/- SE) differences in bone mineral density between the women receiving 10 mg of alendronate daily and those receiving placebo were 8.8 +/- 0.4 percent in the spine, 5.9 +/- 0.5 percent in the femoral neck, 7.8 +/- 0.6 percent in the trochanter, and 2.5 +/- 0.3 percent in the total body (P < 0.001 for all comparisons). The 5-mg dose was less effective than the 10-mg dose, and the regimen of 20 mg followed by 5 mg was similar in efficacy to the 10-mg dose. Overall, treatment with alendronate was associated with a 48 percent reduction in the proportion of women with new vertebral fractures (3.2 percent, vs. 6.2 percent in the placebo group; P = 0.03), a decreased progression of vertebral deformities (33 percent, vs. 41 percent in the placebo group; P = 0.028), and a reduced loss of height (P = 0.005) and was well tolerated. Daily treatment with alendronate progressively increases the bone mass in the spine, hip, and total body and reduces the incidence of vertebral fractures, the progression of vertebral deformities, and height loss in postmenopausal women with osteoporosis.
To update the evidence-based position statement published by The North American Menopause Society (NAMS) in 2006 regarding the management of osteoporosis in postmenopausal women. NAMS followed the general principles established for evidence-based guidelines to create this updated document. A panel of clinicians and researchers expert in the field of metabolic bone diseases and/or women's health was enlisted to review the 2006 NAMS position statement, compile supporting statements, and reach consensus on recommendations. The panel's recommendations were reviewed and approved by the NAMS Board of Trustees. Osteoporosis, which is especially prevalent among older postmenopausal women, increases the risk of fractures. Hip and spine fractures are associated with particularly high morbidity and mortality in this population. Given the health implications of osteoporotic fractures, the primary goal of osteoporosis therapy is to prevent fractures, which is accomplished by slowing or stopping bone loss, maintaining bone strength, and minimizing or eliminating factors that may contribute to fractures. The evaluation of postmenopausal women for osteoporosis risk requires a medical history, physical examination, and diagnostic tests. Major risk factors for postmenopausal osteoporosis (as defined by bone mineral density) include advanced age, genetics, lifestyle factors (such as low calcium and vitamin D intake, smoking), thinness, and menopause status. The most common risk factors for osteoporotic fracture are advanced age, low bone mineral density, and previous fracture as an adult. Management focuses first on nonpharmacologic measures, such as a balanced diet, adequate calcium and vitamin D intake, adequate exercise, smoking cessation, avoidance of excessive alcohol intake, and fall prevention. If pharmacologic therapy is indicated, government-approved options are bisphosphonates, selective estrogen-receptor modulators, parathyroid hormone, estrogens, and calcitonin. Management strategies for postmenopausal women involve identifying those at risk for fracture, followed by instituting measures that focus on reducing modifiable risk factors through dietary and lifestyle changes and, if indicated, pharmacologic therapy.
We compared quantity and structures of food-derived gelatin hydrolysates in human blood from three sources of type I collagen in a single blind crossover study. Five healthy male volunteers ingested type I gelatin hydrolysates from fish scale, fish skin, or porcine skin after 12 h of fasting. Amounts of free form Hyp and Hyp-containing peptide were measured over a 24-h period. Hyp-containing peptides comprised approximately 30% of all detected Hyp. The total area under the concentration-time curve of the fish scale group was significantly higher than that of the porcine skin group. Pro-Hyp was a major constituent of Hyp-containing peptides. Ala-Hyp, Leu-Hyp, Ile-Hyp, Phe-Hyp, and Pro-Hyp-Gly were detected only with fish scale or fish skin gelatin hydrolysates. Ala-Hyp-Gly and Ser-Hyp-Gly were detected only with fish scale gelatin hydrolysate. The quantity and structure of Hyp-containing peptides in human blood after oral administration of gelatin hydrolysate depends on the gelatin source.
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