The SenseWear Pro3 and the SenseWear Mini armbands show promise for accurately measuring daily energy expenditure under free-living conditions. However, more work is needed to improve the ability of these monitors to accurately measure energy expenditure at higher levels of expenditure.

Background:No published studies have directly examined the effect of soy protein with isoflavones on bone or bone turnover in perimenopausal women. Objective: Our objective was to determine the effects of 24 wk of consumption of soy protein isolate with isoflavones (80.4 mg/d) in attenuating bone loss during the menopausal transition. Design: Perimenopausal subjects were randomly assigned, double blind, to treatment: isoflavone-rich soy (SPI+; n = 24), isoflavone-poor soy (SPIϪ; n = 24), or whey (control; n = 21) protein. At baseline and posttreatment, lumbar spine bone mineral density (BMD) and bone mineral content (BMC) were measured by using dual-energy X-ray absorptiometry. At baseline, midtreatment, and posttreatment, urinary N-telopeptides and serum bonespecific alkaline phosphatase (BAP) were measured. Results: The percentage change in lumbar spine BMD and BMC, respectively, did not differ from zero in the SPI+ or SPIϪ groups, but loss occurred in the control group (Ϫ1.28%, P = 0.0041; Ϫ1.73%, P = 0.0037). By regression analysis, SPI+ treatment had a positive effect on change in BMD (5.6%; P = 0.023) and BMC (10.1%; P = 0.0032). Baseline BMD and BMC (P ≤ 0.0001) negatively affected the percentage change in their respective models; baseline body weight (P = 0.0036) and bone-free lean weight (P = 0.016) contributed positively to percentage change in BMD and BMC, respectively. Serum BAP posttreatment was negatively related to percentage change in BMD (P = 0.0016) and BMC (P = 0.019). Contrast coding using analyses of covariance with BMD or BMC as the outcome showed that isoflavones, not soy protein, exerted the effect. Conclusion: Soy isoflavones attenuated bone loss from the lumbar spine in perimenopausal women.Am J Clin Nutr 2000; 72:844-52. KEY WORDSSoy, isoflavones, bone density, lumbar vertebrae, biochemical markers, menopause, bone mineral content, perimenopausal women INTRODUCTIONCurrent therapies for treating osteoporosis include estrogen and hormone replacement therapies (ERT and HRT), bisphosphonates, calcitonin, and raloxifene. Because of possible contraindications of ERT and HRT, such as breast cancer, endometrial adenocarcinoma, and undesirable side effects (1), compliance with hormonal therapy is poor (2), leading to loss of treatment efficacy (3). Continued uterine bleeding and other adverse side effects of HRT cause women to search for alternatives to traditional therapy. Isoflavone-containing soy may be a potential alternative for preventing bone loss during the menopausal transition.Isoflavones, found predominantly in soy products, are estrogen-like substances structurally and functionally similar to 17 ␤-estradiol (4). On the basis of evidence primarily from animal and in vitro studies, isoflavones are thought to exert both estrogenic and antiestrogenic effects, depending on the tissue in which they act (5). Isoflavones may exert a weak antagonistic effect on the estrogen receptor (5), thereby having an antiestrogenic effect on uterine and breast tissue (6), where excess estrogen ...

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Our results do not show a bone-sparing effect of extracted soy isoflavones, except for a modest effect at the femoral neck. This trial was registered at clinicaltrials.gov as NCT00043745.

Phytosterol-supplemented ground beef effectively lowers plasma TC and LDL cholesterol and has the potential to become a functional food to help reduce the risk of cardiovascular disease.

Apigenin has been previously shown to induce G2/M cell-cycle arrest in human colon cancer cell lines. The present study assessed the individual and interactive influence of seven apigenin analogs on cell cycle, cell number, and cell viability in human SW480 and Caco-2 colonic carcinoma cells. Cellular concentration of selected apigenin analogs was further assessed by high-performance liquid chromatography to assess cellular availability. The apigenin analogs studied were acacetin, chrysin, kampherol, luteolin, myricetin, naringenin, and quercetin. DNA flow cytometric analysis indicated that treatment with either chrysin or acacetin at 0 to 80 microM for 48 h resulted in cell-cycle arrest at the G2/M phase in a dose-dependent manner in the SW480 cells but not in the Caco-2 cells. The percentage of SW480 cells at G2/M also increased when cells were treated with kampherol, luteolin, or quercetin between 5 and 30 microM, but the percentage of cells in G2/M decreased at doses greater than 40 microM. Cell number was significantly decreased in a time- and dose-dependent manner following the treatments with each analog except for naringenin and myricetin. The interactive effects of these analogs with apigenin were further assessed by combining each analog at doses from 0 to 80 microM with apigenin at 20 microM, a dose at which apigenin was found to double the proportion of SW480 cells in G2/M. When either acacetin, chrysin, luteolin, kampherol, or quercetin at doses between 5 and 30 microM were combined with apigenin at 20 microM, there was an increase of 22% in the proportion of G2/M cells over that observed with 20 microM apigenin alone (P < 0.05). At doses higher than 40 microM, however, the interaction became antagonistic, and the proportion of cells in G2/M decreased below that observed with apigenin alone. Cell viability, as assessed by Trypan blue exclusion assay, significantly decreased by treatments with high doses of each agent or each agent combined with apigenin. Cellular concentration of apigenin, chrysin, or naringenin in SW480 cells significantly increased at doses of 40 microM or greater, but it was not correlated with their impact on G2/M cell-cycle arrest. The induction of cell-cycle arrest by five of seven tested apigenin analogs and the additive induction by the combination of flavonoids at low doses suggest that apigenin-related flavonoids may cooperatively protect against colorectal cancer through conjoint blocking of cell-cycle progression.

Objective Inadequate vitamin D status is related to increased adiposity, risk of falls, and muscle weakness, particularly in the elderly. We hypothesized that serum 25-hydroxyvitamin D (25(OH)D) is related to physical fitness indices (androidal fat, whole body lean mass, balance, strength) in healthy postmenopausal women. Design Covariates for fitness indices included: age or years since menopause; weight; 25(OH)D; energy expenditure; calcium intake. Overall and regional (androidal fat mass=waist+hip fat) body composition was assessed (N=242) via dual-energy X-ray absorptiometry. Results Regression analyses revealed that 71% of variability (P≤0.0001) in androidal fat mass was accounted for by weight (53.0%, P≤0.0001), white blood cell (WBC) count (2.0%, P≤0.0001), supplemental calcium (1.7%, P=0.0004), years since menopause (1.1%, P=0.0034), 25(OH)D (1.0%, P=0.0051), and vegetable servings (0.6%, P=0.027); 64% of variability (P≤0.0001) in lean mass was accounted for by weight (63.1.%, P≤0.0001), WBC count (1.4%, P=0.0038), and 25(OH)D (1.0%, P=0.013); 12% of variability (P≤0.0001) in balance (right+left leg) was accounted for by age (3.8%, P=0.0019), 25(OH)D (2.0%, P=0.025), and WBC count (1.8%, P=0.032); 14% of variability (P≤0.0001) in hand grip strength (right+left) was accounted for by weight (9.3%, P≤0.0001), 25(OH)D (2.4%, P=0.013), WBC count (2.1%, P=0.019), and age (1.6%, P=0.044); 22% of variability (P≤0.0001) in torso strength was accounted for by site (15.0%, P≤0.0001) and weight (4.6%, P=0.0003). Conclusion Serum 25(OH)D was the common contributor to physical fitness indices (androidal fat mass, lean mass, balance, hand grip strength) in healthy postmenopausal women.

Bone formation and resorption are influenced by inflammatory processes. We examined the relationships among inflammatory markers and bone mineral content and density (BMC, BMD) and determined the contribution of inflammatory markers to 1-year changes in BMC and BMD in Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Additional ContributionsThe SIRBL study team would like to thank all of our participants, since without their dedication, our study could not have been completed. We would like to acknowledge our phlebotomists and students (graduate and undergraduate alike) who reported early and steadfastly for testing at our clinic sites. We would also like to thank the following individuals who worked on various aspects of the NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript healthy postmenopausal women. This analysis included 242 women at baseline from our parent Soy Isoflavones for Reducing Bone Loss (SIRBL) project who were randomly assigned to one of three treatment groups: placebo, 80 mg/d soy isoflavones, or 120 mg/d soy isoflavones. BMD and BMC from the lumbar spine (LS), total proximal femur (hip), and whole body were measured by dual energy x-ray absorptiometry (DXA) and the 4% distal tibia (DT) by peripheral quantitative computed tomography (pQCT). Serum inflammatory markers (C-reactive protein (CRP), interleukin (IL)-1β, IL-6, tumor necrosis factor-alpha (TNF-α), and white blood cell count (WBC)) were measured at baseline, 6 and 12 months. Due to attrition or missing values, data analysis at 12 months includes only 235 women. Significant associations among Il-6, TNF-α, and WBC were observed with percent change in LS, hip, and whole body BMC and BMD. Multiple regression analysis indicated that in combination inflammatory markers accounted for 1.1% to 6.1% of the variance to the observed 12 month changes in BMC and BMD. Our results suggest that modifying inflammatory markers, even in healthy postmenopausal women, may possibly reduce bone loss.