Bone Resorption In Postmenopausal Women Research Articles

Combined Effect of Dietary Acid Load and Cardiometabolic Syndrome on Bone Resorption Marker among Post-Menopausal Women in Malaysia.

This study aimed to investigate factors associated with bone resorption status and determine the independent and interactive effects of dietary acid load (DAL) and cardiometabolic syndrome (CMS) on bone resorption in post-menopausal women. Overall, 211 community-dwelling post-menopausal women were recruited from the National Council of Senior Citizens Organization, Malaysia. DAL was estimated using the potential renal acid load from the food frequency questionnaire. Sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI) and smoking behaviour was assessed using the Global Adult Tobacco Survey 2011. Serum 25(OH) vitamin D levels were determined using the ADVIA Centaur vitamin D assay and serum C-terminal telopeptides of type I collagen (CTX1) were used as surrogate markers to assess bone resorption. CMS was determined based on the harmonised criteria. Age (β = -0.145, t = -2.002, P < 0.05) was negatively associated while DAL (β = 0.142, t = 2.096, P < 0.05) and sleep quality (β = 0.147, t = 2.162, P < 0.05) were positively associated with CTX1. Height was positively correlated with CTX1 (r = 0.136, P <0.05). Conversely, other variables (CMS traits, CMS, serum 25(OH) vitamin D level, years of menopause, years of education and physical activity) were not significantly associated with CTX1 levels. There was no significant interaction between DAL and CMS on bone resorption. Our findings propose that high DAL, but not CMS, is a potential risk factor for bone resorption. The analysis did not demonstrate the combined effects of DAL and CMS on bone resorption.

The Potential of Phytochemicals Lycopene in Prevention of Bone Loss due to Decreased Estrogen Hormone in Humans and Experimental Animals

Osteoporosis is a condition of decreased bone mass and disruption of bone microarchitecture that often occurs in the elderly. One of the causes of osteoporosis is menopause as reduced estrogen secretion increases bone resorption by osteoclasts activity, and the body’s oxidative stress. Currently, osteoporosis is still a major cause of morbidity and mortality in the elderly. Prevention is vital in reducing this disease. Recent studies have shown a reduction in bone loss with lycopene consumption. High serum lycopene is also reported to be associated with decreased protein oxidation and bone resorption in postmenopausal women. This literature aimed to examine and analyze the research results related to the potential of lycopene on bone loss based on molecular and clinical research evidence in preventing osteoporosis in elderly women. Literature review on published papers in English in the last 10 years (2011 – 2021) was conducted using electronic database. Reviewed experimental and cohort studies on elderly women and experimental animals showed influence and effect of lycopene on bone loss. Lycopene may contribute in reduction of oxidative stress caused by reduced secretion of estrogen.

Acute C-Terminal Crosslinking Telopeptide of Type I Collagen (CTX-1) Suppression with Milk Calcium or Calcium Carbonate Is Independent of Visceral Fat in a Randomized Crossover Study in Lean and Overweight Postmenopausal Women

Postmenopausal women with higher visceral adipose tissue (VAT) present with suppressed bone resorption (lower C-terminal crosslinking telopeptide of type I collagen; CTX-1) and turnover (lower osteocalcin) but whether this blunts the effect of calcium is unknown. The primary outcome of this study was the effect of VAT on changes in CTX-1 after intake of 2 forms of calcium. Secondary outcomes included changes in parathyroid hormone (PTH), serum calcium, phosphorus, and alkaline phosphatase (ALP). Randomized open three period crossover trial conducted between 2017 and 2019 at the University of South Australia among 77 lean and overweight postmenopausal women (53-79 y) with BMI <25 kg/m2 and >27 kg/m2, respectively. Participants received a single dose of milk (1000 mg calcium), calcium carbonate tablet (1000 mg calcium), and fruit juice (no calcium) in random order with a 7-d washout period. Blood samples were collected at baseline and hourly for 5 h. Data was analyzed by repeated measures ANOVA of log-transformed data. At baseline, women with higher VAT had significantly lower CTX-1 and higher PTH (44% lower and 30% higher, respectively, between Q4 and Q1, P < 0.0001). VAT had no influence on the acute changes in CTX-1 or PTH with calcium or juice. A suppression of 44% in CTX-1 was seen with calcium carbonate and milk and a suppression of 18% with juice. PTH was suppressed more with calcium carbonate (47%) compared to milk (22%). Milk calcium reduced PTH and CTX-1 at 2 h, whereas calcium carbonate reduced PTH in 1 h. The suppression in CTX-1 was slower with lowest concentrations at 4-5 h. Intake of 1000 mg calcium from milk or from calcium carbonate is effective in acutely suppressing bone resorption in postmenopausal women irrespective of visceral fat. This trial is registered at http://www.ANZCTR.org.au/ACTRN12617000779370.aspx as ACTRN 12617000779370).

Subcutaneous GIP and GLP-2 inhibit nightly bone resorption in postmenopausal women: A preliminary study.

Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-2 (GLP-2) are gut hormones secreted in response to food ingestion, and they have been suggested to regulate bone turnover. In humans, exogenous GIP and GLP-2 acutely inhibit bone resorption as measured by circulating levels of carboxy-terminal type 1 collagen crosslinks (CTX). The objective was to study the individual and combined acute effects of GIP and GLP-2 on bone turnover in postmenopausal women during nighttime - a period of increased bone resorption. Using a randomized, placebo-controlled, double-blinded, crossover design, each participant (n=9) received on four separate study days: GIP, GLP-2, GIP+GLP-2, and placebo (saline) as subcutaneous injections at bedtime. Main outcomes were levels of CTX and procollagen type 1N-terminal propeptide (P1NP). Compared with placebo, GIP and GLP-2 alone significantly inhibited bone resorption (measured by CTX). GIP rapidly reduced CTX levels in the period from 45 to 120min after injection, while GLP-2 had a more delayed effect with reduced CTX levels in the period from 120 to 240min after injection. Combining GIP and GLP-2 showed complementary effects resulting in a sustained inhibition of CTX with reduced levels from 45 to 240min after injection. Furthermore, GIP acutely increased bone formation (measured by P1NP). Both GIP and GLP-2 reduced CTX during the night and had complementary effects when combined.

Immunoexpression pattern of autophagy mediators in alveolar bone osteoclasts following estrogen withdrawal in female rats.

It is known that estrogen deficiency increases osteoclast formation and activity. Autophagy, a cell survival pathway, has been shown to be crucial for osteoclast function. However, little is known about the effects of estrogen depletion on osteoclast autophagy. Here, we evaluated the effects of estrogen deficiency in the immunoexpression of autophagy mediators in alveolar bone osteoclasts of ovariectomized rats. Twelve adult female rats were ovariectomized (OVX-group) or SHAM-operated (SHAM-group). After three weeks, the rats were euthanized and maxillary fragments containing alveolar bone of the first molars were processed for light microscopy or transmission electron microscopy (TEM). Paraffin-sections were subjected to the TRAP method (osteoclast marker) or to the immunohistochemical detections of beclin-1, LC3α, and p62 (autophagy mediators); araldite-sections were processed for TEM. The number of TRAP-positive osteoclasts and the number of immunolabeled-multinucleated cells (MNCs) along the alveolar bone surface of the first molar were computed. The number of TRAP-positive osteoclasts and the number of beclin-1-, LC3α- and p62-immunolabelled osteoclasts were significantly higher in OVX-group than the SHAM-group. MNCs were frequently located juxtaposed to Howship lacunae along the alveolar bone surface, indicating that these cells are osteoclasts. TEM revealed osteoclasts exhibiting autophagosomes. Our data indicate that autophagy plays an important role during estrogen deficiency-induced osteoclastogenesis. Thus, our results contribute to a better understanding on the role of autophagy on osteoclasts under estrogenic deficiency, and reinforce the idea that modulation of autophagy may be a useful tool to inhibit excessive oral bone resorption in post-menopausal women.

Effect of Whey Protein Supplementation on Plasma Bone-Resorption Biomarker in Post-Menopausal Women Submitted to Physical Exercise Training

Abstract Objectives To evaluate the additional effect of whey protein supplementation (WPS) to the physical-exercise training on bone resorption in postmenopausal women. Methods In a prospective, controlled study, 38 postmenopausal women aged 50 to 70 years, were randomized into two groups: with WPS (n = 19) and without WPS (n = 19, control) intervention. The study included amenorrheic women (above 12 months) with normal bone mineral density (T-score ≥ −1.0 SD) not taken bone-related medicines, and practitioners of a physical exercise protocol involving combined walking/jogging and academy/resistance exercises performed under professional supervising, three times a week. Together, there was a weekly dietary counseling along with a daily supplementation of either 25 g of protein (WPS) or placebo. Food intake (24-hour recall), anthropometric, general biochemistry, plasma hormones and bone resorption marker: serum C-terminal cross-linked N-telopeptides of type-I collagen (s-CTX) assessments were undertaken at baseline and after 20-wk intervention. Statistical analysis of the data (P &amp;lt; 0.05) was performed by using a time-repeated measures (ANOVA) followed by the Tukey multiple comparison test adjusted for group x moment interaction, or by gamma distribution (asymmetric variables). Results The groups were anthropometric and biochemical homogeneous, at baseline and after the intervention. Both groups increased similarly the intake of energy and lipids. However, only WPS significantly increased the intake of protein, calcium, phosphates and magnesium, as well as leucine, isoleucine and valine. From a similar baseline plasma values of s-CTX, calcium, phosphorus, alkaline phosphatase and parathormone, only s-CTX responded significantly to the intervention, being reduced in both groups (-34% and −15.2%), statistically significant in the control(non-WPS) group (P = 0.016). Conclusions The reduced plasma marker of bone resorption marker was observed in post-menopause women submitted to a 20-wk lifestyle-modification protocol with physical exercises, independently to the whey protein supplementation. Clinical trial (REBEC): RBR-7KD97. Funding Sources Brazilian foundations CNPq and CAPES.

The Role of Parathyroid Hormone in Alveolar Bone Resorption on Postmenopausal Women

Background: Postmenopausal women exhibit reduced bone mineralization, which causes bone resorption, including that of alveolar bone. Parathyroid hormone has been shown to play a role in alveolar bone resorption. Objective: This study aims to analyze relationships between parathyroid hormone and other factors that may contribute to alveolar bone resorption in postmenopausal women. Methods: This cross-sectional study included 82 postmenopausal women aged 50–74 years, who resided in Central and East Jakarta, Indonesia. Subjects' data were obtained through questionnaires, dental examinations, and blood collection for the examination of parathyroid hormone levels by enzyme-linked immunosorbent assay and using panoramic radiography to measure bone resorption. Results: Spearman correlation analysis showed a significant correlation between parathyroid hormone level (p = 0.005) and extent of alveolar bone resorption, but age (p = 0.292), menopausal duration (p = 0.244), and number of missing teeth (p = 0.517) were not significantly correlated with the extent of alveolar bone resorption. Conclusion: Various factors play a role in the mechanism of bone resorption, so knowing the role of each factor is expected to reduce the effects of alveolar bone resorption that occurs in postmenopause. Among the factors investigated in this study, the parathyroid hormone was the sole factor correlated with postmenopausal alveolar bone resorption.

Relationship of Age, Body Mass Index, Bone Density, and Menopause Duration with Alveolar Bone Resorption in Postmenopausal Women

Objective: To analyze the relationship between age, body mass index (BMI), bone mineral density (BMD), and alveolar bone resorption with menopause duration in postmenopausal women. Material and Methods: A cross-sectional study was developed involving 59 subjects, aged 45 to 80 years and categorized the duration of menopause as ≤5 years and >5 years. Body mass indexmeasurement and menopause duration were collected. Bone loss seen on radiography was measured by drawing a vertical line from the cementoenamel in the distal part of the 36 teeth and the mesial portion of 46 teeth to the base of the bone marked by the lamina dura intact. Categorical determinations of age, BMI, BMD, and alveolar bone resorption were based on receiver operating characteristic (ROC) curves. Were used Pearson correlation and Spearman correlation tests with the significance level set at 5%. Results: The majority of subjects (54.2%) with menopause duration >5 years were aged >54.5 years, most had BMI >24.2 kg/m 2 (39%), had bone resorption >2.95 mm (52.5%), and had bone density ≤73.89 (49.2%). Pearson and Spearman correlation tests showed no significant correlation between age, BMI, bone density, and alveolar bone resorption (p>0.05). Conclusion: The longer the duration of menopause showed a tendency for lower bone density and higher age, BMI, and bone resorption.

Bone Metabolism Markers and Bone Mineral Density in Patients on Long-Term Acenocoumarol Treatment: A Cross-Sectional Study.

The aim of this study was to evaluate levels of osteocalcin (OC), osteoprotegerin (OPG) and total soluble receptor activator of nuclear factor-κB ligand (RANKL), and bone mineral density (BMD) in patients on long-term acenocoumarol (AC) treatment. The cross-sectional study was carried out in 42 patients treated long-term with AC and 28 control subjects. Serum concentrations of OC, OPG, and sRANKL were measured using enzyme linked immunosorbent assay (ELISA) kits, and BMD at the femoral neck and lumbar spine were assessed by dual energy X-ray absorptiometry. A significantly decreased concentration of OC was found in AC users compared to control subjects (4.94 ± 2.22 vs. 10.68 ± 4.5; p < 0.001). Levels of OPG, sRANKL logarithm (log), sRANKL/OPG log ratio, and BMD were comparable between. In female AC users, positive correlations between OC and RANKL log, and between OC and RANKL/OPG log ratio (p = 0.017; p = 0.005, respectively), and a negative correlation between OC and OPG (p = 0.027) were found. Long-term AC anticoagulation significantly decreases OC concentration, but does not affect other bone metabolism markers or BMD. Our results also suggest the possibility that long-term treatment with AC may alleviate bone resorption in postmenopausal women.

Potassium Citrate Decreases Bone Resorption in Postmenopausal Women with Osteopenia: A Randomized, Double-Blind Clinical Trial

Diets rich in animal protein, such as the typical American diet, are thought to create a high acid load. An association between acid load and bone loss has led to the idea that providing positive alkaline salt therapy could have beneficial effects on bone metabolism. The objective of this study was to investigate the effects of potassium citrate (K-citrate), 40 mEq daily, over 1 year on bone resorption and formation. A randomized, double-blind, placebo-controlled trial of 83 women with postmenopausal osteopenia. Levels of bone turnover markers, specifically urinary N-telopeptide of collagen type 1 (u-NTX), amino-terminal propeptide of type 1 procollagen (P1NP), bone-specific alkaline phosphatase (BSAP), and osteocalcin (OC) were compared. Changes in bone mineral density (BMD) were also examined. K-citrate decreased both u-NTX (P = .005) and serum P1NP (P<.001) starting at month 1 and continuing through month 12. No significant change was seen in BSAP or OC. No significant change was seen in lumbar or hip BMD between the 2 groups. In women with postmenopausal osteopenia, treatment with K-citrate for 1 year resulted in a significant decrease in markers of turnover. The effect on markers of bone formation was not consistent. K-citrate may serve as a potential treatment for bone loss that is well tolerated and without any significant known long-term consequences.

Acute effect of a supplemented milk drink on bone metabolism in healthy postmenopausal women is influenced by the metabolic syndrome.

BackgroundDietary factors acutely influence the rate of bone resorption, as demonstrated by changes in serum bone resorption markers. Dietary calcium exerts its effect by reducing parathyroid hormone levels while other components induce gut incretin hormones both of which reduce bone resorption markers. The impact of dietary calcium on bone turnover when energy metabolism is modulated such as in metabolic syndrome has not been explored. This study was designed investigate whether metabolic syndrome or a greater amount of visceral fat influences the impact of dietary calcium on bone turnover.MethodsThe influence of the metabolic syndrome on effects of dietary calcium on bone turnover in community dwelling postmenopausal women was studied. Twenty five volunteers consumed 200 mL of low fat milk with additional 560 mg calcium (one serve of Milo®) in the evening on one occasion. Fasting morning serum biochemistry before and after the milk drink with lumber spine bone density, bone mineral content, fat and lean mass using dual energy X-ray absorptiometry (DXA) and waist circumference were measured. The women were divided into 2 groups using the waist measurement of 88 cm, as a criterion of metabolic syndrome. Student’s t tests were used to determine significant differences between the 2 groups.ResultsThe lumbar spine mineral content was higher in women with metabolic syndrome. After consuming the milk drink, serum bone resorption marker C terminal telopeptide (CTX) was suppressed to a significant extent in women with metabolic syndrome compared to those without.ConclusionsThe results suggests that dietary calcium may exert a greater suppression of bone resorption in post-menopausal women with metabolic syndrome than healthy women. Despite substantial evidence for close links between energy metabolism and bone metabolism this is the first report suggesting visceral fat or metabolic syndrome may influence the effects of dietary calcium on bone metabolism.

SAT0498 Alendronate Inhibits Hyperalgesia and Suppresses Neuropeptide Markers of Pain in A Mouse Model of Osteoporosis

BackgroundOsteoporosis may cause not only fractures but also chronic back pain in elderly women. Iwamoto et al reported that alendronate (ALN) increases bone mineral density of the lumbar spine and...

Effects of Tibolone on Markers of Bone Metabolic Activity in Postmenopausal Women

Effects of Tibolone on Markers of Bone Metabolic Activity in Postmenopausal WomenOsteoporosis, a systemic disease of the bones, is a serious health and socio-economic problem because of its consequences, i.e. broken bones. It is believed that 10% of the world's population suffers from osteoporosis and it affects mostly postmenopausal women (postmenopausal osteoporosis). Tibolone is a synthetic steroid that has estrogenic, androgenic, and progestagenic properties. It has been used primarily for the prevention of postmenopausal osteoporosis and treatment of climacteric symptoms. The research included a group of 40 postmenopausal women with osteopenia treated with tibolone. The control group included 40 postmenopausal women who were not taking any medication. Control group patients were older (54.5 ± 9.84) than the patients treated with tibolone (51.6 ± 6.22). Bone metabolic activity was evaluated using osteocalcin (N-MID osteocalcin) for bone formation and CTX I for bone resorption. Blood samples were taken before therapy was introduced and 3 months after its introduction. The average value of osteocalcin after three months of tibolone therapy was 26.32 ± 3.312 ng/mL compared to the average osteocalcin value prior to therapy of 29.6 ± 3.343 ng/mL. The average value of CTX I three months after tibolone therapy of 0.2870 ± 0.0783 ng/mL was lower compared to the average CTX I value before the therapy of 0.4539 ± 0.1144 ng/mL. Our results show the efficacy of tibolone in preventing bone loss, which was highly statistically significant. They also reveal its suppressive effects on bone formation and resorption, but these effects are statistically less significant. Tibolone significantly reduces the level of bone resorption in postmenopausal women with osteopenia. Its effects on bone formation are less expressed. The parameters of bone metabolic activity are a very useful diagnostic means in the evaluation of tibolone effects on bone metabolic activity and in the prognosis of bone mass loss.

Effects of short-term aerobic exercise with and without external loading on bone metabolism and balance in postmenopausal women with osteoporosis

The aim of this study is to evaluate the effect of submaximal aerobic exercise with and without external loading on bone metabolism and balance in postmenopausal women with osteoporosis (OP). Thirty-six volunteer, sedentary postmenopausal women with OP were randomly divided into three groups: aerobic, weighted vest, and control. Exercise for the aerobic group consisted of 18 sessions of submaximal treadmill walking, 30 min daily, 3 times a week. The exercise program for the weighted-vest group was identical to that of the aerobic group except that the subjects wore a weighted vest (4-8 % of body weight). Body composition, bone biomarkers, bone-specific alkaline phosphatase (BALP) and N-terminal telopeptide of type 1 collagen (NTX), and balance (near tandem stand, NTS, and star-excursion, SE) were measured before and after the 6-week exercise program. Fat decreased (p = 0.01) and fat-free mass increased (p = 0.005) significantly in the weighted-vest group. BALP increased and NTX decreased significantly in both exercise groups (p ≤ 0.05). After 6 weeks of exercise, NTS score increased in the exercise groups and decreased in the control group (aerobic: +49.68 %, weighted vest: +104.66 %, and control: -28.96 %). SE values for all directions increased significantly in the weighted-vest group. Results showed that the two exercise programs stimulate bone synthesis and decrease bone resorption in postmenopausal women with OP, but that exercise while wearing a weighted vest is better for improving balance.

Pro-survival Effects of 17β-Estradiol on Osteocytes Are Mediated by Nitric Oxide/cGMP via Differential Actions of cGMP-dependent Protein Kinases I and II

Estrogens promote bone health in part by increasing osteocyte survival, an effect that requires activation of the protein kinases Akt and ERK1/2, but the molecular mechanisms involved are only partly understood. Because estrogens increase nitric oxide (NO) synthesis and NO can have anti-apoptotic effects, we examined the role of NO/cGMP signaling in estrogen regulation of osteocyte survival. Etoposide-induced death of MLO-Y4 osteocyte-like cells, assessed by trypan blue staining, caspase-3 cleavage, and TUNEL assays, was completely prevented when cells were pre-treated with 17β-estradiol. This protective effect was mimicked when cells were pre-treated with a membrane-permeable cGMP analog and blocked by pharmacological inhibitors of NO synthase, soluble guanylate cyclase, or cGMP-dependent protein kinases (PKGs), supporting a requirement for NO/cGMP/PKG signaling downstream of 17β-estradiol. siRNA-mediated knockdown and viral reconstitution of individual PKG isoforms demonstrated that the anti-apoptotic effects of estradiol and cGMP were mediated by PKG Iα and PKG II. Akt and ERK1/2 activation by 17β-estradiol required PKG II, and cGMP mimicked the effects of estradiol on Akt and ERK, including induction of ERK nuclear translocation. cGMP induced BAD phosphorylation on several sites, and experiments with phosphorylation-deficient BAD mutants demonstrated that the anti-apoptotic effects of cGMP and 17β-estradiol required BAD phosphorylation on Ser(136) and Ser(155); these sites were targeted by Akt and PKG I, respectively, and regulate BAD interaction with Bcl-2. In conclusion, 17β-estradiol protects osteocytes against apoptosis by activating the NO/cGMP/PKG cascade; PKG II is required for estradiol-induced activation of ERK and Akt, and PKG Iα contributes to pro-survival signaling by directly phosphorylating BAD.

Role of serum FSH measurement on bone resorption in postmenopausal women

In vitro and animals models have shown follicle-stimulating hormone (FSH) effects on osteoclastic function, and FSH levels seem to influence bone loss independently of estrogen concentrations in humans. Our aim was to evaluate the role of serum FSH measurement in the assessment of bone resorption in postmenopausal women. We conducted a cross-sectional study including 92 postmenopausal healthy women aged 56.2 (3.6) and 7.2 (4) years since menopause. Serum FSH, luteinizing hormone (LH), estradiol (E2) and bone turnover markers as osteocalcin (OC) and C-terminal telopeptide of type I collagen (CTX) were measured. We analyzed the relationship between serum levels of gonadotropins, E2, and bone turnover markers. Serum levels of OC and CTX were positively related to FSH (r = 0.234, P = 0.047 and r=0.384, P=0.003) and LH (r=0.319, P=0.012 and r=0.273, P=0.038). There was no relationship with E2 levels. When gonadotropins levels were divided into quartiles, we found significant differences in bone turnover markers between the first and the fourth quartile. OC levels were higher in the highest quartile of FSH (P=0.024) and LH (P=0.001). Serum CTX was also higher in the highest quartile of FSH (P=0.004) and LH (P=0.039). FSH levels could explain approximately 14.7% of the chances in CTX. In summary, gonadotropins were related to bone turnover in postmenopausal healthy women. Moreover, the rise in FSH appears to contribute to higher bone resorption. Our results suggest that the measurement of FSH could be usefulness to perform a more comprehensive assessment of bone loss in these women.

Effects of Suppression of Follicle-Stimulating Hormone Secretion on Bone Resorption Markers in Postmenopausal Women

Context: It has recently been proposed that the increase in bone resorption after the menopause may not be due principally to estrogen deficiency but rather to the concomitant increase in circulating FSH levels. Objective: The objective of the study was to test whether suppression of FSH secretion in postmenopausal women reduces levels of bone resorption markers. Design: This was a prospective study. Setting: The study was conducted at a clinical research unit. Participants and Interventions: Postmenopausal women were treated with a GnRH agonist (leuprolide acetate, 7.5 mg im every 28 d; n = 21) or placebo injections (control; n = 20). Both groups received the aromatase inhibitor, letrozole, 2.5 mg/d, to eliminate variations in endogenous estrogen levels as a confounder. Main Outcome Measures: Serum FSH and bone resorption markers [serum C-terminal telopeptide of type I collagen (CTX) and tartrate-resistant acid phosphatase 5b (TRAP5b)] at d 105 (3.5 months) of treatment as compared with baseline. Results: Compared with baseline, serum FSH levels did not change significantly in controls (+6%) but were reduced (−86%, into the premenopausal range) in the GnRH group. Due to the aromatase inhibitor-induced reduction in estrogen production, serum CTX and TRAP5b levels increased significantly in controls (+20 and +10%, respectively). In the GnRH group, suppression of FSH secretion did not reduce serum CTX or TRAP5b levels; rather, both markers also increased in these women (+34 and +15%, respectively; P = 0.161 and 0.266 for comparison of percent changes between groups). Conclusions: This direct interventional study demonstrates that FSH does not regulate bone resorption in postmenopausal women.

Dietary restriction of lycopene for a period of one month resulted in significantly increased biomarkers of oxidative stress and bone resorption in postmenopausal women.

Lycopene is a carotenoid commonly found in tomatoes and tomato products which acts as an antioxidant to decrease oxidative stress and osteoporosis risk. We wanted to determine the effects of a lycopene-restricted diet on oxidative stress parameters and bone turnover markers in postmenopausal women. St. Michael 's Hospital, Toronto, ON, Canada. PARTICIPANTS AND STUDY DESIGN: 23 healthy postmenopausal women, 50-60 years old, provided blood samples at baseline and following a one-month lycopene-depletion period. Serum samples were analyzed for carotenoids; the oxidative stress parameters protein thiols and thiobarbituric-malondialdehyde reactive substances; the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), and the bone turnover markers bone alkaline phosphatase and crosslinked N-telopeptide of type I collagen (NTx). A paired t-test was used to test for significant differences in bone turnover markers, oxidative stress parameters and antioxidant status after lycopene restriction. Dietary lycopene restriction resulted in significantly decreased serum lycopene (p < 0.0001), lutein/zeaxanthin (p < 0.01), and α -/β -carotene (p < 0.05). GPx (p < 0.01), lipid and protein oxidation increased (not significant), while CAT and SOD were significantly depressed (p < 0.05 and p < 0.005, respectively). These changes coincided with significantly increased NTx (p < 0.05). These findings suggest that the daily consumption of lycopene may be important as it acts as an antioxidant to decrease bone resorption in postmenopausal women and may therefore be beneficial in reducing the risk of osteoporosis.

Dietary restriction of lycopene for a period of one month resulted in significantly increased biomarkers of oxidative stress and bone resorption in postmenopausal women

Dietary restriction of lycopene for a period of one month resulted in significantly increased biomarkers of oxidative stress and bone resorption in postmenopausal women

Effects of Suppression of Follicle-Stimulating Hormone Secretion on Bone Resorption Markers in Postmenopausal Women

It has recently been proposed that the increase in bone resorption after the menopause may not be due principally to estrogen deficiency but rather to the concomitant increase in circulating FSH levels. The objective of the study was to test whether suppression of FSH secretion in postmenopausal women reduces levels of bone resorption markers. This was a prospective study. The study was conducted at a clinical research unit. Postmenopausal women were treated with a GnRH agonist (leuprolide acetate, 7.5 mg im every 28 d; n = 21) or placebo injections (control; n = 20). Both groups received the aromatase inhibitor, letrozole, 2.5 mg/d, to eliminate variations in endogenous estrogen levels as a confounder. Serum FSH and bone resorption markers [serum C-terminal telopeptide of type I collagen (CTX) and tartrate-resistant acid phosphatase 5b (TRAP5b)] at d 105 (3.5 months) of treatment as compared with baseline. Compared with baseline, serum FSH levels did not change significantly in controls (+6%) but were reduced (-86%, into the premenopausal range) in the GnRH group. Due to the aromatase inhibitor-induced reduction in estrogen production, serum CTX and TRAP5b levels increased significantly in controls (+20 and +10%, respectively). In the GnRH group, suppression of FSH secretion did not reduce serum CTX or TRAP5b levels; rather, both markers also increased in these women (+34 and +15%, respectively; P = 0.161 and 0.266 for comparison of percent changes between groups). This direct interventional study demonstrates that FSH does not regulate bone resorption in postmenopausal women.