Of the U.S. population, 65% is either overweight or obese, and weight loss is recommended to reduce co-morbid conditions. However, bone mobilization and loss may also occur with weight loss. The risk for bone loss depends on initial body weight, age, gender, physical activity, and conditions of dieting such as the extent of energy restriction and specific levels of nutrient intake. Older populations are more prone to bone loss with weight loss; in women, this is due at least in part to a reduced dietary Ca intake and/or efficiency of absorption. Potential hormonal mechanisms regulating bone loss during weight loss are discussed, including decreases in estrogen, leptin, glucagon-like peptide-2, growth hormone, and insulin-like growth factor-1, or an increase in cortisol. In contrast, the rise in adiponectin and ghrelin with weight reduction should not be detrimental to bone. Combining energy restriction with exercise does not necessarily prevent bone loss, but may attenuate loss as was shown with additional Ca intake or osteoporosis medications. Future controlled weight loss trials should be designed to further address mechanisms influencing the density and quality of bone sites vulnerable to fracture, in the prevention of osteoporosis.
Overweight postmenopausal women may be more susceptible to bone loss with weight reduction than previously studied obese women. The influence of energy restriction and Ca intake on BMD was assessed in 66 individuals. Weight reduction resulted in bone loss at several sites in women consuming 1 g Ca/day and was mitigated with higher calcium intake at 1.7 g/day.Introduction: Bone loss is associated with weight loss in obese postmenopausal women and can be prevented with calcium (Ca) supplementation. However, because bone loss caused by weight loss may be greater in overweight than obese women, it is not clear whether Ca supplementation is also beneficial in overweight women. Materials and Methods:We assessed the influence of caloric restriction at two levels of Ca intake on BMD and BMC in 66 overweight postmenopausal women (age, 61 ± 6 years; body mass index, 27.0 ± 1.8 kg/m
RIEDT, CLAUDIA S., ROBERT E. BROLIN, ROBERT M. SHERRELL, M. PAUL FIELD, AND SUE A. SHAPSES. True fractional calcium absorption is decreased after Roux-en-Y gastric bypass surgery. Obesity. 2006;14: 1940 -1948. Objective: Roux-en-Y gastric bypass (RYGB) is considered to be the gold standard alternative treatment for severe obesity. Weight loss after RYGB results primarily from decreased food intake. Inadequate calcium (Ca) intake and metabolic bone disease can occur after gastric bypass. To our knowledge, whether malabsorption of Ca contributes to an altered Ca metabolism in the RYGB patient has not been addressed previously. Research Methods and Procedures:We recruited 25 extremely obese women in order to study true fractional Ca absorption (TFCA) before and 6 months after RYGB surgery, using a dual stable isotope method ( 42 Ca and 43 Ca) and test load of Ca (200 mg). Hormones regulating Ca absorption and markers of bone turnover were also measured. Results: In 21 women (BMI 52.7 Ϯ 8.3 kg/m 2 , age 43.9 Ϯ 10.4 years) who successfully completed the study, TFCA decreased from 0.36 Ϯ 0.08 to 0.24 Ϯ 0.09 (p Ͻ 0.001) after RYGB. Bone turnover markers increased significantly (p Ͻ 0.01). TFCA correlated with estradiol levels (r ϭ 0.512, p Ͻ 0.02) and tended to correlate with 1,25 (OH) 2 D (r ϭ 0.427, p Ͻ 0.06) at final measurement. Stepwise linear regression indicated that estradiol explained 62% of the variance for TFCA at 6 months post-surgery (p Ͻ 0.01). Discussion: TFCA decreases (0.12 Ϯ 0.08) after RYGB surgery but remains within normal range. Although only some patients were estimated to have low Ca absorption after surgery, all of the patients showed a dramatic increase in markers of bone resorption. The alteration in Ca metabolism after RYGB-induced weight loss appears to be regulated primarily by estradiol levels and might ultimately affect bone mass.
Summary The goal in this study was to determine the relationship between body mass index and trabecular and cortical bone using quantitative computed tomography. A higher body mass index (BMI) was positively associated with trabecular and cortical bone parameters, and serum parathyroid hormone, and negatively associated with cortical volumetric bone mineral density (vBMD) and serum 25-hydroxy-vitamin D. When BMI is greater than 35 kg/m2, adiposity affects vBMD and may explain the higher fracture risk in this population without low BMD. Introduction The influence of adult obesity on the trabecular and cortical bone, geometry, and strength has not been fully addressed. The goal in this study was to determine the relationship between body mass index and trabecular and cortical bone mass and geometry, over a wide range of body weights. Methods We examined 211 women (25–71 years; BMI 18–57 kg/m2) who were classified into three categories of BMI (kg/m2) including normal-weight (BMI<25), overweight and obese-class I (BMI 25–35) and obese-class II–III (BMI>35), and also by menopausal status. Volumetric bone mineral density (mg/cm3), trabecular, and cortical components as well as geometric characteristics at the 4%, 38%, and 66% from the distal tibia were measured by peripheral quantitative computed tomography, and serum was analyzed for parathyroid hormone (PTH) and 25-hydroxy-vitamin D (25OHD). Results Higher BMI was associated with greater values of trabecular bone and cortical BMC and area and PTH (r>0.39, p<0.001), but lower cortical vBMD and 25OHD (r>−0.27, p<0.001). When controlling for lower leg muscle area, fat area was inversely associated with cortical vBMD (r=−0.16, p<0.05). Premenopausal obese women with both higher BMI and PTH had lower cortical vBMD (r<−0.40, p<0.001). While age is a predictor for most bone variables, fat mass explains more variance for vBMD, and lean mass and 25OHD explain greater variance in geometric and strength indices (p<0.05). Conclusions Severe obesity (BMI>35) increases trabecular vBMD and in the presence of a higher PTH is associated with a lower cortical vBMD without compromising bone geometry and strength. Whether or not a lower cortical vBMD in obesity influences fracture risk over time needs to be further explored.
We suggest that WL is associated with elevated calcium requirements that, if not met, could activate the calcium-parathyroid hormone axis to absorb more calcium. Normal intakes of calcium during energy restriction result in inadequate total calcium absorption and could ultimately compromise calcium balance and bone mass.
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