Diabetes and Obesity as Independent Risk Factors for Osteoporosis in Postmenopausal Women: A Population Study

Abstract

We aimed to analyze bone mineralization and the effect of different risk factors for osteoporosis in postmenopausal women. We studied 2,756 postmenopausal subjects out of ≥10,000 records from the ROIS registry in the frame of the PROF Project, a population study carried out in Salento (Taranto, Brindisi, Lecce) from 2009 to 2012. All subjects were assessed by phalangeal Quantitative Ultrasound (QUS) to evaluate their bone mineralization (assessed by Amplitude Dependent Speed of Sound, AD-SoS) and the association between demineralization and the presence of other conditions or risk factors. Mean age was 64±9.5 years and mean BMI was 28.7±3.5 Kg/m2. Pearson correlation analyses revealed a negative association between bone mineralization (AD-SoS) and BMI (P<0.001). By using multivariate logistic regression analysis, we observed significant values of Odds Ratios of osteoporosis (adjusted for age, physical activity and the use of drugs known to increase the risk of fractures) in subjects with diabetes and obesity: 1.39 (CI: 1,05–1,83) and 1.46 (CI: 1.20–1.78), respectively. A statistically significant linear trend of higher Odds Ratios of osteoporosis was found for increasing values of BMI. The percent change in the odds of vertebral fractures per single SD decrease of AD-SoS was 47% (P<0.001). Diabetes and obesity in postmenopausal women are likely to represent independent risk factors for osteoporosis. Phalangeal QUS showed a good power of predictivity in identifying subjects with vertebral fractures.

Hyperbaric oxygen therapy exerts anti‐osteoporotic effects in obese and lean D‐galactose‐induced aged rats

“…8,9 This supports the fact that among the elderly population, a higher proportion of osteoporotic fractures has been observed in the elderly with obesity. 8,10 Increased oxidative stress is a pivotal pathological event that is found in aging-induced osteoporosis. 11,12 With regard to the nine hallmarks of aging, cellular senescence serves as one of the antagonistic hallmarks that exerts a beneficial effect as a protective response to physiologic stress and oxidative damage scavengers, in normal physiological conditions.…”

“…7 Unfortunately, aging-induced bone dyshomeostasis and bone loss are aggravated by obesity. 8,9 This supports the fact that among the elderly population, a higher proportion of osteoporotic fractures has been observed in the elderly with obesity. 8,10 Increased oxidative stress is a pivotal pathological event that is found in aging-induced osteoporosis.…”

“…This phenomenon results in a gradual loss of bone volume fraction and bone mineral density, finally leading to osteoporosis and increased risk of fracture 7 . Unfortunately, aging‐induced bone dyshomeostasis and bone loss are aggravated by obesity 8,9 . This supports the fact that among the elderly population, a higher proportion of osteoporotic fractures has been observed in the elderly with obesity 8,10 …”

“…It has also been observed that increased oxidative stress along with an impairment in antioxidative capacity resulted in hypoxic damage and exacerbated inflammatory responses, resulting in bone dyshomeostasis and bone loss 3,8,9,22 . Those findings indicated that oxidative stress‐induced cellular senescence in the bone ultimately contributed to a senescence‐associated secretory phenotype (SASP), which was characterized by increased proinflammatory cytokine release from the senescent cells 5 .…”