Central and peripheral fat body mass have a protective effect on osteopenia or osteoporosis in adults and elderly?

UNLABELLED: This cross-sectional study involves randomly selected men aged 50 to 99 years and postmenopausal women. Either central fat mass or peripheral fat mass were associated to osteoporosis or osteopenia independently from fat-free body mass and other confounding factors. INTRODUCTION: Obesity and osteoporosis are public health problems that probably share common pathophysiological mechanisms. The question if body fat mass, central or peripheral, is protective or harmful for osteoporosis or osteopenia is not completely resolved. This study aims to investigate the association between osteoporosis or osteopenia, and fat body mass (central and peripheral) independently from fat-free body mass, in men aged 50 to 99 years old and postmenopausal women randomly selected in the community. METHODS: This is a cross-sectional investigation with a random sample of registered population in Niterói Family Doctor Program (FDP), State of Rio de Janeiro, Brazil. Bone mineral density (BMD) and fat-free mass were assessed by dual X-ray absorptiometry (DXA). RESULTS: There was statistically significant bivariate association between bone loss with gender, age, skin color, alcohol consumption at risk dose, use of thiazide, fat-free body mass, and fat body mass (central and peripheral). In the multiple analysis of fat-free body mass, central and peripheral fat body mass showed an independent and protective effect on the presence of osteoporosis or osteopenia (p value <0.001). CONCLUSION: Since both obesity and osteoporosis are public health problems worldwide, strategies aimed at preventing both conditions should be encouraged during aging.

Serum uric acid and disorders of glucose metabolism: the role of glycosuria

Hyperuricemia has been associated with hypertension, diabetes mellitus, and metabolic syndrome. We studied the association between hyperuricemia and glycemic status in a nonrandomized sample of primary care patients. This was a cross-sectional study of adults ≥20 years old who were members of a community-based health care program. Hyperuricemia was defined as a value >7.0 mg/dL for men and >6.0 mg/dL for women. The sample comprised 720 participants including controls (n=257) and patients who were hypertensive and euglycemic (n=118), prediabetic (n=222), or diabetic (n=123). The mean age was 42.4±12.5 years, 45% were male, and 30% were white. The prevalence of hyperuricemia increased from controls (3.9%) to euglycemic hypertension (7.6%) and prediabetic state (14.0%), with values in prediabetic patients being statistically different from controls. Overall, diabetic patients had an 11.4% prevalence of hyperuricemia, which was also statistically different from controls. Of note, diabetic subjects with glycosuria, who represented 24% of the diabetic participants, had a null prevalence of hyperuricemia, and statistically higher values for fractional excretion of uric acid, Na excretion index, and prevalence of microalbuminuria than those without glycosuria. Participants who were prediabetic or diabetic but without glycosuria had a similarly elevated prevalence of hyperuricemia. In contrast, diabetic patients with glycosuria had a null prevalence of hyperuricemia and excreted more uric acid and Na than diabetic subjects without glycosuria. The findings can be explained by enhanced proximal tubule reabsorption early in the course of dysglycemia that decreases with the ensuing glycosuria at the late stage of the disorder.

Serum uric acid and disorders of glucose metabolism: the role of glycosuria.

Hyperuricemia has been associated with hypertension, diabetes mellitus, and metabolic syndrome. We studied the association between hyperuricemia and glycemic status in a nonrandomized sample of primary care patients. This was a cross-sectional study of adults ≥ 20 years old who were members of a community-based health care program. Hyperuricemia was defined as a value >7.0 mg/dL for men and >6.0 mg/dL for women. The sample comprised 720 participants including controls (n=257) and patients who were hypertensive and euglycemic (n=118), prediabetic (n=222), or diabetic (n=123). The mean age was 42.4 ± 12.5 years, 45% were male, and 30% were white. The prevalence of hyperuricemia increased from controls (3.9%) to euglycemic hypertension (7.6%) and prediabetic state (14.0%), with values in prediabetic patients being statistically different from controls. Overall, diabetic patients had an 11.4% prevalence of hyperuricemia, which was also statistically different from controls. Of note, diabetic subjects with glycosuria, who represented 24% of the diabetic participants, had a null prevalence of hyperuricemia, and statistically higher values for fractional excretion of uric acid, Na excretion index, and prevalence of microalbuminuria than those without glycosuria. Participants who were prediabetic or diabetic but without glycosuria had a similarly elevated prevalence of hyperuricemia. In contrast, diabetic patients with glycosuria had a null prevalence of hyperuricemia and excreted more uric acid and Na than diabetic subjects without glycosuria. The findings can be explained by enhanced proximal tubule reabsorption early in the course of dysglycemia that decreases with the ensuing glycosuria at the late stage of the disorder.

Environmental factors, familial aggregation and heritability of total cholesterol, low density lipoprotein-cholesterol and high density lipoprotein-cholesterol in a Brazilian population assisted by the Family Doctor Program.

OBJECTIVES: To estimate familial aggregation and the heritability of total cholesterol (TC), low density lipoprotein-cholesterol (LDL-C) and high density lipoprotein-cholesterol (HDL-C) in families assisted by the Family Doctor Program in a Brazilian city, and to evaluate associations between some environmental factors and familial aggregation of these lipids. STUDY DESIGN: Cross-sectional familial study. METHODS: The association of lipids with sociodemographic factors, lifestyle factors and comorbidities (e.g. physical activity, alcohol consumption, smoking, hypertension, impaired glucose tolerance, body mass index) was estimated using linear models and generalized estimating equations. Correlation of TC, LDL-C and HDL-C between pairs of relatives was estimated with the familial correlation procedure, and heritability was estimated with the ASSOC procedure. RESULTS: All associations were statistically significant. There was familial aggregation of TC (parent/offspring, r=0.33; sibling/sibling, r=0.37), LDL-C (parent/offspring, r=0.29; sibling/sibling, r=0.37) and HDL-C (parent/offspring, r=0.25; sibling/sibling, r=0.48), but less than 3%, 6% and 14%, respectively, which was explained by lifestyle factors. Correlation between pairs with genetic sharing (parent/offspring and sibling/sibling) was higher than that observed between father and mother. Heritability estimates ranged between 0.32 (HDL-C) and 0.50 (TC). Similar results were found for the two approaches used to estimate the contribution of genetic and environmental factors in the correlation of TC, LDL-C and HDL-C between the family pairs. CONCLUSION: The results showed that there is familial aggregation of TC, LDL-C and HDL-C, and point to the predominance of genetic factors because little influence of environmental variables was found.