RESUMEN
BACKGROUND: Several studies point to a correlation between obesity and the severity of depressive and anxiety symptoms in children and adults, but there are still some controversial points about this association. The aim of this study is to investigate the relationship between body composition and the severity of anxiety/depressive symptoms in overweight and obese individuals with Metabolic Syndrome (MS). METHODS: Fifty patients, 18-50 years old, overweight or obese and with the diagnosis of MS based on the International Diabetes Federation (IDF) criteria were selected for this study. Body composition was evaluated using Dual Energy X-ray Absorptiometry (DXA). Depressive symptoms were evaluated using the Hospital Anxiety and Depression Scale (HADS-Depression) and the Beck Depression Inventory (BDI). Anxiety symptoms were evaluated using HADS-Anxiety. RESULTS: No correlation was found between depressive symptoms (HADS-Depression or BDI) and Body Mass Index (BMI) (r = 0.01; p = 0.94 and r = -0.12, p = 0.38; respectively), Waist Circumference (WC) (r = -0.06, p = 0.67 and r = -0.22, p = 0.12; respectively), and Waist-to-Hip Ratio (WHR) (r = -0.12, p = 0.40 and r = -0.17, p = 0.23; respectively). Additionally, no correlation was found among anxiety symptoms (HADS-Anxiety) and BMI (r = -0.15, p = 0.27), and WHR (r = -0.17, p = 0.24). In contrast, a significant correlation was found between percentage of total fat (DXA) and HADS-Depression (r = 0.34, p = 0.019) and HADS-Anxiety (r = 0.30, p = 0.039). Additionally, an inverse and strong correlation was found between lean mass (in grams) and HADS-Depression (r = -0.42, p = 0.004), HADS anxiety (r = -0.57, p < 0.0001), and BDI (r = -0.44, p = 0.026). CONCLUSIONS: In individuals with MS, the percentage of body fat, and not central fat, BMI, WC, or WHR, was associated with an increased severity of anxiety and depressive symptoms. In contrast, total lean mass was strongly associated with fewer anxiety/depressive symptoms, suggesting that body composition might be related to psychiatric comorbidity in overweight individuals with MS.
RESUMEN
BACKGROUND: Adolescent mothers may be at increased risk of irreversible bone loss during pregnancy and lactation, particularly when calcium intake is low. OBJECTIVE: Longitudinal changes in bone mass from lactation to postweaning were evaluated in 10 adolescent mothers aged 15-18 y who habitually consumed <500 mg Ca/d. DESIGN: Total-body bone mineral content (TBBMC), total-body bone mineral density (TBBMD), and lumbar spine bone mineral density (LSBMD) were measured at lactation (6-24 wk postpartum) and after weaning (12-30 mo postpartum). Serum hormones (intact parathyroid hormone, estradiol, and prolactin), serum calcium, and markers of bone turnover [urinary N-telopeptide cross-linking region of type I collagen (NTx) and plasma activity of bone alkaline phosphatase] were measured at lactation. RESULTS: TBBMC, total calcium content, TBBMD, and LSBMD increased from lactation to postweaning (P < 0.01). TBBMD and LSBMD were, respectively, 3.6% and 9.7% lower than predicted at lactation and 0.3% and 4.8% lower than predicted in the postweaning period. The increase in age-matched TBBMD adequacy was correlated with the time after resumption of menses (r = 0.86, P < 0.01). Calcium accretion from lactation to postweaning correlated negatively with estradiol (r = -0.86) and prolactin (r = -0.69) and positively with intact parathyroid hormone (r = 0.72) and NTx (r = 0.84) measured at lactation (P < 0.05). CONCLUSIONS: It appears that adolescent mothers with habitually low calcium intakes recover from lactation-associated bone loss after weaning. The rate of bone accretion, however, may not be sufficient to attain peak bone mass at maturity. Hormones regulating bone turnover during lactation may influence bone recovery in adolescent mothers.
