(1/1519) Persisting benefits 12-18 months after discontinuation of pubertal metformin therapy in low birthweight girls.
BACKGROUND: Discontinuation of metformin therapy, if started beyond menarche in adolescents or young women with hyperinsulinaemia following low birthweight, is rapidly followed by rebound deteriorations in body fat, insulin resistance and blood lipid profile. OBJECTIVE: We hypothesized that early commencement of metformin and its continuation throughout puberty might have more persisting benefits. PATIENTS AND MEASUREMENTS: We followed up on a previously reported randomized study cohort at 12 months and 18 months after treatment discontinuation, including body composition by absorptiometry, fasting insulin, glucose and blood lipids. In that open-labelled, prospective study, 22 low birthweight girls with early normal puberty (Stage 2 breast development at age 8-9 years) were randomized to remain untreated (N = 12] or to receive metformin (850 mg/day; N = 10) for 36 months (between time -36 months to 0 month). RESULTS: The significant improvements previously reported at the end of the 36-month active treatment period in per cent body fat, abdominal fat mass, fasting insulin sensitivity, high density lipoprotein (HDL) cholesterol and triglyceride levels all persisted at follow-up 12 months after treatment discontinuation. Further anthropometry at 18 months off therapy confirmed the persistence of benefits in height, body mass index (BMI) and waist circumference in the previously metformin-exposed girls. CONCLUSION: In low birth weight girls with early normal onset of puberty, metformin treatment for 3 years across puberty resulted in auxological, endocrine and metabolic benefits that persisted for at least 1 year after metformin withdrawal. Further follow-up and longer-term studies are needed to explore the possibility that insulin sensitization therapy during puberty might reprogramme predisposition to metabolic disease. (+info)
(2/1519) Metabolic syndrome in childhood obesity.
OBJECTIVES: We determined the frequency of metabolic risk factors and the prevalence of Metabolic Syndrome in childhood obesity. SUBJECTS: 186 obese children (97 females and 89 males), aged 11.2 +/- 2.8 (6-16) years and 98 healthy children (46 females and 52 males), aged 10.9 +/- 3.2 (6-16) years were recruited for the study, as study and control groups, respectively. METHODS: Subjects were evaluated for anthropometry, blood pressure (BP) and biochemical cardiovascular risk factors. Metabolic syndrome was defined in presence of > or = 3 of the following: (i) fasting triglyceride > or = 100 mg/dL; (ii) high density lipoprotein-cholesterol < 50 mg/dL, except in boys aged 15 to 19 years, in whom the cut-off point was 45 mg/dL; (iii) fasting glucose > or = 110 mg/dL; (iv) waist circumference > 75th percentile for age and gender and (v) systolic BP > 90th percentile. RESULTS: We found that 144 (77.4%) children in the obese group had one, two or more cardiovascular risk factors. Using a pediatric definition, the prevalence of metabolic syndrome was 2.1%. In the control group, the clustering of one, two and three risk factors was very rare. CONCLUSION: Childhood obesity is associated with increased frequency of cardiovascular risk factors and metabolic syndrome. (+info)
(3/1519) Metabolic syndrome in women with polycystic ovary syndrome: prevalence, characteristics and predictors.
The aim of this study was to determine the prevalence of metabolic syndrome in women with polycystic ovary syndrome, as well as its characteristics and predictors. Seventh-three women, with body mass index of 30.4 +/- 7.8 kg/m2 and 25.0 +/- 6.0 years old, subdivided according to body mass index, were studied retrospectively. There was no significant mean age difference among body mass index groups (p = 0.228). Prevalence of metabolic syndrome was 38.4%, with a null prevalence for normal (n = 18), 23.8% for overweight (n = 17), 62.9% for obese (n = 28), and 85.5% for morbidly obese women (n = 7). Women with metabolic syndrome were older than women without metabolic syndrome (27.3 +/- 5.3 vs. 24.2 +/- 4.6 vs. years old; p = 0.031) and presented a higher body mass index (36.3 +/- 7.7 vs. 26.9 +/- 5.4; p < 0.001). There was no difference for degree of hirsutism and menstrual patterns between women with and without metabolic syndrome (p = 0.593 and p = 0.119, respectively). Regarding laboratory parameters, DHEAS was lower (1,646 +/- 1,007 vs. 2,594 +/- 1,563; p = 0.007) and HOMA-IR were higher (9.9 +/- 9.7 vs. 4.6 +/- 4.7; p = 0.004) in women with metabolic syndrome (p = 0.031 and p < 0.001, respectively). The best predictors of metabolic syndrome were waist circumference > 88 cm, HDL-cholesterol < 50 mg/dL and triglycerides >or= 150 mg/dL. (+info)
(4/1519) Validity and reliability of the sagittal abdominal diameter as a predictor of visceral abdominal fat.
OBJECTIVES: To evaluate the reliability of the sagittal abdominal diameter and its validity as a predictor of visceral abdominal fat, as well as to identify the most appropriate cut-off points to identify the area of visceral fat that is known to represent a risk factor for cardiovascular disease. DESIGN: Validation study. SUBJECTS: 92 healthy volunteers (57 women, 35 men), age: 20-83 y, body mass index: 19.3 to 35.9 kg/m2. MEASUREMENTS: Sagittal abdominal diameter (SAD), weight, height, circumferences (waist, hip, and thigh), sub-scapular skinfold thickness, abdominal diameter index, and waist-hip ratio (WHR). METHOD OF CHOICE: Computed tomography (CT). STATISTIC: Receiver operating characteristic (ROC) curve. RESULTS: The reliability for SAD measurement was very high (Inter-class coefficient = 0.99). Visceral fat as measured by VAF through CT was highly correlated with SAD (women r = 0.80; men r = 0.64, p < 0.001), waist circumference (women r = 0.77; men r = 0.73, p < 0.001), and WHR (women r = 0.72; men r = 0.58, p < 0.001). The ROC curve indicated 19.3 cm and 20.5 cm as the threshold values for abdominal sagittal diameter in women and men (sensitivity 85% and 83%, specificity 77% and 82%, respectively). CONCLUSIONS: There was a high correlation between SAD and VAF. The cut-off values identified for SAD presented a sensitivity and specificity that were considered adequate. (+info)
(5/1519) Consumption of red or processed meat does not predict risk factors for coronary heart disease; results from a cohort of British adults in 1989 and 1999.
OBJECTIVES: To investigate whether a high consumption of red or processed meat is associated with increased risk of coronary heart disease (CHD). SUBJECTS/METHODS: The subjects were 517 men and 635 women, who were members of the Medical Research Council National Survey of Health and Development, 1946 birth cohort. Assessment of diet was carried out at two time points 1989 and 1999 with outcome measures collected in 1999. Food intake data were recorded in 5-day diaries. Meat consumption was estimated by adding individual meat portions to the meat fractions of composite dishes. RESULTS: There was no significant association between red or processed meat consumption in 1989 and 1999 and serum cholesterol concentrations and blood pressure measured in 1999. The combined intake of red and processed meat in 1999 had a significant positive association with blood pressure in men only. Red and processed meat intakes in 1989, separately and combined, had a significant positive association with waist circumference in 1999: a 10 g increase in red meat consumption accounted for a 0.3 cm increase in waist circumference; P=0.04 (men), 0.05 (women). CONCLUSIONS: Consumption of red or processed meat assessed separately was not related to the major risk factors for CHD but contributed to increased waist circumference that has also been identified as a risk factor. (+info)
(6/1519) Genetic and non-genetic correlates of vitamins K and D.
OBJECTIVE: To assess the genetic and nongenetic correlates of circulating measures of vitamins K and D status in a community-based sample of men and women. SUBJECTS/METHODS: A cross-sectional study of 1762 participants of the Framingham Offspring Study (919 women; mean age 59 years). Vitamin K status was measured as plasma phylloquinone and serum percent undercarboxylated osteocalcin (ucOC), and vitamin D was measured using plasma 25-hydroxyvitamin D (25(OH)D). Associations between vitamin K status and vitamin D status with biologically plausible nongenetic factors were assessed using stepwise regression. Heritability and linkage were determined using Sequential Oligogenic Linkage Analysis Routines (SOLAR). RESULTS: Nongenetic factors accounted for 20.1 and 12.3% of the variability in plasma phylloquinone in men and women respectively, with triglycerides and phylloquinone intake being the primary correlates. In men 12.2% and in women 14.6% of the variability in %ucOC was explained by nongenetic factors in our models. Heritability estimates for these vitamin K status biomarkers were nonsignificant. Season, vitamin D intake, high-density lipoprotein (HDL) cholesterol and waist circumference explained 24.7% (men) and 24.2% (women) of the variability in plasma 25(OH)D. Of the three vitamins examined, only 25(OH)D was significantly heritable (heritability estimate=28.8%, P<0.01), but linkage analysis of 25(OH)D did not achieve genome-wide significance. CONCLUSIONS: Variability in biomarkers of vitamin K status was attributed to nongenetic factors, whereas plasma 25(OH)D was found to be significantly heritable. Further studies are warranted to investigate genetic loci influencing vitamin D status. (+info)
(7/1519) To treat or not to treat: comparison of different criteria used to determine whether weight loss is to be recommended.
(8/1519) Association of body mass index and abdominal obesity with marital status in adults.