(1/1436) Obesity, abdominal obesity, and clustering of cardiovascular risk factors in South Korea.

The aim of this study was first, to investigate the prevalence of obesity, abdominal obesity, and clustering of cardiovascular (CVD) risk factors, and secondly, to identify the BMI or waist circumference (WC) level at which clustering increases in South Koreans. A population-based, cross-sectional National Health Examination Survey was carried out in 1998. A total of 8,816 subjects (4,029 men and 4,787 women) aged 15-79 y were selected by stratified multistage probability sampling design. The measurements taken of the subjects included: height, weight, waist and hip circumference, blood pressure, fasting glucose, and lipids. The prevalence of BMI > or = 25 kg/m2 was 25.3% for men and 28.3% for women. The prevalence of WC >90 cm in men, and >80 cm in women was 18.5%, and 38.5%, respectively. Clustering of 3 or more CVD risk factors was 22.7% in men ad 21.7% in women. Using <21 kg/m2; as a referent, subjects with BMI of 23 kg/m2; and 27 kg/m2; had an odds ratio of 3.5 and 10.2 in men, and 3.1 and 6.7 in women, respectively for clustering of CVD risk factors. Using <65 cm as a referent, subjects with a WC of > or = 90 cm in men and > or = 85 cm in women had an odds ratio of 13.4, and 13.6, respectively for clustering of CVD risk factors. Considering the significant associations between clustering of CVD risk factors and BMI or WC, the present study suggests that high prevalence of overweight may have important implications for the health care system, even at a lower level of BMI or WC.  (+info)

(2/1436) Impact of obesity on lipid profiles in middle-aged women.

OBJECTIVE: The goal of the study was to analyze the impact of overweight on lipid and apolipoprotein A-I and B (apoA-I, apoB) profiles in the women's blood serum. MATERIAL AND METHODS: Seventy-five women without any symptoms of coronary heart disease were examined. Women were divided into two groups: those with normal weight and the body mass index (BMI) less than 25 (n=34, BMI 22.3+/-1.5; mean age 62+/-8.7 years) and overweight women (n=41, BMI 29.7+/-3.7; mean age 59+/-9.4). Weight and height were measured and blood serum concentrations of total cholesterol, high-density lipoprotein cholesterol, and triglycerides were determined after an overnight fasting. In the same serum samples the levels of apoA-I and B were measured using monoclonal antibodies against apo (Spinreact AA, Sant Esteve De Bas, Spain) by the immunoturbidimetry method. The serum samples were kept frozen at -40 degrees C until used. RESULTS: Total cholesterol and triglycerides levels were similar in the healthy and the overweight women groups (6.49+/-1.25 vs 6.52+/-1.18 mmol/l; p>0.05 and 1.21+/-0.71 vs 1.41+/-0.98 mmol/l; p>0.05, respectively). The concentrations of high-density lipoprotein cholesterol and apoA-I were significantly higher in the normal weight women compared to the overweight women (1.84+/-0.52 vs 1.40+/-0.29 mmol/l, p<0.001 and 1.40+/-0.26 vs 1.24+/-0.23 g/l, p<0.01, respectively). The level of apoB was significantly higher in the overweight female group compared to normal weight women (0.83+/-0.21 vs 0.74+/-0.18 g/l, p=0.049). The apoB/A-I ratio was significantly lower in the normal weight group than in the overweight group (0.055+/-0.15 vs 0.70+/-0.22; p<0.001). Moderate to strong correlations between apoA-I and high-density lipoprotein cholesterol concentrations were found in both groups (r=0.41, p<0.01 in the control female group and r=0.59, p<0.0001 in the overweight group, respectively). A similar level of correlation between apoB and total cholesterol was established in both groups (r=0.54, p<0.0005 and r=0.67, p<0.0001, respectively). CONCLUSION: Obesity in middle-aged women is associated with a significant decrease in serum high-density lipoprotein cholesterol and apoA-I levels, a significant increase in apoB and apoB/A-I ratio, even if serum total cholesterol and triglycerides concentrations are unaltered. Changes of the lipid profile in obese women are indicative of a higher risk of coronary heart disease.  (+info)

(3/1436) Another emerging event occurring during HIV infection treated with any antiretroviral therapy: frequency and role of gynecomastia.

To identify HIV-associated episodes of gynecomastia occurred during antiretroviral therapy in a cohort of around 1,000 patients, and to investigate potential correlations with demographic and epidemiological variables, clinical-laboratory markers of HIV disease, metabolic disturbances, and antiretroviral treatment, a cross-sectional survey of 1.007 patients treated for at least 12 months (669 males: 66.4%), identified all subjects with true (ultrasonography-confirmed) gynecomastia, after exclusion of all other predisposing conditions. Special attention was paid to eventual metabolic alterations, including lipodystrophy syndrome, dyslipidemia, and hyperglycemia, and administered antiretrovirals. Fifteen of the 516 evaluable male subjects (2.9%), developed gynecomastia when aged 12-58 years. A concurrent lipodystrophy was present in all cases, while hypertriglyceridemia, hypercholesterolemia, and hyperglycemia were found in 11, 6, and 3 patients, respectively. Duration of seropositivity and time from start of antiretroviral therapy varied significantly, and no correlation was found with HIV disease progression, but 5 patients never received protease inhibitors, while an efavirenz-based treatment apparently prompted gynecomastia in 4 protease inhibitor-naive patients, and worsened this sign in other 4 patients switching from a protease inhibitor-based HAART. One patient developed gynecomastia while on isolated nucleoside analogue therapy. In the whole patient group, stavudine proved the nucleoside analogue administered more frequently and for a more prolonged time. During the follow-up, no significant ameliorament of gynecomastia was observed despite eventual therapeutic changes. Gynecomastia, as an emerging untoward event of treated HIV infection, deserves further investigation, from an epidemiological, clinical, and especially pathogenetic point of view. The frequent association with metabolic abnormalities suggests some common ethiologic pathway with other HAART-related disturbances.  (+info)

(4/1436) Web-based targeted nutrition counselling and social support for patients at increased cardiovascular risk in general practice: randomized controlled trial.

BACKGROUND: Using the Internet may prove useful in providing nutrition counselling and social support for patients with chronic diseases. OBJECTIVE: We evaluated the impact of Web-based nutrition counselling and social support on social support measures, anthropometry, blood pressure, and serum cholesterol in patients at increased cardiovascular risk. METHODS: We conducted a randomized controlled trial among patients with increased cardiovascular risk in Canadian family practices. During 8 months, patients in the intervention group and control groups received usual care. Patients in the intervention group also had access to a Web-based nutrition counselling and social support tool (Heartweb). Site use during the study was monitored. We measured social support, body mass index, waist/hip ratio, blood pressure, and cholesterol levels at baseline and at 4 and 8 months to assess the effectiveness of the intervention. RESULTS: We randomized 146 patients into the Web-based intervention (n=73) or the control group (n=73). Within the Web-based intervention group, Heartweb was used by only 33% (24/73) of patients, with users being significantly younger than nonusers (P=.03). There were no statistically significant differences between the intervention group and the control group in changes in social support, anthropometry, blood pressure, and serum cholesterol levels. CONCLUSIONS: Uptake of the Web-based intervention was low. This study showed no favourable effects of a Web-based nutrition counselling and social support intervention on social support, anthropometry, blood pressure, and serum cholesterol. Improvements in reach and frequency of site use are needed to increase the effectiveness of Web-based interventions.  (+info)

(5/1436) Rare variant of apolipoprotein E (Arg136 -->Ser) in two normolipidemic individuals.

Through the analysis of the common apolipoprotein (apo) E gene polymorphism in large Caucasian population study with the PCR and subsequent restriction analysis, we have identified carriers of mutant allele Arg136-->Ser. Both of them (71-years-old female and her 43-years-old son) have normal lipid parameters. We suggest that Arg136-->Ser mutation in apoE is not necessarily connected with elevated lipid levels in all cases. Furthermore, so far unidentified factors (environmental and/or genetic) are important for the development of lipid metabolism disorders in apoE Arg136-->Ser mutation carriers.  (+info)

(6/1436) Dynamic genetic architecture of metabolic syndrome attributes in the rat.

The polydactylous rat strain (PD/Cub) is a highly inbred (F > 90) genetic model of metabolic syndrome. The aim of this study was to analyze the genetic architecture of the metabolic derangements found in the PD/Cub strain and to assess its dynamics in time and in response to diet and medication. We derived a PD/Cub x BN/Cub (Brown Norway) F2 intercross population of 149 male rats and performed metabolic profiling and genotyping and multiple levels of genetic linkage and statistical analyses at five different stages of ontogenesis and after high-sucrose diet feeding and dexamethasone administration challenges. The interval mapping analysis of 83 metabolic and morphometric traits revealed over 50 regions genomewide with significant or suggestive linkage to one or more of the traits in the segregating PD/Cub x BN/Cub population. The multiple interval mapping showed that, in addition to "single" quantitative train loci, there are more than 30 pairs of loci across the whole genome significantly influencing the variation of particular traits in an epistatic fashion. This study represents the first whole genome analysis of metabolic syndrome in the PD/Cub model and reveals several new loci previously not connected to the genetics of insulin resistance and dyslipidemia. In addition, it attempts to present the concept of "dynamic genetic architecture" of metabolic syndrome attributes, evidenced by shifts in the genetic determination of syndrome features during ontogenesis and during adaptation to the dietary and pharmacological influences.  (+info)

(7/1436) Effects of cholesteryl ester transfer protein inhibition on high-density lipoprotein subspecies, apolipoprotein A-I metabolism, and fecal sterol excretion.

OBJECTIVE: Pharmacological inhibition of the cholesteryl ester transfer protein (CETP) in humans increases high-density lipoprotein (HDL) cholesterol (HDL-C) levels; however, its effects on apolipoprotein A-I (apoA-I) containing HDL subspecies, apoA-I turnover, and markers of reverse cholesterol transport are unknown. The present study was designed to address these issues. METHODS AND RESULTS: Nineteen subjects, 9 of whom were taking 20 mg of atorvastatin for hypercholesterolemia, received placebo for 4 weeks, followed by the CETP inhibitor torcetrapib (120 mg QD) for 4 weeks. In 6 subjects from the nonatorvastatin cohort, the everyday regimen was followed by a 4-week period of torcetrapib (120 mg BID). At the end of each phase, subjects underwent a primed-constant infusion of (5,5,5-2H3)-L-leucine to determine the kinetics of HDL apoA-I. The lipid data in this study have been reported previously. Relative to placebo, 120 mg daily torcetrapib increased the amount of apoA-I in alpha1-migrating HDL in the atorvastatin (136%; P<0.001) and nonatorvastatin (153%; P<0.01) cohorts, whereas an increase of 382% (P<0.01) was observed in the 120 mg twice daily group. HDL apoA-I pool size increased by 8+/-15% in the atorvastatin cohort (P=0.16) and by 16+/-7% (P<0.0001) and 34+/-8% (P<0.0001) in the nonatorvastatin 120 mg QD and BID cohorts, respectively. These changes were attributable to reductions in HDL apoA-I fractional catabolic rate (FCR), with torcetrapib reducing HDL apoA-I FCR by 7% (P=0.10) in the atorvastatin cohort, by 8% (P<0.001) in the nonatorvastatin 120 mg QD cohort, and by 21% (P<0.01) in the nonatorvastatin 120 mg BID cohort. Torcetrapib did not affect HDL apoA-I production rate. In addition, torcetrapib did not significantly change serum markers of cholesterol or bile acid synthesis or fecal sterol excretion. CONCLUSIONS: These data indicate that partial inhibition of CETP via torcetrapib in patients with low HDL-C: (1) normalizes apoA-I levels within alpha1-migrating HDL, (2) increases plasma concentrations of HDL apoA-I by delaying apoA-I catabolism, and (3) does not significantly influence fecal sterol excretion.  (+info)

(8/1436) Management of dyslipidemia in women in the post-hormone therapy era.

OBJECTIVE: Cardiovascular disease (CVD) is the leading cause of death for women in the United States and is largely preventable. The American Heart Association has recently released evidence-based guidelines for the prevention of CVD in women; these include gender-specific recommendations for the management of dyslipidemia. This article reviews these recommendations and the evidence supporting them. DESIGN: This was a qualitative review of a systematic literature search related to lipid guidelines for women and discussion of rationale and evidence for new clinical recommendations. MAIN RESULTS: Lifestyle modifications are the cornerstone of lipid management. Substantial evidence from randomized clinical trials supports the use of low-density lipoprotein cholesterol-lowering therapy (primarily statins) in all high-risk women and the use of niacin or fibrates when high-density lipoprotein cholesterol is low or non-high-density lipoprotein cholesterol is elevated. Fewer data are available for women at lower or intermediate risk. CONCLUSIONS: Encouragement of lifestyle modification and appropriate use of lipid-altering therapy will have a substantial impact on reducing the burden of cardiovascular disease in women.  (+info)