Differences In Low-density Lipoprotein Cholesterol Research Articles

Association between lipid profiles and osteoporosis in postmenopausal women: a meta-analysis.

To investigate the relationship between blood lipid profiles and osteoporosis in postmenopausal women. A comprehensive search of the literature related to lipid profiles and postmenopausal osteoporosis was conducted in Wanfang Database, CNKI, PubMed (1950-2015) and EMBASE (1974-2015). Appropriate studies were selected according to pre-defined exclusion criteria, and the levels of high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL), triglycerides (TG) and total cholesterol (TC) were compared between osteoporosis and normal density groups. Statistical analysis was performed using RevMan5.3. Ten published articles were selected for meta-analysis. The results showed that the levels of HDL, LDL, TC were higher in the osteoporosis group than the normal density group, whereas the levels of TG were lower in the osteoporosis group (HDL: MD = 2.63, 95% CI: 0.43 to 4.84, p = 0.02; LDL: MD = 9.67, 95% CI: -0.10 to 19.44, p = 0.0532; TG: MD = -0.42, 95% CI: -17.52 to 16.67, p = 0.96; TC: MD = 14.82, 95% CI: 2.84 to 26.80, p = 0.02). There was no statistical difference in LDL and TG. The serum levels of HDL and TC are higher in postmenopausal osteoporosis patients, and may thus be potentially useful indicators to reflect the process of osteoporosis in these women. More research is needed to determine the relationship between LDL, TG and postmenopausal osteoporosis.

Effect of probiotics on metabolic profiles in type 2 diabetes mellitus: A meta-analysis of randomized, controlled trials.

Type 2 diabetes mellitus (T2DM) is a prevalent metabolic disease which is imposing heavy burden on global health and economy. Recent studies indicate gut microbiota play important role on the pathogenesis and metabolic disturbance of T2DM. As an effective mean of regulating gut microbiota, probiotics are live micro-organisms that are believed to provide a specific health benefit on the host. Whether probiotic supplementation could improve metabolic profiles by modifying gut microbiota in T2DM or not is still in controversy.The aim of the study is to assess the effect of probiotic supplementation on metabolic profiles in T2DM.We searched PubMed, EMBASE, and Cochrane Library up to 12 April 2016. Two review authors independently assessed study eligibility, extracted data, and evaluated risk of bias of included studies. Data were pooled by using the random-effect model and expressed as standardized mean difference (SMD) with 95% confidence interval (CI). Heterogeneity was assessed and quantified (I2).A total of 12 randomized controlled trials (RCTs) were included. Lipid profiles (n = 508) and fasting blood glucose (FBG) (n = 520) were reported in 9 trials; the homeostasis model of assessment for insulin resistance index (HOMA-IR) (n = 368) and glycosylated hemoglobin (HbA1c) (n = 380) were reported in 6 trials. Probiotics could alleviate FBG (SMD –0.61 mmol/L, 95% CI [–0.92, –0.30], P = 0.0001). Probiotics could increase high-density lipoprotein-cholesterol (HDL-C) (SMD 0.42 mmol/L, 95% CI [0.08, 0.76], P = 0.01). There were no significant differences in low-density lipoprotein-cholesterol (LDL-C), total cholesterol (TC), triglyceride (TG), HbA1c and HOMA-IR between the treatment group and the control group.Probiotics may improve glycemic control and lipid metabolism in T2DM. Application of probiotic agents might become a new method for glucose management in T2DM.

Effect of dietary vitamin B6on growth, feed utilization, health and non-specific immune of juvenile Pacific white shrimp,Litopenaeus vannamei

Six diets were formulated with vitamin B6 levels (2.6, 32.7, 54.8, 90.7, 119.6 and 247.4 mg kg−1, dry diet) to determine the requirement for juvenile Pacific white shrimp, Litopenaeus vannamei. Triplicate groups of 40 juvenile shrimp (approximately 1.0 g) were provided four times each day to apparent satiation (8 weeks). Weight gain (WG), specific growth rate, feeding efficiency, protein efficiency ratio (PER) and protein productive value of the shrimp were significantly influenced by the vitamin B6 levels. No significant differences in whole-body and muscle composition, except for dry matter and protein contents in whole body. Vitamin B6 concentration in the hepatopancreas significantly increased with the dietary vitamin B6 level increasing from 2.6 to 32.7 mg kg−1. High-density lipoprotein cholesterol in the haemolymph improved with the dietary vitamin B6 levels increasing from 2.6 to 90.7 mg kg−1 diet and no significant differences in low-density lipoprotein cholesterol, cholesterol, glucose and total protein concentrations. Aspartate aminotransferase, alanine aminotransferase, superoxide dismutase, catalase and lysozyme in the haemolymph were significantly influenced by dietary vitamin B6 levels. The optimal dietary vitamin B6 requirements estimated using a two-slope broken-line model based on WG and SGR and an exponential model based on the vitamin B6 concentration in the hepatopancreas were 110.39, 110.08 and 167.5 mg kg−1, respectively.

Efficacy and tolerability of coenzyme A vs pantethine for the treatment of patients with hyperlipidemia: A randomized, double-blind, multicenter study

New, safer, and more effective agents to treat hyperlipidemia and thereby prevent cardiovascular events are under research. To evaluate the lipid-lowering effects and safety of a natural hypolipidemic compound, coenzyme A (CoA) capsule, in Chinese patients with moderate dyslipidemia, compared with pantethine. Overall, 216 subjects (124 males and 92 females; age, 18-75 years) with moderate dyslipidemia (triglyceride [TG], 2.3-6.5 mmol/L) were randomly divided into 2 groups administered CoA 400 U/d (n = 111) or pantethine 600 U/d (n = 105). Blood lipoproteins, liver and renal function, blood glucose, and complete blood count were measured at baseline and after 4- and 8-week treatment. TG reduction was 26.0% with CoA and 17.4% with pantethine after 4 weeks and 33.3% and 16.5% after 8 weeks; compared with baseline, the reduction was significant (P < .01) in both groups. The difference between the 2 groups was significant at both 4 weeks (P = .0413) and 8 weeks (P < .001). Compared with baseline, total cholesterol and non-high-density lipoprotein cholesterol (non-HDL-C) were reduced, whereas HDL-C was increased with CoA after 8 weeks (all P < .05). Compared with pantethine, total cholesterol (P = .026) and non-HDL-C (P = .005) were significantly reduced after 8 weeks of CoA treatment. There was no statistical difference in low-density lipoprotein cholesterol or HDL-C between the 2 groups (P > .05) and no difference in blood glucose, hepatic or renal function, myopathy, or gastrointestinal tract symptoms. CoA can improve TG and other lipoprotein parameters to a greater extent than pantethine in moderate dyslipidemia, with no obvious adverse effects.

Anti-inflammatory and morphologic effects of pitavastatin on carotid arteries and thoracic aorta evaluated by integrated backscatter trans-esophageal ultrasound and PET/CT: a prospective randomized comparative study with pravastatin (EPICENTRE study).

BackgroundWe sought to evaluate the effects of a strong lipophilic statin (pitavastatin) on plaque components and morphology assessed by transesophageal echocardiography (TEE) and transthoracic echocardiography (TTE), as well as plaque inflammation assessed by 18 F-fluorodeoxyglucose (FDG) PET/CT in the thoracic aorta and the carotid artery. Furthermore, we compared the effects of pitavastatin with those of mild hydrophilic statin (pravastatin).MethodsWe examined atherosclerotic plaques in the thoracic aorta by TEE and those in the carotid artery by integrated backscatter (IBS)-TTE and PET/CT. We identified the target plaque, where there was macrophage infiltration and inflammation, by strong FDG uptake in the thoracic aorta and carotid arteries and measured maximum standard uptake values (max SUV) by PET/CT. We measured the intima-media thickness (IMT) and the corrected IBS (cIBS) values in the intima-media complex by TEE and TTE at the same site of FDG accumulation by PET/CT.ResultsPatients were randomly divided into two treatment groups: a pitavastatin group (PI group: n =10, 68.4 ± 5.1 years) and a pravastatin group (PR group: n =10, 63.9 ± 11.2 years). The same examinations were performed after six months at the same site in each patient. We used calculated target-to-background ratio (TBR) to measure max SUV of plaques and evaluated percent change of TBR. There was no significant difference in low density lipoprotein-cholesterol, TBR, IMT and cIBS values in plaques at baseline between the PI and PR groups. After treatment, there was greater improvement in TBR, cIBS values and IMT in the PI group than the PR group.ConclusionsThe pravastatin treatment was less effective on plaque inflammation than pitavastatin treatment. This trend was the same in the carotid arteries and the thoracic aorta. Pitavastatin not only improved the atherosis as measured by IMT and cIBS values but also attenuated inflammation of plaques as measured by max SUV at the same site. The present study indicated that pitavastatin has stronger effects on the regression and stabilization of plaques in the thoracic aorta and carotid arteries compared with pravastatin.

Age- and sex-related difference in lipid profiles of patients hospitalized with acute myocardial infarction in East China.

It was not understood whether age- and sex-related differences were apparent in lipid profiles among acute myocardial infarction (AMI) patients in China. To investigate lipid abnormalities in such AMI patients. A retrospective analysis of 1213 patients hospitalized with a first AMI between May 2007 and July2011. Our data indicated that, compared with the elderly, the nonelderly tended to have higher low-density lipoprotein cholesterol (LDL), total cholesterol (TC), and non-high-density lipoprotein cholesterol (N-HDL) for both males and females. There was significant difference in LDL among various age groups (P<.001): LDL levels in the 50-59 and 60-69 year age groups were higher than those in 70-79 and 80-89 year age groups. Compared with males, females tended to have higher LDL in both the 50-59 and 60-69 year age groups. There was no difference in HDL among various age groups for female AMI patients, but there was significance for males. Compared with males, females had higher HDL in 40-49, 50-59, 60-69, and 70-79 year age groups, respectively. Among various age groups, there was significant difference in triglycerides (TG) for male AMI patients, but no difference in TG for females. The levels of TG were higher in 40-49, 50-59, and 60-69 year age groups than those in 70-79, 80-89, and ≥90 year age groups, respectively, for males. Isolated low HDL (low HDL+normal LDL+normal TG) was the most common type of combined dyslipidemia for male elderly (31.4%), male nonelderly (22.9%), and female elderly (19.2%) patients. We concluded that there was age- and sex-related difference in lipid profiles among AMI patients, with more prevalent dyslipidemia in the nonelderly than the elderly. Perimenopausal women were prone to higher LDL, and low HDL was prevalent among AMI patients in East China.

Decomposing Gender Differences in Low-Density Lipoprotein Cholesterol among Veterans with or at Risk for Cardiovascular Illness

ObjectivesTo measure the extent to which gender differences in poor lipid control among individuals at risk for cardiovascular diseases could be explained by patient-level characteristics. Study DesignCross-sectional analyses of merged Veteran Health Administration (VHA) and Medicare claims data for the fiscal years (FY) 2002 and 2003 consisting of veterans using VHA facilities and were diagnosed with diabetes or heart disease or hypertension during FY 2002 and had recorded LDL cholesterol values in FY2003 (N = 527,568). There were 10,582 women and 516,986 men veterans. Poor lipid control was defined as LDL cholesterol values ≥130 mg/dL. Multivariate techniques consisted of logistic regressions. Based on the parameter estimates and distribution of individual characteristics, we used a decomposition technique to analyze factors that contributed to the gender difference in poor lipid control. Principal FindingsA significantly higher percent of women (27.4%) than men (17.1%) had LDL cholesterol values ≥130 mg/dL. Of the 10.3 percentage point difference in lipid control, 3.4 percentage points were explained by variables included in the model. The gender difference in poor lipid control was mostly explained by age, physical illnesses, use of lipid lowering medications and depression. ConclusionsOnly one-third of the gender difference in poor lipid control could be explained by differences in individual characteristics, some of which are modifiable or could be used to identify groups at risk with poor lipid control. Our findings suggest that gender differences in lipid control could be partially reduced by increasing the prescription of lipid lowering drugs and treating depression among women. Interventions that improve lipid control in the non-elderly will also benefit women. However the largest part of the difference in lipid control between women and men remains unexplained and further research is needed to identify additional modifiable and unmodifiable factors.

Team-Based Care Approach to Cholesterol Management in Diabetes Mellitus

Creative, cost-effective interventions to improve the quality of care of chronic illnesses are needed. This study was designed to evaluate the impact of remote physician-pharmacist team-based care on cholesterol levels in patients with diabetes mellitus (DM). This 2-year prospective, cluster randomized controlled trial was conducted within the Providence Primary Care Research Network in Oregon. Participants at least 18 years of age were identified by a diagnosis of DM. The intervention included remote physician-pharmacist team-based care focused on cholesterol management in DM. All clinicians in the study had access to the health information technology tool CareManager, which provided automated DM-related point-of-care prompts, a Web-based registry, and performance feedback with benchmarking. Study outcomes included the difference in low-density lipoprotein cholesterol (LDL-C) goal attainment, mean LDL-C, prescribed lipid-lowering therapy, and patient satisfaction between the intervention and control arms. A total of 6963 patients with DM cared for by 68 physicians in 9 clinics were evaluated. Patients in the intervention arm were more likely to achieve their target LDL-C levels compared with controls (78% vs 50%; P = .003). The mean LDL-C level was 12 mg/dL lower in the intervention arm compared with the control arm (P < .001). The rate of LDL-C testing was significantly higher in the intervention arm compared with the control arm. Patients in the intervention arm were also 15% more likely to receive a prescription for a lipid-lowering medication (P = .008). There was no significant difference in patient satisfaction between study arms (P = .15). Remotely located physician-pharmacist team-based care resulted in significantly improved LDL-C levels and goal attainment among patients with DM.

One-year soy protein supplementation does not improve lipid profile in postmenopausal women

The risk of heart disease increases significantly in women after menopause mostly because of estrogen deficiency. Soy protein, a good source of isoflavones that are known to bind estrogen receptors, has also been promoted as a dietary means for reducing the risk of heart disease. The aim of this study was to examine the effects of soy protein consumption on heart disease risk in postmenopausal women. Moderately hypercholesterolemic postmenopausal women were randomly assigned to consume soy or control foods daily for 1 year. Serum samples were analyzed for total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, apolipoprotein (Apo) A, and Apo B. Sixty-two women completed the study. There was a trend for total cholesterol and high-density lipoprotein cholesterol levels to increase after 1 year of soy protein supplementation (230.04 +/- 6.1 vs 242.57 +/- 6.2 mg/dL, P < 0.1, and 56.87 +/- 2.5 vs 60.33 +/- 2.5 mg/dL, P < 0.1, respectively). There were no significant differences in low-density lipoprotein cholesterol or triglyceride levels; however, a significant increase in Apo B levels (105.5 +/- 5.9 vs 120.21 +/- 5.9 mg/dL; P = 0.002) and a significant decrease in Apo A levels (189.36 +/- 10 vs 173.21 +/- 10 mg/dL; P = 0.009) were seen. Our data indicate that 1-year soy protein supplementation did not confer cardiovascular benefits, in terms of favorable alterations in the lipid profile, in this cohort of postmenopausal women. These findings, as well as those from other studies, lend credence to the decision of the Food and Drug Administration to reevaluate the soy protein health claim issued a decade ago.

Effects of the Direct Lipoprotein-Associated Phospholipase A 2 Inhibitor Darapladib on Human Coronary Atherosclerotic Plaque

Lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) is expressed abundantly in the necrotic core of coronary lesions, and products of its enzymatic activity may contribute to inflammation and cell death, rendering plaque vulnerable to rupture. This study compared the effects of 12 months of treatment with darapladib (an oral Lp-PLA(2) inhibitor, 160 mg daily) or placebo on coronary atheroma deformability (intravascular ultrasound palpography) and plasma high-sensitivity C-reactive protein in 330 patients with angiographically documented coronary disease. Secondary end points included changes in necrotic core size (intravascular ultrasound radiofrequency), atheroma size (intravascular ultrasound gray scale), and blood biomarkers. =0.37). In contrast, Lp-PLA(2) activity was inhibited by 59% with darapladib (P<0.001 versus placebo). After 12 months, there were no significant differences between groups in plaque deformability (P=0.22) or plasma high-sensitivity C-reactive protein (P=0.35). In the placebo-treated group, however, necrotic core volume increased significantly (4.5+/-17.9 mm(3); P=0.009), whereas darapladib halted this increase (-0.5+/-13.9 mm(3); P=0.71), resulting in a significant treatment difference of -5.2 mm(3) (P=0.012). These intraplaque compositional changes occurred without a significant treatment difference in total atheroma volume (P=0.95). Despite adherence to a high level of standard-of-care treatment, the necrotic core continued to expand among patients receiving placebo. In contrast, Lp-PLA(2) inhibition with darapladib prevented necrotic core expansion, a key determinant of plaque vulnerability. These findings suggest that Lp-PLA(2) inhibition may represent a novel therapeutic approach.

Alternative Splicing of 3-Hydroxy-3-Methylglutaryl Coenzyme A Reductase Is Associated With Plasma Low-Density Lipoprotein Cholesterol Response to Simvastatin

HMGCR(3-Hydroxy-3-methylglutaryl coenzyme A reductase), the direct target of statin inhibition, undergoes alternative splicing of exon 13, which encodes part of the statin-binding domain of the enzyme. We hypothesized that HMGCR alternative splicing might be related to the interindividual variation in plasma low-density lipoprotein cholesterol response to statin treatment. We measured mRNA expression of both the full-length and the alternatively spliced HMGCR transcript lacking exon 13 (HMGCRv_1) in 170 simvastatin-incubated immortalized lymphocyte cell lines derived from participants in the Cholesterol and Pharmacogenetics (CAP) study who were treated with simvastatin 40 mg/d for 6 weeks. Greater upregulation of HMGCRv_1 in vitro was significantly correlated (P<or=0.0001) with smaller in vivo reductions of plasma total cholesterol, low-density lipoprotein cholesterol, apoprotein B, and triglycerides and explained 6% to 15% of the variation in their response to treatment. In contrast, no significant relationship was found between expression of the full-length HMGCR transcript and in vivo response. By siRNA knockdown of the full-length transcript, we found that HMGCR enzyme activity measured in cells enriched in HMGCRv_1 was relatively resistant to statin inhibition, consistent with the association of increased alternative splicing with reduced statin response in the CAP study. In addition, we found that a common HMGCR single-nucleotide polymorphism (rs3846662) located within intron 13 was associated with variation in the proportion of HMGCR mRNA that is alternatively spliced. Variation in the production of an HMGCR isoform with reduced statin sensitivity is a determinant of interindividual differences in low-density lipoprotein cholesterol, apolipoprotein B, and triglyceride response to statin treatment.

Insulin resistance phenotypes and coronary artery disease in a native Pakistani cohort

To determine the relationship between insulin resistance (IR) and atheroma burden in Pakistanis. A prospective case-control study of 400 patients selected for the presence/absence of angiographic disease. Coronary atheroma burden was quantified and IR and cardiovascular risk factors were measured. The patients were divided into two groups by QuickI score. Waist circumference (90 +/- 10 vs. 90 +/- 9 cm; p = 0.7) was similar but the groups differed in body mass index (26.5 +/- 3.7 vs. 24.2 +/- 3.5 kg/m(2); p < 0.001) and waist:hip ratio (0.94 +/- 0.09 vs. 0.90 +/- 0.06; p < 0.001). Lipid parameters showed similar high-density lipoprotein cholesterol (HDL-C) (0.77 +/- 0.23 vs. 0.82 +/- 0.22 mmol/l; p = 0.1) differences in triglycerides [1.32 (0.08-3.98) vs. 1.12 (0.37-3.61) mmol/l; p = 0.01], but no difference in low-density lipoprotein cholesterol (LDL-C) (2.75 +/- 1.00 vs. 2.90 +/- 0.94 mmol/l; p = 0.14). In insulin-resistant patients C-reactive protein (CRP) [6.8 (0.3-175.1) vs. 3.9 (0.2-57.9) mg/l: p < 0.001], sialic acid (82 +/- 14 vs. 77 +/- 15 mg/l; p < 0.001) aspartate transaminase [24 (7-171) vs. 21 (7-83) IU/l; p < 0.001] and gamma-glutamyl transferase [27 (8-482) vs. 21 (7-168) IU/l; p = 0.005] levels were increased. In insulin-resistant patients (n = 187), coronary artery disease (CAD) burden correlated (r = 0.55) with age (beta = 1.62; p < 0.001), HDL-C (beta = -53.2; p < 0.001), lipoprotein (a) (beta = 11.4; p = 0.007), smoking (beta = 7.98; p = 0.004), CRP (beta = 6.06; p = 0.03) and QuickI index (beta = -146; p = 0.04). In contrast in insulin-sensitive patients (n = 178) CAD burden (r = 0.46) correlated with LDL-C (beta = 10.0; p = 0.02), CRP (beta = 7.13; p = 0.03), HDL-C (beta = -38.1; p = 0.03), and weakly with age (beta = 0.73; p = 0.07) and smoking (beta = 5.52; p = 0.09). Indian Asians show a dichotomous insulin-resistance phenotype. Atheroma is associated with low HDL-C and inflammation associated in all but LDL-C is a factor in the insulin sensitive in contrast to age and extent of IR in the insulin resistant.

Analysis of Recent Papers in Hypertension

Analysis of Recent Papers in Hypertension

Ethnic differences in achievement of cholesterol treatment goals. Results from the National Cholesterol Education Program Evaluation Project Utilizing Novel E-Technology II.

African Americans (AA) have the highest coronary heart disease mortality rate of any ethnic group in the United States. Data from the National Cholesterol Education Program Evaluation ProjecT Utilizing Novel E-Technology (NEPTUNE) II survey were used to assess ethnic differences in low-density lipoprotein cholesterol (LDL-C) goal achievement. NEPTUNE II surveyed patients with treated dyslipidemia to assess achievement of treatment goals established by the Adult Treatment Panel III of the National Cholesterol Education Program. United States physicians working in primary care or relevant subspecialties enrolled 10 to 20 consecutive patients (May to September 2003), and patient data were recorded in Personal Digital Assistants and uploaded to a central database via the internet. Among 4,885 patients receiving treatment for dyslipidemia, 79.7% were non-Hispanic white (NHW) and 8.4% were AA. Non-Hispanic white and AA patients had significantly different frequencies of treatment success, with 69.0% and 53.7%, respectively, having achieved their LDL-C goal (P<.001). African-American patients were more likely to be in the highest risk category, and less likely to be using lipid drug therapy, taking high-efficacy statins, and receiving care from a subspecialist, but the difference in goal achievement remained significant (P<.001) after adjustment for these and other predictors of treatment success. The frequency of treatment success in dyslipidemia management was significantly lower in AA than NHW patients. Additional research is needed to elucidate reasons for this disparity and to evaluate strategies for improving goal achievement among AA patients receiving therapy for dyslipidemia.

Effects of Low-Carbohydrate vs Low-Fat Diets on Weight Loss and Cardiovascular Risk Factors

Low-carbohydrate diets have become increasingly popular for weight loss. However, evidence from individual trials about benefits and risks of these diets to achieve weight loss and modify cardiovascular risk factors is preliminary. We used the Cochrane Collaboration search strategy to identify trials comparing the effects of low-carbohydrate diets without restriction of energy intake vs low-fat diets in individuals with a body mass index (calculated as weight in kilograms divided by the square of height in meters) of at least 25. Included trials had to report changes in body weight in intention-to-treat analysis and to have a follow-up of at least 6 months. Two reviewers independently assessed trial eligibility and quality of randomized controlled trials. Five trials including a total of 447 individuals fulfilled our inclusion criteria. After 6 months, individuals assigned to low-carbohydrate diets had lost more weight than individuals randomized to low-fat diets (weighted mean difference, -3.3 kg; 95% confidence interval [CI], -5.3 to -1.4 kg). This difference was no longer obvious after 12 months (weighted mean difference, -1.0 kg; 95% CI, -3.5 to 1.5 kg). There were no differences in blood pressure. Triglyceride and high-density lipoprotein cholesterol values changed more favorably in individuals assigned to low-carbohydrate diets (after 6 months, for triglycerides, weighted mean difference, -22.1 mg/dL [-0.25 mmol/L]; 95% CI, -38.1 to -5.3 mg/dL [-0.43 to -0.06 mmol/L]; and for high-density lipoprotein cholesterol, weighted mean difference, 4.6 mg/dL [0.12 mmol/L]; 95% CI, 1.5-8.1 mg/dL [0.04-0.21 mmol/L]), but total cholesterol and low-density lipoprotein cholesterol values changed more favorably in individuals assigned to low-fat diets (weighted mean difference in low-density lipoprotein cholesterol after 6 months, 5.4 mg/dL [0.14 mmol/L]; 95% CI, 1.2-10.1 mg/dL [0.03-0.26 mmol/L]). Low-carbohydrate, non-energy-restricted diets appear to be at least as effective as low-fat, energy-restricted diets in inducing weight loss for up to 1 year. However, potential favorable changes in triglyceride and high-density lipoprotein cholesterol values should be weighed against potential unfavorable changes in low-density lipoprotein cholesterol values when low-carbohydrate diets to induce weight loss are considered.

Determinants of the Differences in Ldl-Cholesterol After Initiation of Statin Treatment

Randomized clinical trials may not accurately predict drug benefit in clinical practice because the patients and conditions of therapy almost always differ between those settings. To determine whether differences in low-density lipoprotein cholesterol (LDL-C) time curves between clinical trial results and usual care experience after initiation of statin therapy could be explained fully in terms of observable characteristics of patients and practice in usual care. We compared LDL-C measurements for 3 years after initiation of statin treatment in individuals enrolled in a health maintenance organization (HMO), with enrollees in the active treatment arm of the CARE (Cholesterol and Recurrent Events) trial. Analysis of the determinants of variation in LDL-C in the HMO cohort was used to adjust the crude results to the distribution of patient and treatment characteristics in the trial. The mean percent decrease in LDL-C was lower in the HMO cohort (n = 1245) than in the clinical trial at the end of each 6-month period, with the difference diminishing over time. Adjustment of the HMO time curve to the baseline characteristics of the clinical trial cohort did not significantly change the mean estimates at any time point. Assuming optimal adherence in the HMO cohort raised the curve over time, with 95% confidence intervals including the means observed in CARE after 18 months. Fixing treatment to pravastatin 40 mg/day, as in CARE, brought the estimates in the HMO cohort very close to those of the clinical trial, with 95% confidence intervals including the means observed in CARE at all time points. Treatment selection, dosing, and adherence under usual care were the primary reasons for which improvements in LDL-C in practice fell short of expectations that are based on clinical trial findings for statin therapy. Beginning with a low dose of statins and titrating to a satisfactory response can delay effective treatment by 18 months or more. Poor adherence accounts for a further substantial shortfall from maximal effect. Differences between trial populations and the general population of statin users with respect to age, gender, and baseline LDL-C have no measurable impact on discrepancies between predicted and observed LDL-C improvement in usual practice.

Effects of ospemifene and raloxifene on hormonal status, lipids, genital tract, and tolerability in postmenopausal women

To compare ospemifene and raloxifene regarding their effects on hormones, lipids, genital tract, and tolerability in postmenopausal women. A randomized, double-blind study in which 118 healthy postmenopausal women received 30 (n = 29), 60 (n = 30), or 90 mg (n = 30) of ospemifene or 60 mg (n = 29) of raloxifene for 3 months. There were no significant differences in the baseline characteristics between study groups. In comparison with raloxifene, follicle-stimulating hormone levels decreased significantly more in the 90-mg ospemifene group and sex hormone-binding globulin levels increased more in all ospemifene groups. Total cholesterol and low-density lipoprotein cholesterol levels decreased more in raloxifene than in ospemifene groups, although the difference in low-density lipoprotein cholesterol between 90-mg ospemifene and raloxifene was not significant. Endometrial thickness did not change in any study group and endometrial biopsies showed atrophy in the majority of subjects at 3 months. All ospemifene groups demonstrated a clear estrogenic effect on the vaginal epithelium, as seen in Pap smears. This was in sharp contrast to the raloxifene group, which had no effect on the vaginal epithelium. Kupperman index decreased in all study groups during treatment. The adverse events were mild, mainly single cases, and no clustering of events was observed. There were no clinically significant abnormal findings in laboratory safety parameters. Ospemifene, at the dose of 90 mg/day, was more estrogenic than raloxifene, as shown by changes in serum follicle-stimulating hormone and sex hormone-binding globulin levels. Neither agent stimulated endometrium, but in contrast to raloxifene, ospemifene had a clear estrogenic effect in the vagina. Further studies with ospemifene are needed in subjects with vaginal atrophy.

C-Reactive protein levels among women of various ethnic groups living in the United States (from the Women's Health Study)

The distribution of C-reactive protein (CRP) levels was compared among 24,455 white, 475 black, 357 Asian, and 254 Hispanic women, all of whom are participants in the Women's Health Study. Median CRP levels were significantly higher among black women (2.96 mg/L, interquartile range [IQR] 1.19 to 5.86) than among their white (2.02 mg/L, IQR 0.81 to 4.37), Hispanic (2.06 mg/L, IQR 0.88 to 4.88), and Asian (1.12 mg/L, IQR 0.48 to 2.25) counterparts. As expected, women taking hormone replacement therapy had higher baseline CRP levels than women not taking hormone replacement therapy. No differences in low-density lipoprotein cholesterol or total cholesterol levels were observed between ethnic groups. In multivariate regression models, body mass index was a significant (p <0.001) predictor of elevated CRP concentrations among all race/ethnic groups, and control for body mass index substantially attenuated the differences noted in CRP levels across race/ethnic groups, particularly among black women. Control for all measured modifiable risk factors for cardiovascular disease did not entirely explain CRP differences. Among these women, the distribution of CRP levels varied significantly between the various race/ethnic groups.

The changes in plasma lipoproteins in rat with diabetes induced by streptozotocin.

Diabetes was induced in Wistar male rats by streptozotocin given peritoneally. The control rats received the rame volume of buffer. Twelve days after injection of streptozotocin, the levels of plasma triglyceride, total cholesterol and free fatty acid increased significantly as compared with those of the control rats. The plasma very low density lipoprotejn-choleslerol (VLDL-C) of the diabetic rats was twice as much as that of the control rats. No difference in low density lipoprotein-cholesterol (LDL-C) and high density lipoproteincholesterol (HDL-C) was found between the two groups. However, the HDL3 in diabetic rats increased significantly. These results indicated that the degradation of VLDL was reduced in diabetic rats and concurrently the conversion of HDL3 to HDL2 was impaired. Therefore, we are led to assume that the accumulation of VLDL remnants and the impairment of reverse transport of tissue cholesterol may facilitate the development of atherosclerosis in diabetes mellitus.