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Although individual lipid parameters have been frequently examined in association with asymptomatic intracranial arterial stenosis (aICAS), few population-based studies have investigated the lipid profiles associated with aICAS among Chinese adults. This study aims to characterize the lipid profiles associated with aICAS in rural-dwelling adults in China. This population-based study included 2027 persons who were aged ≥40 years and free of stroke. Data were collected via interviews, clinical examinations, and laboratory testing. We diagnosed aICAS by integrating transcranial color Doppler with magnetic resonance angiography. Data were analyzed using binary and multinomial logistic regression models. Of the 2027 participants, 154 were detected with aICAS. The multiadjusted odds ratio (95% confidence interval) of aICAS was 1.41 (0.997–2.00) for high small dense low-density lipoprotein cholesterol, 1.44 (1.02–2.04) for high lipoprotein(a), 1.71 (1.21–2.44) for low apolipoprotein A-1, 1.43 (1.00–2.04) for low high-density lipoprotein cholesterol (HDL-C), 1.61 (1.14–2.27) for high apolipoprotein B/apolipoprotein A-1 ratio, 1.95 (1.38–2.76) for high low-density lipoprotein cholesterol/HDL-C ratio, and 1.51 (1.06–2.14) for high total cholesterol/HDL-C ratio. When severity of aICAS was analyzed, high levels of lipoprotein(a), small dense low-density lipoprotein cholesterol, and lipid ratios were significantly associated with an increased likelihood of moderate-to-severe aICAS (P <.05). An increasing number of abnormal lipid measurements was associated with an increased likelihood of aICAS (P for trend <.001). These findings suggest that lipid profiles for aICAS among rural residents in China are characterized by high atherogenic cholesterol, low antiatherogenic cholesterol, and high ratios of atherogenic-to-antiatherogenic cholesterol or lipoproteins. • We explore lipids associated with asymptomatic intracranial arterial stenosis (aICAS). • Lipid profiles for aICAS are high atherogenic and low antiatherogenic lipids. • Having more abnormal lipid measurements is related to a higher likelihood of aICAS. [ABSTRACT FROM AUTHOR]

Previous studies have demonstrated that elevated cholesterol results in increased white blood cell counts in mouse models. However, there is insufficient evidence to support this in humans. The objective of the study was to investigate the relationship of plasma lipids with white blood cell counts (basophils, eosinophils, monocytes, neutrophils and lymphocytes) in the Multi-Ethnic Study of Atherosclerosis. The analysis included 2873 Multi-Ethnic Study of Atherosclerosis participants with a complete white blood count and differential analysis. The cross-sectional association of total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglyceride levels with different white blood cell counts was analyzed by multivariable linear regression. After adjusting for sociodemographic and confounding factors including red blood cell counts, platelet counts, use of lipid-lowering medication, cardiovascular disease risk factors and other lipid measures, and multiple testing correction, a one–standard deviation increment in total cholesterol and low-density lipoprotein cholesterol was associated with 2.8% and 2.3% lower total white blood cell counts, 3.7% and 3.0% lower monocyte counts, and 3.4% and 2.7% lower neutrophil counts (all P <.01). The same increment in logarithm-transformed triglyceride levels was associated with 2.3% higher total white blood cell counts and 4.5% higher lymphocyte counts (both P <.001). Similar results were obtained after excluding participants taking lipid-lowering medication. A one–standard deviation increase in high-density lipoprotein cholesterol was associated with a 1.5% lower white blood cell count (P =.018) but was not significantly associated with changes in any individual cell type. While significant associations were observed between plasma lipid levels and white blood cell populations, the heterogeneous and modest nature of these relationships makes it hard to support the hypothesis that lipids are in the causal pathway for leukogenesis in humans. [ABSTRACT FROM AUTHOR]

Background--SR-B1 (scavenger receptor class B type 1), encoded by the gene SCARB1, is a lipoprotein receptor that binds both high-density lipoprotein (HDL) and low-density lipoprotein. We reported that SR-B1 is also a receptor for lipoprotein (a) (Lp(a)), mediating cellular uptake of Lp(a) in vitro and promoting clearance of Lp(a) in vivo. Although genetic variants in SCARB1 are associated with variations in HDL level, no SCARB1 variants affecting Lp(a) have been reported. Methods and Results--In an index subject with high levels of HDL cholesterol and Lp(a), SCARB1 was sequenced and demonstrated a missense mutation resulting in an S129L substitution in exon 3. To follow up, 2 cohorts (GeneSTAR, the family-based Genetic Study of Atherosclerosis Risk [n=543], and CCHS, the population-based Copenhagen City Heart Study [n=5835]) were screened for combined HDL cholesterol and Lp(a) elevations. Subjects with the extreme phenotype (HDL >80 mg/dL and Lp(a) >100 nmol/L in GeneSTAR, n=8, and >100 mg/dL in CCHS, n=9) underwent sequencing of SCARB1 exons; 15 of 18 from the combined population demonstrated genetic variants, including rare or uncommon missense or splice site mutations in 9 and homozygous synonymous variants in 6. Functional studies with 4 of the SCARB1 variants (c.386C>T, c.631-14T>G, c.4G>A, and c.631-53mC>T & c.726+55mCG>CA) showed decreased receptor function in vitro. Conclusions--Human SCARB1 gene variants are associated with a new lipid phenotype, characterized by high levels of both HDL cholesterol and Lp(a). SCARB1 exonic variants often result in diminished function of translated SR-B1 via reduced binding/intracellular transport of Lp(a). [ABSTRACT FROM AUTHOR]

Background: Dyslipidemia is associated with chronic cardiovascular disease. However, the effect of dyslipidemia on acute ischemic stroke is unclear. We hypothesized that dyslipidemia could contribute to early neurological deterioration (END) after ischemic stroke.Methods: A total of 410 acute ischemic stroke patients who were admitted to our stroke center within 24 hours after ictus were consecutively included in this study. END was defined as any new neurological symptoms/signs or any neurological worsening occurring during the admission and/or within 3 weeks after the index stroke. Multivariable logistic regression was used to examine the independent association between lipid indices and END.Results: Mean age was 68.2 ± 13.3 years, 241 (58.8%) were male, and 78 (19.0%) experienced END. Almost END occurred within 3 days after admission (n = 70, 89.7%), and the majority of END was stroke progression (n = 68, 87.1%). In univariate analysis, high-density lipoprotein (HDL)-cholesterol levels (per 1 mmol/L; odds ratio [OR] .37; 95% CI .17-.80; P = .012) and apolipoprotein B (apoB)/apoA-I ratio (per 1 increase; OR 3.71; 95% CI 1.48-9.29; P = .005) were associated with END. In the multivariable analysis, adjusted ORs of END for the highest quartile of HDL-cholesterol and apoB/apoA-I ratio were .42 (95% CI .19-.94; P = .034) and 2.37 (95% CI 1.02-5.53; P = .045), respectively. The ratio of apoB/apoA-I was associated with END in large artery atherosclerosis stroke but not in other stroke subtypes.Conclusions: Independent association of low HDL-cholesterol and high apoB/apoA-I ratio with END warrants further research to investigate if correction of the lipid profile during the acute period of ischemic stroke could reduce the risk of END. [ABSTRACT FROM AUTHOR]

There is clear evidence of the effects of sex and age on the prevalence of cardiovascular disease. We investigated the interactions of dietary omega (n)-3 polyunsaturated fatty acids (PUFA), sex, and age on plasma lipids and lipoproteins in the offspring of C57BL/6 mice exposed to high, medium, or low n-3 PUFA at weaning and 16 weeks postweaning. There was an increase in plasma triglycerides from weaning to 16 weeks in male and female offspring; however, the high n-3 PUFA group showed a reduction in triglycerides in both sexes at 16 weeks. High n-3 PUFA caused an increase in plasma LDL-cholesterol from weaning to 16 weeks in male offspring; however, the LDL particle size was significantly larger in the high n-3 PUFA group. Plasma from male mice showed higher cholesterol efflux compared to females; high n-3 PUFA increased cholesterol efflux. Thus the effects of n-3 PUFA are age and sex dependent. [ABSTRACT FROM AUTHOR]

Abstract: Background and aims: Increased plasma phytosterols, which reflect enhanced cholesterol absorption, have been related to an increased risk of cardiovascular disease (CVD). However, high CVD risk conditions, such as obesity, diabetes and the metabolic syndrome (MetS) have been associated with reduced cholesterol absorption. We investigated associations between plasma noncholesterol sterols and MetS components. Methods and results: With a cross-sectional design, we related MetS components to plasma noncholesterol sterol-to-cholesterol ratios measured by gas chromatography in 674 dyslipidemic patients and 361 healthy subjects participating in a prospective cohort study. Plasma phytosterol-to-cholesterol ratios were inversely associated with all components of the MetS. In the dyslipidemic group, multivariable analyses showed that a 1-SD increase in sitosterol-to-cholesterol ratio was associated with a reduced risk for any MetS feature, ranging from 0.57 (95% CI, 0.45 to 0.71) for visceral adiposity to 0.82 (95% CI, 0.69 to 0.98) for high blood pressure. The risk of having MetS was nearly halved, with ORs of 0.49 (95% CI, 0.38 to 0.64) or 0.56 (95% CI, 0.44–0.70), depending on the definition. Results were opposed for plasma lathosterol, a marker of cholesterol synthesis. Most findings were reproduced in the healthy cohort. ApoE genotype was unrelated to plasma noncholesterol sterols. Conclusion: In both dyslipidemic and healthy populations, MetS is associated with increased plasma lathosterol, a cholesterol synthesis marker, and decreased plasma sitosterol, a marker of cholesterol absorption. Elevated plasma phytosterols related to a lower frequency of cardiometabolic risk factors, suggesting that they are associated with a reduced CVD risk. [Copyright &y& Elsevier]

Summary: Background and aim: Small quantities of nuts protect against subsequent cardiovascular risk. There is speculation that the cholesterol lowering effect associated with nut consumption arises primarily from the fatty acid composition of nuts but may be caused by some other component. To evaluate this possibility we compared the effect of various nuts, against a Canola oil based cereal with a comparable fatty acid profile, on lipids, lipoproteins and fatty acids to determine whether the fatty acid profile of nuts explains their cholesterol lowering effects. Methods and results: Twenty-eight men and women with mean (s.d.) levels of total and low density lipoprotein cholesterol of 6.0 (1.1)mmol/L, and 4.1 (1.0)mmol/L, respectively and a mean body mass index (BMI) of 26.9 (3.2)kg/m2 took part in a randomised cross over trial. For two periods of six weeks, separated by a four-week washout, participants were asked to consume a low saturated fat diet, which included either 30g/d nuts (nut diet) or one serving of a cereal containing Canola oil (cereal diet). There were no significant differences in the lipids, lipoproteins, plasma fatty acids or other variables between the two diets at the end of the study. Total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C) were lower on both experimental diets than at baseline, 0.51mmol/L and 0.40mmol/L (p &#60;0.001, p &#60;0.01), respectively on the nut diet and 0.42mmol/L and 0.37mmol/L (p &#60;0.001, p &#60;0.01), respectively on the cereal diet. Conclusion: A 30g serving of nuts, or a serving of a Canola oil enriched cereal with a similar fatty acid composition reduced total and LDL cholesterol to a similar extent when consumed as part of a lipid lowering diet. Results suggest that foods with a similar fatty acid composition to nuts can produce comparable decreases in lipoprotein mediated cardiovascular risk. [Copyright &y& Elsevier]