Background: n−3 Fatty acids influence vascular function, but the effect of individual fatty acids on systemic arterial compliance (SAC) has not been reported. SAC, which reflects arterial elasticity, is emerging as a new cardiovascular risk factor and appears to predict future cardiovascular events. Objective: We tested whether the n−3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) improve SAC in dyslipidemic subjects. Design: Thirty-eight dyslipidemic subjects were randomly assigned to receive 3 g EPA/d (n = 12), 3 g DHA/d (n = 12), or a placebo (n = 14) in a 7-wk parallel, double-blind trial. Arterial functions were measured at the beginning and end of the interventions. Plasma lipids and plasma fatty acids were also measured. Results: Consumption of the n−3 fatty acids significantly increased SAC, whereas consumption of the placebo did not (P = 0.043; repeated-measures analysis of variance across the 3 groups); the increase was 36% with EPA and 27% with DHA. The major components contributing to the increase in SAC (systolic and pulse pressures and total vascular resistance) tended to decrease but not significantly. Plasma total and VLDL triacylglycerol were significantly lower in the n−3 fatty acid groups (P = 0.026 and 0.006, respectively; repeated-measures analysis of variance) than in the placebo group. Conclusion: EPA and DHA increase SAC and tend to reduce pulse pressure and total vascular resistance, effects that may reduce the risk of adverse cardiovascular events.

N−3 Fatty acids have been shown to modify several key risk factors for cardiovascular disease. However, it is not clear whether the apparent protection against cardiovascular disease is directly related to antiatherogenic functions of these fatty acids or is mediated through their modification of the risk factors through mechanisms not directly related to lipids. A major question concerns the importance of lipid modification, which is a potent outcome of fish-oil supplementation. On balance, lipid modification is likely to represent a significant antiatherogenic factor. The benefits include increased HDL₂-cholesterol concentrations, reduced triacylglycerol-rich lipoprotein concentrations, reduced postprandial lipemia, and reduced remnant concentrations. In contrast, LDL-cholesterol concentrations have often been noted to rise and the potential of increased oxidizability of LDLs is potentially adverse with lipid modification, but this potential can be overcome with vitamin E supplementation. The characteristic lipid changes and the underlying mechanisms are reviewed. Additional benefits of fish oils include improved endothelial function and better arterial compliance (elasticity). Future trials will be needed to determine minimum effective dosages of eicosapentaenoic and docosahexaenoic acids over lengthy periods and to show cardiovascular disease reduction through intervention.

BACKGROUND: Low-density lipoprotein cholesterol (LDL-C) and lipoprotein(a) (Lp[a]) levels are independently associated with atherosclerotic cardiovascular disease (ASCVD). However, the relationship between Lp(a) level, LDL-C level, and ASCVD risk at different thresholds is not well defined. METHODS: A participant-level meta-analysis of 27 658 participants enrolled in 6 placebo-controlled statin trials was performed to assess the association of LDL-C and Lp(a) levels with risk of fatal or nonfatal coronary heart disease events, stroke, or any coronary or carotid revascularization (ASCVD). The multivariable-adjusted association between baseline Lp(a) level and ASCVD risk was modeled continuously using generalized additive models, and the association between baseline LDL-C level and ASCVD risk by baseline Lp(a) level by Cox proportional hazards models with random effects. The joint association between Lp(a) level and statin-achieved LDL-C level with ASCVD risk was evaluated using Cox proportional hazards models. RESULTS: Compared with an Lp(a) level of 5 mg/dL, increasing levels of Lp(a) were log-linearly associated with ASCVD risk in statin- and placebo-treated patients. Among statin-treated individuals, those with Lp(a) level >50 mg/dL (≈125 nmol/L) had increased risk across all quartiles of achieved LDL-C level and absolute change in LDL-C level. Even among those with the lowest quartile of achieved LDL-C level (3.1–77.0 mg/dL), those with Lp(a) level >50 mg/dL had greater ASCVD risk (hazard ratio, 1.38 [95% CI, 1.06–1.79]) than those with Lp(a) level ≤50 mg/dL. The greatest risk was observed with both Lp(a) level >50 mg/dL and LDL-C level in the fourth quartile (hazard ratio, 1.90 [95% CI, 1.46–2.48]). CONCLUSIONS: These findings demonstrate the independent and additive nature of Lp(a) and LDL-C levels for ASCVD risk, and that LDL-C lowering does not fully offset Lp(a)-mediated risk.

Background: Legumes are recommended for better glucose control in persons with diabetes. Whether subjects with normal insulin sensitivity would also benefit from legume consumption is not clear. Objective: Our goal was to compare the effects on insulin sensitivity of chickpea-based and wheat-based foods when eaten as single meals or over 6 wk. Design: Acute and long-term studies were conducted in healthy middle-aged men and women. In the acute study (n = 19), plasma glucose, insulin, and calculated homeostasis model assessment (HOMA; an index of insulin sensitivity) were measured on 3 separated days over 3 h after the subjects consumed 50-g available carbohydrate loads from either chickpeas, wheat-based foods, or white bread. The long-term comparison (n = 20) was a randomized, crossover study in which chickpea-based and wheat-based foods were eaten for 6 wk each. Plasma glucose, insulin, and HOMA were measured in the fasting state and 2 h after a 75-g glucose load. Results: After single meals, plasma glucose was substantially lower 30 and 60 min after the chickpea meal than after the other 2 meals (P < 0.05), and plasma insulin and HOMA were lower at 120 min (P < 0.05 for both). Despite this, the long-term study failed to show significant differences in plasma glucose, insulin, or HOMA either in the fasting state or after a glucose load. Conclusion: Compared with a wheat-based meal, a single chickpea-based meal led to a lesser response in plasma glucose and insulin concentrations, but this was not translated into long-term improvement in insulin sensitivity over 6 wk, at least in healthy subjects.