Abstract
BackgroundRecent data suggest that an increased level of high-density lipoprotein cholesterol (HDL-C) is not causally protective against heart disease, shifting focus to other sub-phenotypes of HDL. Prior work on the effects of dietary intakes has focused largely on HDL-C. The goal of this study was to identify the dietary intakes that affect HDL-related measures: HDL-C, HDL-2, HDL-3, and apoA1 using data from a carotid artery disease case–control cohort.MethodsA subset of 1,566 participants with extensive lipid phenotype data completed the Harvard Standardized Food Frequency Questionnaire to determine their daily micronutrient intake over the past year. Stepwise linear regression was used to separately evaluate the effects of dietary covariates on adjusted levels of HDL-C, HDL-2, HDL-3, and apoA1.ResultsDietary folate intake was positively associated with HDL-C (p = 0.007), HDL-2 (p = 0.0011), HDL-3 (p = 0.0022), and apoA1 (p = 0.001). Alcohol intake and myristic acid (14:0), a saturated fat, were each significantly associated with increased levels of all HDL-related measures studied. Dietary carbohydrate and iron intake were significantly associated with decreased levels of all HDL-related measures. Magnesium intake was positively associated with HDL-C, HDL-2, and HDL-3 levels, but not apoA1 levels, while vitamin C was only associated with apoA1 levels. Dietary fiber and protein intake were both associated with HDL-3 levels alone.ConclusionsThis study is the first to report that dietary folate intake is associated with HDL-C, HDL-2, HDL-3, and apoA1 levels in humans. We further identify numerous dietary intake associations with apoA1, HDL-2, and HDL-3 levels. Given the shifting focus away from HDL-C, these data will prove valuable for future epidemiologic investigation of the role of diet and multiple HDL phenotypes in heart disease.
Highlights
Recent data suggest that an increased level of high-density lipoprotein cholesterol (HDL-C) is not causally protective against heart disease, shifting focus to other sub-phenotypes of HDL
The strong inverse association between measures of high density lipoprotein cholesterol (HDL-C) and cardiovascular disease risk [1] has recently prompted several studies to establish the role of HDL-C in the causal pathway of atherosclerosis and its resulting end-organ damage
Recent evidence from the Multi Ethnic Study of Atherosclerosis (MESA) suggests that aspects of the high density lipoprotein particle (HDL-P) not measured by HDL-C may be responsible for the cardioprotective effects of HDL [5]
Summary
Recent data suggest that an increased level of high-density lipoprotein cholesterol (HDL-C) is not causally protective against heart disease, shifting focus to other sub-phenotypes of HDL. The strong inverse association between measures of high density lipoprotein cholesterol (HDL-C) and cardiovascular disease risk [1] has recently prompted several studies to establish the role of HDL-C in the causal pathway of atherosclerosis and its resulting end-organ damage. Mackey et al studied a cohort of 5,598 participants, measured both HDL-P (which reflects the total quantity of HDL and its associated proteins) and HDL-C, and performed multivariate regression on the outcomes of incident coronary heart disease (CHD) and carotid intima media thickening (cIMT) From these analyses, Mackey et al found that when HDL-P was already included in the model, HDL-C measures no longer were protective against cardiovascular disease risk. PON1 is itself atheroprotective [11,12,13,14] and can prevent LDL [15,16] and HDL oxidation [17] (other functions of PON1 are summarized in a recent review article [18])
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