Effects of dietary components on high-density lipoprotein measures in a cohort of 1,566 participants

Nutrition & Metabolism

Gail P Jarvik³  Clement E Furlong³  Jason F Eintracht¹  Leah E Jarvik²  Jane E Ranchalis²  Amber A Burt²  Daniel Seung Kim³ 

[1] Department of General Medicine, Virginia Mason Medical Center, Seattle, WA, USA;Department of Medicine, Division of Medical Genetics, University of Washington School of Medicine, Box 357720, Seattle, WA 98195-7720, USA;Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA, USA

关键词: Cardiovascular disease;    Food frequency questionnaire;    Magnesium;    Fatty acids;    Alcohol;    Folate;    HDL subfractions;    Apolipoprotein A1;    HDL-3;    HDL-2;    HDL-C;    HDL;   

Others  :  1131709
DOI  :  10.1186/1743-7075-11-44

 received in 2014-06-30, accepted in 2014-09-11,  发布年份 2014

【 摘 要 】

Background

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. 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.

Methods

A 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.

Results

Dietary 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.

Conclusions

This 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.

【 授权许可】

   
2014 Kim et al.; licensee BioMed Central Ltd.

【 参考文献 】

• [1]Castelli WP: Cardiovascular disease and multifactorial risk: challenge of the 1980s. Am Heart J 1983, 106:1191-1200.
• [2]Boden WE, Probstfield JL, Anderson T, Chaitman BR, Desvignes-Nickens P, Koprowicz K, McBride R, Teo K, Weintraub W, AIM-HIGH Investigators: Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N Engl J Med 2011, 365:2255-2267.
• [3]Barter PJ, Barter PJ, Caulfield M, Caulfield M, Eriksson M, Eriksson M, Grundy SM, Grundy SM, Kastelein JJP, Kastelein JJP, Komajda M, Komajda M, Lopez-Sendon J, Lopez-Sendon J, Mosca L, Mosca L, Tardif J-C, Tardif J-C, Waters DD, Waters DD, Shear CL, Shear CL, Revkin JH, Revkin JH, Buhr KA, Buhr KA, Fisher MR, Fisher MR, Tall AR, Tall AR, et al.: Effects of Torcetrapib in Patients at High Risk for Coronary Events. N Engl J Med 2007, 357:2109-2122.
• [4]Voight BF, Peloso GM, Orho-Melander M, Frikke-Schmidt R, Barbalic M, Jensen MK, Hindy G, Hólm H, Ding EL, Johnson T, Schunkert H, Samani NJ, Clarke R, Hopewell JC, Thompson JF, Li M, Thorleifsson G, Newton-Cheh C, Musunuru K, Pirruccello JP, Saleheen D, Chen L, Stewart AF, Schillert A, Thorsteinsdottir U, Thorgeirsson G, Anand S, Engert JC, Morgan T, Spertus J, et al.: Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. The Lancet 2012, 380:572-580.
• [5]Mackey RH, Greenland P, Goff DC, Lloyd-Jones D, Sibley CT, Mora S: High-density lipoprotein cholesterol and particle concentrations, carotid atherosclerosis, and coronary events: MESA (multi-ethnic study of atherosclerosis). J Am Coll Cardiol 2012, 60:508-516.
• [6]Asztalos BF, Tani M, Schaefer EJ: Metabolic and functional relevance of HDL subspecies. Curr Opin Lipidol 2011, 22:176-185.
• [7]Asztalos BF, Roheim PS, Milani RL, Lefevre M, McNamara JR, Horvath KV, Schaefer EJ: Distribution of ApoA-I-Containing HDL Subpopulations in Patients With Coronary Heart Disease. Arterioscler Thromb Vasc Biol 2000, 20:2670-2676.
• [8]Asztalos BF, Batista M, Horvath KV, Cox CE, Dallal GE, Morse JS, Brown GB, Schaefer EJ: Change in alpha1 HDL concentration predicts progression in coronary artery stenosis. Arterioscler Thromb Vasc Biol 2003, 23:847-852.
• [9]Kontush A, Chantepie S, Chapman MJ: Small, dense HDL particles exert potent protection of atherogenic LDL against oxidative stress. Arterioscler Thromb Vasc Biol 2003, 23:1881-1888.
• [10]Bergmeier C, Siekmeier R, Gross W: Distribution spectrum of paraoxonase activity in HDL fractions. Clin Chem 2004, 50:2309-2315.
• [11]Mackness MI, Harty D, Bhatnagar D, Winocour PH, Arrol S, Ishola M, Durrington PN: Serum paraoxonase activity in familial hypercholesterolaemia and insulin-dependent diabetes mellitus. Atherosclerosis 1991, 86:193-199.
• [12]Shih DM, Gu L, Xia Y-R, Navab M, Li W-F, Hama S, Castellani LW, Furlong CE, Costa LG, Fogelman AM, Lusis AJ: Mice lacking serum paraoxonase are susceptible to organophosphate toxicity and atherosclerosis. Nature 1998, 394:284-287.
• [13]Bhattacharyya T, Nicholls SJ, Topol EJ, Zhang R, Yang X, Schmitt D, Fu X, Shao M, Brennan DM, Ellis SG: Relationship of paraoxonase 1 (PON1) gene polymorphisms and functional activity with systemic oxidative stress and cardiovascular risk. JAMA 2008, 299:1265-1276.
• [14]Jarvik GP, Rozek LS, Brophy VH, Hatsukami TS, Richter RJ, Schellenberg GD, Furlong CE: Paraoxonase (PON1) Phenotype Is a Better Predictor of Vascular Disease Than Is PON1192 or PON155 Genotype. Arterioscler Thromb Vasc Biol 2000, 20:2441-2447.
• [15]Mackness MI, Arrol S, Abbott C, Durrington PN: Protection of low-density lipoprotein against oxidative modification by high-density lipoprotein associated paraoxonase. Atherosclerosis 1993, 104:129-135.
• [16]Mackness MI, Arrol S, Durrington PN: Paraoxonase prevents accumulation of lipoperoxides in low-density lipoprotein. FEBS Lett 1991, 286:152-154.
• [17]Aviram M, Rosenblat M, Bisgaier CL, Newton RS, Primo-Parmo SL, La Du BN: Paraoxonase inhibits high-density lipoprotein oxidation and preserves its functions. A possible peroxidative role for paraoxonase. J Clin Invest 1998, 101:1581-1590.
• [18]Kim DS, Marsillach J, Furlong CE, Jarvik GP: Pharmacogenetics of paraoxonase activity: elucidating the role of high-density lipoprotein in disease. Pharmacogenomics 2013, 14:1495-1515.
• [19]Kim DS, Burt AA, Rosenthal EA, Ranchalis JE, Eintracht JF, Hatsukami TS, Furlong CE, Marcovina S, Albers JJ, Jarvik GP: HDL-3 is a Superior Predictor of Carotid Artery Disease in a Case–control Cohort of 1725 Participants. J Am Heart Assoc 2014, 3(3):e000902. doi:10.1161/JAHA.114.000902
• [20]Jarvik GP, Hatsukami TS, Carlson C, Richter RJ, Jampsa R, Brophy VH, Margolin S, Rieder M, Nickerson D, Schellenberg GD: Paraoxonase activity, but not haplotype utilizing the linkage disequilibrium structure, predicts vascular disease. Arterioscler Thromb Vasc Biol 2003, 23:1465-1471.
• [21]Kim DS, Burt AA, Ranchalis JE, Richter RJ, Marshall JK, Eintracht JF, Rosenthal EA, Furlong CE, Jarvik GP: Additional Common Polymorphisms in the PON Gene Cluster Predict PON1 Activity but Not Vascular Disease. J Lipids 2012, 2012:476316.
• [22]Krauss RM, Eckel RH, Howard B, Appel LJ, Daniels SR, Deckelbaum RJ, Erdman JW, Kris-Etherton P, Goldberg IJ, Kotchen TA, Lichtenstein AH, Mitch WE, Mullis R, Robinson K, Wylie-Rosett J, St Jeor S, Suttie J, Tribble DL, Bazzarre TL: AHA Dietary Guidelines: Revision 2000: A Statement for Healthcare Professionals From the Nutrition Committee of the American Heart Association. Circulation 2000, 102:2284-2299.
• [23]Lichtenstein AH: Diet and Lifestyle Recommendations Revision 2006: A Scientific Statement From the American Heart Association Nutrition Committee. Circulation 2006, 114:82-96.
• [24]de Lorgeril M, Renaud S, Mamelle N, Salen P, Martin JL, Monjaud I, Guidollet J, Touboul P, Delaye J: Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease. The Lancet 1994, 343:1454-1459.
• [25]Fung TT, Chiuve SE, McCullough ML, Rexrode KM, Logroscino G, Hu FB: Adherence to a DASH-style diet and risk of coronary heart disease and stroke in women. Arch Intern Med 2008, 168:713-720.
• [26]Carter SJ, Roberts MB, Salter J, Eaton CB: Relationship between Mediterranean Diet Score and atherothrombotic risk: findings from the Third National Health and Nutrition Examination Survey (NHANES III), 1988–1994. Atherosclerosis 2010, 210:630-636.
• [27]Jarvik GP, Tsai NT, McKinstry LA, Wani R, Brophy VH, Richter RJ, Schellenberg GD, Heagerty PJ, Hatsukami TS, Furlong CE: Vitamin C and E intake is associated with increased paraoxonase activity. Arterioscler Thromb Vasc Biol 2002, 22:1329-1333.
• [28]Kim DS, Burt AA, Ranchalis JE, Richter RJ, Marshall JK, Nakayama KS, Jarvik ER, Eintracht JF, Rosenthal EA, Furlong CE, Jarvik GP: Dietary cholesterol increases paraoxonase 1 enzyme activity. J Lipid Res 2012, 53:2450-2458.
• [29]Kim DS, Maden SK, Burt AA, Ranchalis JE, Furlong CE, Jarvik GP: Dietary fatty acid intake is associated with paraoxonase 1 activity in a cohort-based analysis of 1,548 subjects. Lipids Health Dis 2013, 12:183. BioMed Central Full Text
• [30]Bachorik PS, Albers JJ: Precipitation methods for quantification of lipoproteins. Methods Enzymol 1986, 129:78-100.
• [31]Marcovina SM, Albers JJ, Henderson LO, Hannon WH: International Federation of Clinical Chemistry standardization project for measurements of apolipoproteins A-I and B. III. Comparability of apolipoprotein A-I values by use of international reference material. Clin Chem 1993, 39:773-781.
• [32]Rimm EB, Giovannucci EL, Stampfer MJ, Colditz GA, Litin LB, Willett WC: Reproducibility and validity of an expanded self-administered semiquantitative food frequency questionnaire among male health professionals. Am J Epidemiol 1992, 135:1114-1126. discussion 1127–36
• [33]Hunter DJ, Hunter DJ, Rimm EB, Rimm EB, Sacks FM, Sacks FM, Stampfer MJ, Stampfer MJ, Colditz GA, Colditz GA, Litin LB, Litin LB, Willett WC, Willett WC: Comparison of measures of fatty acid intake by subcutaneous fat aspirate, food frequency questionnaire, and diet records in a free-living population of US men. Am J Epidemiol 1992, 135:418-427.
• [34]Willett W, Stampfer M, Chu NF, Spiegelman D, Holmes M, Rimm E: Assessment of questionnaire validity for measuring total fat intake using plasma lipid levels as criteria. Am J Epidemiol 2001, 154:1107-1112.
• [35]Dixon WJ, Tukey JW: Approximate behavior of the distribution of Winsorized t (Trimming/Winsorization 2). Technometrics 1968, 10:83-98.
• [36]Pritchard JK, Stephens M, Donnelly P: Inference of population structure using multilocus genotype data. Genetics 2000, 155:945-959.
• [37]Rao MN, Marmillot P, Gong M, Palmer DA, Seeff LB, Strader DB, Lakshman MR: Light, but not heavy alcohol drinking, stimulates paraoxonase by upregulating liver mRNA in rats and humans. Metabolism 2003, 52:1287-1294.
• [38]Djousse L, Ellison RC, Beiser A, Scaramucci A, D’Agostino RB, Wolf PA: Alcohol Consumption and Risk of Ischemic Stroke: The Framingham Study. Stroke 2002, 33:907-912.
• [39]Djoussé L, Dorgan JF, Zhang Y, Schatzkin A, Hood M, D’Agostino RB, Copenhafer DL, Kreger BE, Ellison RC: Alcohol consumption and risk of lung cancer: the Framingham Study. J Natl Cancer Inst 2002, 94:1877-1882.
• [40]Rimm EB, Willett WC, Hu FB, Sampson L, Colditz GA, Manson JE, Hennekens C, Stampfer MJ: Folate and vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women. JAMA 1998, 279:359-364.
• [41]Bazzano LA, He J, Ogden LG, Loria C, Vupputuri S, Myers L, Whelton PK, Kasner SE: Dietary Intake of Folate and Risk of Stroke in US Men and Women: NHANES I Epidemiologic Follow-Up Study * Editorial Comment: NHANES I Epidemiologic Follow-Up Study. Stroke 2002, 33:1183-1189.
• [42]Lowering blood homocysteine with folic acid based supplements: meta-analysis of randomised trials. Homocysteine Lowering Trialists’ Collaboration BMJ 1998, 316:894-898.
• [43]Homocysteine Studies Collaboration: Homocysteine and risk of ischemic heart disease and stroke: a meta-analysis. JAMA 2002, 288:2015-2022.
• [44]Semmler A, Moskau S, Grigull A, Farmand S, Klockgether T, Smulders Y, Blom H, Zur B, Stoffel-Wagner B, Linnebank M: Plasma folate levels are associated with the lipoprotein profile: a retrospective database analysis. Nutr J 2010, 9:31. BioMed Central Full Text
• [45]Söderström E, Eliasson M, Johnson O, Hallmans G, Weinehall L, Jansson J-H, Hultdin J: Plasma folate, but not homocysteine, is associated with Apolipoprotein A1 levels in a non-fortified population. Lipids Health Dis 2013, 12:74. BioMed Central Full Text
• [46]Gaziano JM, Buring JE, Breslow JL, Goldhaber SZ, Rosner B, VanDenburgh M, Willett W, Hennekens CH: Moderate alcohol intake, increased levels of high-density lipoprotein and its subfractions, and decreased risk of myocardial infarction. N Engl J Med 1993, 329:1829-1834.
• [47]Jeppesen J, Schaaf P, Jones C, Zhou MY, Chen YD, Reaven GM: Effects of low-fat, high-carbohydrate diets on risk factors for ischemic heart disease in postmenopausal women. Am J Clin Nutr 1997, 65:1027-1033.
• [48]Abbasi F, McLaughlin T, Lamendola C, Kim HS, Tanaka A, Wang T, Nakajima K, Reaven GM: High carbohydrate diets, triglyceride-rich lipoproteins, and coronary heart disease risk. Am J Cardiol 2000, 85:45-48.
• [49]Salonen JT, Nyyssonen K, Korpela H, Tuomilehto J, Seppanen R, Salonen R: High stored iron levels are associated with excess risk of myocardial infarction in eastern Finnish men. Circulation 1992, 86:803-811.
• [50]Singh RB, Rastogi SS, Sharma VK, Saharia RB, Kulshretha SK: Can dietary magnesium modulate lipoprotein metabolism? Magnes Trace Elem 1990, 9:255-264.
• [51]He K: Magnesium Intake and Incidence of Metabolic Syndrome Among Young Adults. Circulation 2006, 113:1675-1682.
• [52]Stampfer MJ, Hu FB, Manson JE, Rimm EB, Willett WC: Primary prevention of coronary heart disease in women through diet and lifestyle. N Engl J Med 2000, 343:16-22.
• [53]Kromhout D: Prevention of Coronary Heart Disease by Diet and Lifestyle: Evidence From Prospective Cross-Cultural, Cohort, and Intervention Studies. Circulation 2002, 105:893-898.
• [54]Zock PL, de Vries JH, Katan MB: Impact of myristic acid versus palmitic acid on serum lipid and lipoprotein levels in healthy women and men. Arterioscler Thromb Vasc Biol 1994, 14:567-575.
• [55]Müller H, Lindman AS, Brantsaeter AL, Pedersen JI: The serum LDL/HDL cholesterol ratio is influenced more favorably by exchanging saturated with unsaturated fat than by reducing saturated fat in the diet of women. J Nutr 2003, 133:78-83.
• [56]Hu FB, Stampfer MJ, Manson JE, Rimm E, Colditz GA, Rosner BA, Hennekens CH, Willett WC: Dietary fat intake and the risk of coronary heart disease in women. N Engl J Med 1997, 337:1491-1499.
• [57]Hooper L, Kroon PA, Rimm EB, Cohn JS, Harvey I, Le Cornu KA, Ryder JJ, Hall WL, Cassidy A: Flavonoids, flavonoid-rich foods, and cardiovascular risk: a meta-analysis of randomized controlled trials. Am J Clin Nutr 2008, 88:38-50.
• [58]Costa LG, Tait L, Laat R, Dao K, Giordano G, Pellacani C, Cole TB, Furlong CE: Modulation of Paraoxonase 2 (PON2) in Mouse Brain by the Polyphenol Quercetin: A Mechanism of Neuroprotection? Neurochem Res 2013, 38:1809-1818.