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51. Docosahexaenoic acid-enriched canola oil increases adiponectin concentrations: A randomized crossover controlled intervention trial

Author

Baril-Gravel, L., primary, Labonté, M.-E., additional, Couture, P., additional, Vohl, M.-C., additional, Charest, A., additional, Guay, V., additional, Jenkins, D.A., additional, Connelly, P.W., additional, West, S., additional, Kris-Etherton, P.M., additional, Jones, P.J., additional, Fleming, J.A., additional, and Lamarche, B., additional

Published
2015
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52. Discordance analysis and the Gordian Knot of LDL and non-HDL cholesterol versus apoB

Author

Sniderman, A.D., Lamarche, B., Contois, J.H., Graaf, J. de, Sniderman, A.D., Lamarche, B., Contois, J.H., and Graaf, J. de

Abstract

Item does not contain fulltext, PURPOSE OF REVIEW: Conventional methods, comparing the concentration of cholesterol to particle number as indices of cardiovascular risk, have not produced consistent results, in large part, because they treat these variables as independent and unrelated. However, although highly correlated, apolipoprotein B particles may contain a normal mass of cholesterol or may be cholesterol-depleted or cholesterol-enriched. Discordance analysis compares the predictive power of LDL-C and non-HDL-C to apolipoprotein B and LDL particle numbers in patients in whom they differ, that is, in whom they are discordant. The advantage of discordance analysis is that the results are not diluted by concordant data in which risk predictions cannot differ. RECENT FINDINGS: The evidence, to date, consistently demonstrates that apolipoprotein B and LDL particle numbers are more accurate indices of cardiovascular risk than LDL-C or non-HDL-C. SUMMARY: Discordance analysis is a methodological advance that allows the clinical value of closely correlated variables to be determined and demonstrates that cardiovascular risk is more closely related to the number of atherogenic particles than to the total mass of cholesterol within them.

Published
2014

54. Systematically missing confounders in individual participant data meta-analysis of observational cohort studies

Author

Fibrinogen Studies Collaboration, Jackson, D, White, I, Kostis, JB, Wilson, AC, Folsom, AR, Wu, K, Chambless, L, Benderly, M, Goldbourt, U, Willeit, J, Kiechl, S, Yarnell, JW, Sweetnam, PM, Elwood, PC, Cushman, M, Psaty, BM, Tracy, RP, Tybjaerg-Hansen, A, Haverkate, F, de Maat, MP, Thompson, SG, Fowkes, FG, Lee, AJ, Smith, FB, Salomaa, V, Harald, K, Rasi, V, Vahtera, E, Jousilahti, P, D'Agostino, R, Kannel, WB, Wilson, PW, Tofler, G, Levy, D, Marchioli, R, Valagussa, F, Rosengren, A, Wilhelmsen, L, Lappas, G, Eriksson, H, Cremer, P, Nagel, D, Curb, JD, Rodriguez, B, Yano, K, Salonen, J, Nyyssönen, K, Tuomainen, TP, Hedblad, B, Engström, G, Berglund, G, Loewel, H, Koenig, W, Hense, HW, Meade, TW, Cooper, JA, De Stavola, B, Knottenbelt, C, Miller, GJ, Bauer, KA, Rosenberg, RD, Sato, S, Kitamura, A, Naito, Y, Iso, H, Palosuo, T, Ducimetiere, P, Amouyel, P, Arveiler, D, Evans, AE, Ferrieres, J, Juhan-Vague, I, Bingham, A, Schulte, H, Assmann, G, Cantin, B, Lamarche, B, Despres, JP, Dagenais, GR, Tunstall-Pedoe, H, Lowe, GD, Woodward, M, Ben-Shlomo, Y, Davey Smith, G, Palmieri, V, Yeh, JL, Rudnicka, A, Brennan, P, Ridker, P, Rodeghiero, F, Tosetto, A, Shepherd, J, Ford, I, Robertson, M, Brunner, E, Shipley, M, Feskens, EJ, Di Angelantonio, E, Kaptoge, S, Lewington, S, Sarwar, N, Walker, M, Watson, S, White, IR, Wood, AM, and Danesh, J

Abstract

One difficulty in performing meta-analyses of observational cohort studies is that the availability of confounders may vary between cohorts, so that some cohorts provide fully adjusted analyses while others only provide partially adjusted analyses. Commonly, analyses of the association between an exposure and disease either are restricted to cohorts with full confounder information, or use all cohorts but do not fully adjust for confounding. We propose using a bivariate random-effects meta-analysis model to use information from all available cohorts while still adjusting for all the potential confounders. Our method uses both the fully adjusted and the partially adjusted estimated effects in the cohorts with full confounder information, together with an estimate of their within-cohort correlation. The method is applied to estimate the association between fibrinogen level and coronary heart disease incidence using data from 154,012 participants in 31 cohorts

Published
2009

55. Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality

Author

Tipping, R.W. Ford, C.E. Simpson, L.M. Walldius, G. Jungner, I. Folsom, A.R. Chambless, L. Panagiotakos, D. Pitsavos, C. Chrysohoou, C. Stefanadis, C. Goldbourt, U. Benderly, M. Tanne, D. Whincup, P. Wannamethee, S.G. Morris, R.W. Kiechl, S. Willeit, J. Santer, P. Mayr, A. Wald, N. Ebrahim, S. Lawlor, D. Yarnell, J. Gallacher, J. Casiglia, E. Tikhonoff, V. Nietert, P.J. Sutherland, S.E. Bachman, D.L. Cushman, M. Psaty, B.M. Tracy, R. Tybjærg-Hansen, A. Nordestgaard, B.G. Frikke-Schmidt, R. Kamstrup, P.R. Giampaoli, S. Palmieri, L. Panico, S. Vanuzzo, D. Pilotto, L. De La Cámara, A.G. Gómez Gerique, J.A. Simons, L. McCallum, J. Friedlander, Y. Fowkes, F.G.R. Lee, A. Smith, F.B. Taylor, J. Guralnik, J.M. Phillips, C.L. Wallace, R.B. Blazer, D.G. Brenner, H. Raum, E. Müller, H. Rothenbacher, D. Jansson, J.-H. Wennberg, P. Nissinen, A. Donfrancesco, C. Salomaa, V. Harald, K. Jousilahti, P. Vartiainen, E. Woodward, M. D’Agostino, R.B. Wolf, P.A. Vasan, R.S. Pencina, M.J. Bladbjerg, E.-M. Jørgensen, T. Møller, L. Jespersen, J. Dankner, R. Chetrit, A. Lubin, F. Rosengren, A. Wilhelmsen, L. Lappas, G. Eriksson, H. Björkelund, C. Lissner, L. Bengtsson, C. Cremer, P. Nagel, D. Tilvis, R.S. Strandberg, T.E. Rodriguez, B. Dekker, J. Nijpels, G. Stehouwer, C.D.A. Rimm, E. Pai, J.K. Sato, S. Iso, H. Kitamura, A. Noda, H. Salonen, J.T. Nyyssönen, K. Tuomainen, T.-P. Deeg, D.J.H. Poppelaars, J.L. Hedblad, B. Berglund, G. Engström, G. Verschuren, W.M.M. Blokstra, A. Döring, A. Koenig, W. Meisinger, C. Mraz, W. Bueno-De-Mesquita, H.B. Kuller, L.H. Grandits, G. Selmer, R. Tverdal, A. Nystad, W. Gillum, R.F. Mussolino, M. Hankinson, S. Manson, J.E. Cooper, J.A. Bauer, K.A. Naito, Y. Holme, I. Nakagawa, H. Miura, K. Ducimetiere, P. Jouven, X. Luc, G. Crespo, C.J. Garcia Palmieri, M.R. Amouyel, P. Arveiler, D. Evans, A. Ferrieres, J. Schulte, H. Assmann, G. Shepherd, J. Packard, C.J. Sattar, N. Ford, I. Cantin, B. Lamarche, B. Després, J.-P. Dagenais, G.R. Barrett-Connor, E. Daniels, L.B. Laughlin, G.A. Gudnason, V. Aspelund, T. Sigurdsson, G. Thorsson, B. Trevisan, M. Witteman, J. Kardys, I. Breteler, M.M.B. Hofman, A. Tunstall-Pedoe, H. Tavendale, R. Lowe, G. Ben-Shlomo, Y. Davey-Smith, G. Howard, B.V. Zhang, Y. Best, L. Umans, J. Onat, A. Njølstad, I. Mathiesen, E.B. Løchen, M.-L. Wilsgaard, T. Ingelsson, E. Sundström, J. Lind, L. Lannfelt, L. Gaziano, J.M. Stampfer, M. Ridker, P.M. Ulmer, H. Diem, G. Concin, H. Tosetto, A. Rodeghiero, F. Marmot, M. Clarke, R. Collins, R. Fletcher, A. Brunner, E. Shipley, M. Buring, J. Cobbe, S. Robertson, M. He, Y. Ibañez, A.M. Feskens, E. Kromhout, D. Walker, M. Watson, S. Di Angelantonio, E. Erqou, S. Kaptoge, S. Lewington, S. Orfei, L. Pennells, L. Perry, P.L. Ray, K.K. Sarwar, N. Alexander, M. Thompson, A. Thompson, S.G. Wensley, F. White, I.R. Wood, A.M. Danesh, J.

Abstract

Context Circulating concentration of lipoprotein(a) (Lp[a]), a large glycoprotein attached to a low-density lipoprotein–like particle, may be associated with risk of coronary heart disease (CHD) and stroke. Objective To assess the relationship of Lp(a) concentration with risk of major vascular and nonvascular outcomes. Study Selection Long-term prospective studies that recorded Lp(a) concentration and subsequent major vascular morbidity and/or cause-specific mortality published between January 1970 and March 2009 were identified through electronic searches of MEDLINE and other databases, manual searches of reference lists, and discussion with collaborators. Data Extraction Individual records were provided for each of 126 634 participants in 36 prospective studies. During 1.3 million person-years of follow-up, 22 076 firstever fatal or nonfatal vascular disease outcomes or nonvascular deaths were recorded, including 9336 CHD outcomes, 1903 ischemic strokes, 338 hemorrhagic strokes, 751 unclassified strokes, 1091 other vascular deaths, 8114 nonvascular deaths, and 242 deaths of unknown cause. Within-study regression analyses were adjusted for within-person variation and combined using meta-analysis. Analyses excluded participants with known preexisting CHD or stroke at baseline. Data Synthesis Lipoprotein(a) concentration was weakly correlated with several conventional vascular risk factors and it was highly consistent within individuals over several years. Associations of Lp(a) with CHD risk were broadly continuous in shape. In the 24 cohort studies, the rates of CHD in the top and bottom thirds of baseline Lp(a) distributions, respectively, were 5.6 (95% confidence interval [CI], 5.4-5.9) per 1000 personyears and 4.4 (95% CI, 4.2-4.6) per 1000 person-years. The risk ratio for CHD, adjusted for age and sex only, was 1.16 (95% CI, 1.11-1.22) per 3.5-fold higher usual Lp(a) concentration (ie, per 1 SD), and it was 1.13 (95% CI, 1.09-1.18) following further adjustment for lipids and other conventional risk factors. The corresponding adjusted risk ratios were 1.10 (95% CI, 1.02-1.18) for ischemic stroke, 1.01 (95% CI, 0.98-1.05) for the aggregate of nonvascular mortality, 1.00 (95% CI, 0.97-1.04) for cancer deaths, and 1.00 (95% CI, 0.95-1.06) for nonvascular deaths other than cancer. Conclusion Under a wide range of circumstances, there are continuous, independent, and modest associations of Lp(a) concentration with risk of CHD and stroke that appear exclusive to vascular outcomes. ©2009 American Medical Association. All rights reserved.

Published
2009

57. Systematically missing confounders in individual participant data meta-analysis of observational cohort studies

Author

Jackson, D, White, I, Kostis, JB, Wilson, AC, Folsom, AR, Wu, K, Chambless, L, Benderly, M, Goldbourt, U, Willeit, J, Kiechl, S, Yarnell, JW, Sweetnam, PM, Elwood, PC, Cushman, M, Psaty, BM, Tracy, RP, Tybjaerg-Hansen, A, Haverkate, F, de Maat, MP, Thompson, SG, Fowkes, FG, Lee, AJ, Smith, FB, Salomaa, V, Harald, K, Rasi, V, Vahtera, E, Jousilahti, P, D'Agostino, R, Kannel, WB, Wilson, PW, Tofler, G, Levy, D, Marchioli, R, Valagussa, F, Rosengren, A, Wilhelmsen, L, Lappas, G, Eriksson, H, Cremer, P, Nagel, D, Curb, JD, Rodriguez, B, Yano, K, Salonen, J, Nyyssönen, K, Tuomainen, TP, Hedblad, B, Engström, G, Berglund, G, Loewel, H, Koenig, W, Hense, HW, Meade, TW, Cooper, JA, De Stavola, B, Knottenbelt, C, Miller, GJ, Bauer, KA, Rosenberg, RD, Sato, S, Kitamura, A, Naito, Y, Iso, H, Palosuo, T, Ducimetiere, P, Amouyel, P, Arveiler, D, Evans, AE, Ferrieres, J, Juhan-Vague, I, Bingham, A, Schulte, H, Assmann, G, Cantin, B, Lamarche, B, Despres, JP, Dagenais, GR, Tunstall-Pedoe, H, Lowe, GD, Woodward, M, Ben-Shlomo, Y, Davey Smith, G, Palmieri, V, Yeh, JL, Rudnicka, A, Brennan, P, Ridker, P, Rodeghiero, F, Tosetto, A, Shepherd, J, Ford, I, Robertson, M, Brunner, E, Shipley, M, Feskens, EJ, Di Angelantonio, E, Kaptoge, S, Lewington, S, Sarwar, N, Walker, M, Watson, S, White, IR, Wood, AM, and Danesh, J

Subjects
Statistics and Probability, Male, Nutrition and Disease, Epidemiology, Coronary Disease, Bivariate analysis, Logistic regression, 01 natural sciences, survival analysis, Cohort Studies, 010104 statistics & probability, 03 medical and health sciences, 0302 clinical medicine, Meta-Analysis as Topic, Voeding en Ziekte, Statistics, Medicine, Humans, Computer Simulation, 030212 general & internal medicine, 0101 mathematics, observational studies, patient data, Survival analysis, time, VLAG, Models, Statistical, aggregate data, model, business.industry, Incidence (epidemiology), Confounding, Fibrinogen, confounders, event outcomes, meta-analysis, Meta-analysis, Data Interpretation, Statistical, missing covariates, logistic-regression analysis, Observational study, Female, heterogeneity, business, Demography, Cohort study, Research Article
Abstract

One difficulty in performing meta-analyses of observational cohort studies is that the availability of confounders may vary between cohorts, so that some cohorts provide fully adjusted analyses while others only provide partially adjusted analyses. Commonly, analyses of the association between an exposure and disease either are restricted to cohorts with full confounder information, or use all cohorts but do not fully adjust for confounding. We propose using a bivariate random-effects meta-analysis model to use information from all available cohorts while still adjusting for all the potential confounders. Our method uses both the fully adjusted and the partially adjusted estimated effects in the cohorts with full confounder information, together with an estimate of their within-cohort correlation. The method is applied to estimate the association between fibrinogen level and coronary heart disease incidence using data from 154 012 participants in 31 cohorts.† Copyright © 2009 John Wiley & Sons, Ltd.

Published
2009

58. Plasma fibrinogen level and the risk of major cardiovascular diseases and nonvascular mortality: an individual participant meta-analysis

Author

Fibrinogen Studies Collaboration, Danesh, John, Lewington, Sarah, Thompson, Simon G, Lowe, Gordon DO, Collins, Rory, Kostis, JB, Wilson, AC, Folsom, AR, Wu, K, Benderly, M, Goldbourt, U, Willeit, J, Kiechl, S, Yarnell, JWG, Sweetnam, PM, Elwood, PC, Cushman, M, Psaty, BM, Tracy, RP, Tybjaerg-Hansen, A, Haverkate, F, de Maat, MPM, Fowkes, FGR, Lee, AJ, Smith, FB, Salomaa, V, Harald, K, Rasi, R, Vahtera, E, Jousilahti, P, Pekkanen, J, D'Agostino, R, Kannel, WB, Wilson, PWF, Tofler, G, Arocha-Piñango, CL, Rodriguez-Larralde, A, Nagy, E, Mijares, M, Espinosa, R, Rodriquez-Roa, E, Ryder, E, Diez-Ewald, MP, Campos, G, Fernandez, V, Torres, E, Marchioli, R, Valagussa, F, Rosengren, A, Wilhelmsen, L, Lappas, G, Eriksson, H, Cremer, P, Nagel, D, Curb, JD, Rodriguez, B, Yano, K, Salonen, JT, Nyyssönen, K, Tuomainen, T-P, Hedblad, B, Lind, P, Loewel, H, Koenig, W, Meade, TW, Cooper, JA, De Stavola, B, Knottenbelt, C, Miller, GJ, Bauer, KA, Rosenberg, RD, Sato, S, Kitamura, A, Naito, Y, Palosuo, T, Ducimetiere, P, Amouyel, P, Arveiler, D, Evans, AE, Ferrieres, J, Juhan-Vague, I, Bingham, A, Schulte, H, Assmann, G, Cantin, B, Lamarche, B, Després, J-P, Dagenais, GR, Tunstall-Pedoe, H, Woodward, M, Ben-Shlomo, Y, Davey Smith, G, Palmieri, V, Yeh, JL, Rudnicka, A, Ridker, P, Rodeghiero, F, Tosetto, A, Shepherd, J, Ford, I, Robertson, M, Brunner, E, Shipley, M, Feskens, EJM, Kromhout, D, Dickinson, A, Ireland, B, Juzwishin, K, Kaptoge, S, Lewington, S, Memon, A, Sarwar, N, Walker, M, Wheeler, J, White, I, and Wood, A

Abstract

CONTEXT: Plasma fibrinogen levels may be associated with the risk of coronary heart disease (CHD) and stroke. OBJECTIVE: To assess the relationships of fibrinogen levels with risk of major vascular and with risk of nonvascular outcomes based on individual participant data. DATA SOURCES: Relevant studies were identified by computer-assisted searches, hand searches of reference lists, and personal communication with relevant investigators. STUDY SELECTION: All identified prospective studies were included with information available on baseline fibrinogen levels and details of subsequent major vascular morbidity and/or cause-specific mortality during at least 1 year of follow-up. Studies were excluded if they recruited participants on the basis of having had a previous history of cardiovascular disease; participants with known preexisting CHD or stroke were excluded. DATA EXTRACTION: Individual records were provided on each of 154,211 participants in 31 prospective studies. During 1.38 million person-years of follow-up, there were 6944 first nonfatal myocardial infarctions or stroke events and 13,210 deaths. Cause-specific mortality was generally available. Analyses involved proportional hazards modeling with adjustment for confounding by known cardiovascular risk factors and for regression dilution bias. DATA SYNTHESIS: Within each age group considered (40-59, 60-69, and > or =70 years), there was an approximately log-linear association with usual fibrinogen level for the risk of any CHD, any stroke, other vascular (eg, non-CHD, nonstroke) mortality, and nonvascular mortality. There was no evidence of a threshold within the range of usual fibrinogen level studied at any age. The age- and sex- adjusted hazard ratio per 1-g/L increase in usual fibrinogen level for CHD was 2.42 (95% confidence interval [CI], 2.24-2.60); stroke, 2.06 (95% CI, 1.83-2.33); other vascular mortality, 2.76 (95% CI, 2.28-3.35); and nonvascular mortality, 2.03 (95% CI, 1.90-2.18). The hazard ratios for CHD and stroke were reduced to about 1.8 after further adjustment for measured values of several established vascular risk factors. In a subset of 7011 participants with available C-reactive protein values, the findings for CHD were essentially unchanged following additional adjustment for C-reactive protein. The associations of fibrinogen level with CHD or stroke did not differ substantially according to sex, smoking, blood pressure, blood lipid levels, or several features of study design. CONCLUSIONS: In this large individual participant meta-analysis, moderately strong associations were found between usual plasma fibrinogen level and the risks of CHD, stroke, other vascular mortality, and nonvascular mortality in a wide range of circumstances in healthy middle-aged adults. Assessment of any causal relevance of elevated fibrinogen levels to disease requires additional research.

Published
2005

64. Effect of Sitagliptin therapy on postprandial lipoprotein levels in patients with type 2 diabetes

Author

Tremblay, AJ, Lamarche, B, Deacon, Carolyn F., Weisnagel, SJ, Couture, P, Tremblay, AJ, Lamarche, B, Deacon, Carolyn F., Weisnagel, SJ, and Couture, P

Abstract

Aim: Recent studies indicate that type 2 diabetes is associated with an increased secretion of both hepatic and intestinal lipoproteins, leading to the accumulation of atherogenic triglyceride (TG)-rich lipoproteins. Sitagliptin is a selective inhibitor of dipeptidyl peptidase-4 that has been shown to reduce fasting and postprandial glucose levels in patients with type 2 diabetes presumably through incretin hormone-mediated improvements in islet function. The objective of the present study is to examine the effects of treatment with sitagliptin on postprandial lipid and incretin hormone levels as well as glucose homeostasis in patients with type 2 diabetes. Methods: Thirty-six subjects with type 2 diabetes (30 men/6 postmenopausal women with a mean age of 58.1 ± 6.4 years and a body mass index of 30.7 ± 4.9 kg/m2) were recruited in this double-blind cross-over study using sitagliptin 100 mg/day or placebo for a 6-week period each, with a 4-week washout period between the two phases. At the end of each phase of treatment, patients underwent an oral lipid tolerance test providing 35 g of fat per m2 of body surface area and blood samples were taken over an 8-h period. Results: Sitagliptin therapy significantly decreased the postprandial area under the curves (AUCs) for plasma apolipoprotein (apo)B (-5.1%, p = 0.002), apoB-48 (-7.8%, p = 0.03), TG (-9.4%, p = 0.006), very low-density lipoprotein (VLDL)-cholesterol (-9.3%, p = 0.001), free fatty acids (FFAs) (-7.6%, p = 0.005) and glucose (-9.7%, p < 0.0001). Furthermore, the postprandial AUCs for plasma intact glucagonlike peptide-1 (+67.8%, p < 0.0001) and glucose-dependent insulinotropic polypeptide (+67.3%, p < 0.0001) were significantly increased following treatment with sitagliptin, whereas the AUC for plasma glucagon was reduced by -9.7% (p = 0.001) with no significant changes in the AUCs for plasma insulin and C-peptide. Sitagliptin th

Published
2011

65. Systematically missing confounders in individual participant data meta-analysis of observational cohort studies

Author

Jackson, D., White, I., Kostis, J.B., Wilson, A.C., Folsom, A.R., Wu, K., Chambless, L., Benderly, M., Goldbourt, U., Willeit, J., Kiechl, S., Yarnell, J.W., Sweetnam, P.M., Elwood, P.C., Cushman, M., Psaty, B.M., Tracy, R.P., Tybjaerg-Hansen, A., Haverkate, F., Maat, M.P. de, Thompson, S.G., Fowkes, F.G., Lee, A.J., Smith, F.B., Salomaa, V., Harald, K., Rasi, V., Vahtera, E., Jousilahti, P., D'Agostino, R., Kannel, W.B., Wilson, P.W., Tofler, G., Levy, D., Marchioli, R., Valagussa, F., Rosengren, A., Wilhelmsen, L., Lappas, G., Eriksson, H., Cremer, P., Nagel, D., Curb, J.D., Rodriguez, B., Yano, K., Salonen, J.T., Nyyssonen, K., Tuomainen, T.P., Hedblad, B., Engstrom, G., Berglund, G., Loewel, H., Koenig, W., Hense, H.W., Meade, T.W., Cooper, J.A., Stavola, B. De, Knottenbelt, C., Miller, G.J., Bauer, K.A., Rosenberg, R.D., Sato, S., Kitamura, A., Naito, Y., Iso, H., Palosuo, T., Ducimetiere, P., Amouyel, P., Arveiler, D., Evans, A.E., Ferrieres, J., Juhan-Vague, I., Bingham, A., Schulte, H., Assmann, G., Cantin, B., Lamarche, B., Despres, J.P., Dagenais, G.R., Tunstall-Pedoe, H., Lowe, G.D., Woodward, M., Ben-Shlomo, Y., Smith, G. Davey, Palmieri, V., Yeh, J.L., Rudnicka, A., Brennan, P., Ridker, P., Rodeghiero, F., Tosetto, A., Shepherd, J., Ford, I., Robertson, M., Brunner, E., Shipley, M., Feskens, E.J., Angelantonio, E. Di, Kaptoge, S., Lewington, S., Sarwar, N., Walker, M., Watson, S., White, I.R., Wood, A.M., Danesh, J., Jackson, D., White, I., Kostis, J.B., Wilson, A.C., Folsom, A.R., Wu, K., Chambless, L., Benderly, M., Goldbourt, U., Willeit, J., Kiechl, S., Yarnell, J.W., Sweetnam, P.M., Elwood, P.C., Cushman, M., Psaty, B.M., Tracy, R.P., Tybjaerg-Hansen, A., Haverkate, F., Maat, M.P. de, Thompson, S.G., Fowkes, F.G., Lee, A.J., Smith, F.B., Salomaa, V., Harald, K., Rasi, V., Vahtera, E., Jousilahti, P., D'Agostino, R., Kannel, W.B., Wilson, P.W., Tofler, G., Levy, D., Marchioli, R., Valagussa, F., Rosengren, A., Wilhelmsen, L., Lappas, G., Eriksson, H., Cremer, P., Nagel, D., Curb, J.D., Rodriguez, B., Yano, K., Salonen, J.T., Nyyssonen, K., Tuomainen, T.P., Hedblad, B., Engstrom, G., Berglund, G., Loewel, H., Koenig, W., Hense, H.W., Meade, T.W., Cooper, J.A., Stavola, B. De, Knottenbelt, C., Miller, G.J., Bauer, K.A., Rosenberg, R.D., Sato, S., Kitamura, A., Naito, Y., Iso, H., Palosuo, T., Ducimetiere, P., Amouyel, P., Arveiler, D., Evans, A.E., Ferrieres, J., Juhan-Vague, I., Bingham, A., Schulte, H., Assmann, G., Cantin, B., Lamarche, B., Despres, J.P., Dagenais, G.R., Tunstall-Pedoe, H., Lowe, G.D., Woodward, M., Ben-Shlomo, Y., Smith, G. Davey, Palmieri, V., Yeh, J.L., Rudnicka, A., Brennan, P., Ridker, P., Rodeghiero, F., Tosetto, A., Shepherd, J., Ford, I., Robertson, M., Brunner, E., Shipley, M., Feskens, E.J., Angelantonio, E. Di, Kaptoge, S., Lewington, S., Sarwar, N., Walker, M., Watson, S., White, I.R., Wood, A.M., and Danesh, J.

Abstract

One difficulty in performing meta-analyses of observational cohort studies is that the availability of confounders may vary between cohorts, so that some cohorts provide fully adjusted analyses while others only provide partially adjusted analyses. Commonly, analyses of the association between an exposure and disease either are restricted to cohorts with full confounder information, or use all cohorts but do not fully adjust for confounding. We propose using a bivariate random-effects meta-analysis model to use information from all available cohorts while still adjusting for all the potential confounders. Our method uses both the fully adjusted and the partially adjusted estimated effects in the cohorts with full confounder information, together with an estimate of their within-cohort correlation. The method is applied to estimate the association between fibrinogen level and coronary heart disease incidence using data from 154,012 participants in 31 cohorts Udgivelsesdato: 2009/4/15

Published
2009

66. A reappraisal of the impact of dairy foods and milk fat on cardiovascular disease risk

Author

German, J.B., Gibson, R.A., Krauss, R.M., Nestel, P., Lamarche, B., van Staveren, W.A., Steijns, J.M., de Groot, C.P.G.M., Lock, A.L., Destaillats, F., German, J.B., Gibson, R.A., Krauss, R.M., Nestel, P., Lamarche, B., van Staveren, W.A., Steijns, J.M., de Groot, C.P.G.M., Lock, A.L., and Destaillats, F.

Abstract

Background This review provides a reappraisal of the potential effects of dairy foods, including dairy fats, on cardiovascular disease (CVD)/coronary heart disease (CHD) risk. Commodities and foods containing saturated fats are of particular focus as current public dietary recommendations are directed toward reducing the intake of saturated fats as a means to improve the overall health of the population. A conference of scientists from different perspectives of dietary fat and health was convened in order to consider the scientific basis for these recommendations. Aims This review and summary of the conference focus on four key areas related to the biology of dairy foods and fats and their potential impact on human health: (a) the effect of dairy foods on CVD in prospective cohort studies; (b) the impact of dairy fat on plasma lipid risk factors for CVD; (c) the effects of dairy fat on non-lipid risk factors for CVD; and (d) the role of dairy products as essential contributors of micronutrients in reference food patterns for the elderly. Conclusions Despite the contribution of dairy products to the saturated fatty acid composition of the diet, and given the diversity of dairy foods of widely differing composition, there is no clear evidence that dairy food consumption is consistently associated with a higher risk of CVD. Thus, recommendations to reduce dairy food consumption irrespective of the nature of the dairy product should be made with caution.

Published
2009

68. JAMA: Effect of a dietary portfolio of cholesterol-lowering foods given at 2 levels of intensity of dietary advice on serum lipids in hyperlipidemia: a randomized controlled trial

Author

Jenkins, D.J., Jones, P.J., and Lamarche, B.

Subjects
Dietetic foods -- Health aspects -- Research, Hyperlipidemia -- Diet therapy -- Research, Health
Abstract

CONTEXT: Combining foods with recognized cholesterol-lowering properties (dietary portfolio) has proven highly effective in lowering serum cholesterol under metabolically controlled conditions. OBJECTIVE: To assess the effect of a dietary portfolio [...]

Published
2011

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