HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: clinchem.2007.097907v1 54/1/11    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Ridker, P. M Search for Related Content PubMed PubMed Citation Articles by Ridker, P. M Related Collections Perspective

Fasting versus Nonfasting Triglycerides and the Prediction of Cardiovascular Risk: Do We Need to Revisit the Oral Triglyceride Tolerance Test?

¹ Center for Cardiovascular Disease Prevention, Brigham and Women’s Hospital, Boston, MA.

^aAddress correspondence to the author at: Center for Cardiovascular Disease Prevention, Brigham and Women’s Hospital, 900 Commonwealth Ave. East, Boston, MA 02215. Fax 617-734-1508; e-mail pridker@partners.org.

The first 300 words of the full text of this article appear below.

Historically, triglycerides have been measured in the fasting state for 2 reasons. First, because of the marked increase in triglycerides after fat ingestion, the variability in triglyceride measurements is much smaller in the fasting state. Second, before the availability of direct assays for LDL cholesterol (LDL-C),¹ estimation of LDL-C was performed in clinical practice almost exclusively by use of the Friedewald equation, which requires that both the HDL-C concentration and the fasting triglyceride concentration divided by 5 be subtracted from the total cholesterol concentration.

The recommendations to measure triglycerides in the fasting state did not, however, derive from a consistent set of prospective cohort studies showing that fasting concentrations were superior to nonfasting concentrations for the detection of cardiovascular risk. Instead, following screening guidelines, most epidemiologic investigations simply relied on fasting triglycerides. Taken as a whole, such studies indicate that fasting triglycerides are a univariate predictor of vascular disease. Controversy exists, however, regarding the clinical usefulness of fasting triglycerides as an independent predictor of risk, because adjustment for other covariates—in particular HDL-C—markedly decreases both the magnitude and significance of observed epidemiologic effects (1). The extent to which investigators have sought to avoid nonfasting triglycerides as a method for risk detection is evident in a recent metaanalysis that limited evaluation only to those epidemiologic studies that measured fasting triglycerides, specifically "to exclude the possibility of postprandial effects" (2).

Is it possible, then, that recommendations to measure triglycerides in the fasting state have systematically underestimated the impact of hypertriglyceridemia in clinical practice? Atherosclerosis has long been hypothesized to be a disorder influenced by postprandial effects. As early as 1950, J. R. Moreton, writing in the Journal of Laboratory and Clinical Medicine, suggested a linkage between chylomicronemia, fat tolerance, and atherosclerosis (3). A major source of . . . [Full Text of this Article]

The following articles in journals at HighWire Press have cited this article:

				J. Yang, Y. Park, H. Zhang, X. Gao, E. Wilson, W. Zimmer, L. Abbott, and C. Zhang Role of MCP-1 in tumor necrosis factor-{alpha}-induced endothelial dysfunction in type 2 diabetic mice Am J Physiol Heart Circ Physiol, October 1, 2009; 297(4): H1208 - H1216. [Abstract] [Full Text] [PDF]

				G. R. Warnick and K. Nakajima Fasting versus Nonfasting Triglycerides: Implications for Laboratory Measurements Clin. Chem., January 1, 2008; 54(1): 14 - 16. [Full Text] [PDF]