Glycemic Index, Glycemic Load, and Thrombogenesis

Jennie Brand-Miller; Scott Dickinson; Alan Barclay; Margaret Allman-Farinelli

doi:10.1055/s-0029-1214154

Seminars in Thrombosis and Hemostasis, Table of Contents

Semin Thromb Hemost 2009; 35(1): 111-118
DOI: 10.1055/s-0029-1214154

Glycemic Index, Glycemic Load, and Thrombogenesis

Jennie Brand-Miller¹ , Scott Dickinson¹ , Alan Barclay¹ , Margaret Allman-Farinelli¹

¹Institute of Obesity, Nutrition and Exercise, and Department of Medicine, University of Sydney and Royal Prince Alfred Hospital, Camperdown, NSW, Australia

Abstract

ABSTRACT

Hyperglycemia and insulin resistance are independent risk factors for cardiovascular disease (CVD). Postprandial glycemic “spikes” adversely affect vascular structure and function via multiple mechanisms including oxidative stress, inflammation, low-density lipoprotein oxidation, protein glycation, and procoagulant activity. Glycemic responses can be reliably predicted by considering both the quantity and quality of carbohydrate. The glycemic index (GI), a measure of carbohydrate quality, has provided insights that knowledge of the sugar or starch content has not. In prospective observational studies, dietary GI and/or glycemic load (GL; the product of the amount of carbohydrate and GI) independently predict CVD, with relative risk ratios of 1.2 to 1.9 comparing highest and lowest quartiles. In randomized controlled trials in overweight subjects, diets based on low GI carbohydrates have decreased plasminogen activator inhibitor-1 activity and other CVD risk factors over and above that of conventional low-fat diets. Taken together, the findings suggest that clinicians may be able to improve CVD outcomes by recommending the judicious use of low GI/GL foods.

KEYWORDS

Glycemic index - cardiovascular disease - carbohydrates - glycemic load - postprandial glycemia

Full Text

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Prof. J. Brand-Miller

Human Nutrition Unit (G08), University of Sydney, Camperdown

NSW 2006, Australia

Email: j.brandmiller@mmb.usyd.edu.au