ORIGINAL COMMUNICATION Individual saturated fatty acids and nonfatal acute myocardial infarction in Costa Rica EK Kabagambe 1 , A Baylin 1 , X Siles 2 and H Campos 1,2 * 1 Department of Nutrition, Harvard School of Public Health, Boston, MA USA; and 2 Centro Centroamericano de Poblacio´n, Universidad de Costa Rica, San Pedro de Montes de Oca, Costa Rica Background: Epidemiological studies on the effect of individual saturated fatty acids (SFAs) on cardiovascular disease, especially in developing countries with different dietary patterns, are scarce. Objective: To determine the risk of nonfatal acute myocardial infarction (MI) associated with consumption of individual SFAs and their food sources in Costa Rica. Design: The cases (n ¼ 485) were survivors of a first acute MI and were matched by age, sex and area of residence to population controls (n ¼ 508). Data on anthropometrical measurements, lifestyle and diet were collected using interviewer-administered questionnaires. Results: In analyses adjusted for confounders, consumption of total and individual SFAs was associated with an increased risk of MI. The odds ratio (OR) (95% confidence intervals) for 1% increase in energy from total saturated fat was 1.12 (1.03–1.21) while it was 1.51 (1.03–2.22) for lauric acid þ myristic acid, 1.14 (1.01–1.30) for palmitic acid and 2.00 (1.34–3.00) for stearic acid. Although lauric and myristic acids were associated with increased risk of MI, they were consumed in small amounts and most of the saturated fat (87%) came from palmitic and stearic acids, which derived mainly from red meat and fried foods. Consumption of cheese (1–2 vs 0 servings/day) was associated with increased risk of MI (OR ¼ 3.07; 95% confidence interval: 1.74–5.39; P for trend o0.0001), while consumption of low-fat milk was not. Conclusion: Increased consumption of total and individual SFAs is associated with increased risk of MI. Lauric, myristic and stearic acids were more potent than palmitic acid. Sponsorship: National Institutes of Health Grant HL 49086 and HL 60692. European Journal of Clinical Nutrition (2003) 57, 1447–1457. doi:10.1038/sj.ejcn.1601709 Keywords: diet; fatty acids; coronary disease; risk factors; epidemiology Introduction Increased saturated fat intake is a risk factor for cardiovas- cular disease (CVD) (Hu et al, 1999, 2001), the leading cause of death in many Western and Latin American countries (Anon, 2002; Reddy & Yusuf, 1998). Although the effect of saturated fat on CVD risk has been mainly attributed to its ability to raise total and low-density lipoprotein (LDL) cholesterol (Kris-Etherton & Yu, 1997), it could be due, in part, to low-fiber intake among consumers of high-fat diets (Ascherio et al, 1996). Studies in Nigeria suggest that the effects of saturated fat on serum cholesterol depend on the subject’s physical activity level, total fat and total energy intakes (Kesteloot et al, 1989; Glew et al, 2001). Most studies on saturated fat have been experimental and compared individual saturated fatty acids (SFAs) to carbohydrates and/ or oleic acid with regard to changes in serum lipid profiles (Katan et al, 1995; Kris-Etherton & Yu, 1997). Most of these studies showed that lauric, myristic and palmitic acids were hypercholesterolemic and that myristic acid was the most potent (Denke & Grundy, 1992; Zock et al, 1994; Katan et al, 1995) while stearic acid and the short-chain SFAs were considered to be neutral (Grundy & Denke, 1990; Yu et al, 1995; Kris-Etherton & Yu, 1997; Judd et al, 2002). Epidemiological studies on saturated fat and CVD end points are few (Garcia-Palmieri et al, 1980; Shekelle et al, 1981; McGee et al, 1984; Kushi et al, 1985; Kromhout et al, 1995; Ascherio et al, 1996; Pietinen et al, 1997; Hu et al, 1999; Suh et al, 2001); most were conducted in industrialized countries and did not investigate individual SFAs (Garcia- Palmieri et al, 1980; Shekelle et al, 1981; McGee et al, 1984; Kushi et al, 1985; Ascherio et al, 1996; Pietinen et al, 1997). A large prospective cohort (Hu et al, 1999) of mainly US Received 13 September 2002; revised 21 October 2002; accepted 6 December 2002 *Correspondence: H Campos, Department of Nutrition, Room 353A, Harvard School of Public Health, Boston, MA 02115, USA. E-mail: hcampos@hsph.harvard.edu European Journal of Clinical Nutrition (2003) 57, 1447–1457 & 2003 Nature Publishing Group All rights reserved 0954-3007/03 $25.00 www.nature.com/ejcn