Coronary heart disease (CHD) is primarily a disease of occidental culture, being more prevalent in populations that have adopted a high-fat, high-cholesterol diet, who smoke and do not engage in sufficient physical activity. 1 The Islamic religion prescribes fasting during Ramadan for all healthy Muslims for ostensibly moral and spiritual reasons. It may, however, be viewed as an effective model for CHD risk profile modulation.The effect of Ramadan fasting on cardiovascular risk factors is still a matter of debate. Energy intake decreases during Ramadan, 2-5 as do weight 2-5 and body fat percentage. 3,5 The effect of Ramadan fasting on serum lipid profile is not so clear, however. Numerous studies report improvements in serum lipoproteins, while a few report a deterioration in the LDL:HDL cholesterol ratio during Ramadan. 4 There seems to be a reduction in the number of hospitalizations for acute coronary events during the month of Ramadan, 6 although this cannot be entirely or necessarily attributed to the physical restrictions, which the faithful endure during this month.This study was performed to evaluate alterations in CHD risk profile during the holy month of Ramadan.
Materials and MethodsNinety-one healthy volunteers aged 20.8±3.1 years from two seminary schools in Rey, south of Tehran, took part in this study during Ramadan 2000 (1442 in the lunar calendar). The sample consisted of 50 men (age 19.9±1.8 years) and 41 women (age 21.9±3.9 years). All participants had the same diet and level of physical activity. Participants fasted from sunrise to sunset for at least 25 days during Ramadan. Dietary intake was recorded using a semi-quantitative food frequency questionnaire on days zero and 14 of fasting. None of the students smoked or was taking any medication at the time of the study.Blood samples were collected twice: first, one week before Ramadan after a 12-hour overnight fast (baseline) and then on the 28 th day of Ramadan, just before sunset. Anthropometric measures were performed at the same time as blood sampling.Biochemical measurements took place at the laboratory of the Endocrine and Metabolism Research Centre, affiliated to the Tehran University of Medical Sciences.Blood samples were centrifuged and the supernatant plasma stored at -25°C. All blood samples were analyzed in a single batch to avoid day-to-day laboratory variation. Glucose, total cholesterol (T-C) and triglyceride (TG) levels were measured by auto-analyser (Hitachi 911, Böhringer Mannheim, Germany) with standard reagents supplied by the company. High-density lipoprotein cholesterol (HDL-C) was measured enzymatically from the supernatant obtained after precipitation of apolipoprotein B-containing lipoproteins (very low-density lipoprotein [VLDL] and LDL) by dextran sulphate and Mg ++ (HDL-Cholesterol kit, Sigma Diagnostics, USA). The intra-assay and inter-assay variation coefficients were less than 1%. Low-density lipoprotein (LDL-C) levels were then calculated using the Friedwald formula (all participants had TG values <400 mg/dl)....