BACKGROUND: Patients with hypertriglyceridemia (HTG) are generally advised to avoid alcohol, even though moderate alcohol consumption is cardioprotective. Alcohol increases plasma triglyceride concentration transiently in normolipidemic subjects, but whether alcohol consumption per se increases triglyceride concentrations in patients with HTG is unclear. OBJECTIVE: To assess whether baseline fasting triglyceride concentration determines plasma triglyceride concentration after acute oral alcohol intake. METHODS: Twelve persons with fasting triglyceride concentrations of 2.3 to 8.5 mmol/L (200-750 mg/dL) and 12 persons as a non-HTG group were enrolled. Obesity, current smoking, and history of hypertension, diabetes, or excessive alcohol use were exclusionary. Fasted subjects consumed 38 mL of ethanol in water (equivalent, 2 alcoholic drinks); blood samples were collected at baseline and at intervals thereafter for 10 hours. No less than 1 week later, the subjects consumed water alone in a control test. RESULTS: Mean triglyceride values were 4.04+/-0.41 mmol/L (358+/-36.9 mg/dL) and 1.00+/-0.11 mmol/L (89+/-10.2 mg/dL) for the HTG and non-HTG groups, respectively. Despite similar changes with alcohol feeding in plasma ethanol, nonesterified fatty acid, and acetate concentrations, the groups differed in triglyceride response. At 6 hours (peak) compared with baseline, triglyceride concentration increased only 3% in the HTG group but 53% in the non-HTG group. The former change was not significantly different from the effect with water alone (-9.2% from baseline; P = .43), whereas the latter was (-8.0%; P = .003). CONCLUSIONS: Acute alcohol intake alone is not an important determinant of plasma triglyceride concentration in individuals with HTG. Other factors, such as the contemporaneous consumption of fat and alcohol, known to increase triglyceride concentrations synergistically in non-HTG individuals, may be more important.
BACKGROUND:Patients with hypertriglyceridemia (HTG) are generally advised to avoid alcohol, even though moderate alcohol consumption is cardioprotective. Alcohol increases plasma triglyceride concentration transiently in normolipidemic subjects, but whether alcohol consumption per se increases triglyceride concentrations in patients with HTG is unclear. OBJECTIVE: To assess whether baseline fasting triglyceride concentration determines plasma triglyceride concentration after acute oral alcohol intake. METHODS: Twelve persons with fasting triglyceride concentrations of 2.3 to 8.5 mmol/L (200-750 mg/dL) and 12 persons as a non-HTG group were enrolled. Obesity, current smoking, and history of hypertension, diabetes, or excessive alcohol use were exclusionary. Fasted subjects consumed 38 mL of ethanol in water (equivalent, 2 alcoholic drinks); blood samples were collected at baseline and at intervals thereafter for 10 hours. No less than 1 week later, the subjects consumed water alone in a control test. RESULTS: Mean triglyceride values were 4.04+/-0.41 mmol/L (358+/-36.9 mg/dL) and 1.00+/-0.11 mmol/L (89+/-10.2 mg/dL) for the HTG and non-HTG groups, respectively. Despite similar changes with alcohol feeding in plasma ethanol, nonesterified fatty acid, and acetate concentrations, the groups differed in triglyceride response. At 6 hours (peak) compared with baseline, triglyceride concentration increased only 3% in the HTG group but 53% in the non-HTG group. The former change was not significantly different from the effect with water alone (-9.2% from baseline; P = .43), whereas the latter was (-8.0%; P = .003). CONCLUSIONS: Acute alcohol intake alone is not an important determinant of plasma triglyceride concentration in individuals with HTG. Other factors, such as the contemporaneous consumption of fat and alcohol, known to increase triglyceride concentrations synergistically in non-HTG individuals, may be more important.