Kwiterovich Peter O, Vining Eileen P G, Pyzik Paula, Skolasky Richard, Freeman John M
Lipid Research Atherosclerosis Division, Department of Neurology, The Johns Hopkins Medical Institutions, Baltimore, Md, USA.
JAMA. 2003 Aug 20;290(7):912-20. doi: 10.1001/jama.290.7.912.
Little prospective long-term information is available on the effect of a ketogenic diet on plasma lipoproteins in children with difficult-to-control seizures.
To determine the effect in children with intractable seizures of a high-fat ketogenic diet on plasma levels of the major apolipoprotein B (apoB)-containing lipoproteins, low-density lipoprotein (LDL) and very LDL (VLDL); and the major apolipoprotein A-I (apoA-I)-containing lipoprotein, high-density lipoprotein (HDL).
DESIGN, SETTING, AND PATIENTS: A 6-month prospective cohort study of 141 children (mean [SD] age, 5.2 [3.8] years for 70 boys and 6.1 [4.4] years for 71 girls) with difficult-to-treat seizures who were hospitalized for initiation of a high-fat ketogenic diet and followed up as outpatients. This cohort constituted a subgroup of the 371 patients accepted into the ketogenic diet program between 1994 and 2001. A subset of the cohort was also studied after 12 (n = 59) and 24 (n = 27) months.
A ketogenic diet consisting of a high ratio of fat to carbohydrate and protein combined (4:1 [n = 102], 3.5:1 [n = 7], or 3:1 [n = 32]). After diet initiation, the calories and ratio were adjusted to maintain ideal body weight for height and maximal urinary ketosis for seizure control.
Differences at baseline and 6-month follow-up for levels of total, VLDL, LDL, HDL, and non-HDL cholesterol; triglycerides; total apoB; and apoA-I.
At 6 months, the high-fat ketogenic diet significantly increased the mean plasma levels of total (58 mg/dL [1.50 mmol/L]), LDL (50 mg/dL [1.30 mmol/L]), VLDL (8 mg/dL [0.21 mmol/L]), and non-HDL cholesterol (63 mg/dL [1.63 mmol/L]) (P<.001 vs baseline for each); triglycerides (58 mg/dL [0.66 mmol/L]) (P<.001); and total apoB (49 mg/dL) (P<.001). Mean HDL cholesterol decreased significantly (P<.001), although apoA-I increased (4 mg/dL) (P =.23). Significant but less marked changes persisted in children observed after 12 and 24 months.
A high-fat ketogenic diet produced significant increases in the atherogenic apoB-containing lipoproteins and a decrease in the antiatherogenic HDL cholesterol. Further studies are necessary to determine if such a diet adversely affects endothelial vascular function and promotes inflammation and formation of atherosclerotic lesions.
关于生酮饮食对难以控制癫痫发作儿童血浆脂蛋白影响的前瞻性长期信息较少。
确定高脂肪生酮饮食对难治性癫痫儿童血浆中主要含载脂蛋白B（apoB）的脂蛋白，即低密度脂蛋白（LDL）和极低密度脂蛋白（VLDL）；以及主要含载脂蛋白A-I（apoA-I）的脂蛋白，即高密度脂蛋白（HDL）水平的影响。
设计、地点和患者：对141名儿童进行为期6个月的前瞻性队列研究（70名男孩的平均[标准差]年龄为5.2[3.8]岁，71名女孩为6.1[4.4]岁），这些儿童因开始高脂肪生酮饮食而住院，并作为门诊患者进行随访。该队列是1994年至2001年接受生酮饮食计划的371名患者中的一个亚组。该队列的一个子集在12个月（n = 59）和24个月（n = 27）后也进行了研究。
一种脂肪与碳水化合物和蛋白质组合比例较高的生酮饮食（4:1[n = 102]、3.5:1[n = 7]或3:1[n = 32]）。开始饮食后，调整热量和比例以维持身高的理想体重和最大尿酮症以控制癫痫发作。
基线和6个月随访时总胆固醇、VLDL、LDL、HDL和非HDL胆固醇水平；甘油三酯；总apoB；以及apoA-I的差异。
6个月时，高脂肪生酮饮食显著提高了总胆固醇（58mg/dL[1.50mmol/L]）、LDL（50mg/dL[1.30mmol/L]）、VLDL（8mg/dL[0.21mmol/L]）和非HDL胆固醇（63mg/dL[1.63mmol/L]）的平均血浆水平（每项与基线相比P<.001）；甘油三酯（58mg/dL[0.66mmol/L]）（P<.001）；以及总apoB（49mg/dL）（P<.001）。平均HDL胆固醇显著降低（P<.001），尽管apoA-I升高了（4mg/dL）（P = 0.23）。在12个月和24个月后观察的儿童中，显著但不太明显的变化仍然存在。
高脂肪生酮饮食使致动脉粥样硬化的含apoB脂蛋白显著增加，而抗动脉粥样硬化的HDL胆固醇降低。需要进一步研究以确定这种饮食是否会对内皮血管功能产生不利影响并促进炎症和动脉粥样硬化病变的形成。
