Little prospective long-term information is available on the effect
of a ketogenic diet on plasma lipoproteins in children with difficult-to-control
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
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)
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.
Main Outcome Measures
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.