Cardiometabolic risk and effectiveness of the modified Atkins Ketogenic Diet for adult patients with pharmacoresistant epilepsies in a middle-income country.

A ketogenic diet may be a therapeutic option for approximately one third of patients with epilepsy. These patients continue to have seizures despite suitable pharmacological treatment. Regardless of the diet's therapeutic potential regarding seizure control, adverse events may coexist. This requires constant monitoring of the patient as comorbidities may emerge. A prospective, nonrandomized and uncontrolled study was conducted to evaluate the effect of a ketogenic diet on cardiometabolic parameters (lipid profile, glycemic profile and body composition variables) and seizure control in adult patients with pharmacoresistant epilepsies. Patients followed the Modified Atkin's Diet (MAD), with a restriction of 20 g of carbohydrates per day, adequate protein amounts and fats ad libitum for 24 weeks. Fourteen eligible patients were enrolled in the study, however, only eight completed the treatment (four women with an average age of 33.5 ± 9.9 years and four men with an average age of 27.5 ± 9.0 years; p = 0.386). The median of focal impaired awareness seizures decreased from 9.0 (interquartile range [IQR] 4.0-28.0) seizures per month pre-diet to 4.0 (IQR 0.5-11.2) seizures per month in 12 weeks (p = 0.028), i.e. a 55.5% reduction. Total cholesterol (19,711 ± 1373 mg/dL to 28,427 ± 2545 mg/dL; p = 0.016), LDL (131.47 ± 1319 mg/dL to 194.85 ± 20.41 mg/dL; p = 0.037), and non-HDL (140.20 ± 13.04 mg/dL to 219.75 ± 28.53 mg/dL; p = 0.028) levels increased progressively over the intervention period, being significant at 24 weeks (n = 6). A significant reduction in blood glucose (89.70 ± 2.20 mg/dL to 82.62 ± 1.45 mg/dL at week 24, p < 0.001, n = 6), insulin (11.02 ± 1.78 μUI/mL to 6.20 ± 0.71 μUI/mL at week 12, p < 0.001, n = 6) and HOMA-IR index was observed (1.46 ± 0.29 to 0.91 ± 0.23 at week 24, p < 0.001, n = 5). The estimated cardiovascular risk after treatment was low for all patients (less than 10 %). A significant reduction in body weight (76.28 ± 6.62 kg to 69.14 ± 5.63 kg; p < 0.001), body mass index (26.41 ± 1.79 kg/m² to 24.05 ± 1.58 kg/m²; p = 0.001), and waist (87.40 ± 4.98 cm to 78.61 ± 3.94 cm; p < 0.001) and arm circumferences (32.12 ± 1.97 cm to 28.98 ± 1.30 cm; p < 0.001) was observed (n = 8), as well as reduction in fat mass (26.85 ± 3.15 g to 21.54 ± 2.64 g; p < 0.001) and fat free mass (48.01 ± 2.75 g to 46.60 ± 2.29 g; p < 0.001), n = 7. Adverse events were generally mild and treatable, with the following being the most common: headache (50 %), weakness (50 %), and gastrointestinal symptoms (37.5 %). Potentially atherogenic lipid profile changes were observed; however, improved glycemic control and reduced body weight and waist circumference demonstrated an improvement in cardiometabolic parameters. Framingham score and the QRISK3 showed lower cardiovascular disease risk for some of the patients. Our data suggests MAD could be an appropriate therapeutic choice for adults with pharmacoresistant epilepsies.