Severe Hyperlipidemia With LDL Cholesterol of 393 Milligrams per Decilitre After 7 Months of High Fat Ketogenic Diet: A Rare Case Report

Introduction: Ketogenic diet (KD) is now a popular weight-loss diet with other proclaimed health benefits. KD is largely safe in the short-term especially if done under medical supervision to monitor for well-described side effects like hyperlipidemia among others. We report a case of KD-induced drastic elevation in LDL cholesterol. Clinical Case: An otherwise healthy 41-year-old male with obesity and a BMI of 35.8 kg/m(2) followed KD to help with weight loss. His lipid panel 18 months prior to initiation of KD showed total cholesterol (TC) 171 mg/dL (reference <200 preferred), HDL cholesterol (HDL-C) 49 mg/dL (reference >60 preferred), LDL cholesterol (LDL-C) 99 mg/dL (reference <100 optimal), and a triglyceride (TG) 145 mg/dL (reference <200). During his KD journey, he lost 40 pounds and his BMI became 29.5 kg/m(2) after seven months. While on KD, he reported more mental clarity, improved sleep quality, higher energy level, and complete resolution of chronic cystic acne. Seven months after starting KD, his lipid panel showed TC 488.7 mg/dL, HDL-C 54.4 mg/dL, LDL-C 393 mg/dL, VLDL-C 41.5 mg/dL, and triglyceride 207.5 mg/dL. Lipid panel was repeated in 2 days to exclude a possible laboratory error but it confirmed the previous result and repeat LDL-C was 380 mg/dL. Fasting plasma glucose (FPG) was 91 mg/dL. HbA1c was normal at 5.0%. Uric acid was elevated at 8.9 mg/dL (reference 3.4–7.0). High sensitivity C-reactive protein was not elevated at 0.13 mg/dL (reference <0.5). Total 25 hydroxy-vitamin D level was normal at 43.9 ng/mL (reference 30–100). CBC, renal function, and liver function tests were all normal. Since the patient declined statin therapy, he was counseled to decrease saturated fat (e.g. animal-based) intake and to liberalize his carbohydrate intake (i.e. 30% of total calorie intake instead of his baseline of 5–10%). Two weeks after doing so, lipid panel was remarkable for TC 371.2 mg/dL, HDL-C 49.7 mg/dL, LDL-C 279.0 mg/dL, VLDL-C 42.26 mg/dL and TG 211.3 mg/dL. Six weeks from the initial lipid panel, repeat testing showed TC 266.2 mg/dL, HDL-C 54.4 mg/dL, LDL-C 190.0 mg/dL, VLDL-C 21.64 mg/dL and TG 108.2 mg/dL. The patient remained without any major symptoms, namely no symptoms of cardiovascular disease. Conclusion: To the best of our knowledge, our patient had the highest reported KD-induced increase in LDL-C (297% increase) despite normal baseline and no history of familial hypercholesterolemia. Dietary modification alone resulted in 29% decrease in 2 weeks and 52% decrease in six weeks. A limitation to this case report is the lack of lipid panel subfractionation as previous studies showed KD to result in a decrease in small LDL particles (atherogenic) and an increase in large LDL particles (non-atherogenic). More research is needed on the long-term health consequences of KD. Despite guidelines on how to manage KD-induced hyperlipidemia are greatly needed, they are lacking.