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Introduction <p>Ketogenic diet (KD) therapy is effective for refractory epilepsy but significantly impacts carbohydrate and lipid metabolism. We previously encountered a patient who developed diabetes during KD; metabolic abnormalities were undetected by conventional criteria for diabetes, suggesting standard criteria are inapplicable. This study aimed to establish specialized metabolic reference ranges for patients on KD.</p> Methods <p>We retrospectively analyzed laboratory data from 18 pediatric patients with refractory epilepsy treated with KD. Geometric means and reference ranges (mean ± 2SD) were calculated using mixed-effects models to account for repeated measures.</p> Results <p>Before KD, geometric means (reference ranges) were: random plasma glucose (RPG), 96.7 (79.1–118.3) mg/dL; HbA1c (NGSP), 4.76% (4.22–5.36); HbA1c (IFCC), 29 (23–35) mmol/mol; total cholesterol (T-Cho), 159.1 (98.8–256.5) mg/dL; and triglycerides (TG), 107.3 (41.4–277.8) mg/dL. During KD, values were: RPG, 77.6 (59.8–100.6) mg/dL; HbA1c (NGSP), 4.09% (3.58–4.69); HbA1c (IFCC), 21 (16–28) mmol/mol; T-Cho, 184.5 (113.3–300.7) mg/dL; and TG, 155.5 (48.2–501.7) mg/dL. Multiple mixed-effects models showed that KD significantly lowered HbA1c and RPG but increased T-Cho, HDL-Cho, TG, and free fatty acids. Changes in LDL-Cho were not statistically significant.</p> Conclusion <p>KD therapy significantly lowers HbA1c and RPG while increasing lipid profiles. Consequently, impaired glucose tolerance may be masked by “normal” values if conventional criteria are used. To avoid delayed diagnosis, patients on KD should be evaluated using specialized reference ranges specific to their dietary therapy.</p>

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Risks of using standard reference ranges for carbohydrate and lipid metabolism in low-carbohydrate diets: insights from ketogenic diet therapy in children with refractory epilepsy

  • 期刊论文

  • 发表日期：

    2026年5月15日

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  • Katsuyuki Matsui,
  • Mioko Mori,
  • Tomohiro Kumada

摘要

Introduction

Ketogenic diet (KD) therapy is effective for refractory epilepsy but significantly impacts carbohydrate and lipid metabolism. We previously encountered a patient who developed diabetes during KD; metabolic abnormalities were undetected by conventional criteria for diabetes, suggesting standard criteria are inapplicable. This study aimed to establish specialized metabolic reference ranges for patients on KD.

Methods

We retrospectively analyzed laboratory data from 18 pediatric patients with refractory epilepsy treated with KD. Geometric means and reference ranges (mean ± 2SD) were calculated using mixed-effects models to account for repeated measures.

Results

Before KD, geometric means (reference ranges) were: random plasma glucose (RPG), 96.7 (79.1–118.3) mg/dL; HbA1c (NGSP), 4.76% (4.22–5.36); HbA1c (IFCC), 29 (23–35) mmol/mol; total cholesterol (T-Cho), 159.1 (98.8–256.5) mg/dL; and triglycerides (TG), 107.3 (41.4–277.8) mg/dL. During KD, values were: RPG, 77.6 (59.8–100.6) mg/dL; HbA1c (NGSP), 4.09% (3.58–4.69); HbA1c (IFCC), 21 (16–28) mmol/mol; T-Cho, 184.5 (113.3–300.7) mg/dL; and TG, 155.5 (48.2–501.7) mg/dL. Multiple mixed-effects models showed that KD significantly lowered HbA1c and RPG but increased T-Cho, HDL-Cho, TG, and free fatty acids. Changes in LDL-Cho were not statistically significant.

Conclusion

KD therapy significantly lowers HbA1c and RPG while increasing lipid profiles. Consequently, impaired glucose tolerance may be masked by “normal” values if conventional criteria are used. To avoid delayed diagnosis, patients on KD should be evaluated using specialized reference ranges specific to their dietary therapy.