Effect of classic ketogenic diet treatment on lipoprotein subfractions in children and adolescents with refractory epilepsy

Abstract Objective To evaluate the impact of the classic ketogenic diet (KD) on low density lipoprotein (LDL) and high density lipoprotein (HDL) subfractions in children and adolescents with refractory epilepsy. Methods This prospective study recruited epileptic children and adolescents of either se...

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Veröffentlicht in:Nutrition (Burbank, Los Angeles County, Calif.) Los Angeles County, Calif.), 2017-01, Vol.33, p.271-277
Hauptverfasser: de Lima, Patricia Azevedo, Prudêncio, Mariana Baldini, Murakami, Daniela Kawamoto, de Brito Sampaio, Leticia Pereira, Neto, Antônio Martins Figueiredo, Damasceno, Nágila Raquel Teixeira
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Sprache:eng
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Zusammenfassung:Abstract Objective To evaluate the impact of the classic ketogenic diet (KD) on low density lipoprotein (LDL) and high density lipoprotein (HDL) subfractions in children and adolescents with refractory epilepsy. Methods This prospective study recruited epileptic children and adolescents of either sex, whose epilepsy was refractory to treatment with multiple drugs; to be included, the patients had to have an indication for treatment with the KD and be treated as an outpatient. At baseline and after 3 and 6 months of the KD, lipid profile (total cholesterol [TC], triglycerides [TG], low density lipoprotein [LDL-C] cholesterol, and high density lipoprotein [HDL-C] cholesterol), apolipoproteins (APOA-I and APOB), 10 subfractions of HDL, 7 subfractions of LDL, LDL phenotype, and LDL size were analyzed using the Lipoprint system. Results The lipid profile components (TC, TG, LDL-C, HDL-C, APOA-I, and APOB) increased during the 3-month follow-up, and remained consistent after 6 months of treatment. Similarly, non-HDL-C, TC/HDL-C, LDL-C/HDL-C, and APOB/APOA-I ratios, represented atherogenic particles, significantly increased. In contrast, qualitative lipoprotein characteristics progressively changed during the follow-up period. Small LDL subfractions increased, and this profile was related with reduced LDL size (27.3 nm to 26.7 nm). The LDL phenotype became worse; 52.1% of the patients had a non-A phenotype after 6 months of the KD. Small HDL subfractions decreased only after 6 months of the KD. Conclusions KD treatment promotes negative changes in lipoprotein size and phenotype, contributing to atherogenic risk in these patients.
ISSN:0899-9007
1873-1244
DOI:10.1016/j.nut.2016.06.016