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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container_title Nutrition (Burbank, Los Angeles County, Calif.)
container_volume 33
creator de Lima, Patricia Azevedo
Prudêncio, Mariana Baldini
Murakami, Daniela Kawamoto
de Brito Sampaio, Leticia Pereira
Neto, Antônio Martins Figueiredo
Damasceno, Nágila Raquel Teixeira
description 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.
doi_str_mv 10.1016/j.nut.2016.06.016
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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.</description><identifier>ISSN: 0899-9007</identifier><identifier>EISSN: 1873-1244</identifier><identifier>DOI: 10.1016/j.nut.2016.06.016</identifier><identifier>PMID: 27712963</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adolescent ; Adolescent Nutritional Physiological Phenomena ; Adolescents ; Apolipoproteins ; Atherosclerosis - epidemiology ; Atherosclerosis - etiology ; Atherosclerosis - prevention &amp; control ; Atoms &amp; subatomic particles ; Biomarkers - blood ; Body mass index ; Brazil - epidemiology ; Carbohydrates ; Cardiovascular disease ; Child ; Child Nutritional Physiological Phenomena ; Children ; Cholesterol ; Convulsions &amp; seizures ; Diet ; Diet, Atherogenic - adverse effects ; Diet, Ketogenic - adverse effects ; Disease Progression ; Drug dosages ; Drug Resistant Epilepsy - blood ; Drug Resistant Epilepsy - diet therapy ; Drug Resistant Epilepsy - physiopathology ; Dyslipidemia ; Dyslipidemias - etiology ; Dyslipidemias - physiopathology ; Epilepsy ; Female ; Follow-Up Studies ; Gastroenterology and Hepatology ; Genotype &amp; phenotype ; Hormone replacement therapy ; Humans ; Ketogenic diet ; Laboratories ; LDL size ; Lipids ; Lipoprint ; Lipoprotein subfractions ; Lipoproteins, HDL - blood ; Lipoproteins, LDL - blood ; Low density lipoprotein ; Male ; Metabolism ; Particle size ; Plasma ; Prospective Studies ; Proteins ; Risk ; Teenagers</subject><ispartof>Nutrition (Burbank, Los Angeles County, Calif.), 2017-01, Vol.33, p.271-277</ispartof><rights>2016 Elsevier Inc.</rights><rights>Copyright © 2016 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Jan 01, 2017</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c469t-429cfa5188cdc216e978c069146da0e579c83dedd103ec324ec980d2452e1faa3</citedby><cites>FETCH-LOGICAL-c469t-429cfa5188cdc216e978c069146da0e579c83dedd103ec324ec980d2452e1faa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1847428974?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>315,781,785,3551,27929,27930,46000,64390,64392,64394,72474</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27712963$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>de Lima, Patricia Azevedo</creatorcontrib><creatorcontrib>Prudêncio, Mariana Baldini</creatorcontrib><creatorcontrib>Murakami, Daniela Kawamoto</creatorcontrib><creatorcontrib>de Brito Sampaio, Leticia Pereira</creatorcontrib><creatorcontrib>Neto, Antônio Martins Figueiredo</creatorcontrib><creatorcontrib>Damasceno, Nágila Raquel Teixeira</creatorcontrib><title>Effect of classic ketogenic diet treatment on lipoprotein subfractions in children and adolescents with refractory epilepsy</title><title>Nutrition (Burbank, Los Angeles County, Calif.)</title><addtitle>Nutrition</addtitle><description>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.</description><subject>Adolescent</subject><subject>Adolescent Nutritional Physiological Phenomena</subject><subject>Adolescents</subject><subject>Apolipoproteins</subject><subject>Atherosclerosis - epidemiology</subject><subject>Atherosclerosis - etiology</subject><subject>Atherosclerosis - prevention &amp; control</subject><subject>Atoms &amp; subatomic particles</subject><subject>Biomarkers - blood</subject><subject>Body mass index</subject><subject>Brazil - epidemiology</subject><subject>Carbohydrates</subject><subject>Cardiovascular disease</subject><subject>Child</subject><subject>Child Nutritional Physiological Phenomena</subject><subject>Children</subject><subject>Cholesterol</subject><subject>Convulsions &amp; seizures</subject><subject>Diet</subject><subject>Diet, Atherogenic - adverse effects</subject><subject>Diet, Ketogenic - adverse effects</subject><subject>Disease Progression</subject><subject>Drug dosages</subject><subject>Drug Resistant Epilepsy - blood</subject><subject>Drug Resistant Epilepsy - diet therapy</subject><subject>Drug Resistant Epilepsy - physiopathology</subject><subject>Dyslipidemia</subject><subject>Dyslipidemias - etiology</subject><subject>Dyslipidemias - physiopathology</subject><subject>Epilepsy</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Gastroenterology and Hepatology</subject><subject>Genotype &amp; phenotype</subject><subject>Hormone replacement therapy</subject><subject>Humans</subject><subject>Ketogenic diet</subject><subject>Laboratories</subject><subject>LDL size</subject><subject>Lipids</subject><subject>Lipoprint</subject><subject>Lipoprotein subfractions</subject><subject>Lipoproteins, HDL - blood</subject><subject>Lipoproteins, LDL - blood</subject><subject>Low density lipoprotein</subject><subject>Male</subject><subject>Metabolism</subject><subject>Particle size</subject><subject>Plasma</subject><subject>Prospective Studies</subject><subject>Proteins</subject><subject>Risk</subject><subject>Teenagers</subject><issn>0899-9007</issn><issn>1873-1244</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkk2LFDEQhhtR3HH1B3iRgBcvPear0wmCsCzrByx4UM8hm1S7me1JxiStDP55a5xVYQ8iFKQCz1tU1Vtd95TRNaNMvdys09LWHNM1xWDqXrdiehQ941Le71ZUG9MbSseT7lGtG0opM8o87E74ODJulFh1Py6mCXwjeSJ-drVGT26g5S-QMAsRGmkFXNtCQiaROe7yruQGMZG6XE3F-RZzqgT__jrOoUAiLgXiQp6hepRV8j22a1LgF5zLnsAuzrCr-8fdg8nNFZ7cvqfd5zcXn87f9Zcf3r4_P7vsvVSm9ZIbP7mBae2D50yBGbWnyjCpgqMwjMZrESAERgV4wSV4o2ngcuDAJufEaffiWBc7_7pAbXYbsbV5dgnyUi3TAx01Z0z_ByoGgRsWI6LP76CbvJSEgyAlR8m1GSVS7Ej5kmvFJdhdiVtX9pZRezDRbiyaaA8mWorBFGqe3VZerrYQ_ih-u4bAqyMAuLVvEYqtPkLyEGJBM23I8Z_lX99R-zmi3W6-gT3Uv1PYyi21Hw9XdDgilFImBiV-ArV2w3k</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>de Lima, Patricia Azevedo</creator><creator>Prudêncio, Mariana Baldini</creator><creator>Murakami, Daniela Kawamoto</creator><creator>de Brito Sampaio, Leticia Pereira</creator><creator>Neto, Antônio Martins Figueiredo</creator><creator>Damasceno, Nágila Raquel Teixeira</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RQ</scope><scope>7RV</scope><scope>7TS</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88C</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>ASE</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FPQ</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K6X</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M0T</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20170101</creationdate><title>Effect of classic ketogenic diet treatment on lipoprotein subfractions in children and adolescents with refractory epilepsy</title><author>de Lima, Patricia Azevedo ; 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seizures</topic><topic>Diet</topic><topic>Diet, Atherogenic - adverse effects</topic><topic>Diet, Ketogenic - adverse effects</topic><topic>Disease Progression</topic><topic>Drug dosages</topic><topic>Drug Resistant Epilepsy - blood</topic><topic>Drug Resistant Epilepsy - diet therapy</topic><topic>Drug Resistant Epilepsy - physiopathology</topic><topic>Dyslipidemia</topic><topic>Dyslipidemias - etiology</topic><topic>Dyslipidemias - physiopathology</topic><topic>Epilepsy</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Gastroenterology and Hepatology</topic><topic>Genotype &amp; phenotype</topic><topic>Hormone replacement therapy</topic><topic>Humans</topic><topic>Ketogenic diet</topic><topic>Laboratories</topic><topic>LDL size</topic><topic>Lipids</topic><topic>Lipoprint</topic><topic>Lipoprotein subfractions</topic><topic>Lipoproteins, HDL - blood</topic><topic>Lipoproteins, LDL - blood</topic><topic>Low density lipoprotein</topic><topic>Male</topic><topic>Metabolism</topic><topic>Particle size</topic><topic>Plasma</topic><topic>Prospective Studies</topic><topic>Proteins</topic><topic>Risk</topic><topic>Teenagers</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>de Lima, Patricia Azevedo</creatorcontrib><creatorcontrib>Prudêncio, Mariana Baldini</creatorcontrib><creatorcontrib>Murakami, Daniela Kawamoto</creatorcontrib><creatorcontrib>de Brito Sampaio, Leticia Pereira</creatorcontrib><creatorcontrib>Neto, Antônio Martins Figueiredo</creatorcontrib><creatorcontrib>Damasceno, Nágila Raquel Teixeira</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Career &amp; 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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.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>27712963</pmid><doi>10.1016/j.nut.2016.06.016</doi><tpages>7</tpages></addata></record>
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source MEDLINE; Access via ScienceDirect (Elsevier); ProQuest Central UK/Ireland
subjects Adolescent
Adolescent Nutritional Physiological Phenomena
Adolescents
Apolipoproteins
Atherosclerosis - epidemiology
Atherosclerosis - etiology
Atherosclerosis - prevention & control
Atoms & subatomic particles
Biomarkers - blood
Body mass index
Brazil - epidemiology
Carbohydrates
Cardiovascular disease
Child
Child Nutritional Physiological Phenomena
Children
Cholesterol
Convulsions & seizures
Diet
Diet, Atherogenic - adverse effects
Diet, Ketogenic - adverse effects
Disease Progression
Drug dosages
Drug Resistant Epilepsy - blood
Drug Resistant Epilepsy - diet therapy
Drug Resistant Epilepsy - physiopathology
Dyslipidemia
Dyslipidemias - etiology
Dyslipidemias - physiopathology
Epilepsy
Female
Follow-Up Studies
Gastroenterology and Hepatology
Genotype & phenotype
Hormone replacement therapy
Humans
Ketogenic diet
Laboratories
LDL size
Lipids
Lipoprint
Lipoprotein subfractions
Lipoproteins, HDL - blood
Lipoproteins, LDL - blood
Low density lipoprotein
Male
Metabolism
Particle size
Plasma
Prospective Studies
Proteins
Risk
Teenagers
title Effect of classic ketogenic diet treatment on lipoprotein subfractions in children and adolescents with refractory epilepsy
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