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Impact of the ketogenic diet on linear growth in children: a single-center retrospective analysis of 34 cases
ОглавлениеFerraris C1, Guglielmetti M1, Pasca L2,3, De Giorgis V2, Ferraro OE3, Brambilla I4, Leone A5, De Amicis R5, Bertoli S5, Veggiotti P6,7, Tagliabue A1
1Human Nutrition and Eating Disorder Research Center, Department of Public Health, Experimental and Forensic Medicine, University of Pavia, Pavia, Italy; 2Department of Child Neurology and Psychiatry, IRCCS Mondino Foundation, Pavia, Italy; 3Unit of Biostatistics and Clinical Epidemiology, Department of Public Health, Experimental and Forensic Medicine, University of Pavia, Pavia, Italy; 4Department of Pediatrics, Fondazione I.R.C.C.S. Policlinico San Matteo, University of Pavia, Pavia, Italy; 5International Center for the Assessment of Nutritional Status (ICANS), Department of Food Environmental and Nutritional Sciences (DeFENS), University of Milan, Milan, Italy; 6Pediatric Neurology Unit, Vittore Buzzi Hospital, Milan, Italy; 7Biomedical and Clinical Sciences Department, Luigi Sacco Hospital, University of Milan, Milan, Italy
Nutrients 2019;11:1442
Abstract: Data on the impact of the ketogenic diet (KD) on children’s growth remain controversial. Here, we retrospectively investigated the occurrence of linear growth retardation in 34 children (47% males; age range: 2–17 years) diagnosed with drug-resistant epilepsy (n = 14) or glucose transporter type 1 deficiency syndrome (n = 20) who had been treated with the KD for 12 months. The general characteristics of children with and without growth retardation were also compared. All participants received a full-calorie, traditional KD supplemented with vitamins, minerals, and citrate. Most children (80%; 11/14 in the drug-resistant epilepsy subgroup and 16/20 in the glucose transporter type 1 deficiency syndrome subgroup) treated with the KD did not show growth retardation at 12 months. Although participants with and without delay of growth did not differ in terms of baseline clinical characteristics, dietary prescriptions, or supplementation patterns, marked ketosis at 12 months tended to occur more frequently in the latter group. Altogether, our results indicate that growth retardation may occur in a minority of children treated with the KD. However, further research is required to identify children at risk and to clarify how increased ketones levels may affect endocrine pathways regulating growth during KD administration.
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Comments | Even after the present study, the question “does ketogenic diet interfere with children’s growth?” remains without a proper answer. The prospective nature of this study: mixed population, number of patients in each group, and the different age groups as well as the Tanner stage, make it difficult to draw definite conclusions from the results. So, I agree with the authors that prospective big studies are needed to answer this important question and not just for patients with drug-resistant epilepsy or glucose transporter type 1 deficiency syndrome. Many children in the world are trying different degrees of ketogenic diets for off-labeled indications, and their caregivers should know what it does to their growth during childhood and adolescence. |