Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/17710
Title: The effect of the ketogenic diet on the developing skeleton.
Austin Authors: Simm, Peter J;Bicknell-Royle, Jillian;Lawrie, Jock;Nation, Judy;Draffin, Kellie;Stewart, Karen G;Cameron, Fergus J;Scheffer, Ingrid E ;Mackay, Mark T
Affiliation: Royal Children's Hospital Melbourne, Australia
Murdoch Childrens Research Institute, Melbourne, Australia
Department of Nutrition and Dietetics, Austin Health, Heidelberg, Victoria, Australia
Department of Paediatrics, Austin Health, Heidelberg, Victoria, Australia
Department of Paediatrics, University of Melbourne, Australia
Department of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia
Issue Date: Oct-2017
Date: 2017-07-26
Publication information: Epilepsy research 2017; 136: 62-66
Abstract: The ketogenic diet (KD) is a medically supervised, high fat, low carbohydrate and restricted protein diet which has been used successfully in patients with refractory epilepsy. Only one published report has explored its effect on the skeleton. We postulated that the KD impairs skeletal health parameters in patients on the KD. Patients commenced on the KD were enrolled in a prospective, longitudinal study, with monitoring of Dual-energy X-ray absorptiometry (DXA) derived bone parameters including bone mineral content and density (BMD). Areal BMD was converted to bone mineral apparent density (BMAD) where possible. Biochemical parameters, including Vitamin D, and bone turnover markers, including osteocalcin, were assessed. Patients were stratified for level of mobility using the gross motor functional classification system (GMFCS). 29 patients were on the KD for a minimum of 6 months (range 0.5-6.5 years, mean 2.1 years). There was a trend towards a reduction in lumbar spine (LS) BMD Z score of 0.1562 (p=0.071) per year and 20 patients (68%) had a lower BMD Z score at the end of treatment. While less mobile patients had lower baseline Z scores, the rate of bone loss on the diet was greater in the more mobile patients (0.28 SD loss per year, p=0.026). Height adjustment of DXA data was possible for 13 patients, with a mean reduction in BMAD Z score of 0.19 SD. Only two patients sustained fractures. Mean urinary calcium-creatinine ratios were elevated (0.77), but only 1 patient developed renal calculi. Children on the KD exhibited differences in skeletal development that may be related to the diet. The changes were independent of height but appear to be exaggerated in patients who are ambulant. Clinicians should be aware of potential skeletal side effects and monitor bone health during KD treatment. Longer term follow up is required to determine adult/peak bone mass and fracture risk throughout life.
URI: https://ahro.austin.org.au/austinjspui/handle/1/17710
DOI: 10.1016/j.eplepsyres.2017.07.014
ORCID: 0000-0002-2311-2174
Journal: Epilepsy research
PubMed URL: 28778055
Type: Journal Article
Subjects: Bone density
Ketosis
Mobility
Appears in Collections:Journal articles

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