PMID- 19064531
OWN - NLM
STAT- MEDLINE
DCOM- 20090113
LR  - 20230318
IS  - 1938-3207 (Electronic)
IS  - 0002-9165 (Linking)
VI  - 88
IP  - 6
DP  - 2008 Dec
TI  - Progressive bone mineral content loss in children with intractable epilepsy 
      treated with the ketogenic diet.
PG  - 1678-84
LID - 10.3945/ajcn.2008.26099 [doi]
AB  - BACKGROUND: The ketogenic diet (KD) is a high-fat, low-carbohydrate, and protein 
      diet that effectively treats intractable epilepsy (IE). OBJECTIVE: The purpose of 
      this study was to measure the change in bone mineral content (BMC) in children 
      with IE treated with the KD for 15 mo. DESIGN: Prepubertal children >or=5 y of 
      age with IE were eligible. A 4:1 ketogenic diet was maintained for 15 mo, and 
      whole-body and spine BMCs were measured with dual-energy X-ray absorptiometry. Z 
      scores were generated by comparing the children with IE with a cohort of 847 
      healthy children. Other measurements included demographics, anthropometry, serum 
      25-hydroxyvitamin D (25-OHD), intact parathyroid hormone, electrolytes, and 
      dietary intake. All measurements were performed at baseline and at 3, 6, 12, and 
      15 mo. Longitudinal mixed effects models were used to analyze change in BMC over 
      time. RESULTS: Twenty-five children (9 girls, 16 boys) with IE [age (x +/- SD): 
      7.3 +/- 1.9 y] participated. Growth and bone health status were suboptimal as 
      were serum 25-OHD concentrations and dietary intake of calcium and vitamin D. 
      Whole-body and spine BMC-for-age both declined by 0.6 z score/y and whole-body 
      and spine BMC-for-height declined 0.7 z score/y and 0.4 z score/y, respectively. 
      Height declined 0.5 z score/y. Body mass index (BMI; in kg/m(2)) z score, age, 
      and ambulation were positive predictors of BMC, which declined sharply over 15 mo 
      of KD treatment. CONCLUSION: Bone health in children with IE was poor, 
      particularly for younger nonambulatory children with low BMI status. The KD 
      resulted in progressive loss of BMC. The mechanism is unclear. Further studies 
      are needed.
FAU - Bergqvist, A G Christina
AU  - Bergqvist AG
AD  - Division of Neurology, The Children's Hospital of Philadelphia, Philadelphia, PA 
      19104, USA. bergqvist@email.chop.edu
FAU - Schall, Joan I
AU  - Schall JI
FAU - Stallings, Virginia A
AU  - Stallings VA
FAU - Zemel, Babette S
AU  - Zemel BS
LA  - eng
GR  - K-23 RR16074/RR/NCRR NIH HHS/United States
GR  - UL1-RR-024134/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Clin Nutr
JT  - The American journal of clinical nutrition
JID - 0376027
RN  - 0 (Calcium, Dietary)
RN  - 1406-16-2 (Vitamin D)
RN  - 21343-40-8 (25-Hydroxyvitamin D 2)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - 25-Hydroxyvitamin D 2/blood
MH  - Absorptiometry, Photon/methods
MH  - Body Mass Index
MH  - *Bone Density/drug effects/physiology
MH  - Bone and Bones/*metabolism
MH  - Calcium/blood
MH  - Calcium, Dietary/administration & dosage/metabolism
MH  - Child
MH  - Diet, Ketogenic/*adverse effects
MH  - Epilepsy/complications/*diet therapy
MH  - Female
MH  - Humans
MH  - Ketosis/*metabolism
MH  - Longitudinal Studies
MH  - Male
MH  - Nutritional Status
MH  - Osteoporosis/epidemiology/etiology
MH  - Vitamin D/administration & dosage/blood
EDAT- 2008/12/10 09:00
MHDA- 2009/01/14 09:00
CRDT- 2008/12/10 09:00
PHST- 2008/12/10 09:00 [pubmed]
PHST- 2009/01/14 09:00 [medline]
PHST- 2008/12/10 09:00 [entrez]
AID - S0002-9165(23)23386-9 [pii]
AID - 10.3945/ajcn.2008.26099 [doi]
PST - ppublish
SO  - Am J Clin Nutr. 2008 Dec;88(6):1678-84. doi: 10.3945/ajcn.2008.26099.