VITAMIN D STATUS IN CHILDREN WITH INTRACTABLE EPILEPSY TREATED WITH THE CLASSIC OR MEDIUM-CHAIN TRIGLYCERIDE (MCT) KETOGENIC DIET
Abstract number :
2.097
Submission category :
4. Clinical Epilepsy
Year :
2009
Submission ID :
9814
Source :
www.aesnet.org
Presentation date :
12/4/2009 12:00:00 AM
Published date :
Aug 26, 2009, 08:12 AM
Authors :
Yeou-mei Liu, M. Zak, V. Chan and E. Donner
Rationale: In 2008, professional pediatrics associations in North America recommended that the minimum vitamin D intake for children be doubled to 400 IU per day. While vitamin D is known to be essential for promoting calcium absorption, maintenance of serum calcium and phosphate concentrations and bone health, it has recently garnered more attention as a supplement for preventative health, including the prevention of some cancers and autoimmune diseases. Anticonvulsant medications put children with epilepsy at an increased risk for vitamin D deficiency. Children treated with the ketogenic diets are at further risk, as these diets are nutritionally incomplete, particularly those in northern climates and with limited sun exposure. The objective of this study is to assess the vitamin D status of children treated with the classic and MCT ketogenic diets in Toronto, Canada. Methods: Fifty-two children, aged 0.5-14 years (mean±SD=5.9±3.3), were treated with a ketogenic diet from January 1998 to May 2009. Thirty-seven children (age: mean±SD=5.1±3.0) were treated with the classic diet and 17 children (age: mean±SD=7.5±3.6) were treated with the MCT diet. Vitamin D status was determined by serum 25-hydroxy vitamin D (25(OH)D) levels. All children received a multivitamin containing 400 IU of vitamin D. Children with a documented vitamin D deficiency prior to or during diet therapy were given an additional 400-1000 IU of vitamin D in order to achieve normal serum levels. Serum levels were measured prior to diet initiation, and at 6, 12, 18, 24 and every 12 months during diet treatment. Results: In 37 children treated with the classic ketogenic diet, the mean serum 25(OH)D prior to initiating the classic ketogenic diet was 62.4 nmol/L (SD=±12.4) and 102.6 nmol/L (SD=±28.0) at follow-up. One child (3%) had a low 25(OH)D level (44 nmol/L) prior to initiating the classic ketogenic diet. At all points of follow-up no child treated with the classic ketogenic diet had a low 25(OH)D level. In 17 children treated with the MCT ketogenic diet, the mean serum 25(OH)D level was 68.7 nmol/L (SD=±26.4) prior to diet initiation and 79.6 nmol/L (SD=±28.8) at follow-up. Three children (18%) had a low 25(OH)D level (mean±SD=44.7±8.3 nmol/L) prior to initiating the MCT diet. At follow-up 2 children (12%) had low 25(OH)D levels (mean±SD=43.5±3.5 nmol/L). Conclusions: The majority of children treated with a ketogenic diet maintained serum 25(OH)D levels within the therapeutic range with vitamin D supplementation. However, children treated with the MCT ketogenic diet had lower serum 25(OH)D levels than those treated with the classic ketogenic diet, despite tailored vitamin D supplementation. This is an unexpected finding, as the MCT diet permits a greater variety of foods and can be more nutritionally complete. Given the recent attention to the role of vitamin D in disease prevention and the increased minimum daily intake recommendations, it is critical that all children with epilepsy be monitored for vitamin D deficiency, particularly those treated with a ketogenic diet.
Clinical Epilepsy