Ketogenic diet

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The ketogenic diet is a very high fat diet that relies on inducing a state of ketosis. It is most commonly used for the treatment of pediatric epilepsy, to lose body fat, and is also under early research for the treatment of cancer (see External Links). The diet typically provides 3-4 grams of fat for every 1 gram of carbohydrate and protein combined. A likely ketogenic diet comprises about 88% fat, 10% proteins and 2% of carbohydrate energy.


The diet prescribes foods high in fat, and heavily restricts carbohydrate intake. As fats become the body's primary source of metabolic energy, ketones accumulate in the brain, which can alleviate epileptic symptoms. The diet is often perceived as more effective in children than adults, particularly when anticonvulsant drug therapy is ineffective (20%-30% of patients) or contraindicated, however, data from the 1920s and 1930s, as well as recently, shows similar results. However, the ketogenic diet is more restrictive for adults.

Foods used in the diet include high-triglyceride dairy products (e.g., butter, cream), mayonnaise and peanut butter. Carbohydrates, found in breads and starches, are eliminated in the diet, and liquid and calorie intake are often restricted as well in order to aid ketone accumulation. Though superficially similar, this is not the same as the Atkins diet. This has been used as well for some patients with epilepsy, as well as a low-glycemic index diet. [1] Possible long-term side effects of the diet include:

The diet is typically supplemented with calcium, vitamin D, iron, and folic acid.

Among the possible reasons the diet has not been widely adopted by doctors:

  • Lack of double blind studies. (see below)
  • Concerns about patient compliance with diet
  • Concerns about potential nutritional deficiency
  • It is possible that early anti-convulsants were statistically more effective than diets as treatment for new patients but that they worked on separate population groups.
  • Lack of knowledge and a dietitian to help manage children on the diet

Scientific studies

A study conducted by Johns Hopkins reported that 50% of those patients starting the ketogenic diet reported a decrease in seizures of 50% or more, with 29% of patients reporting a 90% reduction in symptoms; these patients had previously tried an average of six anticonvulsant drugs. The success rate on patients who responded to anticonvulsants was not measured in that study (and appears to be lacking in other recent studies as well - there appears to be reluctance to try the diet on subjects except as a last resort). The success rate of the diet on those who are successfully treated with anti-convulsants may be higher, lower, or the same as those who do not respond. It may be that the diet and anti-convulsants are effective on different segments of the population. This has continued to be the statistics today, with approximately half of patients having at least half of their seizures improve.

The ketogenic diet has been reported to work in cases where multiple epilepsy drugs have failed. There may also be cases where the ketogenic diet has failed and epilepsy drugs succeeded. When one epilepsy drug fails, there is a high likelihood that other drugs will also fail. When the diet works, the response is often rapid and dramatic.

Related studies regarding the safety of low-carborhydrate, ketogenic diets in general can be found here.

Double blind studies

Lack of double blind studies is an issue preventing wider acceptance by the medical profession. Reliance on proper studies rather than anecdotal evidence or flawed studies is important. Double blind studies help eliminate:

  • Placebo effect
  • Spontaneous remission
  • Researchers' expectations prejudicing their observations
  • Researchers inadvertently prejudicing patients through body language, tone of voice, etc.

A double blind study of the Ketogenic Diet has been completed and is being analyzed.

Research and variants

The diet usually referred to in the context of epilepsy treatment is the classic 4:1 fat to protein plus carbohydrate ratio Johns Hopkins Hospital protocol,[1],[2] but there is more than one type of ketogenic diet. There's also the Sanggye Paik Hospital protocol (also 4:1) developed by Drs. Kim and Park, the medium chain triglyceride diet,[3] the Atkins diet,[4] and supplementation with polyunsaturated fats.[5]

Kim Dong Wook and colleagues at the Inje University Sanggye Paik Hospital Epilepsy Center found that patients treated with the nonfasting, introduce high-fat foods to existing diet gradually protocol (August 1999-February 2001) achieved urinary ketosis just as fast, with just as much improvement in seizures, as patients using the initial fasting Johns Hopkins protocol (July 1995-July 1999), with 1/6 the dehydration and a shorter average hospital stay.[6] A team led by Dr. Inna I. Vaisleib reported that same year that the 4:1 diet could also be done outpatient and with no caloric restrictions.[7] According to Freeman et al, the ketogenic diet reduces atonic and myoclonic seizures by over 50% immediately.[8] </ref>-->

Like any other therapeutic intervention, the ketogenic diet is not without adverse effects. In 2004, Drs. Hoon Chul Kang, Da Eun Chung, Dong Wook Kim, and Heung Dong Kim reported that out of 129 patients who were on the diet at the Epilepsy Center at Inje University Sanggye Paik Hospital between July 1995 and October 2001, 46.5% experienced—in the 4-week trial period—dehydration, 38.8% experienced gastrointestinal symptoms (diarrhea (32.6%), nausea/vomiting (27.9%), and constipation (2.3%)), hypertriglyceridemia in 27.1%, hyperuricemia in 26.4%, hypercholesterolemia (14.7%), infections (pneumonia, cystitis, etc) in 9.3%, symptomatic hypoglycemia (7.0%), hypoproteinemia (5.4%), hypomagnesemia (4.7%), repetitive hyponatremia (4.7%), HDL hypocholesterolemia (3.9%), lipoid pneumonia due to aspiration (2.3%), hepatitis (2.3%), acute pancreatitis and persistent metabolic acidosis.[9] After those first four weeks, the side effects, in descending order of prevalence, were gastrointestinal discomfort (27.9%), infectious disease (20.9%), hypertriglyceridemia (20.2%), hypercholesterolemia (19.4%), osteopenia (14.7%), hypomagnesemia (10.9%), hyperuricemia (7.8%), hepatitis (5.4%), lipoid pneumonia due to aspiration (4.7%), hypoproteinemia (3.9%), kidney stone(s) (3.1%), iron-deficiency anemia (1.6%), secondary hypocarnitinemia (1.6%), HDL hypocholesterolemia (0.8%), symptomatic hypoglycemia (0.8%), hydronephrosis (0.8%), and cardiomyopathy (0.8%).[10] The person who had cardiomyopathy died, along with three other people, one with lipoid pneumonia and the other two with sepsis.[11]

The majority of side effects of the diet are transient and can be addressed without diet discontinuation. Kidney stones can be treated with extra hydration and oral citrates. Hypercholesterolemia is improved with lowering the diet ratio and substituting higher amounts of polyunsaturated fats. Weight loss can be corrected with extra calories.

Recent work on the mechanism of action for ketogenic diet as a treatment for epilepsy have investigated the role of glycolysis in the disease [2]. The glycolytic inhibitor 2-Deoxy-D-glucose has been proposed as a mimic for the ketogenic diet, and shows great promise as a new anti-epileptic drug.


  1. James Wheless (1996). "A Practical Approach". Special Meeting: Controversies in Epilepsy - The Ketogenic Diet. Retrieved 22 February. Unknown parameter |accessyear= ignored (|access-date= suggested) (help); Check date values in: |accessdate= (help)
  2. Vining, Eileen P. G. (1998). "A Multicenter Study of the Efficacy of the Ketogenic Diet". Archives of Neurology. 55 (11): 1433–7. PMID 9823827. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  3. P. R. Huttenlocher (1971). "Medium-chain triglycerides as a therapy for intractable childhood epilepsy". Neurology. 21 (11): 1097–103. PMID 5166216. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  4. Kossoff, Eric H. (23 December, 2003). "Efficacy of the Atkins diet as therapy for intractable epilepsy". Neurology. 61 (12): 1789–91. PMID 14694049. Unknown parameter |coauthors= ignored (help); Check date values in: |date= (help)
  5. Yuen, Alan W.C. (2005). "Omega-3 fatty acid supplementation in patients with chronic epilepsy: A randomized trial". Epilepsy & Behavior. 7 (2): 253–8. doi:10.1016/j.yebeh.2005.04.014. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  6. Dong Wook, Kim. "Benefits of the Nonfasting Ketogenic Diet Compared With the Initial Fasting Ketogenic Diet". Pediatrics. 114 (6): 1627–30. doi:10.1542/peds.2004-1001. Unknown parameter |coauthors= ignored (help)
  7. Vaisleib, Inna I. (2004). "Ketogenic diet: Outpatient initiation, without fluid, or caloric restrictions". Pediatric Neurology. 31 (3): 198–202. doi:10.1016/j.pediatrneurol.2004.03.007. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  8. Freeman JM, Vining EP (1999). "Seizures decrease rapidly after fasting: preliminary studies of the ketogenic diet". Archives of Pediatrics & Adolescent Medicine. 153 (9): 946–9. PMID 10482210.
  9. Kang HC, Chung da E, Kim DW, Kim HD (2004). "Early- and late-onset complications of the ketogenic diet for intractable epilepsy". Epilepsia. 45 (9): 1116–23. PMID 15329077. Fulltext options
  10. see Kang et al., 2004.
  11. see Kang et al., 2004.

See also

External links


de:Ketogene Diät id:Diet ketogenik

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