Information about Ketogenic Diet
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.
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:
Among the possible reasons the diet has not been widely adopted by doctors:
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.
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]-->
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.
..... Click the link for more information.
The double blind method is an important part of the scientific method, used to prevent research outcomes from being 'influenced' by either the placebo effect or the observer bias.
..... Click the link for more information.
The double blind method is an important part of the scientific method, used to prevent research outcomes from being 'influenced' by either the placebo effect or the observer bias.
..... Click the link for more information.
..... Click the link for more information.
Description
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:
- kidney stones
- abnormal liver function
- high cholesterol
- weight loss
- dehydration
- bone thinning
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.
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]-->
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.
Footnotes
1. ^ James Wheless (1996). A Practical Approach. Special Meeting: Controversies in Epilepsy - The Ketogenic Diet. Retrieved on 22 February, 2006.
2. ^ Vining, Eileen P. G.; John M. Freeman, MD; Karen Ballaban-Gil, MD; Carol S. Camfield, MD; Peter R. Camfield, MD; Gregory L. Holmes, MD; Shlomo Shinnar, MD, PhD; Robert Shuman, MD; Edwin Trevathan, MD; James W. Wheless, MD; and The Ketogenic Diet Multi-Center Study Group (November 1998). "A Multicenter Study of the Efficacy of the Ketogenic Diet". Archives of Neurology 55 (11): 1433-7. PubMed.
3. ^ P. R. Huttenlocher; A. J. Wilbourn and J. M. Signore (November 1971). "Medium-chain triglycerides as a therapy for intractable childhood epilepsy". Neurology 21 (11): 1097-103. PubMed.
4. ^ Kossoff, Eric H.; Gregory L. Krauss, Jane R. McGrogan and John M. Freeman (23 December, 2003). "Efficacy of the Atkins diet as therapy for intractable epilepsy". Neurology 61 (12): 1789-91. PubMed.
5. ^ Yuen, Alan W.C.; Josemir W. Sander, Dominique Fluegel, Philip N. Patsalos, Gail S. Bell, Tony Johnson and Matthias J. Koepp (September 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.
6. ^ Dong Wook, Kim; Hoon Chul Kang, Jung Chae Park, and Heung Dong 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.
7. ^ Vaisleib, Inna I.; Jeffrey R. Buchhalter and Mary L. Zupanc (September 2004). "Ketogenic diet: Outpatient initiation, without fluid, or caloric restrictions". Pediatric Neurology 31 (3): 198-202. doi:10.1016/j.pediatrneurol.2004.03.007.
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. PubMed.
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.
2. ^ Vining, Eileen P. G.; John M. Freeman, MD; Karen Ballaban-Gil, MD; Carol S. Camfield, MD; Peter R. Camfield, MD; Gregory L. Holmes, MD; Shlomo Shinnar, MD, PhD; Robert Shuman, MD; Edwin Trevathan, MD; James W. Wheless, MD; and The Ketogenic Diet Multi-Center Study Group (November 1998). "A Multicenter Study of the Efficacy of the Ketogenic Diet". Archives of Neurology 55 (11): 1433-7. PubMed.
3. ^ P. R. Huttenlocher; A. J. Wilbourn and J. M. Signore (November 1971). "Medium-chain triglycerides as a therapy for intractable childhood epilepsy". Neurology 21 (11): 1097-103. PubMed.
4. ^ Kossoff, Eric H.; Gregory L. Krauss, Jane R. McGrogan and John M. Freeman (23 December, 2003). "Efficacy of the Atkins diet as therapy for intractable epilepsy". Neurology 61 (12): 1789-91. PubMed.
5. ^ Yuen, Alan W.C.; Josemir W. Sander, Dominique Fluegel, Philip N. Patsalos, Gail S. Bell, Tony Johnson and Matthias J. Koepp (September 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.
6. ^ Dong Wook, Kim; Hoon Chul Kang, Jung Chae Park, and Heung Dong 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.
7. ^ Vaisleib, Inna I.; Jeffrey R. Buchhalter and Mary L. Zupanc (September 2004). "Ketogenic diet: Outpatient initiation, without fluid, or caloric restrictions". Pediatric Neurology 31 (3): 198-202. doi:10.1016/j.pediatrneurol.2004.03.007.
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. PubMed.
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
- Ketogenic Diet Ketones charitable donation
- Epilepsy Action: The Ketogenic Diet
- The Ketogenic Diet Johns Hopkins
- Ketogenic Diet for people with ALS - A recent study (April 4th, 2006) by Mount Sinai School of Medicine shows KD diet may prevent progression of ALS
- NICUS: Ketogenic Diet: Fact or Fiction?
- MATTHEWS FRIENDS : An online ketogenic diet support group
- Can a High-Fat Diet Beat Cancer? Monday, Sep. 17, 2007 By Richard Friebe, Time magazine
- "The calorically restricted ketogenic diet, an effective alternative therapy for malignant brain cancer" in Nutrition and Metabolism, 2007
- Ketogenesis, Ketogenic Diet, And Prostate Cancer Progression, Stephen Friedland, Duke University Medical Center
- Targeting energy metabolism in brain cancer: review and hypothesis, Thomas N Seyfried, Purna Mukherjee, Biology Department, Boston College, Chestnut Hill, MA 02467, USA
- Brain Cancer - Seyfried Lab, Boston College
- Ketogenic Diet Prevents Seizures By Enhancing Brain Energy Production, Increasing Neuron Stability, Science Daily, November 2005
Studies
- Abstract: Clinical efficacy of the ketogenic diet.
- Abstract: The ketogenic diet in children, adolescents and young adults with refractory epilepsy: an Italian multicentric experience.
- Abstract: Implementing a ketogenic diet based on medium-chain triglyceride oil in pediatric patients with cancer., Nebeling LC, Lerner E.
- Abstract Ketogenic treatment reduces deleted mitochondrial DNAs in cultured human cells
Ketosis (IPA pronunciation: [ki'tosɪs]) is a stage in metabolism occurring when the liver converts fat into fatty acids and ketone bodies which can be used by the body for energy. It was identified by Dr.
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Epilepsy
Classification & external resources
ICD-10 G 40. -G 41.
ICD-9 345
DiseasesDB 4366
MedlinePlus 000694
eMedicine neuro/415
MeSH D004827
Epilepsy
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Classification & external resources
ICD-10 G 40. -G 41.
ICD-9 345
DiseasesDB 4366
MedlinePlus 000694
eMedicine neuro/415
MeSH D004827
Epilepsy
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Fat
Fat may refer to:- Fat, a group of compounds that are generally soluble in organic solvents and largely insoluble in water
- Adipose tissue, an anatomical term for loose connective tissue composed of adipocytes
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In animals, the brain or encephalon (Greek for "in the skull"), is the control center of the central nervous system, responsible for behavior. The brain is located in the head, protected by the skull and close to the primary sensory apparatus of vision, hearing,
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In medicine, a contraindication is a condition or factor that increases the risks involved in using a particular drug, carrying out a medical procedure or engaging in a particular activity.
The opposite of contraindication is indication.
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The opposite of contraindication is indication.
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Triglyceride (more properly known as triacylglycerol or triacylglyceride
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Butter is a dairy product, made by churning fresh or fermented cream or milk. Butter is used as a spread and a condiment, as well as in cooking applications such as baking, sauce making, and frying.
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Cream (from Greek chrisma) is a dairy product that is composed of the higher-butterfat layer skimmed from the top of milk before homogenization. In un-homogenized milk, over time, the lighter fat rises to the top.
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Mayonnaise (or Mayo in its abbreviated form) is a thick sauce made primarily from vegetable oil and egg yolks.[1] Whitish-yellow in color, it is a stable emulsion formed from the oil and the yolks and is generally flavored with mustard, lemon juice and/or vinegar,
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fougasse or as fouace in the rest of southern France. It is usually seasoned with olive oil and herbs, and often either topped with cheese or stuffed with meat or vegetables. Focaccia doughs are similar in style and texture to pizza doughs.
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A calorie is a unit of measurement for energy. Calorie is French and derives from the Latin calor (heat). In most fields, it has been replaced by the joule, the SI unit of energy.
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The Atkins Nutritional Approach, popularly known as the Atkins Diet or just Atkins, is the most marketed and well-known low-carbohydrate diet. It was adapted by Dr.
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Kidney stone
Classification & external resources
Ultrasonic instrument and kidney stone
ICD-10 N 20.0
ICD-9 592.0
DiseasesDB 11346
MedlinePlus 000458
eMedicine med/1600 Kidney stones, or Renal calculi
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Classification & external resources
Ultrasonic instrument and kidney stone
ICD-10 N 20.0
ICD-9 592.0
DiseasesDB 11346
MedlinePlus 000458
eMedicine med/1600 Kidney stones, or Renal calculi
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Low-density lipoprotein (LDL) belongs to the lipoprotein particle family. Its size is approx. 22 nm but since LDL particles contain a changing number of fatty acids they actually have a mass and size distribution.
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MeSH D015431 Weight loss, in the context of medicine or health or physical fitness, is a reduction of the total body weight, due to a mean loss of fluid, body fat or adipose tissue and/or lean mass, namely bone mineral deposits, muscle, tendon and other connective tissue.
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Dehydration
Classification & external resources
ICD-10 E 86.
ICD-9 276.5
Dehydration (hypohydration) is the removal of water (hydro in ancient Greek) from an object.
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Classification & external resources
ICD-10 E 86.
ICD-9 276.5
Dehydration (hypohydration) is the removal of water (hydro in ancient Greek) from an object.
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Calcium (IPA: /ˈkalsiəm/) is the chemical element in the periodic table that has the symbol Ca and atomic number 20. It has an atomic mass of 40.078.
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Vitamin D is a group of fat-soluble prohormones, the two major forms of which are vitamin D2 (or ergocalciferol) and vitamin D3 (or cholecalciferol).[1] The term vitamin D also refers to metabolites and other analogues of these substances.
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3, 4, 6
(amphoteric oxide)
Electronegativity 1.83 (Pauling scale)
Ionization energies
(more) 1st: 762.5 kJmol−1
2nd: 1561.9 kJmol−1
3rd: 2957 kJmol−1
Atomic radius 140 pm
Atomic radius (calc.
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(amphoteric oxide)
Electronegativity 1.83 (Pauling scale)
Ionization energies
(more) 1st: 762.5 kJmol−1
2nd: 1561.9 kJmol−1
3rd: 2957 kJmol−1
Atomic radius 140 pm
Atomic radius (calc.
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Folic acid and folate (the anion form) are forms of the water-soluble Vitamin B9. These occur naturally in food and can also be taken as supplements. Folate gets its name from the Latin word folium ("leaf").
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For the communication paradox, see .
The double blind method is an important part of the scientific method, used to prevent research outcomes from being 'influenced' by either the placebo effect or the observer bias.
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355:1991-2002.
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For the communication paradox, see .
The double blind method is an important part of the scientific method, used to prevent research outcomes from being 'influenced' by either the placebo effect or the observer bias.
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Placebo effect is the term applied by medical science to the therapeutical and healing effects of inert medicines and/or ritualistic or faith healing manipulations.[1] [2].
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Spontaneous remission is a common term in medicine, it is defined as recoveries without reason or cause.[1] Spontaneous remission are usual in many health disorders [2] and are more commonplace than it is generally assumed[1]
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Fat
Fat may refer to:- Fat, a group of compounds that are generally soluble in organic solvents and largely insoluble in water
- Adipose tissue, an anatomical term for loose connective tissue composed of adipocytes
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Proteins are large organic compounds made of amino acids arranged in a linear chain and joined together by peptide bonds between the carboxyl and amino groups of adjacent amino acid residues.
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