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2.
Int J Mol Sci ; 22(10)2021 May 15.
Article in English | MEDLINE | ID: mdl-34063366

ABSTRACT

The high-fat, low-carbohydrate (ketogenic) diet has grown in popularity in the last decade as a weight loss tool. Research into the diet's effects on the body have revealed a variety of other health benefits. The use of exogenous ketone supplements to confer the benefits of the diet without strict adherence to it represents an exciting new area of focus. Synthetic ketogenic compounds are of particular interest that has received very little emphasis and is an untapped area of focus for chemical synthesis. In this review, we summarize the chemical basis for ketogenicity and opportunities for further advancement of the field.


Subject(s)
Diet, Ketogenic , Dietary Supplements , Ketone Bodies , Diet, Ketogenic/history , Dietary Fats/pharmacology , Energy Metabolism , Epilepsy/diet therapy , Glycolysis , History, Ancient , Humans , Ketone Bodies/metabolism , Ketosis/chemically induced
4.
Curr Nutr Rep ; 8(4): 340-346, 2019 12.
Article in English | MEDLINE | ID: mdl-31713719

ABSTRACT

PURPOSE OF REVIEW: To review the available literature/evidence on low carbohydrate/high fat (LCHF) and low carbohydrate ketogenic (LCKD) diets' effects on human athletic performance and to provide a brief review of the physiology and history of energy systems of exercise. RECENT FINDINGS: Multiple studies have been conducted in an attempt to answer this question, many within the last 3-5 years. Studies are heterogenous in design, intervention, and outcome measures. Current available data show that LCHF and LCKD do not significantly enhance or impair performance in endurance or strength activities. However, there is a trend towards improved body composition (greater percent lean body mass) across multiple studies. While this may not translate to enhanced performance in the primarily laboratory conditions in the reviewed studies, there could be a benefit in sports in which an athlete's strength-to-weight ratio is a significant determinant of outcome.


Subject(s)
Athletes , Athletic Performance , Diet, Ketogenic , Body Composition , Diet, Carbohydrate-Restricted , Diet, Ketogenic/history , History, 20th Century , History, 21st Century , Humans , Nutritional Status , Physical Endurance , Sports
5.
Epilepsy Behav ; 101(Pt A): 106588, 2019 12.
Article in English | MEDLINE | ID: mdl-31677579

ABSTRACT

In the ketogenic diet (KD) history, Wilder is often mentioned as the first author to report on the use of KD for patients with epilepsy. Our article aimed to understand how Wilder formulated the hypothesis of the KD effectiveness for patients with epilepsy, and how the KD was used and spread in the 1920s. In 1921, Wilder published two articles on the effects of ketonemia on epilepsy. He first reported on the interest of fasting for patients with epilepsy, suggesting that the benefits of fasting on seizures might be dependent on ketonemia. He then hypothesized that equally good results could be obtained with a KD, very rich in fat and very low in carbohydrate, which would provoke ketogenesis, and observed the effects of this diet on three patients for the first time. Following the publication of Wilder articles, 9 papers on KD were published during the 1920s, involving more than 400 patients with epilepsy. Ketogenic diet therapies (KDT) are now evidence-based treatments of epilepsy. Available experimental data do not confirm the role of ketosis as the unique mechanism of the KD. The KD is still explored to understand all the underlying mechanisms.


Subject(s)
Diet, Ketogenic , Epilepsy/diet therapy , Diet, Ketogenic/history , Diet, Ketogenic/methods , History, 20th Century , Humans , Seizures/diet therapy
6.
Epilepsy Behav ; 94: 277-280, 2019 05.
Article in English | MEDLINE | ID: mdl-30999258

ABSTRACT

We analyzed the article of Guelpa & Marie, published in 1911 and often quoted in the history of dietary treatment, as the basis for the use of ketogenic diet to mimic fasting. In this paper, the authors treated 21 patients with a diet consisting of daily administration of 30 g of sodium sulphate for 4 days, with unlimited aqueous beverage and no food, followed by a vegetarian diet restricted to half of the ordinary intake. This is the first report of intermittent fasting as treatment strategy for epilepsy. In this case series, 15 patients did not follow properly the diet while 2 improved temporary before they quitted the diet and 4 presented an improvement.


Subject(s)
Diet, Ketogenic/history , Epilepsy/diet therapy , Fasting , Cathartics/therapeutic use , Diet Therapy/history , Epilepsy/history , Female , History, 20th Century , Humans , Male , Research Design , Sulfates/therapeutic use
7.
Indian J Pediatr ; 85(11): 1000-1005, 2018 Nov.
Article in English | MEDLINE | ID: mdl-30242606

ABSTRACT

About one-third of childhood epilepsy ultimately becomes drug resistant epilepsy. Only about one-third of drug resistant epilepsy is amenable for epilepsy surgery. Epilepsy surgery and vagal nerve stimulation is still beyond the reach of huge proportion of children with pharmacoresistant epilepsy. Ketogenic diet (KD) has been in use for almost a century now all over the world for drug resistant epilepsy, although in between there was a decline in its popularity with advent of newer antiepileptic drugs like valproate, phenytoin and carbamazepine. Again from 1990s there was resurgence of interest in KD for pharmacoresistant epilepsy and in the last two decades several randomized controlled trials and systemic reviews have proved its efficacy beyond any suspicion. Ketogenic diet is a high fat low carbohydrate and low protein diet, which has been found to reduce epileptogenesis in body most probably by production of ketone bodies. Modified Atkin's Diet (MAD) first introduced in 2003 and Low Glycemic Index Treatment (LGIT) first introduced in 2005 are another two dietary therapies, which are less restrictive, more palatable with fewer adverse effects and comparable efficacy. MAD is also a high fat, low carbohydrate diet, in which high sugar foods are discouraged and protein and fluids are unrestricted. In LGIT, only carbohydrates with Glycemic Index <50 are allowed and carbohydrate intake is restricted to 40-60 g per day. Medium Chain Triglyceride KD (MCT KD) is another alternative, in which there are more food choices as compared to classic KD, with comparable efficacy.


Subject(s)
Diet, Ketogenic , Drug Resistant Epilepsy/diet therapy , Child , Diet, Ketogenic/adverse effects , Diet, Ketogenic/history , Dietary Fats/administration & dosage , Drug Resistant Epilepsy/metabolism , Glycemic Index , History, 20th Century , History, 21st Century , History, Ancient , Humans , Ketone Bodies/biosynthesis , Triglycerides/administration & dosage
8.
Rev. GASTROHNUP ; 13(2, Supl.1): S11-S19, mayo-ago. 2011. tab
Article in Spanish | LILACS | ID: lil-645145

ABSTRACT

Históricamente se describió al ayuno como tratamiento de la epilepsia. La dieta cetogénica (DC), es alta enlípidos, baja en proteínas y en hidratos de carbono, es decir, se invierte el cociente normal con la finalidad deproducir y mantener un estado de cetosis. La DC debe producir cuerpos cetónicos debido a la oxidación incompleta de los lípidos. Casi todos los estudios han logrado establecer una asociación entre cetonemia yeficacia anticonvulsiva. Mientras muchos estudios han sugerido que la cetosis persistente es esencial para laprotección anticonvulsiva de la DC, otros han propuesto que la restricción de glucosa es la clave. Los PUFAs, se cree que actúan a nivel cardíaco sobre los canales de sodio y calcio, encuentros similares se han descrito en tejido neuronal.


Historically described fasting as a treatment for epilepsy. The ketogenic diet (KD), is high in fat, low inprotein and carbohydrates, that is, the normal ratio is reversed in order to produce and maintain a state ofHistorically described fasting as a treatment forepilepsy. The ketogenic diet (KD), is high in fat, low inprotein and carbohydrates, that is, the normal ratio isreversed in order to produce and maintain a state ofketosis. The KD should produce ketone bodies due tothe incomplete oxidation of lipids. Almost all studieshave established an association between ketonemia andanticonvulsant efficacy. While many studies havesuggested that persistent ketosis is essential for theprotection of the KD anticonvulsant, others haveproposed that glucose restriction is the key. ThePUFAs, are thought to act at the heart of the sodium andcalcium channels, similar events have been describedin neuronal tissue.


Subject(s)
Humans , Male , Female , Child , Diet, Ketogenic/classification , Diet, Ketogenic/history , Diet, Ketogenic/methods , Diet, Ketogenic , Epilepsy/diagnosis , Epilepsy/history , Anticonvulsants/classification , Glucose/pharmacology , Glucose , Lipids
9.
Epilepsia ; 49 Suppl 8: 3-5, 2008 Nov.
Article in English | MEDLINE | ID: mdl-19049574

ABSTRACT

Fasting and other dietary regimens have been used to treat epilepsy since at least 500 BC. To mimic the metabolism of fasting, the ketogenic diet (KD) was introduced by modern physicians as a treatment for epilepsy in the 1920s. For two decades this therapy was widely used, but with the modern era of antiepileptic drug treatment its use declined dramatically. By the end of the twentieth century this therapy was available in only a small number of children's hospitals. Over the past 15 years, there has been an explosion in the use, and scientific interest in the KD. This review traces the history of one of the most effective treatments for childhood epilepsy.


Subject(s)
Diet, Ketogenic/history , Animals , History, 15th Century , History, 16th Century , History, 17th Century , History, 18th Century , History, 19th Century , History, 20th Century , History, Ancient , History, Medieval
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