Cybermedlife - Therapeutic Actions Dietary Modification - High-Fat-Low-Carbohydrate

High-fat and ketogenic diets in amyotrophic lateral sclerosis. 📎

Abstract Title: High-fat and ketogenic diets in amyotrophic lateral sclerosis. Abstract Source: J Child Neurol. 2013 Aug ;28(8):989-92. Epub 2013 May 10. PMID: 23666040 Abstract Author(s): Sabrina Paganoni, Anne-Marie Wills Article Affiliation: Sabrina Paganoni Abstract: Amyotrophic lateral sclerosis is a fatal neurodegenerative disease. Epidemiologic data suggest that malnutrition is a common feature in amyotrophic lateral sclerosis and being overweight or obese confers a survival advantage in this patient population. In amyotrophic lateral sclerosis mouse models, a high-fat diet has been shown to lead to weight gain and prolonged survival. However, little research has been conducted to test whether nutritional interventions might ameliorate the disease course in humans. Here we review the currently available evidence supporting the potential role of dietary interventions as a therapeutic tool for amyotrophic lateral sclerosis. Ultimately, determining whether a high-fat or ketogenic diet could be beneficial in amyotrophic lateral sclerosis will require large randomized, placebo-controlled clinical trials. Article Published Date : Jul 31, 2013

Dietary treatment of diabetes mellitus in the pre-insulin era (1914-1922).

Abstract Title: Dietary treatment of diabetes mellitus in the pre-insulin era (1914-1922). Abstract Source: Perspect Biol Med. 2006;49(1):77-83. PMID: 16489278 Abstract Author(s): [No authors listed] Abstract: Before the discovery of insulin, one of the most common dietary treatments of diabetes mellitus was a high-fat, low-carbohydrate diet. A review of Frederick M. Allen's case histories shows that a 70% fat, 8% carbohydrate diet could eliminate glycosuria among hospitalized patients. A reconsideration of the role of the high-fat, low-carbohydrate diet for the treatment of diabetes mellitus is in order. Article Published Date : Jan 01, 2006
Therapeutic Actions DIETARY MODIFICATION High-Fat-Low-Carbohydrate

NCBI pubmed

Dietary Therapies: Emerging Paradigms in Therapy of Drug Resistant Epilepsy in Children : Based on 6th Dr. I. C. Verma Excellence in Research Award Oration.

Related Articles Dietary Therapies: Emerging Paradigms in Therapy of Drug Resistant Epilepsy in Children : Based on 6th Dr. I. C. Verma Excellence in Research Award Oration. Indian J Pediatr. 2018 Sep 21;: Authors: Gulati S 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. PMID: 30242606 [PubMed - as supplied by publisher]