Keto diet helps with inflammatory response

By | July 12, 2020

keto diet helps with inflammatory response

Ketogenic diets are well-established as a successful anticonvulsant therapy. Based on overlap between mechanisms postulated to underlie pain and inflammation, and mechanisms postulated to underlie therapeutic effects of ketogenic diets, recent studies have explored the ability for ketogenic diets to reduce pain. Pain is one of the most commonly indicated health-related factors leading to poor quality of life. Here we review correlative and direct evidence that ketogenic diets could offer a non-pharmacological option for reducing pain and inflammation. High-fat ketogenic diets have long been known to be effective against seizures, 4, 5 and metabolically the high fat, very low carbohydrate and restricted protein content limits available glucose and forces utilization of ketones for cell energy. Similar to epilepsy, pain is a condition that encompasses diverse underlying conditions. Why would one propose that ketogenic diets might also be useful in treating pain, a seemingly disparate condition? There are several lines of evidence, outlined below, that strongly suggest that metabolic approaches to pain could provide new clinical opportunities. Some of these mechanisms have been tested directly and additional research is ongoing.

Our products are not intended to diagnose, treat, cure, or prevent any disease. Please see our guide on cholesterol and low carb to get a more in-depth answer. Some studies in animal models have highlighted the role of HDACs inhibitors in enhancing mnesic processes suggesting their potential use in the treatment of cognitive diseases. Persistent pain and well-being: a World Health Organization study in primary care. Number of subjects is 12 in all groups. There is a lot about the gut microbiome. HDAC plays an important role in the pathogenesis of AD by altering chromatin structure and accessibility [ 96 ]. Ohnuma T. In the cell there is a constant balance between the mitophagy of damaged mitochondria and the biogenesis to renew mitochondria population [ 75 ]. These inflammatory mediators, in turn, act on target tissues and alter their functional states, promoting elimination of the inducers, adaptation to the noxious state, and restoration of normal tissue function. This is because there are many perhaps dozens of different isoprostane molecules that result from the random attacks of ROS on membrane fatty acids.

The main activity of the ketogenic diet has been related to improved mitochondrial function and decreased oxidative stress. Furthermore, the ketogenic diet performs anti-inflammatory activity by inhibiting nuclear factor kappa-light-chain-enhancer of activated B cells NF-kB activation and nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 NLRP3 inflammasome as well as inhibiting histone deacetylases HDACs, improving memory encoding. According to the World Alzheimer Report , there are 47 million people worldwide suffering from dementia, and this number will rise to million by due to population aging. This data also implies a great economic impact, which is expected to be one billion dollars worldwide by Based on this consideration, much effort is aimed at the development of effective prevention lines: so far many non-pharmacological treatments have been proposed, including lifestyle interventions such as targeted nutritional protocols, caloric restriction and exercise, as well as mental challenges and socialization [ 1 ]. The brain hypometabolism was associated to a reduced glucose utilization, detected by fluorodeoxyglucose positron emission tomography FDG-PET, but several alteration in amino acids and lipids metabolic pathways have been recently identified through modern metabolomics techniques [ 7, 8, 9, 10, 11 ]. When there is a decreased expression of these transporters, as it has been shown in AD, Ketone Bodies KBs become the alternative energy source to glucose for the brain due to their ability to cross the BBB carried by specific transporters that are not down-regulated during AD.

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