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Read how KETONES can reduce and eliminate the inflammation that causes pain, and debilitation with ARTHRITIS

The ketone metabolite β-hydroxybutyrate blocks the NLRP3 inflammasome-mediated inflammatory disease

Youm YH1, Nguyen KY1, Grant RW2, Goldberg EL1, Bodogai M3, Kim D4, D.Agostino D5, Planavsky N6, Lupfer C7, Kannaganti TD7, Kang S8, Horvath TL1, Crawford PA9, Biragyn A3, Alnemri E8, Dixit VD10.

Citation: Nat. Med. 2015 Mar; 21(3):263-9 doi: 10.1038/nm.3804. Epud 2015 Feb 16.

Link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4352123/


The Ketone bodies β-hydroxybutyrate (BHB) and acetoacetate support mammalian survival during states of energy deficit by serving as alternative source of ATP1. BHB levels are elevated during starvation, high-intensity exercise or by the low carbohydrate ketogenic diet2. Prolonged caloric restriction or fasting reduces inflammation as immune system adapts to low glucose supply and energy metabolism switches towards mitochondrial fatty acid oxidation, ketogenesis and ketolysis2-6. However, role of ketones bodies in regulation of innate immune response is unknown. We report that BHB, but neither acetoacetate nor structurally-related short chain fatty acids, butyrate and acetate, suppresses activation of the NLRP3 inflammasome in response to several structurally unrelated NLRP3 activators, without impacting NLRC4, AIM2 or non-canonical caspase-11 inflammasome activation. Mechanistically, BHB inhibits NLRP3 inflammasome by preventing K+ efflux and reducing ASC oligomerization and speck formation. The inhibitory effects of BHB on NLRP3 were not dependent on chirality or classical starvation regulated mechanisms like AMPK, reactive oxygen species (ROS), autophagy or glycolytic inhibition. BHB blocked NLRP3 inflammasome without undergoing oxidation in TCA cycle, independently of uncoupling protein-2 (UCP2), Sirt2, receptor Gpr109a and inhibition of NLRP3 did not correlate with magnitude of histone acetylation in macrophages. BHB reduced the NLRP3 inflammasome mediated IL-1β and IL-18 production in human monocytes. In vivo, BHB attenuates caspase-1 activation and IL-1β secretion in mouse models of NLRP3-mediated diseases like Muckle-Wells Syndrome (MWS), Familial Cold Autoinflammatory syndrome (FCAS) and urate crystal induce body cavity inflammation. Taken together, these findings suggest that the anti-inflammatory effects of caloric restriction or ketogenic diets may be mechanistically linked to BHB-mediated inhibition of the NLRP3 inflammasome, and point to the potential use of interventions that elevate circulating BHB against NLRP3-mediated proinflammatory diseases.

Not only do ketones IMPROVE BLOOD SUGAR LEVELS, but also cholesterol levels, and all of this WITHOUT DRUGS!

Effects of exogenous ketone supplementation on blood ketone, glucose, triglyceride, and lipoprotein levels in Sprague-Dawley rats.

Kesl SL, Poff AM, Ward NP, Fiorelli TN, Ari C, Van Putten AJ, Sherwood JW, Arnold P, D’Agostino, DP.

Citation: Nutr Metab (Lond). 2016 Feb 4;13:19. doi:10.1186/s12986-016-0069-y. eCollection 2016.

Link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4743170/



Nutritional ketosis induced by the ketogenic diet (KD) has therapeutic applications for many disease states. We hypothesized that oral administration of exogenous ketone supplements could produce sustained nutritional ketosis (>0.5 mM) without carbohydrate restriction.


We tested the effects of 28-day administration of five ketone supplements on blood glucose, ketones, and lipids in male Sprague–Dawley rats. The supplements included: 1,3-butanediol (BD), a sodium/potassium β-hydroxybutyrate (βHB) mineral salt (BMS), medium chain triglyceride oil (MCT), BMS + MCT 1:1 mixture, and 1,3 butanediol acetoacetate diester (KE). Rats received a daily 5–10 g/kg dose of their respective ketone supplement via intragastric gavage during treatment. Weekly whole blood samples were taken for analysis of glucose and βHB at baseline and, 0.5, 1, 4, 8, and 12 h post-gavage, or until βHB returned to baseline. At 28 days, triglycerides, total cholesterol and high-density lipoprotein (HDL) were measured.


Exogenous ketone supplementation caused a rapid and sustained elevation of βHB, reduction of glucose, and little change to lipid biomarkers compared to control animals.


This study demonstrates the efficacy and tolerability of oral exogenous ketone supplementation in inducing nutritional ketosis independent of dietary restriction.

If you or a loved one is suffering with Dementia or Alzheimer’s you need to read how a ketone supplement can improve their cognitive abilities, their mood, and improve their “self care”! 

A new way to produce hyperketonemia: Use of ketone ester in a case of Alzheimer’s disease.

Newport MT, VanItallie TB, Kashiwaya Y, King MT, Veech RL.

Citation: Alzheimer’s Dement. 2015 Jan; 11(1):99-101. doi: 10.1016/j.jalz.2014.01.006. Epub 2014 Oct 7.

Link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4300286/



Providing ketone bodies to the brain can bypass metabolic blocks to glucose utilization and improve function in energy-starved neurons. For this, plasma ketones must be elevated well above the ≤ .02 mM default concentrations normally prevalent. Limitations of dietary methods currently used to produce therapeutic hypertonemia have stimulated the search for better approaches.


Describe herein is a new way to produce therapeutic hypertonemia, entailing prolonged oral administration of a potent ketogenic agent—ketone monoester (KME)—to a patient with Alzheimer’s disease dementia and a pretreatment Mini-Mental State Examination score of 12.


*The patient improved markedly in mood, affect, self-care, and cognitive and daily activity performance.* The KME was well tolerated throughout the 20-month treatment period. Cognitive performance tracked plasma-hydroxybutyrate concentrations, with noticeable improvements in conversation and interaction as the higher levels, compared with predose levels.


KME- Induced hyperketonemia is robust, convenient, and safe, and the ester can be taken as an oral supplement without changing the habitual diet. 

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