lower caloric content than LCTs
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Medium Chain Triglycerides (MCTs) | Nutrition Review - 0 views
nutritionreview.org/...edium-chain-triglycerides-mcts
MCT medium chain fatty acids medium chain triglycerides
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A Branched-Chain Amino Acid-Related Metabolic Signature that Differentiates Obese and L... - 0 views
www.ncbi.nlm.nih.gov/...PMC3640280
metabolism insulin resistance high protein diet obesity branched chain overload hypothesis
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The role of long chain fatty acids in regulating food intake and cholecystokinin releas... - 0 views
www.ncbi.nlm.nih.gov/...PMC1727908
LCFA long-chain fatty acids cholecystokinin calorie restriction calorie obesity overweight food intake
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Update on branched-chain amino acid supplementation in liver... : Current Opinion in Ga... - 0 views
journals.lww.com/...nched_chain_amino_acid.12.aspx
branched chain amino acids liver cirrhosis hepatitis amino acids protein BCCA
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Branched-chain amino acid metabolism in cancer - 0 views
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Role of Gut Microbiota and Short Chain Fatty Acids in Modulating Energy Harvest and Fat... - 0 views
press.endocrine.org/...jc.2016-1797
obesity gut gut flora gut microbiome gut microbiota butyrate firmicutes_bacteroidetes firmicutes bacteroidetes
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effects of beta-hydroxybutyrate on cognition in memory-impaired adults - 0 views
w.numedica.net/...Reger%202004.pdf
ketogenic diet ketone bodies ketosis Alzheimer's disease neurodegenerative disease MCT medium chain fatty acids
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Those with Alzheimer's disease have associated dysfunction of glucose metabolism in the brain, particularly in the hippocampus. It has been reported that a ketogenic diet can improve cognitive function in these individuals. In this study, the ketone bodies were initiated through a diet high in medium chain fatty acids. The ketone bodies served as an alternative fuel source for the brain.
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Interplay between lipids and branched-chain amino acids in development of insulin resis... - 0 views
www.ncbi.nlm.nih.gov/...PMC3695706
protein high diet insulin resistance metabolism obesity diabetes fatty acids essential
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Branched Chain Amino Acid Supplementation for Patients with Cirrhosis | Clinical Correl... - 0 views
www.clinicalcorrelations.org/?p=3544
BCCA branched chain amino acids liver cirrhosis hepatitis amino acids
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low level of BCAAs in patients with cirrhosis is hypothesized to be one of multiple factors responsible for development of hepatic encephalopathy
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supplementation of BCAAs is thought to facilitate ammonia detoxification by supporting synthesis of glutamine, one of the non-branched chain amino acids, in skeletal muscle and in the brain as well as diminishing the influx of AAAs across the blood-brain barrier
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oral BCAA supplementation is more useful in chronic encephalopathic patients than is parenteral BCAA supplementation in patients with acute encephalopathy
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Studies show that administration of amino acid formulas enriched with BCAAs can reduce protein loss, support protein synthesis, and improve nutritional status of patients with chronic liver disease
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Leucine has been shown to be the most effective of the BCAAs because it acts via multiple pathways to stimulate protein synthesis
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BCAAs (particularly leucine) help to reverse the catabolic, hyperglucagonemic state of cirrhosis both by stimulating insulin release from the pancreatic β cells and by decreasing insulin resistance allowing for better glucose utilization
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BCAA supplementation improves protein-energy malnutrition by improving utilization of glucose, thereby diminishing the drive for proteolysis, inhibiting protein breakdown, and stimulating protein synthesis
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Cirrhotic patients have impaired immune defense, characterized by defective phagocytic activity and impaired intracellular killing activity
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another effect of BCAA supplementation is improvement of phagocytic function of neutrophils and possibly improvement in natural killer T (NKT) cell lymphocyte activity
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BCAA supplementation may reduce the risk of infection in patients with advanced cirrhosis not only through improvement in protein-energy malnutrition but also by directly improving the function of the immune cells themselves
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A proposed mechanism for improved liver regeneration is the stimulatory effect of BCAAs (particularly leucine) on the secretion of hepatocyte growth factor by hepatic stellate cells
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BCAAs activate rapamycin signaling pathways which promotes albumin synthesis in the liver as well as protein and glycogen synthesis in muscle tissue
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Chemical improvement with BCAA treatment is demonstrated by recovery of serum albumin and lowering of serum bilirubin levels
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long-term oral BCAA supplementation was useful in staving off malnutrition and improving survival by preventing end-stage fatal complications of cirrhosis such as hepatic failure and gastrointestinal bleeding
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The incidence of death by any cause, development of liver cancer, rupture of esophageal varices, or progression to hepatic failure was decreased in the group that received BCAA supplementation
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Patients receiving BCAA supplementation also have a lower average hospital admission rate, better nutritional status, and better liver function tests
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BCAAs have been shown to mitigate hepatic encephalopathy, cachexia, and infection rates, complications associated with the progression of hepatic cirrhosis
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Highest levels are found in casein whey protein of dairy products and vegetables, such as corn and mushrooms. Other sources include egg albumin, beans, peanuts and brown rice bran
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Oral supplementation tends to provide a better hepatic supply of BCAAs for patients able to tolerate PO nutrition as compared with IV supplementation, especially when treating symptoms of hepatic encephalopathy
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Coadministration of BCAAs with carnitine and zinc has also been shown to increase ammonia metabolism further reducing the encephalopathic symptoms
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Cirrhotic patients benefit from eating frequent, small meals that prevent long fasts which place the patient in a catabolic state
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the best time for BCAA supplementation is at bedtime to improve the catabolic state during starvation in early morning fasting
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A late night nutritional snack reduces symptoms of weakness and fatigability, lowers postprandial hyperglycemia, increases skeletal muscle mass,[25] improves nitrogen balance, and increases serum albumin levels.[26] Nocturnal BCAAs even improve serum albumin in cirrhotic patients who show no improvement with daytime BCAAs
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Protein-energy malnutrition (PEM), with low serum albumin and low muscle mass, occurs in 65-90% of cases of advanced cirrhosis
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BCAAs are further depleted from the circulation due to increased uptake by skeletal muscles that use the BCAAs in the synthesis of glutamine, which is produced in order to clear the ammonia that is not cleared by the failing liver
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patients with chronic liver disease, particularly cirrhosis, routinely have decreased BCAAs and increased aromatic amino acids (AAAs) in their circulation
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Maintaining a higher serum albumin in patients with cirrhosis is associated with decreased mortality and improved quality of life
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Leucine Regulates Translation Initiation of Protein Synthesis in Skeletal Muscle after ... - 0 views
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Serum Free Light Chain in Waldenstrom Macroglobulinemia. | Blood Journal - 0 views
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The Role of Serum Immunoglobulin Free Light Chain in Response and Progression in Walden... - 0 views
clincancerres.aacrjournals.org/...3013.long
Waldenstrom lymphoma "waldenstrom's macroglobulinemia" Cancer
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Serum immunoglobulin free light chain correlates with tumor burden markers in Waldenstr... - 1 views
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Toxicity of the spike protein of COVID-19 is a redox shift phenomenon: A novel therapeu... - 0 views
www.sciencedirect.com/...S0891584923005014
COVID19 COVID-19 cancer inflammation SARS-CoV-2 spike proteins COVID spikeopathy
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Lipoic acid and Methylene Blue have been shown to enhance the mitochondrial activity, relieve the Warburg effect and increase catabolism
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Lipoic acid and Methylene Blue have been shown to enhance the mitochondrial activity, relieve the Warburg effect and increase catabolism
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Lipoic acid and Methylene Blue have been shown to enhance the mitochondrial activity, relieve the Warburg effect and increase catabolism
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Methylene Blue, Chlorine dioxide and Lipoic acid may help reduce long-term Covid-19 effects by stimulating the catabolism
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Methylene Blue, Chlorine dioxide and Lipoic acid may help reduce long-term Covid-19 effects by stimulating the catabolism
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Methylene Blue, Chlorine dioxide and Lipoic acid may help reduce long-term Covid-19 effects by stimulating the catabolism
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direct consequence of redox iMeBalance, itself a consequence of decreased energy yield by the mitochondria
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direct consequence of redox iMeBalance, itself a consequence of decreased energy yield by the mitochondria
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mitochondrial dysfunction and increased levels of lactate, which are important characteristics of metabolic shift and Warburg effect in many diseases
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mitochondrial dysfunction and increased levels of lactate, which are important characteristics of metabolic shift and Warburg effect in many diseases
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cell division is the most sophisticated way to release entropy
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redox signaling plays an important role in regulating immune function and inflammation, and disruptions in this signaling can lead to excessive cytokine production and immune system activation
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reduced extracellular environment in the elderly and the increased susceptibility to Covid-19 infection
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reduced extracellular environment in the elderly and the increased susceptibility to Covid-19 infection
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Redox signaling tightly modulates the inflammatory response and oxidative stress has been reported in acute Covid-19
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People at high risk are the elderly, patients suffering from metabolic syndrome such as obesity, or those suffering from chronic diseases such as cancer or inflammation
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COVID-19 patients with severe disease have higher levels of oxidative stress markers and lower antioxidant levels
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oxidative stress can activate the NLRP3 inflammasome, which is a protein complex that plays a key role in the cytokine storm
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inflammation leads to the formation of ROS and RNS, while redox iMeBalance results in cellular damage, which in turn triggers an inflammatory response
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persistently elevated mtROS triggers endothelial dysfunction and inflammation, which results in a vicious loop involving ROS, inflammation, and mitochondrial dysfunction
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IL-2 is highly up-regulated in Covid-19 patients [37], and IL-2 is known to significantly stimulate the generation of NO in patients
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Elevated levels of lactate, a characteristic of the Warburg effect, were also reported in the high-risk Covid-19
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vaccinated with RNA or DNA vaccines triggering the synthesis of the viral spike protein in human cells
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viral reactivation in varicella-zoster virus [55] or hepatitis [56], coagulopathy and resulting stroke and myocarditis following both DNA-based vaccines [57] and RNA-based vaccines
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characteristic of the Warburg effect is present in almost every disease and appears to be a central feature in most of the hallmarks of cancer
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inflammation, mitochondrial dysfunction and increased lactate concentrations in the extracellular fluid
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As the mitochondria are impaired, the infected cell cannot catabolize efficiently. It will release lactic acid in the blood stream
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Striking similarities are seen between cancer, Alzheimer's disease and Covid-19, all related to the Warburg effect
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Cancer, inflammation, Alzheimer's, and Parkinson's diseases share a common peculiarity, the inability of the cell to export entropy outside the body in the harmless form of heat
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MEB relieves the Warburg effect [87], improves memory [77], is active in the treatment of depressive episodes [79,80] and reduces the importance of ischemic strokes
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MEB relieves the Warburg effect [87], improves memory [77], is active in the treatment of depressive episodes [79,80] and reduces the importance of ischemic strokes
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It has been shown that Covid-19-patients treated with MEB, have a significant reduction in hospital stay duration and mortality
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MeB + can take a pair of electrons (of H atoms) and MeBH can release this pair easily, so that MeB is partially recycled like a catalyst
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MeB acts as an electron bridge between a donor (FADH2, FMNH, NADH) and an acceptor (complex IV of ETC or oxygen itself)
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As a coenzyme of pyruvate dehydrogenase (PDH), alpha-lipoic acid (ALA) initiates the formation of acetyl-CoA to feed the TCA cycle
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ALA enhances the catabolism of carbon. cycle and therefore may reduce the Warburg effect and consequently, lactate production
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Methylene Blue plays a similar role after the TCA cycle, by carrying electrons to complex IV of the electron transport chain
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Drugs such as lipoic acid and MeB, which target the metabolism, decrease the redox shift by increasing catabolism
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The role of short-chain fatty acids in the interplay between diet, gut microbiota, and ... - 0 views
www.ncbi.nlm.nih.gov/...PMC3735932
SCFA gut gut health diet nutrition metabolism gut flora gut microbiota
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Acetate, propionate, and butyrate are present in an approximate molar ratio of 60:20:20 in the colon and stool
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SCFAs might play a key role in the prevention and treatment of the metabolic syndrome, bowel disorders, and certain types of cancer
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SCFA administration positively influenced the treatment of ulcerative colitis, Crohn's disease, and antibiotic-associated diarrhea
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Gut bacteria in the cecum and large intestine produce SCFAs mainly from nondigestible carbohydrates that pass the small intestine unaffected
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colonocytes, the first host cells that take up SCFAs and which depend largely on butyrate for their energy supply
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the microbiota act as a metabolic organ that can break down otherwise indigestible food components, degrade potentially toxic food compounds like oxalate, and synthesize certain vitamins and amino acids
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The general idea is that colonocytes prefer butyrate to acetate and propionate, and oxidize it to ketone bodies and CO2
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Exogenous acetate formed by colonic bacterial fermentation enters the blood compartment and is mixed with endogenous acetate released by tissues and organs (103, 104). Up to 70% of the acetate is taken up by the liver (105), where it is not only used as an energy source, but is also used as a substrate for the synthesis of cholesterol and long-chain fatty acids and as a cosubstrate for glutamine and glutamate synthesis
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SCFAs regulate the balance between fatty acid synthesis, fatty acid oxidation, and lipolysis in the body.
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obese animals in this study showed a 50% reduction in relative abundance of the Bacteroidetes (i.e., acetate and propionate producers), whereas the Firmicutes (i.e., butyrate producers) were proportionally increased compared with the lean counterparts.
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In humans the distinct relation between the Firmicutes:Bacteroidetes ratio and obesity is less clear.
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Is administrating branched-chain amino acid-enriched nutrition achieved symptom-free in... - 0 views
www.ncbi.nlm.nih.gov/...PMC3882488
BCAA branched chain amino acids NH3 metabolism muscle glutamine glutamate glutamic acid liver cirrhosis disease nutrition
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Effects of oral branched-chain amino acids o... [Nutr Clin Pract. 2013] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...23945292
BCAA branched chain amino acids liver disease cirrhosis hepatic encephalopathy mild
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Branched-chain amino acids increase arterial blood ammonia in spite of enhanced intrins... - 0 views
ajpgi.physiology.org/...G269
BCAA branched chain amino acids NH3 ammonia liver disease cirrhosis alpha-ketoglutarate
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Branched-chain amino acids and muscle ammoni... [Metab Brain Dis. 2013] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...23315357
NH3 muscle brain urea cycle metabolism BCAA branched chain amino acids liver cirrhosis disease
shared by Nathan Goodyear on 10 Feb 14
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BCAA metabolism may improve muscle net ammonia removal by supplying carbon skeletons for formation of alfa-ketoglutarate that combines with two ammonia molecules to become glutamine