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Nathan Goodyear

Effects of oral branched-chain amino acids o... [Nutr Clin Pract. 2013] - PubMed - NCBI - 0 views

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    BCAA aid NH3 metabolism in the muscle in those with liver cirrhosis.  This specifically can aid hepatic encephalopathy and mild hepatic encephalopathy.
Nathan Goodyear

Hepatic Encephalopathy - 0 views

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    Good discussion on the underlying mechanisms, as currently known, that contribute to hepatic encephalopathy.
Nathan Goodyear

Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy following Repetitiv... - 0 views

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    discussion of chronic traumatic encephalopathy.  Good discussion of the neuropathological findings in 3 athletes.
Nathan Goodyear

Chronic traumatic encephalopathy in a National ... [Neurosurgery. 2005] - PubMed - NCBI - 0 views

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    chronic traumatic encephalopathy in football players is felt to play a role in the cognitive changes seen long-term.
Nathan Goodyear

Chronic Traumatic Encephalopathy: Chronic Degenerative Disease - 0 views

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    Good discussion on chronic traumatic encephalopathy. CTE is a condition found in the military and sports related head trauma. This is usually the result of low, repetitive impact injuries to the brain. Though, genetic susceptibility is discussed as well.
Nathan Goodyear

Wernicke's Encephalopathy in Colon Cancer - 0 views

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    Wernicke's encephalopathy in colon cancer relieved with thiamine support
Nathan Goodyear

Branched-chain amino acids for people with hepatic encephalopathy. - PubMed - NCBI - 0 views

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    BCAA beneficial in hepatic encephalopathy, but no benefit in mortality, QOL measures, or nutritional parameters due to studies included.
Nathan Goodyear

Probiotics for patients with hepatic encephalopathy. - PubMed - NCBI - 0 views

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    cochrane review finds equivical evidence for probiotics in hepatic encephalopathy despite improved ammonia metabolism.
Nathan Goodyear

Branched Chain Amino Acid Supplementation for Patients with Cirrhosis | Clinical Correl... - 0 views

  • low level of BCAAs in patients with cirrhosis is hypothesized to be one of multiple factors responsible for development of hepatic encephalopathy
  • 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
  • oral BCAA supplementation is more useful in chronic encephalopathic patients than is parenteral BCAA supplementation in patients with acute encephalopathy
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  • malnutrition progressing to cachexia is another common manifestation of cirrhosis
  • Malnutrition can be mitigated with BCAA supplementation
  • 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
  • Leucine has been shown to be the most effective of the BCAAs because it acts via multiple pathways to stimulate protein synthesis
  • BCAAs metabolites inhibit proteolysis
  • Patients with cirrhosis have both insulin deficiency and insulin resistance
  • 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
  • Coadministration of BCAAs and glucose has been found to be particularly useful
  • BCAA supplementation improves protein-energy malnutrition by improving utilization of glucose, thereby diminishing the drive for proteolysis, inhibiting protein breakdown, and stimulating protein synthesis
  • Cirrhotic patients have impaired immune defense, characterized by defective phagocytic activity and impaired intracellular killing activity
  • another effect of BCAA supplementation is improvement of phagocytic function of neutrophils and possibly improvement in natural killer T (NKT) cell lymphocyte activity
  • 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
  • BCAA administration has also been shown to have a positive effect on liver regeneration
  • 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
  • BCAAs activate rapamycin signaling pathways which promotes albumin synthesis in the liver as well as protein and glycogen synthesis in muscle tissue
  • Chemical improvement with BCAA treatment is demonstrated by recovery of serum albumin and lowering of serum bilirubin levels
  • 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
  • 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
  • Patients receiving BCAA supplementation also have a lower average hospital admission rate, better nutritional status, and better liver function tests
  • patients taking BCAA supplementation report improved quality of life
  • BCAAs have been shown to mitigate hepatic encephalopathy, cachexia, and infection rates, complications associated with the progression of hepatic cirrhosis
  • BCAAs make up 20-25% of the protein content of most foods
  • 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
  • In addition to BCAAs from diet, oral supplements of BCAAs can be used
  • 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
  • Coadministration of BCAAs with carnitine and zinc has also been shown to increase ammonia metabolism further reducing the encephalopathic symptoms
  • Cirrhotic patients benefit from eating frequent, small meals that prevent long fasts which place the patient in a catabolic state
  • the best time for BCAA supplementation is at bedtime to improve the catabolic state during starvation in early morning fasting
  • 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
  • Protein-energy malnutrition (PEM), with low serum albumin and low muscle mass, occurs in 65-90% of cases of advanced cirrhosis
  • hyperglucagonemia results in a catabolic state eventually producing anorexia and cachexia
  • 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
  • patients with chronic liver disease, particularly cirrhosis, routinely have decreased BCAAs and increased aromatic amino acids (AAAs) in their circulation
  • Maintaining a higher serum albumin in patients with cirrhosis is associated with decreased mortality and improved quality of life
  • the serum BCAA concentration is strongly correlated with the serum albumin level
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    great review of cirrhosis and BCCA supplementation.
Nathan Goodyear

American Journal of Gastroenterology - Abstract of article: Effects of Branched-Chain A... - 0 views

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    BCAA supplementation does not inhibit recurrences of hepatic encephalopathy, but it does improve muscle mass.
Nathan Goodyear

Immunoexcitotoxicity as a central mechanism in chronic traumatic encephalopathy-A unify... - 0 views

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    great analysis of immunoexcitoxicity and it's pathophysiologic role in CTE.
Nathan Goodyear

Endotoxemia-induced inflammation and the effect on... [Crit Care. 2010] - PubMed - NCBI - 0 views

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    LPS endotoxemia shown to induce brain inflammation.  In this study, the inflammatory cytokine upregulation did not fully explain the septic encephalopathy so often found.  It was associated with elevated cortisol, which has been shown to shrink the hippocampus
Nathan Goodyear

Is administrating branched-chain amino acid-enriched nutrition achieved symptom-free in... - 0 views

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    BCAA improve NH3 metabolism.  This is via muscle metabolism as reported in other studies.  This study highlighted the differences in BCAA supplementation.  One caveat is that high glutamine is the result from glutamate and this can increase hepatic encephalopathy.
Nathan Goodyear

Absence of chronic traumatic encephalopat... [Front Hum Neurosci. 2013] - PubMed - NCBI - 0 views

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    Study finds that not all football players with a history of multiple concussions and neurologic symptoms have CTE.
Nathan Goodyear

Three targets of branched-chain amino acid supplementation in the treatment of liver di... - 0 views

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    BCAA supplementation in those individuals with liver cirrhosis improves hyperammonemia, nutritional status, hepatic encephalopathy, liver regeneration, and hepatic cachexia.
Nathan Goodyear

Effect of long-term oral supplementation with branched-chain amino acid granules on the... - 0 views

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    long term BCAA supplementation (defined as > 6 months) shown to be safe and effective in liver cirrhosis malnutrition, liver failure and hepatic encephalopathy.
Nathan Goodyear

Branched-chain amino acids in liver diseases - 0 views

  • Serum concentrations of BCAAs are decreased, while the concentrations of the aromatic amino acids (AAAs) phenylalanine and tyrosine are increased, in patients with advanced liver diseases, resulting in a low ratio of BCAAs to AAAs, a ratio called the Fischer ratio
  • BCAAs were reported to stimulate the production of hepatocyte growth factor
  • a simplified Fischer ratio, the BCAA to tyrosine ratio (BTR), has been reported useful for predicting serum albumin concentration one year later
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  • BCAA supplementation was shown to delay the progression of CCl4-induced chronic liver injury in a rat model by reducing hepatic apoptosis
  • BCAAs promoted hepatocyte regeneration in a rat model of hepatectomy
  • BCAA supplementation for advanced cirrhotic patients improves nutritional status and quality of life
  • A low Fischer ratio has been associated with hepatic encephalopathy
  • BCAAs were shown to improve homeostasis model assessment scores for insulin resistance (HOMA-IR) and beta cell function (HOMA-%B) in patients with chronic liver disease, indicating that BCAAs can ameliorate insulin resistance
  • Several clinical trials have suggested that BCAA supplementation improves the prognosis of cirrhotic patients
  • BCAAs activate mTOR and subsequently increase the production of eukaryotic initiation factor 4E-binding protein-1 and ribosomal protein S6 kinase, which upregulate the synthesis of albumin
  • Treatment with BCAAs may therefore have a beneficial effect on patients with hepatic encephalopathy mainly by compensating decreased ratio of BCAAs to AAAs, but not by reducing serum ammonia levels
  • Two randomized studies also showed that BCAAs did not clearly prevent HE in patients with advanced cirrhosis, although BCAAs prevented the progression of hepatic failure
  • a systematic review with meta-analyses on the effect of oral BCAAs for the treatment of HE was published[66]. The review has revealed that supplementation of oral BCAAs in cirrhotic patients inhibits the manifestation of HE, especially in patients with overt HE rather than those with minimal HE, but showed no effect on the survival of those patients[66]. Thus, oral administration of BCAAs is the treatment of choice in cirrhotic patients with HE
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    good review of BCAA and liver disease: both mechanisms and therapy.
Nathan Goodyear

The epidemiology of sports-related tra... [J Head Trauma Rehabil. 1998] - PubMed - NCBI - 0 views

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    analysis of sports related TBI
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