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Nathan Goodyear

Branched-chain amino acids and ammonia metabolism in liver disease: Therapeutic implica... - 0 views

www.sciencedirect.com/...S0899900713000907

BCAA branched chain amino acids glutamate glutamic acid glutamine alpha-ketoglutarate NH3 ammonia liver disease cirrhosis

shared by Nathan Goodyear on 10 Feb 14 - No Cached
  • Nathan Goodyear on 10 Feb 14
     
    BCAA are low in patients with liver cirrhosis due to increased glutamate production from glutamine.  The addition of BCAA in these patients is not without side effects--increased NH3 production.  The addition of alpha ketoglutarate should alleviate this risk.
Nathan Goodyear

Metabolite profiles and the risk of developing diabetes : Nature Medicine : Nature Publ... - 0 views

www.nature.com/...nm.2307.html

diabetes metabolism branch chain overload hypothesis branched chain amino acids amino acids protein isoleucine leucine valine tyrosine phenylalanine

shared by Nathan Goodyear on 21 Oct 13 - No Cached
  • Nathan Goodyear on 21 Oct 13
     
    High amino acid intake associated with 5 fold higher risk of Diabetes.  The risk required 3 out of 5 amino acids isoleucine, leucine, valine, tyrosine, and phenylalanine.
Nathan Goodyear

Hypometabolism as a therapeutic target in Alzheimer's disease - 0 views

www.ncbi.nlm.nih.gov/...PMC2604900

cocconut oil brain Alzheimer's disease ketones

shared by Nathan Goodyear on 11 Nov 13 - No Cached
  • Nathan Goodyear on 11 Nov 13
     
    Medium chain fatty acids, such as cocconut oil, benefit brain with glucose hypometabolism problems such as in Alzheimer's disease.
Nathan Goodyear

PLOS ONE: Depletion of Brain Docosahexaenoic Acid Impairs Recovery from Traumatic Brain... - 0 views

journals.plos.org/...article

DHA TBI traumatic brain injury omega 3 brain injury brain omega-3

shared by Nathan Goodyear on 31 Aug 15 - No Cached
  • The polyunsaturated fatty acids linoleic (LA, 18:2n-6) and linolenic acid (LNA, 18:3n-3) are essential fatty acids that cannot be synthesized by the body.
  • LNA serves as the precursor for long chain omega-3 fatty acids such as docosahexaenoic acid (DHA) while LA is converted into long chain omega-6 fatty acids such as arachidonic acid (AA)
  • DHA and AA are abundantly found in the brain, where these are stored mainly in membrane phospholipids
  • ...10 more annotations...
  • DHA has been shown to increase neurite outgrowth and synaptogenesis, and promotes glutamatergic neurotransmission through increase in glutamate receptor subunit expression
  • DHA has been shown to be converted to anti-inflammatory, proresolving and neuroprotective mediators, such as resolvins [7] and protectins
  • AA is converted by cyclooxygenases into 2-series prostaglandins and 4-series leukotrienes, most of which exert pro-inflammatory effects
  • Supplementation of DHA exerts neuroprotective effects and has been reported to afford protection from diffuse axonal injury [11] and mixed brain injury [12] as well
  • severe depletion of membrane DHA in the brain renders mice significantly more susceptible to TBI and impairs recovery following the injury
  • Omega-3 fatty acids may serve as nutraceutical agents and precondition the brain to make it more resilient to injury
  • it can be suggested that enriching DHA in the brain may be prophylactic and protective against brain injury
  • severe DHA deficiency in the brain impairs functional recovery from TBI in terms of vestibulo-motor and cognitive deficits
  • DHA deficiency further elevates TBI-induced production of SBDPs
  • less neurons were found around the injury site of DHA deficient brain after TBI compared to the omega-3 fatty acid adequate group
  • Nathan Goodyear on 31 Aug 15
     
    mouse study finds prolonged recovery in DHA deficient mice compared to controls.
Nathan Goodyear

Branched-chain amino acids as a protein- and energy-source in liver cirrhosis. - PubMed... - 0 views

www.ncbi.nlm.nih.gov/...14684176

BCAA branched chain amino acids liver cirrhosis hepatitis ammonia

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • Nathan Goodyear on 05 Oct 15
     
    BCAA for liver cirrhosis to improve ammonia clearance.  Increased glutamine is a means to compensate for the decreased ammonia clearance as well as a means to improve energy balance often present in these clients.  Night time dosing prevents fasting catabolic exacerbations.
Nathan Goodyear

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

www.ncbi.nlm.nih.gov/...20071143

BCAA branched chain amino acids liver cirrhosis amino acids

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • Nathan Goodyear on 05 Oct 15
     
    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

www.ncbi.nlm.nih.gov/...2606303

BCAA branched chain amino acids liver cirrhosis amino acids

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • Nathan Goodyear on 05 Oct 15
     
    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 Acid Supplementation in Patients with Liver Diseases - 0 views

jn.nutrition.org/...1596S.long

BCAA branched chain amino acids amino acids liver cirrhosis

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • the optimum amount of BCAA supplements for liver disease has not been determined,
  • BCAAs not only provide substrates for protein synthesis but also accelerate the biochemical machinery, which facilitates liver regeneration, compensating for progressive liver-cell death
  • rapamycin signaling in the liver, a well-demonstrated effect of BCAAs, promotes albumin synthesis in the liver
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  • the amount of BCAAs supplied in the various studies is extremely variable
  • Nathan Goodyear on 05 Oct 15
     
    BCAA effective in patients with liver cirrhosis, liver cancer, and liver transplant.  BCAA improve the liver regenerative capacity.
Nathan Goodyear

Nutritional supplementation with branched-chain amino acids in advanced cirrhosis: a do... - 0 views

www.ncbi.nlm.nih.gov/...12806613

BCAA branched chain amino acids liver cirrhosis amino acids

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • Nathan Goodyear on 05 Oct 15
     
    BCAA beneficial in malnutrition, anorexia, and QOL measures in patients with liver failure.
Nathan Goodyear

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

www.ncbi.nlm.nih.gov/...25715177

BCAA branched chain amino acids hepatic encephalopathy liver cirrhosis

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • Nathan Goodyear on 05 Oct 15
     
    BCAA beneficial in hepatic encephalopathy, but no benefit in mortality, QOL measures, or nutritional parameters due to studies included.
Nathan Goodyear

Branched-Chain Amino Acid Enriched Supplements as Therapy for Liver Disease - 0 views

jn.nutrition.org/...295S.long

BCAA branched chain amino acids liver cirrhosis disease amino acids

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • The most compelling basis for a more widespread prescription of BCAA supplements to patients with cirrhosis is the potential to avert general hepatic decompensation and subsequent death and liver transplantation
  • Nathan Goodyear on 05 Oct 15
     
    Good review of the evidence of BCAA therapy and liver disease.
Nathan Goodyear

A randomized pilot trial of oral branched-chain amino acids in early cirrhosis: Validat... - 0 views

onlinelibrary.wiley.com/...full

BCAA branched chain amino acids liver cirrhosis disease

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • Nathan Goodyear on 05 Oct 15
     
    BCAA slows cirrhosis progression.  This may prolong the waiting time period for those awaiting transplant.
Nathan Goodyear

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

www.nature.com/...ajg20119a.html

BCAA branched chain amino acids Muscle mass hepatic encephalopathy liver cirrhosis disease

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • Nathan Goodyear on 05 Oct 15
     
    BCAA supplementation does not inhibit recurrences of hepatic encephalopathy, but it does improve muscle mass.
Nathan Goodyear

Nutritional supplementation with branched-chain amino acids in advanced cirrhosis: a do... - 0 views

www.sciencedirect.com/...S0016508503003238

BCAA branched chain amino acids liver cirrhosis disease

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • Nathan Goodyear on 05 Oct 15
     
    BCAA useful in advanced liver cirrhosis.
Nathan Goodyear

Potential role of branched-chain amino acids in glucose metabolism through the accelera... - 0 views

www.ncbi.nlm.nih.gov/...20506195

BCAA branched chain amino acids liver cirrhosis disease GLUT2 glucose metabolism

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • Nathan Goodyear on 05 Oct 15
     
    BCAA improve glucose metabolism via, in part, up regulation of GLUT2 receptors in the liver
Nathan Goodyear

Branched-chain amino acids in liver diseases - 0 views

www.ncbi.nlm.nih.gov/...PMC3837260

BCAA branched chain amino acids liver cirrhosis disease

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • 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
  • 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
  • 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
  • A low Fischer ratio has been associated with hepatic encephalopathy
  • 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
  • Nathan Goodyear on 05 Oct 15
     
    good review of BCAA and liver disease: both mechanisms and therapy.
Nathan Goodyear

Is docosahexaenoic acid, an n-3 long-chain polyunsaturated fatty acid, required for dev... - 0 views

www.ajcn.org/...281.abstract

long-chain fatty acid brain development function behavioral DHA Omega-3

shared by Nathan Goodyear on 06 Sep 11 - No Cached
  • Nathan Goodyear on 06 Sep 11
     
    changes in brain concentrations of DHA (omega-3) are positively associated with changes in cognitive or behavioral performance
Nathan Goodyear

Hyperammonemia-induced depletion of glutamate and branched-chain am... - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...8938556

ammonia NH3 BCCA branched chain amino acids glutamine

shared by Nathan Goodyear on 18 Nov 14 - No Cached
  • Nathan Goodyear on 18 Nov 14
     
    Elevated ammonia depletes glutamate and BCCA in muscle and plasma.  A decrease in BCCA is through an up regulation of glutamine in an attempt to eliminate ammonia.
Nathan Goodyear

Acute hyperammonemia activates branched-chain amino acid catabolism... - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...20614225

ammonia BCCA branched chain amino acids

shared by Nathan Goodyear on 18 Nov 14 - No Cached
  • Nathan Goodyear on 18 Nov 14
     
    elevated ammonia levels reduce BCCA levels and increase glutamine levels in an attempt to eliminate ammonia.
Nathan Goodyear

Press-pulse: a novel therapeutic strategy for the metabolic management of cancer | Nutr... - 0 views

nutritionandmetabolism.biomedcentral.com/...s12986-017-0178-2

ketogenic diet ketogenic press-pulse hyperbaric oxygen therapy HBOTnutrition diet cancer HBOT IVC IV vitamin C DCA dichloracetic acid cancer therapy cancer treatment alternative cancer treatment

shared by Nathan Goodyear on 09 Jul 17 - No Cached
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  • A “press” disturbance was considered a chronic environmental stress on all organisms in an ecological community
  • “pulse” disturbances were considered acute events that disrupted biological communities to produce high mortality
  • Neoplasia involving dysregulated cell growth is the biological endpoint of the disease
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  • Data from the American Cancer Society show that the rate of increase in cancer deaths/year (3.4%) was two-fold greater than the rate of increase in new cases/year (1.7%) from 2013 to 2017
  • cancer is predicted to overtake heart disease as the leading cause of death in Western societies
  • cancer can also be recognized as a metabolic disease.
  • glucose is first split into two molecules of pyruvate through the Embden–Meyerhof–Parnas glycolytic pathway in the cytosol
  • Aerobic fermentation, on the other hand, involves the production of lactic acid under normoxic conditions
  • persistent lactic acid production in the presence of adequate oxygen is indicative of abnormal respiration
  • Otto Warburg first proposed that all cancers arise from damage to cellular respiration
  • The Crabtree effect is an artifact of the in vitro environment and involves the glucose-induced suppression of respiration with a corresponding elevation of lactic acid production even under hyperoxic (pO2 = 120–160 mmHg) conditions associated with cell culture
  • the Warburg theory of insufficient aerobic respiration remains as the most credible explanation for the origin of tumor cells [2, 37, 51, 52, 53, 54, 55, 56, 57].
  • The main points of Warburg’s theory are; 1) insufficient respiration is the predisposing initiator of tumorigenesis and ultimately cancer, 2) energy through glycolysis gradually compensates for insufficient energy through respiration, 3) cancer cells continue to produce lactic acid in the presence of oxygen, and 4) respiratory insufficiency eventually becomes irreversible
  • Efraim Racker coined the term “Warburg effect”, which refers to the aerobic glycolysis that occurs in cancer cells
  • Warburg clearly demonstrated that aerobic fermentation (aerobic glycolysis) is an effect, and not the cause, of insufficient respiration
  • all tumor cells that have been examined to date contain abnormalities in the content or composition of cardiolipin
  • The evidence supporting Warburg’s original theory comes from a broad range of cancers and is now overwhelming
  • respiratory insufficiency, arising from any number mitochondrial defects, can contribute to the fermentation metabolism seen in tumor cells.
  • data from the nuclear and mitochondrial transfer experiments suggest that oncogene changes are effects, rather than causes, of tumorigenesis
  • Normal mitochondria can suppress tumorigenesis, whereas abnormal mitochondria can enhance tumorigenesis
  • In addition to glucose, cancer cells also rely heavily on glutamine for growth and survival
  • Glutamine is anapleurotic and can be rapidly metabolized to glutamate and then to α-ketoglutarate for entry into the TCA cycle
  • Glucose and glutamine act synergistically for driving rapid tumor cell growth
  • Glutamine metabolism can produce ATP from the TCA cycle under aerobic conditions
  • Amino acid fermentation can generate energy through TCA cycle substrate level phosphorylation under hypoxic conditions
  • Hif-1α stabilization enhances aerobic fermentation
  • targeting glucose and glutamine will deprive the microenvironment of fermentable fuels
  • Although Warburg’s hypothesis on the origin of cancer has created confusion and controversy [37, 38, 39, 40], his hypothesis has never been disproved
  • Warburg referred to the phenomenon of enhanced glycolysis in cancer cells as “aerobic fermentation” to highlight the abnormal production of lactic acid in the presence of oxygen
  • Emerging evidence indicates that macrophages, or their fusion hybridization with neoplastic stem cells, are the origin of metastatic cancer cells
  • Radiation therapy can enhance fusion hybridization that could increase risk for invasive and metastatic tumor cells
  • Kamphorst et al. in showing that pancreatic ductal adenocarcinoma cells could obtain glutamine under nutrient poor conditions through lysosomal digestion of extracellular proteins
  • It will therefore become necessary to also target lysosomal digestion, under reduced glucose and glutamine conditions, to effectively manage those invasive and metastatic cancers that express cannibalism and phagocytosis.
  • Previous studies in yeast and mammalian cells show that disruption of aerobic respiration can cause mutations (loss of heterozygosity, chromosome instability, and epigenetic modifications etc.) in the nuclear genome
  • The somatic mutations and genomic instability seen in tumor cells thus arise from a protracted reliance on fermentation energy metabolism and a disruption of redox balance through excess oxidative stress.
  • According to the mitochondrial metabolic theory of cancer, the large genomic heterogeneity seen in tumor cells arises as a consequence, rather than as a cause, of mitochondrial dysfunction
  • A therapeutic strategy targeting the metabolic abnormality common to most tumor cells should therefore be more effective in managing cancer than would a strategy targeting genetic mutations that vary widely between tumors of the same histological grade and even within the same tumor
  • Tumor cells are more fit than normal cells to survive in the hypoxic niche of the tumor microenvironment
  • Hypoxic adaptation of tumor cells allows for them to avoid apoptosis due to their metabolic reprograming following a gradual loss of respiratory function
  • The high rates of tumor cell glycolysis and glutaminolysis will also make them resistant to apoptosis, ROS, and chemotherapy drugs
  • Despite having high levels of ROS, glutamate-derived from glutamine contributes to glutathione production that can protect tumor cells from ROS
    • Nathan Goodyear
      Nathan Goodyear on 08 Feb 18
       
      reason to eliminate glutamine in cancer patients and even GSH with cancer patients
  • It is clear that adaptability to environmental stress is greater in normal cells than in tumor cells, as normal cells can transition from the metabolism of glucose to the metabolism of ketone bodies when glucose becomes limiting
  • Mitochondrial respiratory chain defects will prevent tumor cells from using ketone bodies for energy
  • glycolysis-dependent tumor cells are less adaptable to metabolic stress than are the normal cells. This vulnerability can be exploited for targeting tumor cell energy metabolism
  • In contrast to dietary energy reduction, radiation and toxic drugs can damage the microenvironment and transform normal cells into tumor cells while also creating tumor cells that become highly resistant to drugs and radiation
  • Drug-resistant tumor cells arise in large part from the damage to respiration in bystander pre-cancerous cells
  • Because energy generated through substrate level phosphorylation is greater in tumor cells than in normal cells, tumor cells are more dependent than normal cells on the availability of fermentable fuels (glucose and glutamine)
  • Ketone bodies and fats are non-fermentable fuels
  • Although some tumor cells might appear to oxidize ketone bodies by the presence of ketolytic enzymes [181], it is not clear if ketone bodies and fats can provide sufficient energy for cell viability in the absence of glucose and glutamine
  • Apoptosis under energy stress is greater in tumor cells than in normal cells
  • A calorie restricted ketogenic diet or dietary energy reduction creates chronic metabolic stress in the body
  • . This energy stress acts as a press disturbance
  • Drugs that target availability of glucose and glutamine would act as pulse disturbances
  • Hyperbaric oxygen therapy can also be considered another pulse disturbance
  • The KD can more effectively reduce glucose and elevate blood ketone bodies than can CR alone making the KD potentially more therapeutic against tumors than CR
  • Campbell showed that tumor growth in rats is greater under high protein (>20%) than under low protein content (<10%) in the diet
  • Protein amino acids can be metabolized to glucose through the Cori cycle
  • The fats in KDs used clinically also contain more medium chain triglycerides
  • Calorie restriction, fasting, and restricted KDs are anti-angiogenic, anti-inflammatory, and pro-apoptotic and thus can target and eliminate tumor cells through multiple mechanisms
  • Ketogenic diets can also spare muscle protein, enhance immunity, and delay cancer cachexia, which is a major problem in managing metastatic cancer
  • GKI values of 1.0 or below are considered therapeutic
  • The GKI can therefore serve as a biomarker to assess the therapeutic efficacy of various diets in a broad range of cancers.
  • It is important to remember that insulin drives glycolysis through stimulation of the pyruvate dehydrogenase complex
  • The water-soluble ketone bodies (D-β-hydroxybutyrate and acetoacetate) are produced largely in the liver from adipocyte-derived fatty acids and ketogenic dietary fat. Ketone bodies bypass glycolysis and directly enter the mitochondria for metabolism to acetyl-CoA
  • Due to mitochondrial defects, tumor cells cannot exploit the therapeutic benefits of burning ketone bodies as normal cells would
  • Therapeutic ketosis with racemic ketone esters can also make it feasible to safely sustain hypoglycemia for inducing metabolic stress on cancer cells
    • Nathan Goodyear
      Nathan Goodyear on 08 Feb 18
       
      Ketones are much more than energy adaptabilit, but actually are therapeutic.
  • ketone bodies can inhibit histone deacetylases (HDAC) [229]. HDAC inhibitors play a role in targeting the cancer epigenome
  • Therapeutic ketosis reduces circulating inflammatory markers, and ketones directly inhibit the NLRP3 inflammasome, an important pro-inflammatory pathway linked to carcinogenesis and an important target for cancer treatment response
  • Chronic psychological stress is known to promote tumorigenesis through elevations of blood glucose, glucocorticoids, catecholamines, and insulin-like growth factor (IGF-1)
  • In addition to calorie-restricted ketogenic diets, psychological stress management involving exercise, yoga, music etc. also act as press disturbances that can help reduce fatigue, depression, and anxiety in cancer patients and in animal models
  • Ketone supplementation has also been shown to reduce anxiety behavior in animal models
  • This physiological state also enhances the efficacy of chemotherapy and radiation therapy, while reducing the side effects
  • lower dosages of chemotherapeutic drugs can be used when administered together with calorie restriction or restricted ketogenic diets (KD-R)
  • Besides 2-DG, a range of other glycolysis inhibitors might also produce similar therapeutic effects when combined with the KD-R including 3-bromopyruvate, oxaloacetate, and lonidamine
    • Nathan Goodyear
      Nathan Goodyear on 08 Feb 18
       
      oxaloacetate is a glycolytic inhibitor, as is doxycycline, and IVC.
  • A synergistic interaction of the KD diet plus radiation was seen
  • It is important to recognize, however, that the radiotherapy used in glioma patients can damage the respiration of normal cells and increase availability of glutamine in the microenvironment, which can increase risk of tumor recurrence especially when used together with the steroid drug dexamethasone
  • Poff and colleagues demonstrated that hyperbaric oxygen therapy (HBOT) enhanced the ability of the KD to reduce tumor growth and metastasis
  • HBOT also increases oxidative stress and membrane lipid peroxidation of GBM cells in vitro
  • The effects of the KD and HBOT can be enhanced with administration of exogenous ketones, which further suppressed tumor growth and metastasis
  • Besides HBOT, intravenous vitamin C and dichloroacetate (DCA) can also be used with the KD to selectively increase oxidative stress in tumor cells
  • Recent evidence also shows that ketone supplementation may enhance or preserve overall physical and mental health
  • Some tumors use glucose as a prime fuel for growth, whereas other tumors use glutamine as a prime fuel [102, 186, 262, 263, 264]. Glutamine-dependent tumors are generally less detectable than glucose-dependent under FDG-PET imaging, but could be detected under glutamine-based PET imaging
  • GBM and use glutamine as a major fuel
  • Many of the current treatments used for cancer management are based on the view that cancer is a genetic disease
  • Emerging evidence indicates that cancer is a mitochondrial metabolic disease that depends on availability of fermentable fuels for tumor cell growth and survival
  • Glucose and glutamine are the most abundant fermentable fuels present in the circulation and in the tumor microenvironment
  • Low-carbohydrate, high fat-ketogenic diets coupled with glycolysis inhibitors will reduce metabolic flux through the glycolytic and pentose phosphate pathways needed for synthesis of ATP, lipids, glutathione, and nucleotides
  • Nathan Goodyear on 09 Jul 17
     
    Cancer is a mitochondrial disease? So says the well published Dr Seyfried. Glucose and glutamine drive cancer growth.
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