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Nathan Goodyear

Obesity - Amelioration of Lipid Abnormalities by [alpha]-Lipoic acid Through Antioxidat... - 0 views

www.nature.com/...oby2011121a.html

ALA alpha-lipoic-acid lipoic acid obesity insulin oxidative stress damage inflammation inflammatory markers cytokine cytokines TNF-alpha IL-6 adiponectin IV intravenous oxidized LDL

shared by Nathan Goodyear on 01 Aug 12 - No Cached
  • Nathan Goodyear on 01 Aug 12
     
    alpha lipoic acid found to improve insulin sensitivity and reduce oxidative stress and inflammatory markers.  In this study, IV ALA was given daily for 2 weeks, and the result was reduced oxidized LDL and all other lipids, improved insulin sensitivity, reduced TNF-alpha, IL-6, and 8-iso-prostaglandin, and increased adiponectin.
Nathan Goodyear

Urinary Estrogens and Estrogen Metabolites and Subsequent Risk of Breast Cancer among P... - 0 views

cancerres.aacrjournals.org/...696.full

estrogen metabolites estrogen metabolism ER estrogen receptors ROS hormones cancer breast cancer

shared by Nathan Goodyear on 07 Oct 15 - No Cached
  • both 2- and 4-catechol estrogen metabolites bind to the ER with affinities comparable with estradiol, 4-catechol estrogen metabolites have lower dissociation rates than estradiol and an enhanced ability to upregulate ER-dependent processes
  • 2-catechol estrogen metabolites act as either weak mitogens (39) or weak inhibitors of cell proliferation
  • While 16α-hydroxyestrone binds to the ER with lower affinity than estradiol, it binds covalently (41) and leads to a constitutively activated ER
  • ...15 more annotations...
  • 4-hydroxyestradiol and 16α-hydroxyestrone increasing proliferation and decreasing apoptosis in a manner similar to estradiol; however, these effects were achieved only at concentrations 10-fold higher than estradiol (39). In contrast, 2-hydroxyestradiol did not have substantial proliferative or antiapoptotic effects
  • In our study, the associations with both 2-hydroxyestrone and 16α-hydroxyestrone were nonsignificantly inverse and we did not observe a consistent trend or significant associations between the 2-hydroxyestrone:16α-hydroxyestrone ratio and breast cancer risk
  • Ratios of the 3 hydroxylation pathways were not significantly associated with risk although the 2:16-pathway and 4:16-pathway ratios were suggestively inversely associated
  • a significant inverse association with the ratio of parent estrogens to estrogen metabolites
  • several potentially estrogenic and genotoxic mechanisms
  • Estrogen metabolites also can be genotoxic
  • Catechol estrogens can be oxidized into quinones and induce DNA damage directly through the formation of DNA adducts, or indirectly via redox cycling and generation of reactive oxygen species
  • the oxidized forms of the catechol estrogens differ in their ability to damage DNA through adducts, with oxidized 2-catechols forming stable and reversible DNA adducts and oxidized 4-catechols forming unstable adducts, which lead to depurination and mutations
  • 2- and 4-catechols have been shown to produce reactive oxygen species and induce oxidative DNA damage
  • act independently from the ER
  • 16α-Hydroxyestrone also may be genotoxic
  • While the catechol estrogens have estrogenic and genotoxic potential, the methylated catechol estrogens, which are catechol estrogens with one hydroxyl group methylated, have been hypothesized to lower the risk of breast cancer
  • The suggested mechanisms are indirect, by decreasing circulating levels of catechol estrogens and thereby the opportunity for catechols to exert genotoxic or proliferative effects, or direct, by inhibiting tumor growth and inducing apoptosis
  • the balance between phase I (oxidation) and phase II (methylation) metabolism of estrogen may be important in hormonally related cancer development.
  • Despite the estrogenic and genotoxic potential of many of the estrogen metabolites, we only observed a significantly increased breast cancer risk with one estrogen metabolite, 17-epiestriol, which has particularly strong estrogenic activity and binds to both ERα and ERβ with an affinity comparable with estradiol
  • Nathan Goodyear on 07 Oct 15
     
    review of estrogen metabolites and breast cancer risk in premenopausal women.
Nathan Goodyear

The two faces of α- and γ-tocopherols: an in ... [J Nutr Biochem. 2011] - Pub... - 0 views

www.ncbi.nlm.nih.gov/...21715151

Vitamin E tocopherols anti-oxidants pro-oxidants

shared by Nathan Goodyear on 29 Sep 11 - No Cached
  • Nathan Goodyear on 29 Sep 11
     
    Vitamin E shown to have pro-oxidant effects with HDL and anti-oxidant effects with LDL and vLDL
Nathan Goodyear

ScienceDirect - Food and Chemical Toxicology : Neuroprotective effect of ginger on anti... - 0 views

www.sciencedirect.com/science

Ginger diabetes oxidative stress

shared by Nathan Goodyear on 27 Apr 11 - No Cached
  • A marked decrease in anti-oxidant marker enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), reduced glutathione (GSH) and increase in malondialdehyde (MDA) was observed in the diabetic rats
  • inger may be used as therapeutic agent in preventing complications in diabetic patients.
  • These results suggest that ginger exhibit a neuroprotective effect by accelerating brain anti-oxidant defense mechanisms and down regulating the MDA levels to the normal levels in the diabetic rats
  • Nathan Goodyear on 27 Apr 11
     
    Ginger reduces oxidative stress in diabetic rat model
Nathan Goodyear

Lead exposure, polymorphisms in genes related to oxidative stress and risk of adult bra... - 0 views

www.ncbi.nlm.nih.gov/...PMC2750838

meningioma CNS tumor tumors glioblastoma brain oxidative damage oxidative stress

shared by Nathan Goodyear on 04 Mar 13 - No Cached
  • Nathan Goodyear on 04 Mar 13
     
    another study that showed that lead exposure in susceptible individuals increased risk of CNS tumors, including menngiomas, and gliomas.  The apparent mechanism in this study was proposed through oxidative damage.  
Nathan Goodyear

Acute prooxidant effects of vitamin C in... [Free Radic Biol Med. 2005] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...15917185

IV vitamin C antioxidant pro-oxidant EDTA EDTA chelation vitamin C vitamin

shared by Nathan Goodyear on 05 Jun 13 - No Cached
  • Nathan Goodyear on 05 Jun 13
     
    This study found a pro oxidant effect of the addition of 5 grams of IV vitamin C with EDTA chelation.  As dosing of IV vitamin C goes, 5 grams is quite small.  Vitamin C has been shown to have varying effects (pro oxidant versus antioxidant) dictated by the dosage.  One wonders if higher dosing IV vitamin C provides antioxidant effects?
Nathan Goodyear

EDTA chelation therapy, without added vitamin C, decreases oxidative DNA damage and lip... - 0 views

www.altmedrev.com/...56.pdf

EDTA EDTA chelation vitamin C IV vitamin C CVD cardiovascular disease Diabetes

shared by Nathan Goodyear on 05 Jun 13 - No Cached
  • Nathan Goodyear on 05 Jun 13
     
    This study found that the elimination of hight dose vitamin C in EDTA chelation removed the pro oxidant effect. This provided an antioxidant effect only from EDTA chelation, which is beneficial in the oxidative damage diseases like CVD and Diabetes
Nathan Goodyear

alpha-Lipoic acid and ascorbate prevent LDL... [Mol Cell Biochem. 2008] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...18026819

alpha lipoic acid vitamin C oxidized LDL LDL cholesterol CVD cardiovascular disease

shared by Nathan Goodyear on 20 Feb 13 - No Cached
  • Nathan Goodyear on 20 Feb 13
     
    Alpha lipoic acid and vitamin C shown to protect against oxidized LDL.  When discussing the negative effects of LDL, the real risk associated with LDL is whether it is oxidized or not.  Alpha lipoic acid and Vitamin C prevent this and thus protect the vascular endothelium.
Nathan Goodyear

T3 increases mitochondrial ATP production in oxidative muscle despite increased express... - 0 views

ajpendo.physiology.org/...E761.full.pdf

T3 hypothyroid hypothyroidism Cancer

shared by Nathan Goodyear on 28 Jun 13 - No Cached
  • Nathan Goodyear on 28 Jun 13
     
    T3 increases mitochondrial oxidative phosphorylation. This has huge impacts on which hypothyroidism is currently managed (only evaluate TSH and T4) and disease implication. We know that decoupling of oxidative phosporylation and a shift to glycolysis and glutaminolysis (substrate-level phosphorylation) results in genomic mutability and cancer, then a low T3 has implications in cancer prevention
Nathan Goodyear

Oxidative Stress and Stress-Activated Signaling Pathways: A Unifying Hypothesis of Type... - 0 views

edrv.endojournals.org/...599.long

free radicals oxidative stress damage inflammation type II DM alpha lipoic acid alpha-lipoic-acid diabetes

shared by Nathan Goodyear on 02 Aug 12 - No Cached
  • In patients with diabetes, LA levels are reduced (48, 74, 103). LA has long been used for the treatment of diabetic neuropathy in Germany
  • evidence indicates that it increases insulin sensitivity in patients with type 2 diabetes
  • LA has been shown to 1) quench free radicals, 2) prevent singlet oxygen-induced DNA damage, 3) exhibit chelating activity, 4) reduce lipid peroxidation, 5) increase intracellular glutathione levels, and 6) prevent glycation of serum albumin (73, 74). LA is able to reduce oxidative stress-mediated NF-κB activation in vitro (74, 108, 109) and in patients with type 2 diabetes
  • ...2 more annotations...
  • Activation of NF-κB can also be blocked by several other thiol-containing antioxidants including N-acetyl-l-cysteine (NAC)
  • Other clinically available antioxidants reported to have antiinflammatory, antioncogenic, and/or antiatherogenic properties that have been shown to block the activation of NF-κB include resveratrol (115, 116), (-)-epicatechin-3-gallate (117), pycnogenol (118), silymarin (119), and curcumin (120)
  • Nathan Goodyear on 02 Aug 12
     
    Great read!  If you want to see how free radicals and oxidative stress contribute to inflammation and disease (DM in this case), read this article.
Nathan Goodyear

Apolipoprotein E allele-dependent antioxidant activity in brains with Alzheimer's disease - 0 views

www.neurology.org/...2319.abstract

antioxidant alzheimer disease brains neurology brain TBARS oxidative stress lipid peroxidation

shared by Nathan Goodyear on 13 Jun 12 - No Cached
  • Nathan Goodyear on 13 Jun 12
     
    TBARS were found elevated in Alzheimer's individuals.  TBARS are the result of oxidative stress.  Thus TBARS can be used to evaluate lipid peroxidation (oxidative damage) in the brain.
Nathan Goodyear

Polysaccharides from Cordyceps sinensis mycelium ... [Pharm Biol. 2014] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...24047103

Cordyceps Cordyceps sinensis exercise performance oxidative stress

shared by Nathan Goodyear on 27 Jan 14 - No Cached
  • Nathan Goodyear on 27 Jan 14
     
    Mouse model finds that Cordyceps increased the interval to exhaustive exercise induced oxidative stress.  SOD, Cat, and GPx were increased in the low, intermediate, and high dose Cordyceps groups.  Oxidative stress markers MDA and 8-OHdG were lower in all groups
Nathan Goodyear

Oxidative Stress in Autism - 0 views

www.modernhcp.com/...imcj%208061.pdf

oxidative stress autism ASD oxidative stress selenium detoxification

shared by Nathan Goodyear on 14 Aug 13 - No Cached
  • Nathan Goodyear on 14 Aug 13
     
    high oxidative stress in autism will compromise detoxification. OR is it the other way around? Low Selenium is commonly found in those with autism.
Nathan Goodyear

Urinary estrogens and estrogen metabolites and subsequent risk of breast cancer among p... - 0 views

www.ncbi.nlm.nih.gov/...PMC3271178

estrogen metabolites estrogen metabolites cancer hormones

shared by Nathan Goodyear on 04 Oct 15 - No Cached
  • While the catechol estrogens have estrogenic and genotoxic potential, the methylated catechol estrogens, which are catechol estrogens with one hydroxyl group methylated, have been hypothesized to lower risk of breast cancer.
  • Despite the estrogenic and genotoxic potential of many of the EM, we only observed a significantly increased breast cancer risk with one EM, 17-epiestriol, which has particularly strong estrogenic activity and binds to both ERα and ERβ with an affinity comparable to estradiol
  • We did not observe reduced risk for higher concentrations of 2-pathway EM relative to 16-pathway EM, nor did we observe a consistent benefit of higher concentrations of methylated catechol EM compared with catechol EM.
  • ...4 more annotations...
  • EM also can be genotoxic, but the individual EM vary in their ability to induce DNA damage
  • Catechol estrogens can be oxidized into quinones and induce DNA damage directly through the formation of DNA adducts, or indirectly via redox cycling and generation of reactive oxygen species
  • the oxidized forms of the catechol estrogens differ in their ability to damage DNA through adducts, with oxidized 2-catechols forming stable and reversible DNA adducts and oxidized 4-catechols forming unstable adducts, which lead to depurination and mutations
  • 2- and 4-catechols have been shown to produce reactive oxygen species and induce oxidative DNA damage (46). These catechols also induce neoplastic transformation in ER-cells, and thus act independently from the ER
  • Nathan Goodyear on 04 Oct 15
     
    Estrogen metabolites.
Nathan Goodyear

Role of oxidative stress from mitochondria on agin... [Cornea. 2007] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...17881913

oxidative mitochondria stress cancer

shared by Nathan Goodyear on 08 Feb 11 - No Cached
  • t is suggested that oxidative stress from mitochondria plays an important role in apoptosis, which leads to precocious aging and cancer.
  • Nathan Goodyear on 08 Feb 11
     
    oxidative stress, mitochondrial death, and cancer 
Nathan Goodyear

5-Hydroxytrytophan Inhibits tert-Butylhydroperoxide (t-BHP)-Induced Oxidative... - 0 views

pubs.acs.org/...jf904201h

5 hydroxytrytophan 5-HTP glutathione NF-kappaB

shared by Nathan Goodyear on 27 May 11 - No Cached
  • Nathan Goodyear on 27 May 11
     
    5-HTP, precursor to serotonin, shows anti-oxidant activity, reduces oxidative damage, suppressed pro-inflammatory p38MAPK and NF-kappaB, and helps to prevent glutathione depletion
Nathan Goodyear

Journal of Clinical Investigation -- Oxidation of tetrahydrobiopterin leads to uncoupli... - 0 views

www.jci.org/14172

tetrahydrobiopterin cardiovascular disease hypertension

shared by Nathan Goodyear on 29 Apr 11 - No Cached
  • Tetrahydrobiopterin is a critical cofactor for the NO synthases
  • at hypertension produces a cascade involving production of ROSs from the NADPH oxidase leading to oxidation of tetrahydrobiopterin and uncoupling of endothelial NO synthase (eNOS). This decreases NO production and increases ROS production from eNOS
  • Tetrahydrobiopterin oxidation may represent an important abnormality in hypertension
  • ...1 more annotation...
  • Treatment strategies that increase tetrahydrobiopterin or prevent its oxidation may prove useful in preventing vascular complications of this common disease.
  • Nathan Goodyear on 29 Apr 11
     
    tetrahydrobiopterin deficiency plays role in cardiovasular disease
Nathan Goodyear

Metabolic biomarkers of increased oxidative stress... [Am J Clin Nutr. 2004] - PubMed r... - 0 views

www.ncbi.nlm.nih.gov/...15585776

ASD autism spectrum disorder detoxification children SAMe SAH homocysteine cystathionine glutathione adenosine

shared by Nathan Goodyear on 05 Jul 11 - No Cached
  • children with autism had significantly lower baseline plasma concentrations of methionine, SAM, homocysteine, cystathionine, cysteine, and total glutathione and significantly higher concentrations of SAH, adenosine, and oxidized glutathione
  • This metabolic profile is consistent with impaired capacity for methylation (significantly lower ratio of SAM to SAH) and increased oxidative stress (significantly lower redox ratio of reduced glutathione to oxidized glutathione) in children with autism
  • increased vulnerability to oxidative stress and a decreased capacity for methylation may contribute to the development and clinical manifestation of autism.
  • Nathan Goodyear on 05 Jul 11
     
    detoxification impairment and the markers to assess it in children with ASD
Nathan Goodyear

Unveiling the Mechanisms for Decreased Glutathione in Individuals with HIV Infection - 0 views

connection.ebscohost.com/...ione-individuals-hiv-infection

glutathione GSH Nrf2 GSSG HIV inflammation oxidative Stress

shared by Nathan Goodyear on 07 Jan 15 - No Cached
  • Nathan Goodyear on 07 Jan 15
     
    men with HIV have GSH depleted macrophages.  GSH is the reduced, ready to act form of Glutathione.  In contrast, the macrophages were high in the oxidized form of Glutathione--GSSG.  In HIV, the high inflammation increased oxidative stress, likely overwhelmed Nrf2 activation and resulted in decreased GSH synthase transcription and thus decreased Glutathione production balance.
Nathan Goodyear

Frontiers | Management of Glioblastoma Multiforme in a Patient Treated With Ketogenic M... - 0 views

www.frontiersin.org/...full

press-pulse therapy hyperbaric ketogenic metabolic therapy cancer ketogenic diet Glioblastoma glioblastoma multiforme HBOT nutrition

shared by Nathan Goodyear on 01 Apr 18 - No Cached
  • The SOC for GBM was modified in this patient to initiate KMT prior to surgical resection, to eliminate steroid medication, and to include HBOT as part of the therapy
  • the greatest therapeutic benefit for patients (near 1.0)
  • The observed reduction in blood glucose in our patient would reduce lactic acid fermentation in the tumor cells, while the elevation of ketone bodies would fuel normal cells thus protecting them from hypoglycemia and oxidative stress
  • ...30 more annotations...
  • Previous studies showed that GBM survival and tumor growth was correlated with blood glucose levels
  • Evidence indicates that glioma cells cannot effectively use ketone bodies for energy due to defects in the number, structure, and function of their mitochondria
  • The accuracy of the GKI as a predictor for therapeutic efficacy, however, is better when ketone bodies are measured from the blood than when measured from the urine
  • A reduction of glucose-driven lactic acid fermentation would not only increase tumor cell apoptosis, but would also reduce inflammation and edema in the tumor microenvironment thus reducing tumor cell angiogenesis and invasion
  • Besides serving as a metabolic fuel for GBM, glutamine is also an essential metabolite for normal immune cells
  • therapies that inhibit glutamine availability and utilization must be strategically employed to avoid inadvertent impairment of immune cell functions
  • we used the non-toxic green tea extract, EGCG, and chloroquine in an attempt to limit glutamine availability to the tumor cells
  • EGCG is thought to target the glutamate dehydrogenase activity that facilitates glutamine metabolism in GBM cells
  • Chloroquine, on the other hand, will inhibit lysosomal digestion thus restricting fermentable amino acids and carbohydrates from phagocytosed materials in the tumor microenvironment
  • HBOT to increase oxidative stress in the tumor cells
  • As glucose and glutamine fermentation protect tumor cells from oxidative stress, reduced availability of these metabolites under ketosis could enhance the therapeutic action of HBOT, as we recently described
  • Prior to subtotal tumor resection and standard of care (SOC), the patient conducted a 72-h water-only fast
  • Following the fast, the patient initiated a vitamin/mineral-supplemented ketogenic diet (KD) for 21 days that delivered 900 kcal/day
  • KD (increased to 1,500 kcal/day at day 22
  • the patient received metformin (1,000 mg/day), methylfolate (1,000 mg/day), chloroquine phosphate (150 mg/day), epigallocatechin gallate (400 mg/day), and hyperbaric oxygen therapy (HBOT) (60 min/session, 5 sessions/week at 2.5 ATA)
  • Biomarkers showed reduced blood glucose and elevated levels of urinary ketones with evidence of reduced metabolic activity (choline/N-acetylaspartate ratio) and normalized levels of insulin, triglycerides, and vitamin D
  • This is the first report of confirmed GBM treated with a modified SOC together with KMT and HBOT, and other targeted metabolic therapies
  • Glioblastoma multiforme (GBM) is the most common and malignant of the primary adult brain cancers
  • less than 20% of younger adults generally survive beyond 24 months
  • glucose and glutamine are the primary fuels that drive the rapid growth of most tumors including GBM
  • Glucose drives tumor growth through aerobic fermentation (Warburg effect), while glutamine drives tumor growth through glutaminolysis
  • The fermentation waste products of these molecules, i.e., lactic acid and succinic acid, respectively, acidify the tumor microenvironment thus contributing further to tumor progression
  • Glucose and glutamine metabolism is also responsible for the high antioxidant capacity of the tumor cells thus making them resistant to chemo- and radiotherapies
  • The reliance on glucose and glutamine for tumor cell malignancy comes largely from the documented defects in the number, structure, and function of mitochondria and mitochondrial-associated membranes
  • These abnormalities cause the neoplastic GBM cells to rely more heavily on substrate level phosphorylation than on oxidative phosphorylation for energy
  • dexamethasone not only increases blood glucose levels but also increases glutamine levels through its induction of glutamine synthetase activity
    • Nathan Goodyear
      Nathan Goodyear on 21 May 18
       
      use mannitol instead
  • Calorie restriction and restricted KD are anti-angiogenic, anti-inflammatory, anti-invasive, and also kill tumor cells through a proapoptotic mechanism
  • Evidence also shows that therapeutic ketosis can act synergistically with several drugs and procedures to enhance cancer management improving both progression free and overall survival
  • hyperbaric oxygen therapy (HBOT) increases oxidative stress on tumor cells especially when used alongside therapies that reduce blood glucose and raise blood ketones
  • The glutamine dehydrogenase inhibitor, epigallocatechin gallate (EGCG) is also proposed to target glutamine metabolism
  • Nathan Goodyear on 01 Apr 18
     
    Case study of Glioblastoma treated with ketogenic metabolic therapy as an adjuct to modified standard therapy.
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