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Nathan Goodyear

Treatment of chronic hepatitis C virus ... [J Clin Gastroenterol. 2005] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...16082287

IV vitamin C hepatitis IV intravenous vitamin C antioxidant therapy antioxidants

shared by Nathan Goodyear on 25 Sep 13 - No Cached
  • Nathan Goodyear on 25 Sep 13
     
    Treatment of chronic Hepatitis with antioxidants, particularly IV vitamin C with glutathione, B complex and glycyrrhizin results in normalization of liver enzymes in 44% of patients with elevated enzymes with HCV.
Nathan Goodyear

From the Cover: Pharmacologic doses of ascorbate act as a prooxidant and decrease growt... - 0 views

www.ncbi.nlm.nih.gov/...PMC2516281

cancer IV intravenous vitamin C IV vitamin C

shared by Nathan Goodyear on 18 Sep 13 - No Cached
  • An extensive panel of 43 tumor and 5 normal cell lines were exposed to ascorbate in vitro for ≤2 h to mimic clinical pharmacokinetics
  • effective concentration that decreased survival 50% (EC50) was determined. EC50 was <10 mM for 75% of tumor cells tested, whereas cytotoxicity was not evident in normal cells with >20 mM ascorbate
  • The addition of catalase to the medium ameliorated death of ovarian carcinoma (Ovcar5), pancreatic carcinoma (Pan02), and glioblastoma (9L) cells exposed to 10 mM ascorbate (1 h), indicating cytotoxicity was mediated by H2O2
  • ...8 more annotations...
  • A treatment dose of 4 g ascorbate/kg body weight either once or twice daily did not produce any discernible adverse effects
  • Xenograft experiments showed that parenteral ascorbate as the only treatment significantly decreased both tumor growth and weight by 41–53%
  • Peak plasma concentrations of ascorbate approached 30 mM
  • Pharmacologic concentrations of ascorbate decreased tumor volumes 41–53% in diverse cancer types known for both their aggressive growth and limited treatment options.
  • Our findings showed that pharmacologic ascorbic acid concentrations were cytotoxic to many types of cancer cells in vitro (Fig. 1A) and significantly impeded tumor progression in vivo without toxicity to normal tissues
  • The amelioration of ascorbate cytotoxicity in vitro by the addition of catalase was consistent among sensitive cancer cells (Fig. 1B) and points unambiguously to H2O2 generation in the extracellular medium
  • the current in vivo data support that pharmacologic ascorbate concentrations, which can readily be achieved in humans (Fig. 3E), diminished growth of several aggressive cancer types in mice (Fig. 2) without causing apparent adverse effects.
  • These intratumoral H2O2 concentrations of >125 μM persisted for >3 h after ascorbate administration
  • Nathan Goodyear on 18 Sep 13
     
    Tumor xenograft model in mice finds reduction in growth rates of ovarian cancer, pancreatic cancer, and glioblastoma with daily IV vitamin C.
Nathan Goodyear

The Nitrilosides(Vitamin B-17) - 1 views

users.navi.net/krebs3.htm

Laetrile vitamin B17 amygdalin cancer nitrilosides

shared by Nathan Goodyear on 16 Apr 18 - No Cached
  • Nathan Goodyear on 16 Apr 18
     
    Dr. Krebs' Jr paper on nitrilosides i.e. laetril or vitamin B17 in its use in the fight against cancer.  This is a reprint from the Journal of Applied Nutrition from 1970.
Justin Tantrum

Perfect Body Building Supplements - 3 views

I can honestly recommend Body Workshop Supplements to anyone who is aiming for a high quality protein source supplement. I have taken their offered product immediately after my work-out and it prov...

supplements

started by Justin Tantrum on 28 Mar 12 no follow-up yet
Nathan Goodyear

S-adenosylmethionine reduces the progress of... [Neurobiol Aging. 2012] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...22221883

SAMe Alzheimer's disease Alzheimer's aging

shared by Nathan Goodyear on 27 Jun 12 - No Cached
  • Nathan Goodyear on 27 Jun 12
     
    SAMe helps to correct disordered homocysteine metabolism due to B- vitamin deficiency found in Alzheimer's disease.  SAMe show to reduce amyloid production, improve memory, decrease Tau, and reduced plaque formation.  Now, this was in a mice model, but SAMe as a methyl donor can benefit clients with dementia with minimal side effects.
Nathan Goodyear

S-adenosylmethionine prevents oxidative str... [J Alzheimers Dis. 2010] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...20413874

SAMe Alzheimer's disease Alzheimer's

shared by Nathan Goodyear on 27 Jun 12 - No Cached
  • Nathan Goodyear on 27 Jun 12
     
    SAMe shown to be neuroprotective by increasing SOD activity, increasing glutathione production and decreasing homocysteine levels in Alzheimer's even in the presence of vitamin B deficiency.
olivehealthcare

Blood Tests | Blood Test at Home | Mobile Phlebotomy - 0 views

www.olivehealthandtravel.co.uk/blood-tests

Blood Tests Blood test at home TB test

shared by olivehealthcare on 18 Jun 18 - No Cached
  • olivehealthcare on 18 Jun 18
     
    We offers the full range of blood tests with results available as early as 48 hours. Home-visits (mobile phlebotomy) offered for blood sample collection for both NHS and Private blood tests. Pregnancy HCG, Hepatitis B Immunity, Tuberculosis, Occupational Health, Vitamin tests, Glucose, Cholesterol, etc.
Nathan Goodyear

Normal Flora - Medical Microbiology - NCBI Bookshelf - 0 views

www.ncbi.nlm.nih.gov/...NBK7617

flora gut flora gut microbiome gut microbiota

shared by Nathan Goodyear on 05 May 15 - No Cached
  • Concentrations of 109 to 1011 bacteria/g of contents are frequently found in human colon
  • more than 400 species have been identified
  • 95 to 99 percent belong to anaerobic genera such as Bacteroides, Bifidobacterium, Eubacterium, Peptostreptococcus, and Clostridium
  • ...2 more annotations...
  • hese genera proliferate, occupy most available niches, and produce metabolic waste products such as acetic, butyric, and lactic acids
  • Anaerobic bacteria can then deconjugate bile acids in this region and bind available vitamin B12 so that the vitamin and fats are malabsorbed
  • Nathan Goodyear on 05 May 15
     
    normal flora of the body
Nathan Goodyear

Prooxidative inhibition against NF-κB-mediated inflammation by pharmacologica... - 0 views

www.sciencedirect.com/...S0891584922000181

vitamin C nuclear factor kappa B NF-KappaB v nuclear factor κB inflammation ascorbic acid NF-κB

shared by Nathan Goodyear on 16 Jul 22 - No Cached
  • Nathan Goodyear on 16 Jul 22
     
    The title tells it all.
Nathan Goodyear

Quantitative data on the magnitude of the systemic inflammatory response and its effect... - 0 views

www.ajcn.org/...64.abstract

inflammation micronutrients Vitamin A B-6 C D

shared by Nathan Goodyear on 01 Feb 12 - No Cached
  • Nathan Goodyear on 01 Feb 12
     
    As systemic inflammation goes up: the reliability of plasma micronutrients goes down.  The micronutrients listed in this study (Se, A, B-6, C and D) decreased as inflammation increased.  The take home is, the reliability of micronutrient testing must take into account inflammation
Nathan Goodyear

Homocysteine and MTHFR Mutations - 0 views

circ.ahajournals.org/...e289.full

homocysteine MTHFR CVD cardiovascular death CAD c677T A1298c

shared by Nathan Goodyear on 02 Feb 15 - No Cached
  • The most common MTHFR mutation is called the MTHFR C677T mutation
  • Another common mutation is called MTHFR A1298C
  • Having only one mutation, ie, being heterozygous, is, from a medical perspective, irrelevant. Even when 2 MTHFR mutations are present (eg, 2 C677T mutations, or one C677T mutation and one A1298C mutation)
  • ...4 more annotations...
  • Although these mutations do impair the regulation of homocysteine, adequate folate levels essentially “cancel out” this defect.
  • Regardless of whether you have an MTHFR mutation in both genes or not, the treatment for elevated homocysteine is the same—dietary intervention and supplementation with folic acid and vitamins B6 and B12
  • Overall, evidence from these studies indicates that, so long as the homocysteine level is normal, MTHFR mutations do not significantly increase the risk of heart attack or stroke
  • Studies investigating the association of MTHFR mutations and venous blood clots have been inconsistent, with some studies showing a slight association, but most studies have not shown any association
  • Nathan Goodyear on 02 Feb 15
     
    Good review of MTHFR and homocysteine.
Nathan Goodyear

Folate | Linus Pauling Institute | Oregon State University - 0 views

lpi.oregonstate.edu/...folate

Folate folic acid MTHFR micronutrients

shared by Nathan Goodyear on 23 Aug 15 - No Cached
  • Nathan Goodyear on 23 Aug 15
     
    Nice review on the difference b/t Folate and Folic acid.  Also, brief but worthy of a read, review of the MTHFR polymorphism 677.
Nathan Goodyear

Promising role for Gc-MAF in cancer immunotherapy: from bench to bedside - 0 views

www.ncbi.nlm.nih.gov/...PMC5686300

nagalase Gc-MAF cancer

shared by Nathan Goodyear on 29 Jan 18 - No Cached
  • MAF precursor activity has also been lost or reduced after Gc-globulin treatment in some cancer cell lines
  • This appears to result from the deglycosylated ɑ-N-acetylgalactosaminidase (nagalase) secreted from cancerous cells
  • Nagalase has been detected in many cancer patients, but not in healthy individuals
  • ...31 more annotations...
  • Studies have shown that the production of nagalase has a mutual relationship with Gc-MAF level and immunosuppression
  • It has been demonstrated that serum levels of nagalase are good prognosticators of some types of cancer
  • The nagalase level in serum correlates with tumor burden and it has been shown that Gc-MAF therapy progresses, nagalase activity decreases
  • It has been shown that Gc-MAF can inhibit the angiogenesis induced by pro-inflammatory prostaglandin E1
  • The effect of Gc-MAF on chemotaxis or activation of tumoricidal macrophages is likely the main mechanism against angiogenesis.
  • Administration of Gc-MAF stimulates immune-cell progenitors for extensive mitogenesis, activates macrophages and produces antibodies. “This indicates that Gc-MAF is a powerful adjuvant for immunization.”
  • Cancer cell lines do not develop into tumor genes in mouse models after Gc-MAF-primed immunization (29-31) and the effect of Gc-MAF has been approved for macrophage stimulation for angiogenesis, proliferation, migration and metastatic inhibition on tumors induced by MCF-7 human breast cancer cell line
  • The protocol included: "a high dose of second-generation Gc-MAF (0.5 ml) administered twice a week intramuscularly for a total of 21 injections.”
  • Yamamoto et al. showed that the administration of Gc-MAF to 16 patients with prostate cancer led to improvements in all patients without recurrence
  • Inui et al. reported that a 74-year-old man diagnosed with prostate cancer with multiple bone metastases was in complete remission nine months after initiation of GcMAF therapy simultaneously with hyper T/NK cell, high-dose vitamin C and alpha lipoic acid therapy
  • It has also been approved for non-neoplastic diseases such as autism (41), multiple sclerosis (42, 43), chronic fatigue syndrome (CFS) (40), juvenile osteoporosis (44) and systemic lupus erythematous (45).
  • Gc-MAF has been verified for use in colon, thyroid (38), lung (39), liver, thymus (36), pancreatic (40), bladder and ovarian cancer and tongue squamous carcinoma
  • Prostate, breast, colon, liver, stomach, lung (including mesothelioma), kidney, bladder, uterus, ovarian, head/neck and brain cancers, fibrosarcomas and melanomas are the types of cancer tested thus far
  • weekly administration of 100 ng Gc-MAF to cancer at different stages and types showed curative effects at different follow-up times
  • this treatment has been suggested for non-anemic patients
  • Studies have shown that weekly administration of 100 ng Gc-MAF to cancer patients had curative effects on a variety of cancers
  • Because the half-life of the activated macrophages is approximately one week, it must be administered weekly
  • In vivo weekly intramuscular administration of Gc-MAF (100 ng) for 16-22 weeks was used to treat patients with breast cancer
  • individuals harboring different VDR genotypes had different responses to Gc-MAF and that some genotypes were more responsive than others
  • Administration of Gc-MAF for cancer patients exclusively activates macrophages as an important cell in adaptive immunity
  • Gc-MAF supports humoral immunity by producing, developing and releasing large quantities of antibodies against cancer. Clinical evidence from a human model of breast cancer patients supports this hypothesis
  • There is also evidence that confirms the tumoricidal role of Gc-MAF via Fc-receptor mediation
  • It is likely that the best therapeutic responses will be observed when the nutritional and inflammatory aspects are taken together with stimulation of the immune system
  • it should be noted that no harmful side effects of Gc-MAF treatment have been reported, even when it was successfully administered to autistic children
  • The natural activation mechanism of macrophages by Gc-MAF is so natural and it should not have any side effects on humans or animal models even in cell culture
  • Besides the Gc-MAF efficacy on macrophage activity, it can be a potential anti-angiogenic agent (28) and an inhibitor of the migration of cancerous cells in the absence of macrophages (47).
  • Activating or modifying natural killer cells, dendritic cells, DC, CTL, INF and IL-2 have all been recommended for cancer immunotherapy
  • It has been reported that nagalase cannot deglycosylate Gc-MAF as it has specificity for Gc globulin alone
  • inflammation-derived macrophage activation with the participation of B and T lymphocytes is the main mechanism
  • macrophages highly-activated by the addition of Gc-MAF can show tumoricidal activity
  • Previous clinical investigations have confirmed the efficacy of Gc-MAF. In addition to activating existing macrophages, Gc-MAF is a potent mitogenic factor that can stimulate the myeloid progenitor cells to increase systemic macrophage cell counts by 40-fold in four days
  • Nathan Goodyear on 29 Jan 18
     
    great review on Gc-MAF in cancer.  An increase in nagalase blocks Gc-protein to Gc-MAF activity leaving the host immune system compromised.
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