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Oxidal - Liquid Dietary Supplement For Oxidation Support

Discussion in 'IdeaLabs' started by haidut, May 8, 2015.

  1. Jsaute21

    Jsaute21 Member

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    Thanks i will run those tests and let you know the feedback i receive.
     
  2. Jsaute21

    Jsaute21 Member

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    @haidut oxidal has become one of my favorite supplements. At what dose have you been using lately? I usually just do two drops per day but i am thinking about adding two in with lunch as well.
     
  3. OP
    haidut

    haidut Member

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    I out a drop in every bottle of soda I drink, so maybe a total of about 3 drops daily. Sometimes, I do not take it during the day and then take 2 drops at night.
     
  4. tca300

    tca300 Member

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    Biol Psychiatry. 2014 May 1;75(9):678-85.
    Benzoate, a D-amino acid oxidase inhibitor, for the treatment of early-phase
    Alzheimer disease: a randomized, double-blind, placebo-controlled trial.
    Lin CH(1), Chen PK(2), Chang YC(3), Chuo LJ(4), Chen YS(5), Tsai GE(6), Lane
    HY(7).
    (1)Institute of Clinical Medical Science, China Medical University, Taichung,
    Taiwan; Department of Psychiatry, Kaohsiung Chang Gung Memorial Hospital, Chang
    Gung University College of Medicine, Kaohsiung, Taiwan. (2)Institute of Clinical
    Medical Science, China Medical University, Taichung, Taiwan; Department of
    Psychiatry, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College
    of Medicine, Kaohsiung, Taiwan; Department of Neurology, Lin-Shin Hospital,
    Taichung, Taiwan. (3)Department of Mathematics, Tamkang University, Taipei,
    Taiwan. (4)Department of Psychiatry, Taichung Veterans General Hospital,
    Taichung, Taiwan. (5)Department of Mathematics, Tamkang University, Taipei,
    Taiwan; Department of Psychiatry, China Medical University Hospital, Taichung,
    Taiwan. (6)Department of Psychiatry, Harbor-UCLA Medical Center, Torrance,
    California. (7)Institute of Clinical Medical Science, China Medical University,
    Taichung, Taiwan; Department of Psychiatry, China Medical University Hospital,
    Taichung, Taiwan. Electronic address: hylane@gmail.com.
    BACKGROUND: N-methyl-D-aspartate receptor (NMDAR)-mediated neurotransmission is
    vital for learning and memory. Hypofunction of NMDAR has been reported to play a
    role in the pathophysiology of Alzheimer disease (AD), particularly in the early
    phase. Enhancing NMDAR activation might be a novel treatment approach. One of the
    methods to enhance NMDAR activity is to raise the levels of NMDA coagonists by
    blocking their metabolism. This study examined the efficacy and safety of sodium
    benzoate, a D-amino acid oxidase inhibitor, for the treatment of amnestic mild
    cognitive impairment and mild AD.
    METHODS: We conducted a randomized, double-blind, placebo-controlled trial in
    four major medical centers in Taiwan. Sixty patients with amnestic mild cognitive
    impairment or mild AD were treated with 250-750 mg/day of sodium benzoate or
    placebo for 24 weeks. Alzheimer's Disease Assessment Scale-cognitive subscale
    (the primary outcome) and global function (assessed by Clinician Interview Based
    Impression of Change plus Caregiver Input) were measured every 8 weeks.
    Additional cognition composite was measured at baseline and endpoint.
    RESULTS: Sodium benzoate produced a better improvement than placebo in
    Alzheimer's Disease Assessment Scale-cognitive subscale (p = .0021, .0116, and
    .0031 at week 16, week 24, and endpoint, respectively), additional cognition
    composite (p = .007 at endpoint) and Clinician Interview Based Impression of
    Change plus Caregiver Input (p = .015, .016, and .012 at week 16, week 24, and
    endpoint, respectively). Sodium benzoate was well-tolerated without evident
    side-effects.
    CONCLUSIONS: Sodium benzoate substantially improved cognitive and overall
    functions in patients with early-phase AD. The preliminary results show promise
    for D-amino acid oxidase inhibition as a novel approach for early dementing
    processes.



    J Immunol. 2009 Nov 1; 183(9): 5917–5927.
    Sodium Benzoate, a Metabolite of Cinnamon and a Food Additive, Reduces Microglial and Astroglial Inflammatory Responses1
    Saurav Brahmachari, Arundhati Jana, and Kalipada Pahan2
    Author information ► Copyright and License information ►
    The publisher's final edited version of this article is available free at J Immunol
    See other articles in PMC that cite the published article.
    Activation of glial cells (microglia and astroglia) has been implicated in the pathogenesis of a variety of neurodegenerative diseases, including Alzheimer's disease (AD), 3 Parkinson's disease, Creutzfeld-Jacob disease, HIV-associated dementia (HAD), stroke, and multiple sclerosis (MS) (1, 2). It has been found that activated microglia and astroglia accumulate at sites of injury or plaques in neurodegenerative CNS (1–7). Although activated microglia scavenge dead cells from the CNS and secrete different neurotrophic factors for neuronal survival, it is believed that severe activation causes various autoimmune responses leading to neuronal death and brain injury (1–7). During activation, microglia and astroglia express various genes related to inflammation, such as proinflammatory cytokines, proinflammatory enzymes, and proinflammatory adhesion molecules (1–9). Therefore, characterization of signaling pathways required for the activation of glial cells is an active area of investigation since compounds capable of antagonizing such signaling steps may have therapeutic effect in neurodegenerative disorders.

    Cinnamon contains three major compounds (cinnamaldehyde, cinnamyl acetate and cinnamyl alcohol), which are converted into cinnamic acid by oxidation and hydrolysis, respectively. In the liver, this cinnamic acid is β-oxidized to benzoate (10) that exists as sodium salt (sodium benzoate; NaB) or benzoyl-CoA. It has been reported that minor amount of NaB is also excreted in the urine of humans (11, 12). NaB is of medical importance because it is a component of Ucephan, a Food and Drug Administration (FDA)-approved drug used in the treatment for hepatic metabolic defects associated with hyperammonemia such as urea cycle disorder in children (13, 14). It is also widely used as a preservative in broad range of foods and cosmetic products (15). It is nontoxic and can be administered as a solution in drinking water. It has been reported that 2% solution of NaB in drinking water is safe for lifelong treatment in mice without any noticeable side effects (16). Because Ayurvedic as well as Yunani medicines have been using cinnamon as vital medicines for inflammatory diseases like arthritis for centuries, we were prompted to test the effect of NaB on the expression of proinflammatory molecules in glial cells.

    Here we provide the first evidence that NaB attenuates the expression of inducible NO synthase (iNOS) and proinflammatory cytokines in microglia, astrocytes, and macrophages. Although NaB reduced the level of cholesterol in vivo in mice, it was not the cause behind the anti-inflammatory activity of NaB. Alternatively, hydroxymethylglutaryl-CoA (HMG-CoA), mevalonate, and farnesylpyrophosphate reversed NaB-mediated inhibition of iNOS, indicating the involvement of intermediates, but not the end product, of the mevalonate pathway in the anti-inflammatory effect of NaB. Consistently, inhibition of the expression of iNOS and the production of NO by farnesylpyrophosphate transferase inhibitor, suppression of p21ras activation by NaB and induction of iNOS by the activated p21ras alone suggest that NaB exerts its anti-inflammatory effect in glial cells via modulating farnesylation and activation of p21ras. Our findings raise a possibility that NaB, a component of a prescribed drug for human urea cycle disorder and a widely used food preservative, may find further application in neuroinflammatory and neurodegenerative disorders.
     
  5. Jsaute21

    Jsaute21 Member

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    Yeah, i have it with my mexican coke as well.

    My last concern is that I have seen the prior posts regarding MB & Coffee synergism potentially exacerbating a MAO toxicity...do you still drink coffee despite this possibility?
     
  6. OP
    haidut

    haidut Member

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    Thanks, great find. I think this is the same group that published on Ceylon cinnamon as treatment for Parkinson by lowering NO.
     
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