Oxidal - Liquid Redox Modulator

Jsaute21

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In adrenal failure, not much pregnenolone would be present, and neither will adrenaline. There are blood and urine tests for adrenaline metabolites which can rule that out. In adrenal failure, ACTH is usually very high, so that can tested as well.

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

Jsaute21

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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.
 
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haidut

haidut

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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.

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.
 
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tca300

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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: [email protected].
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.
 

Jsaute21

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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.
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?
 
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haidut

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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: [email protected].
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.

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

Progesterone

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Loving Oxidal so far, too early to speak on overall effects, I will keep monitoring and report back though.

Interesting to note I get a more pronounced effect when dropping 1 drop on my tongue and swallowing VS taking 3 drops in carbonated beverage.

The easier and deeper breathing effect comes on almost right away and is quite apparent from oral dosing directly in mouth.
 

Xisca

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I can see that most of you take it orally, I thought it was fine to have it through the skin!
I have a blue belly button now....
lol I have always loved that color!
and my belly is B-yellow...
 

Nokoni

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Messages
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Back pain reduced with Oxidal.

This may belong elsewhere, but I get great relief from back pain with Oxidal.

Had a major back attack recently, started antibiotics, topical Oxidal, and red light. Didn't get desired results.

Started additional drop of oral Oxidal in morning, noticed almost immediate improvement. (Need helper for topical on back, not available first thing.)

Still tough getting up until my oral dose, so tried additional drop at bedtime despite concern it would interfere with sleep. But sleep actually improved and morning stiffness was much reduced.

Dropped red light, substituted oral for topical Oxidal, now taking half dozen drops throughout the day. Back feels great (and so do I), though I'm still babying it.

Antibiotics and bunch of other stuff are confounds, but the take drop/feel relief association is strong. Back pain episodes can be so debilitating, to me this stuff's miraculous.
 

Obi-wan

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Now that you are used to Oxidal, wait until you take Panquinone. Taken once a day in the morning will give you open breathing and energy all day long! In addition I will also do 2 drops of Oxidal late afternoon. Both are great for oxidative metabolism and as Haidut stated, Panquinone is in a league of it's own!
 

Progesterone

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haidut,
Now that you are used to Oxidal, wait until you take Panquinone. Taken once a day in the morning will give you open breathing and energy all day long! In addition I will also do 2 drops of Oxidal late afternoon. Both are great for oxidative metabolism and as Haidut stated, Panquinone is in a league of it's own!

How is MB for hair and erectile function, in your experience?

I will look into Panquinone, thanks.
 

Obi-wan

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MB is more of a quick oxidator and immediate systems are clear breathing and deeper breathing which indicates better carbon dioxide production. I don't see any correlation with hair of erectile function. Panquinone is not MB by the way. Read the Panquinone thread.
 

Progesterone

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MB is more of a quick oxidator and immediate systems are clear breathing and deeper breathing which indicates better carbon dioxide production. I don't see any correlation with hair of erectile function. Panquinone is not MB by the way. Read the Panquinone thread.

I am aware of that. I am noticing better erection quality though since using Oxidal.

I was asking because of it's effects on NO.

MB does a lot of different things... we probably don't know of everything it does, yet.

MB increases autophagy and decreases cellular senescence as well.. which should be beneficial for hair.
 

Obi-wan

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I still like taking MB in the afternoon even though I take Panquinone in the morning. How many drops of MB do you take? I do 2 drops (Oxidal) at a time. I am up to the recommended 8 drops of Panquinone. The late afternoon combo of Oxidal (2 drops), B1 (100mg), Niacinamide (500mg), Aspirin (325mg), and Caffeine (200mg) is a great energy boost by the way. More carbon dioxide = less NO in my opinion.
 

Owen B

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I've been using the Oxidal for a couple of months and noticed few effects. No more than 2 mgs a day.

I always end up having to take any medicines in very small doses because my system is highly stressed out (two traumas). I just cannot get anything into my system without getting a negative effects/blowback.

But I went to 3 mgs the other day and the effect was tremendous. Improved working memory, mood and energy. I also took 1 mg before sleep and found I slept better and had less sleep hangover the next AM.

I had a series of killer catalepsies in April and I just could not think well at all. Had I taken say 5 mgs after each collapse, plus more niancinamide I think I would have recovered much quicker.

I have my fingers crossed but I think I'll be able to use this regularly. It's the best I've tried of all the Peat/Haidut substances so far.

THANKS!
 

Lee Simeon

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I've been using the Oxidal for a couple of months and noticed few effects. No more than 2 mgs a day.

I always end up having to take any medicines in very small doses because my system is highly stressed out (two traumas). I just cannot get anything into my system without getting a negative effects/blowback.

But I went to 3 mgs the other day and the effect was tremendous. Improved working memory, mood and energy. I also took 1 mg before sleep and found I slept better and had less sleep hangover the next AM.

I had a series of killer catalepsies in April and I just could not think well at all. Had I taken say 5 mgs after each collapse, plus more niancinamide I think I would have recovered much quicker.

I have my fingers crossed but I think I'll be able to use this regularly. It's the best I've tried of all the Peat/Haidut substances so far.

THANKS!
Which others Haidut supplements have you previously used/use?
 

Owen B

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Which others Haidut supplements have you previously used/use?
I've used Progestene, Cypro, Pansterone, Estroban, Tyromix, Gonadin etc. I just don't get sustained results or the feeling of restabilizing. I want to go for Diamant or Metergoline; maybe some Preg with added Prog.
 
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haidut

haidut

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haidut,


How is MB for hair and erectile function, in your experience?

I will look into Panquinone, thanks.

Have not used it for hair, and also have not found that it interferes with erection despite the claims that anything lowering NO will create problems down there.
 
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haidut

haidut

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Back pain reduced with Oxidal.

This may belong elsewhere, but I get great relief from back pain with Oxidal.

Had a major back attack recently, started antibiotics, topical Oxidal, and red light. Didn't get desired results.

Started additional drop of oral Oxidal in morning, noticed almost immediate improvement. (Need helper for topical on back, not available first thing.)

Still tough getting up until my oral dose, so tried additional drop at bedtime despite concern it would interfere with sleep. But sleep actually improved and morning stiffness was much reduced.

Dropped red light, substituted oral for topical Oxidal, now taking half dozen drops throughout the day. Back feels great (and so do I), though I'm still babying it.

Antibiotics and bunch of other stuff are confounds, but the take drop/feel relief association is strong. Back pain episodes can be so debilitating, to me this stuff's miraculous.

Great, thanks for the feedback. I actually use Oxidal for sleep myself. I find that it works much better than even glycine/GABA. MB is not a stimulant so it not expected to create problems with sleep but quite the opposite due to improved metabolism and higher CO2.
 
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haidut

haidut

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I've been using the Oxidal for a couple of months and noticed few effects. No more than 2 mgs a day.

I always end up having to take any medicines in very small doses because my system is highly stressed out (two traumas). I just cannot get anything into my system without getting a negative effects/blowback.

But I went to 3 mgs the other day and the effect was tremendous. Improved working memory, mood and energy. I also took 1 mg before sleep and found I slept better and had less sleep hangover the next AM.

I had a series of killer catalepsies in April and I just could not think well at all. Had I taken say 5 mgs after each collapse, plus more niancinamide I think I would have recovered much quicker.

I have my fingers crossed but I think I'll be able to use this regularly. It's the best I've tried of all the Peat/Haidut substances so far.

THANKS!

Incredible, thanks! Please keep us posted on progress.
 

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