Succinic Acid Supplementation

griesburner

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sounds very nice. would like to try some succinic acid too. Anyone know of a good source you can buy from germany? i only found some stuff from a russian company or some company where you have to buy 25kg at once.
 

LeeLemonoil

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Short-term succinic acid treatment mitigates cerebellar mitochondrial OXPHOS dysfunction, neurodegeneration and ataxia in a Purkinje-specific spinocerebellar ataxia type 1 (SCA1) mouse model

Abstract

Mitochondrial dysfunction plays a significant role in neurodegenerative disease including ataxias and other movement disorders, particularly those marked by progressive degeneration in the cerebellum. In this study, we investigate the role of mitochondrial oxidative phosphorylation (OXPHOS) deficits in cerebellar tissue of a Purkinje cell-driven spinocerebellar ataxia type 1 (SCA1) mouse. Using RNA sequencing transcriptomics, OXPHOS complex assembly analysis and oxygen consumption assays, we report that in the presence of mutant polyglutamine-expanded ataxin-1, SCA1 mice display deficits in cerebellar OXPHOS complex I (NADH-coenzyme Q oxidoreductase). Complex I genes are upregulated at the time of symptom onset and upregulation persists into late stage disease; yet, functional assembly of complex I macromolecules are diminished and oxygen respiration through complex I is reduced. Acute treatment of postsymptomatic SCA1 mice with succinic acid, a complex II (succinate dehydrogenase) electron donor to bypass complex I dysfunction, ameliorated cerebellar OXPHOS dysfunction, reduced cerebellar pathology and improved motor behavior. Thus, exploration of mitochondrial dysfunction and its role in neurodegenerative ataxias, and warrants further investigation.
 

LeeLemonoil

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Succinic acid studied for mito disease. Fumaric acid also

This was copy pasted from a website in Russian, as they have more info on succinic acid in their country than in English countries. The website is in the public domain.
Янтарная кислота, свойства, применение, противопоказания : Нетрадиционная медицина

In Western countries, the coenzyme Q10 is very popular. In some experiments, coenzyme Q10 showed the ability to express prolonged life. But here that is interesting; There is a drug that plays in the body a role similar to coenzyme Q10. It is also, and perhaps more effective, at a price that is about 10 times cheaper. It's succinic acid. Perhaps, it is because of such a low price that amber acid is not promoted to the market.

We should pay special attention to succinic acid (hereinafter YaK)! By the ratio of price / effectiveness, this thing is almost the leader among the means to prolong life. Yak is a natural substance (present in all organisms), has a powerful healing effect, without causing side effects and addictive. There are many reasons for this, but there are basic reasons.
Amber acid:
 
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There is a russian drug 50mg of citric acid + 200mg of succinic acid. Should be dissolved in alkaline mineral water or with addition of baking soda. I can vouch for it. Two days of illicit amphetamine binge without sleep or even shutting your mouth lets say 500mg+ when it comes off you still cant sleep but your brain is so tired you cant speak anymore, brain fog, zombie like state. 2 tablets of this drug dissolved in cheap highly mineralized water brings you back from zombieland for a couple of hours. The effect is that profound that probably you will continue to binge if something remains.

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LeeLemonoil

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Succinate supplementation improves metabolic performance of mixed glial cell cultures with mitochondrial dysfunction


Scientific Reportsvolume 7, Article number: 1003 (2017)

Mitochondrial dysfunction, the inability to efficiently utilise metabolic fuels and oxygen, contributes to pathological changes following traumatic spinal cord or traumatic brain injury (TBI). In the present study, we tested the hypothesis that succinate supplementation can improve cellular energy state under metabolically stressed conditions in a robust, reductionist in vitro model of mitochondrial dysfunction in which primary mixed glial cultures (astrocytes, microglia and oligodendrocytes) were exposed to the mitochondrial complex I inhibitor rotenone. Cellular response was determined by measuring intracellular ATP, extracellular metabolites (glucose, lactate, pyruvate), and oxygen consumption rate (OCR). Rotenone produced no significant changes in glial ATP levels. However, it induced metabolic deficits as evidenced by lactate/pyruvate ratio (LPR) elevation (a clinically-established biomarker for poor outcome in TBI) and decrease in OCR. Succinate addition partially ameliorated these metabolic deficits. We conclude that succinate can improve glial oxidative metabolism, consistent our previous findings in TBI patients’ brains. The mixed glial cellular model may be useful in developing therapeutic strategies for conditions involving mitochondrial dysfunction, such as TBI.
 

LeeLemonoil

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Mitochondrial Complex II Prevents Hypoxic but Not Calcium- and Proapoptotic Bcl-2 Protein-induced Mitochondrial Membrane Potential Loss

Mitochondrial Complex II Prevents Hypoxic but Not Calcium- and Proapoptotic Bcl-2 Protein-induced Mitochondrial Membrane Potential Loss*

Mitochondrial membrane potential loss has severe bioenergetic consequences and contributes to many human diseases including myocardial infarction, stroke, cancer, and neurodegeneration. However, despite its prominence and importance in cellular energy production, the basic mechanism whereby the mitochondrial membrane potential is established remains unclear. Our studies elucidate that complex II-driven electron flow is the primary means by which the mitochondrial membrane is polarized under hypoxic conditions and that lack of the complex II substrate succinate resulted in reversible membrane potential loss that could be restored rapidly by succinate supplementation. Inhibition of mitochondrial complex I and F0F1-ATP synthase induced mitochondrial depolarization that was independent of the mitochondrial permeability transition pore, Bcl-2 (B-cell lymphoma 2) family proteins, or high amplitude swelling and could not be reversed by succinate. Importantly, succinate metabolism under hypoxic conditions restores membrane potential and ATP levels. Furthermore, a reliance on complex II-mediated electron flow allows cells from mitochondrial disease patients devoid of a functional complex I to maintain a mitochondrial membrane potential that conveys both a mitochondrial structure and the ability to sequester agonist-induced calcium similar to that of normal cells. This finding is important as it sets the stage for complex II functional preservation as an attractive therapy to maintain mitochondrial function during hypoxia.
 

haidut

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Mitochondrial Complex II Prevents Hypoxic but Not Calcium- and Proapoptotic Bcl-2 Protein-induced Mitochondrial Membrane Potential Loss

Mitochondrial Complex II Prevents Hypoxic but Not Calcium- and Proapoptotic Bcl-2 Protein-induced Mitochondrial Membrane Potential Loss*

Mitochondrial membrane potential loss has severe bioenergetic consequences and contributes to many human diseases including myocardial infarction, stroke, cancer, and neurodegeneration. However, despite its prominence and importance in cellular energy production, the basic mechanism whereby the mitochondrial membrane potential is established remains unclear. Our studies elucidate that complex II-driven electron flow is the primary means by which the mitochondrial membrane is polarized under hypoxic conditions and that lack of the complex II substrate succinate resulted in reversible membrane potential loss that could be restored rapidly by succinate supplementation. Inhibition of mitochondrial complex I and F0F1-ATP synthase induced mitochondrial depolarization that was independent of the mitochondrial permeability transition pore, Bcl-2 (B-cell lymphoma 2) family proteins, or high amplitude swelling and could not be reversed by succinate. Importantly, succinate metabolism under hypoxic conditions restores membrane potential and ATP levels. Furthermore, a reliance on complex II-mediated electron flow allows cells from mitochondrial disease patients devoid of a functional complex I to maintain a mitochondrial membrane potential that conveys both a mitochondrial structure and the ability to sequester agonist-induced calcium similar to that of normal cells. This finding is important as it sets the stage for complex II functional preservation as an attractive therapy to maintain mitochondrial function during hypoxia.

Succinic acid works even better when combined with methylene blue (MB) as the combination can bypass any mitochondrial damage and produce ATP/CO2 even in very sick people. The Russian drug Cytoflavin combines succinic acid with riboflavin as the FAD from B2 can play the role of electron acceptor from succinic acid, but MB can perform that role even better and had other benefits B2 does not.
 
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Succinic acid works even better when combined with methylene blue (MB) as the combination can bypass any mitochondrial damage and produce ATP/CO2 even in very sick people. The Russian drug Cytoflavin combines succinic acid with riboflavin as the FAD from B2 can play the role of electron acceptor from succinic acid, but MB can perform that role even better and had other benefits B2 does not.

So what is theoretical dosage for MB + SA supplementation?
 

haidut

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So what is theoretical dosage for MB + SA supplementation?

Same doses as what Peat recommended for each separately - 200mg x 2 daily for succinic acid and maybe 1mg MB with each dose succinic acid.
 

LeeLemonoil

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Succincic Acid, around ~300mg two times a day for 4 days now.

Most noticeable effect: cognition and clearheadedness are impacted positively, I feel a bit fresher mentally.
And, very striking: Football session and a bit of running uphill 2 days later. I hardly got out of breath: dradticallly increased stamina. Didn’t expect that
 

Lokzo

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Human Metabolome Database: Showing metabocard for Succinic acid (HMDB0000254)

Is anyone able to explain why this link is claiming that succinic acid can be described as a 'cancer causing' metabolite?

I've just started to take it, and I have noticed grater energy. But reading this link worries me. This succinic acid does make me feel almost borderline manic, actually. I'm taking 800mg per day. I'm always suspicious of something that makes me feel 'too good'. It's definitely doing something.

@haidut, sorry I don't suppose you might have an opinion on what this link says about succinic acid? I know you've mentioned malic acid as a chelating agent in another thread (in recent times). Maybe I should just stick with that one instead (along with the large quantities of coffee that I drink).


How was succinic acid for you in the end?! I am interested in exploring it.
 

RobertJM

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How was succinic acid for you in the end?! I am interested in exploring it.

From what I can remember it had those energising effects but I had to stop taking it as I misplaced it, and never found it again. So not sure what happened to it.
 

managing

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Got to try finally. After 2 days (125mg 2xd) I started to really feel the effects of the chelation. Neuropathic symptoms in extremities like foot pain, elbow/ulnar twitch. No eye twitch. Feeling a tad run down. No kidney symptoms which is good. I stopped it for now. But I do feel pretty strongly that it is indeed chelating minerals. Anybody know a way to determine if it is removing bad metals and not just good stuff? It ought to have an affinity for polyvalent cations like al, mb, he, etc.
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

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