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Ethanol, krebs/TCA cycle and the mitochndrial causes of addiction.

Discussion in 'Mitochondrial Rx' started by Oskar Q-NRG, Jan 28, 2020.

  1. Oskar Q-NRG

    Oskar Q-NRG New Member

    I have noticed that I feel significanlty less fatigue after I have had few drinks and even the next day I feel better than normal and have more energy - despite the hangover if I happen to over do it.

    Alcohol gets metabolized to acetate, which is a ketone body so I wonder if this provides brain with dysfunctional mitochondria a more usable form of fule and acts as a neuroprotection in short term with obvious negative long term side effects?

    And then there is the acetyl-coA story: https://www.ncbi.nlm.nih.gov/pubmed/30245009
    From what I can take away from this abstract is that acetate is an important mechanism to secure acetyl coA pools in damaged mitochondria and de novo synthesis of acetate plays big role in this. Synthesis of acetate from puryvate happens when excess glucose is present - so maybe the sugar binges that I and most likely many other people experience are part of this? And alcohol intake of course can help big time to generate acetate - the only problem is that if you consume too much the intermediate metabolite acetaldehyde bilds up to toxic levels and braking it down waists all the NAD+ reserves leaving you feel like a train wreck.

    So hence I have a hypothesis that many people that are addicted to alcohol might just have dysfunctional mitochondria. It looks even more likely as the most successful therapy against alcoholism and opiate addiction is IV NAD+ which among other things will likely fix the link between krebs cycle and ETC.

    I have heard Jack Kruse mentione that amphetamines (meth etc) lower mitochondrial membrane potential making them to burn fatty acids like craizy to avoid collaps of the potential and resulting death of mitochondria and eventually cell death. This looks lika another way of squeesing sufficient energy output from dysfunctional mitochondria.

    Then there are opioids, bnzos and other sedatives that calms the brain down. This is a way to reduce energy requirement of neurons so that energy supply can meet demand reducing the overwhelm in mitochondria and resulting oxydative stress. Oxydative stress is a hallmark of all the major mental disorders (depression skizo, anxitety etc) according to Dr William Walsh. Again, the fact that you can treat these addictions with IV NAD+ speaks about mitochondrial dysfunction IMO.

    Anyway, if any of you have any input into this theory it will be appreaciated. Aslo if it rises interest in anyone who is a member and can post to "Ask Jack" section of the forum please do so - I'd like to have the master expert's take on this issue but I'm not a paying member and dont have money to become one at the moment.

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