Understanding Ray Peat's Model Of Redox

Ray Peat often write and talks about this, and so does haidut, but I find this a hard topic to really understand. Many people say that Ray Peat's view about PUFA is the most controversial, but I think his opinion about how redox works is even more controversial. I have been studying this now, and this how I understand it, please feel free to correct me.

The main idea of Ray Peat's model is that as long as the cell is doing oxidative phosphorylation and makes a generous amount of ATP than the cell is healthy and able to withstand many biological problems.

If for some reason, oxidative phosphorylation is impaired, then the cell becomes unhealthy. It could become cancerous, it could become diabetic, it could become lipofuscin etc. etc. Overgeneralizing.

Now the big problem is, how can you make oxidative phosphorylation work again, if it is impaired. Well, oxidative phosphorylation works with a lot of redox reactions. Where high energy molecules/electron donors/reducers give their electrons to low energy molecules/electron acceptors/oxidizers.

Here reducers are molecules such as NADPH, NADH, GSH, vitamin E, vitamin C etc. They often act directly or indirectly as an anti oxidant, as they give their energy to GSH which is the "master antioxidant" that guards against oxidative stress. But they also, when a reducers loses its energy in a redox reaction, they can fuel ADP to ATP, which is the molecule where it is all about. This is the molecule that is needed to keep the cell in a health differentiated gell like state, but also the molecule that the organism needs to meets its energetic demands in the sense of mental and physical activity.

Now oxidants are molecules such as O2, quinones, NAD, MB, ROS. Those are molecules that ask for electrons. Some are highly unstable, such as ROS, which causes oxidative stress.

Now many diseases are marked by oxidative stress, which is why many people believe that you probably need to raise GSH, NADPH, vitamin C, vitamin E etc. to combat those. This would ensure that DNA, membranes, PUFA etc. all don't get damaged from oxidative stress.

However, it is well known that if you want to kill cancer, this is impossible if your anti oxidants are high. Cell apoptosis requires ROS, and anti oxidants neutralise the action of ROS. So many people think that you want high anti oxidants levels, which means a lot of reducers such as NADPH, NADH, GSH, vitamin E etc, except if you have cancer, because otherwise cancer therapies won't be effective in killing it.

Now, here is where Ray Peat differs. He seems to reason that not only in cancer, but everywhere where metabolism is impaired, there is actually a buildup of those electron donors, causing reductive stress. And to restore the flow of molecules, you don't need more of those electron donors, but less, and you need more oxidants, such as O2 (which indirectly means CO2), NAD and quinones, to make sure the electrons start flowing again from donor to acceptor until it fuels ATP, and the cell gets back in its differentiated, gell like state.

Of you course you need reducers for redox, but too much of them seems to impair the enzymes in the mitochrondia, too much GSH impairs cytochrome C, too much NAPDH impairs PDH. Ray Peat seems to think that injury, cancer, inflammation has this reductive swarm around it, which impairs metabolism.

Please correct me if I'm wrong, or if you have more to add to this.

 

Thank you for posting your thoughts @Mufasa. One part of me is an electrical engineer so I can understand the concepts of electron flow from one molecule to another. Through Ray's writings on Gilbert Ling, I've also become fascinated with Ling's ideas on how cells work at the tiniest level which Ling refers to as a nano-protoplasm unit (NPU). There he give a precise description (and diagram) of how ATP is used at the NPU level.

http://www.gilbertling.org/pdf/A 400 Word Summary of the Association-Induction Hypothesis.pdf