Chris Masterjohn

So mitochondria produce usable energy from food in the form of ATP.

When they do that, they have a bunch of different pathways through which electrons flow.

And methylene blue is able to grab those electrons and put them somewhere else.

So they call it a redox cycler.

So it's taking an electron here, it's shuttling it over there, it's taking an electron here, it's shuttling over there.

And so if you have this, let's say the normal way for your mitochondria to produce energy has a main road where the electrons just flow straight through.

Methylene blue is coming in and it's just taking that electron over here, it's throwing it in over there and so on.

So if you've got a road that goes like this and you've got a blockage right here and methylene blue is just taking something out there and it's putting it over there, you actually wind up getting better energy with it.

But if you don't have a blockage, you're just creating random chaos in the mitochondria.

And in animal experiments, what they've done is they've said, okay, let's give these animals inhibitors of their mitochondria at specific locations and see what methylene blue does.

And if you don't have any inhibitors, and if the animal is genetically healthy,

then you add methylene blue, they get less ATP.

So the mitochondria is less effective at converting food to usable energy.

But if they do have an inhibitor, their ATP production goes down, you add methylene blue, it goes back up, right?

So if there's a blockage to get around, methylene blue helps.

So I think what's important if you really want to make sure that people are using methylene blue right is

to actually do mitochondrial testing that will tell you whether there was specific blockages are there.

I ran a biochemical optimization program a while back and one of the clients that I had in there, he tried methylene blue and he only got up to a half a milligram or a milligram and his mood was worse, his fatigue was worse, he had more anxiety, a bunch of problems that

The dose was too low to say it was doing a pharmacological messing with his neurotransmitters.

And so I think it was just making his mitochondrial function worse.