[Tim]: I've been thinking about it also because cancer generally . . . by the time you're
40, we all have pre-cancerous little cells.
But the question is do they grow?
Do they then metastasize or become a problem, or do they just remain these little mutations
that don't cause any particular harm among other things obviously?
For me, I've become also interested in . . . I'd love to get your opinion on metformin.
There are people who'd say, "Well, if you want to try to dodge that cancer bullet, we
know that cancer cells, they love sustaining themselves anaerobically . . . or let me rephrase
that, with glucose.
They love glucose.
So if we can dramatically lower, whether it's storage of glycogen, plasma, glucose, whatever
it might be, then in theory, we should be able to lower the risk of cancer and limit
cancer growth, cancer cell growth.
What are your thoughts on metformin and why are you taking it or not taking it?
[Rhonda]: I'm not taking it.
The reason I'm not taking it . . . I think it has been shown, like you said, it can possibly
prophylactically prevent cancer so far.
I think the studies that have shown that have been pretty short-term.
My concern with metformin is the feedback mechanisms that happen when you're taking
this drug.
How is that going to affect other cells and how they respond to glucose and things like
that over the long-term, like 15 years down the line?
I think that limiting your sugar intake is probably . . . if you haven't damaged yourself
by eating a bunch of crap, a bunch of processed sugars and carbohydrates and things like that,
then I think limiting your sugar intake is probably good, good enough.
To a certain component, there's a certain component of cancer that there is a genetic
component.
What I mean by that is not that you're born with it but . . . so, downstream of a cell
that's glycolytic, that's only using glucose to make ATP through this glycolysis pathway
is inflammation again.
I come back to it because it's just downstream of everything.
And inflammation damages DNA and eventually you get it in the right gene that's saying,
"Oh, this gene usually protects," whenever there's any damage, it kills a cell.
It's called a tumor suppressor gene.
You get it in that tumor suppressor gene, you're screwed.
Now any time you get damaged, that pathway isn't activated to go, "Whoa, wait a minute,
this is not good.
I'm going to die.
And it just keeps living."
[Tim]: Yeah.
[Rhonda]: If you look at, for example, our lymphocytes, our lymphocytes are glycolytic
and they're not cancer.
So it's not as simple as a glycolytic cell is going to give you cancer.
[Tim]: No, no.
[Rhonda]: But definitely starving . . . I think before you get to the point where you're
starving a cancer cell, you can kill the damaged cell before it becomes to that point where
it's shifted its metabolism.
[Tim]: What do the lymphocytes do in a ketotic state?
[Rhonda]: I don't know.
[Tim]: Do they derive glucose form lactate or something?
[Rhonda]: Yes.
They do get it from lactate.
Lactate is something that they do use.
Yeah.
[Tim]: Cool.
[Rhonda]: It's interesting because lactate also is much like ketone bodies, energetically
thermodynamically favorable.
So it takes less energy to make energy.
[Tim]: Yeah.
[Rhonda]: So you're consuming less oxygen because you don't need as many ATP molecules
to make ATP.