[Rhonda]: So your biomarkers tend to be a lot of performance-related biomarkers.
[Tim]: Yeah.
And I've done the genetic stuff.
So I know, let's just say that I'm a poor methylator, the motherfucker gene, as they
say.
[Rhonda]: Yes, MTHFR.
[Tim]: Yeah.
I'm not in an ideal spot.
So taking, say, l-methylfolate could be a good option for me and I've experimented with
that in the past, looking at how that can lower homocysteine or things like that.
[Rhonda]: Have you noticed any differences after experimented with 5-methylfolate, L-5-methylfolate,
methylcobalamin?
[Tim]: Yeah.
I haven't noticed many changes in blood markers and I haven't noticed subjective changes in,
say, performance or clarity or anything like that.
[Rhonda]: Yeah.
[Tim]: It doesn't mean it isn't doing things.
[Rhonda]: Yeah.
I have an anecdotal story.
So I'm very into looking at different gene polymorphisms.
23andMe is a great service that can do that.
So my friends, family, etc., I'm telling everyone to do it.
So my mother-in-law got genotyped and we found out that she is homozygous for MTHFR, meaning
that her MTHFR enzyme only is working at about 10 to 20% efficiency.
She's always had really high blood pressure, to the point where doctors were wanting to
get her on medicine for it and she's always refused.
Nothing she did . . . she's done various diets, lots of exercise, lots of things she's tried,
nothing has gotten her into a normal range until we identified she had MTHFR, got her
supplementing with 5-methylfolate and methylcobalamin.
But she's been taking pretty high doses of it.
But now her blood pressure for the first time is in like a normal range.
So I was kind of curious if you had ever . . . [Tim]: I have very consistently what you would
consider excellent blood pressure.
So I haven't looked closely at that.
The question that comes to mind for me always because I've noticed . . . so, I'm a big fan
of Richard Feynman.
Richard Feynman, and I'm not saying this is the case with your, you said mother-in-law?
[Rhonda]: Yes.
[Tim]: But the importance of not tricking yourself because you're the easiest person
to fool, basically, is what he would say.
I know that what I have initially thought were sort of causal relationships with high
correlative value . . . for instance, I've talked to people who have gone on fill in
the blank diet.
They're like, "This thing changed.
I'm so glad I found this diet."
I'm like, "So you haven't changed anything else?"
"No, no, no.
I started running in the morning.
I started doing this.
I started doing that."
I'm like, "Hell yeah" . . . because like one, it's so hard.
That's where the observational data gets so challenging, when you look at, say anything,
whether it's the China study or whatever.
We don't need to get into that one.
That's a sensitive one.
But any observational self-reporting and so on, the data is almost always so flawed because
humans almost never change just one thing.
[Rhonda]: Yeah.
I think that's why it's so important when you're looking at epi studies that are associative
that are not a clinical, randomizable trial, coupling that data with mechanistic data done
on animal models or lower organisms, I think coupling the two is very important because
then you go, "Oh, okay.
We've noticed this observational data and here we've done X, Y or Z to manipulate it
in a worm or in a fly or a mouse."
[Tim]: Right.
So you have a plausible mechanism.
[Rhonda]: Right.
So you have a mechanism.
That's where I think looking comprehensibly at the whole . . .
[Tim]: At the intersection.
[Rhonda]: Yeah, scientific is very important.