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Speaker 1: Yeah, So mixing it up a little bit, I think

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Speaker 1: is really important. Let's die, Let's get back to the

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Speaker 1: SGL two inhibitors now. Is interesting to hear you say that.

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Speaker 1: I'll give you a little bit of background. So January

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Speaker 1: this year, I had open heart surgery for a dodgy

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Speaker 1: valve that I was born with. I was born with

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Speaker 1: a bi cuspan aortic valve. But it's all good. But

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Speaker 1: the upshot of this is the one drug that they've

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Speaker 1: put me on is an SGL two inhibitor. And actually,

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Speaker 1: when I dug into it, I went, you know what,

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Speaker 1: that's a drug. I'm not basically a big fan of

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Speaker 1: taking drugs, but I'm like, I'm actually happy that they

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Speaker 1: put me on an SGL two inhibitor. It's essentially a

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Speaker 1: diabetes drug or our drug for managing your blood sugar

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Speaker 1: slice insulin, but it also has benefits for heart and

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Speaker 1: so I'm actually pretty happy to be on an SGL

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Speaker 1: to inhibitor. That's a nice unintended consequence of my being

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Speaker 1: born with the doachi for help, So tell our listeners

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Speaker 1: what and because actually, out of the interventional's testing program,

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Speaker 1: a lot of them, the drugs that were successful controlled

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Speaker 1: inchilin our and or glucose, which is an interesting thread, right,

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Speaker 1: But one of them, and canaga flows in and is

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Speaker 1: an sgl TO inhibitor. So talk to our listeners about

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Speaker 1: what an sgl TO inhibitor is and why you think

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Speaker 1: it's interesting from a longevity slice health span perspective.

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Speaker 2: Yeah, well, so the reason I'm excited about these is

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Speaker 2: just the abundance of data that we have suggesting that

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Speaker 2: they can be beneficial. And it's We've talked about the

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Speaker 2: issues with mouse studies. They do extend lifespan in my

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Speaker 2: least in mail lice, yes, but you know that's just

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Speaker 2: the beginning of the data. We have tons of data

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Speaker 2: for many, many thousands of patients taking these drugs in

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Speaker 2: the real world showing that it generates positive health outcomes

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Speaker 2: and reduces the incidents of negative health outcomes. They appear

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Speaker 2: to be very protective for the heart, like you mentioned,

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Speaker 2: also the kidneys. There's also a lot of data emerging

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Speaker 2: to suggest that they're very good for the brain. So

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Speaker 2: we have that piece of data saying, you know, patients

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Speaker 2: that are on these for diabetes tend to exhibit better

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Speaker 2: health outcomes over time, even outcomes unrelated to diabetes. Yes,

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Speaker 2: and then there's this other piece that you don't often

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Speaker 2: get for a longevity intervention, and this comes from studies,

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Speaker 2: these Mendelian randomization studies, which can you take me.

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Speaker 1: Take a step back and explain what those are and

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Speaker 1: why they're actually useful.

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Speaker 2: Yeah, so these are sort of a clever way of

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Speaker 2: modeling the impact of different interventions, in this case the

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Speaker 2: drug intervection and intervention by looking at sort of a

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Speaker 2: natural experiment that genetics have given us. So we all

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Speaker 2: have this protein called SGLT two that's the target of

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Speaker 2: this drug, right, and it's a channel. It's a channel

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Speaker 2: that recovers glucose in your kidney so that you don't

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Speaker 2: have glucose in your urine and we're keeping it in

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Speaker 2: the body where we need it because glucose is a

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Speaker 2: nutrient that we need. It's important for energy production. But

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Speaker 2: we have different genetic variants in SGLT two. So you know,

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Speaker 2: most of us have a fully functional version, but there

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Speaker 2: are rare genetic variants where you have a dysfunctional SGLT

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Speaker 2: two protein that doesn't come glucose as efficiently. So that's

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Speaker 2: very similar to what the drugs doing.

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Speaker 3: Right.

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Speaker 2: If the drug inhibits. And then there are some people

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Speaker 2: that have just been operating this way their whole lives,

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Speaker 2: their SGLT two never worked efficiently. You can look at

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Speaker 2: what happens to those people have a pretty good idea

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Speaker 2: of what the drug's gonna do. Right, Have I blamed

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Speaker 2: this in.

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Speaker 3: A way in a minute you have? Yeah, you've explained

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Speaker 3: really well.

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Speaker 2: So, yeah, that's that's an Ndelian randomization. And when you

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Speaker 2: look at it for SGLT two and you look at

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Speaker 2: studies sort of modeling the impact of these drugs, you

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Speaker 2: see really cool stuff. You see longer life span in

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Speaker 2: males just like the ip saw and mail mice. You

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Speaker 2: see increased intelligence, which is kind of a surprising one, right,

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Speaker 2: like why would having h this dysfunctional glucose channel increase

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Speaker 2: or intelligence? But it's probably doing really good things for

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Speaker 2: brain health and that's probably why.

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Speaker 3: Yeah.

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Speaker 2: But so we sort of have this natural experiment that

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Speaker 2: tells us, hey, you know, if you're worried about taking

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Speaker 2: this drug and inhibiting this protein, there are many people

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Speaker 2: walking around their whole lives with the equivalent of the

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Speaker 2: impact of this drug. It may have very good health outcomes.

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Speaker 2: So for me personally, that just sort of gives me

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Speaker 2: more reassurance that this could be a really good thing.

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Speaker 3: Yeah, uh, I think it's a.

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Speaker 1: I think it's a it's a it's a pretty deep

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Speaker 1: level of reassurance whenever you see real humans with a

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Speaker 1: genetic change that that seems to then have good outcomes,

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Speaker 1: and then we understand the process by which it happens

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Speaker 1: as well, and then we have a drug that that

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Speaker 1: mimics that process, that has a low side effect profile.

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Speaker 1: You're starting to get towards slam dunk interventions, right, Yeah.

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Speaker 2: I mean it's it's a lot of data. You don't

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Speaker 2: you don't have that for any other longevity drug. Yeah,

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Speaker 2: the Mendelian randomization. You have to get lucky. There has

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Speaker 2: to be a gene that can model the impact of

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Speaker 2: the drug that in the human population. Most of the

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Speaker 2: time there isn't one, but we got lucky. That's JILT too,

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Speaker 2: But yeah, that I think the strongest data really is

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Speaker 2: just what's see seeing what's happening to the patients who

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Speaker 2: are taking it, how how they go on after many

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Speaker 2: years of taking this drug, and they have lower incidences

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Speaker 2: of heart failure, of a chronic kidney disease. It they're

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Speaker 2: really really impactful drugs, and it seems to be occurring

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Speaker 2: through the mechanism that makes them useful diabetes drugs. It's

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Speaker 2: decreasing blood ghos. We haven't talked about how these drugs work.

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Speaker 2: We kind of hinted at it with the function of

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Speaker 2: the protein. But at the most basic way to explain

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Speaker 2: how these work is they make you pee out some sugar.

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Speaker 2: Not what they do, because two different.

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Speaker 1: Diabetes strugs have different effects and will probably come on

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Speaker 1: the Tall Apartment form and as well. So, but to

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Speaker 1: think this is important, right, is that that that process.

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Speaker 3: By which they work.

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Speaker 2: Yep, absolutely, yeah, they in this case. I mean, there's

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Speaker 2: different ways you can decrease blood sugar, right. One way

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Speaker 2: is to let more of it out in the urine

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Speaker 2: and with sglt too. And it's a substantial amount. I'm

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Speaker 2: not the best with numbers all the time. I can't

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Speaker 2: remember how many grams of sugar it is that you

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Speaker 2: lose per day, but it's substantial. It's something like I

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Speaker 2: want to say it's fifty grams that don't quote me

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Speaker 2: on that, but you're losing a substantial amount of sugar

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Speaker 2: in your urine. It's higher in a diabetic that has

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Speaker 2: high blood sugar to begin with, but it happens in

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Speaker 2: healthy individuals too, So you're basically taking taking your blood

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Speaker 2: sugar level, which you know you have your stable zones

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Speaker 2: and your spikes, and you're just shifting all of it down.

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Speaker 2: You're just decreasing the basal tone in that blood sugar level.

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Speaker 2: You're making the blood sugar spikes less spiky, so it's

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Speaker 2: I'm presumably john then less inchillin exactly, then you get

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Speaker 2: less insulin signaling. So in some ways it's sort of

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Speaker 2: mimicking what happens with chloric restriction, which is sort of

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Speaker 2: a gold standard intervention for lifespan extension, right, So at

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Speaker 2: a fundamental level, that's at least one of the things

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Speaker 2: they're doing is decreasing blood sugar, which has onstream benefits

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Speaker 2: throughout the body. In the kidney I mentioned, they have

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Speaker 2: sort of a protective effect on the kidney. One of

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Speaker 2: the by products of inhibiting that sodia well glucose and

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Speaker 2: also it inhibits sodium re uptake in the kidney is

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Speaker 2: that you decrease the pressure in your kidney, so you're

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Speaker 2: just putting less stress on it over time. So people

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Speaker 2: don't think about kidneys in terms of longevity so often,

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Speaker 2: but it's important to realize as we get older, all

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Speaker 2: of our kidneys are starting to fail. Your kidney function

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Speaker 2: is never going up, it's always going down. So if

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Speaker 2: you have a drug that can stop that, and that's

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Speaker 2: exactly what these do, They stop the decline of kidney function,

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Speaker 2: that's that's potentially a very good thing.

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Speaker 3: Kidneys are really interesting.

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Speaker 1: I remember I went to the Ukena was sitting beside

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Speaker 1: an nephrologist and we had a long chat about kidneys

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Speaker 1: and kidney health and basically they're a window into your

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Speaker 1: cardiovascular system, which I'd never thought about because he said

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Speaker 1: that the amount of blood vessels concentrated in the kidney,

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Speaker 1: so he said, in nerve research, they see a lot

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Speaker 1: of cardiovascular issues appearing in the kidney first.

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Speaker 3: That's the place that they can look for them.

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Speaker 2: That makes sense. I mean, kidneys they're not a regenerative organ.

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Speaker 2: So you knows, as you lose the filtering units in

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Speaker 2: your kidneys as you get older, you're never getting them

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Speaker 2: aer back. And they're also very susceptible to stress. You know,

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Speaker 2: things like high blood pressure, high blood sugar. It stresses

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Speaker 2: the kidney and you start to lose more of that function.

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Speaker 2: So yeah, I mean it makes sense that you could

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Speaker 2: free it that way.

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Speaker 1: Yeah. Okay, So we've talked about SGL two inhibitors and

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Speaker 1: and that that they and I completely agree with you

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Speaker 1: that they seem to be the one drug. I think

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Speaker 1: that data is much clearer for humans than wrappamacin. Let's

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Speaker 1: then talk about mett Foreman, right, because it's it's interesting

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Speaker 1: when as I've talked about longevity before in topics, and

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Speaker 1: I've had you know, molecules that or drugs that are

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Speaker 1: really interesting, and then I had a category of yen nah.

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Speaker 3: It's a it's a kind of an Australian thing.

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Speaker 1: Yeah nah, yeah, the same, right, And so I had

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Speaker 1: put met forman in the yen nah and now it's

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Speaker 1: in the yen na maybe camp for me, right and

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Speaker 1: reason So the reason I'll give you for that was

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Speaker 1: you you'll probably be more over this than me. But

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Speaker 1: there was that early experiment that showed and correct me

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Speaker 1: if I'm I get the details wrong here, John, but

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Speaker 1: people who were at diabetics who were taking met Foreman

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Speaker 1: and appeared to live longer, and then people who were

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Speaker 1: non diabetics and not on met forman right in this

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Speaker 1: one particular study, and then there was all of this

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Speaker 1: creas about met forman being a longevity molecular longevity drug.

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Speaker 1: And then another study came out which actually criticized some

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Speaker 1: of the methodology in the first study and that that

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Speaker 1: some of the people who were excluded were because they

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Speaker 1: had disease, and it was like, well, you can't really

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Speaker 1: do that. And this intervention where they included everybody and

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Speaker 1: showed that there was no longevity benefit to the people

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Speaker 1: who were diabetic taking met forms So there was a

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Speaker 1: bit of a ooh dob squid, but they and some

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Speaker 1: interesting stuff has come out about met forming recently in

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Speaker 1: terms of other health benefits, which I'm sure you're more

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Speaker 1: over than me, and and lots of animal So talk

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Speaker 1: us through met forming and your take on met forming

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Speaker 1: and and.

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Speaker 3: It's yeah, is it a year na? Is it a yeah?

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Speaker 1: Nah?

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Speaker 3: Yeah, yeah, work.

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Speaker 2: I'm kind of gonna eat I guess it's a yeah.

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Speaker 1: No.

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Speaker 2: I think I think there's reason to believe that could

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Speaker 2: be beneficial, but we don't have, you know, the rock

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Speaker 2: solid data that I think we have for SGLT too inhibitors.

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Speaker 2: So yeah, met foreman, I've I've tried met Foreman as

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Speaker 2: a longevity intervention myself.

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Speaker 3: I think, how did you how did you find that?

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Speaker 3: What would they also that any positive SETI negatives that

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Speaker 3: you noticed.

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Speaker 1: You're running reasonably tightly controlled experiments as much as you

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Speaker 1: can in a free living human.

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Speaker 2: Yeah, I'd try to change a million things at once,

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Speaker 2: and you know, take good notes on my biomarkers and

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Speaker 2: how I feel and that sort of thing. Met Foreman,

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Speaker 2: It's one of those that. So there there are some

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Speaker 2: drugs that I've noticed when I've taken, like an SGLT

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Speaker 2: two inhibitor. I feel fantastic when I when I take

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Speaker 2: an SGLT two inhibitor, and I think it's probably because

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Speaker 2: I wake up in ketosis. I have these keytnes going

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Speaker 2: into my brain in the morning, and I just feel

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Speaker 2: crystal clear and energetic. And I notice when I'm taking

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Speaker 2: one of those drugs and it feels very good. Met Foreman.

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Speaker 2: Kind of is the other way. I don't feel the

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Speaker 2: greatest met Foreman, I feel kind of sleepy and then

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Speaker 2: like I have a little bit less energy. So that's

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Speaker 2: that's a turn off, right. I don't like to feel

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Speaker 2: that way. Yeah, And I've tried to you know, tweaking

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Speaker 2: the dose a little bit, seeing if I can find

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Speaker 2: a low enough dose where it's doing something. But I

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Speaker 2: don't have those side effects and that that does help.

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Speaker 2: But you know, everybody's different. That's probably just a me thing.

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Speaker 2: I don't think everybody's going to be leepy if they

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Speaker 2: take a low dose in that form, and I think

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Speaker 2: maybe I'm just kind of sensitive to some of the

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Speaker 2: downstream effects of that one. But for that reason, it's

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Speaker 2: not my favorite. But I do think there's good data

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Speaker 2: to support that it's doing positive things for health, absolutely, but.

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Speaker 1: It's in exercise interference. Yeah, do you do you think

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Speaker 1: that's real?

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Speaker 2: I think it's real if you are the type of

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Speaker 2: subject that that study was run on, if you're if

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Speaker 2: you're an elderly person who is at risk of frailty

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Speaker 2: and you're not resistance training. Yeah, I mean, I think

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Speaker 2: there's a risk that then you take a drug like

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Speaker 2: Matt Foreman that is going to decrease your blood sugar

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Speaker 2: levels and lead to some muscle atrophy.

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Speaker 3: Yeah.

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Speaker 2: I think that's a real risk For someone who is

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Speaker 2: regularly in the gym, they're you know, eating enough protein

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Speaker 2: to build some muscle. Maybe they've already built some muscle.

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Speaker 2: I think it's, you know, probably not a concern. I

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Speaker 2: think the benefits of that resistance training are going to

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Speaker 2: outweigh any any slight negative exercise adaptation effects of a

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Speaker 2: drug like that.

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Speaker 1: Okay, interesting, and now I interesting you mentioned with the

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Speaker 1: SGL two inhibitor you wake up in kontosis. I've been

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Speaker 1: recently thinking about intermittent fasting, right, So I used to

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Speaker 1: do intimittent fasting. Used to do sometimes sixteen it's sometimes

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Speaker 1: fourteen ten whatever, But I would just push.

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Speaker 3: My breakfast out.

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Speaker 1: And then I stopped doing it because I was having

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Speaker 1: DEXA scans every sort of six months to a year

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Speaker 1: and I had lost with it. But I'd lost significant

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Speaker 1: amounts of muscle, right, and so I stopped intermittent fasting.

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Speaker 1: And then I find out that I had a bicusp

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Speaker 1: of iotic valve and significant regurgitation, which probably explained my

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Speaker 1: muscle loss right over and above the intermittent fasting. So

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Speaker 1: I'm not like, ah shit, maybe that was any you know,

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Speaker 1: you have seen some of the data coming out. Some

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Speaker 1: of the concern about the intermittent fasting is obviously that

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Speaker 1: you fast overnight, that you've only you don't have a

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Speaker 1: big amino acid storage pull in your body. So if

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Speaker 1: you're fasting twelve, thirteen, fourteen hours, your body is going

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Speaker 1: to be breaking down muscle to get those amino acids

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Speaker 1: that are very critical for cellular function.

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Speaker 3: Right.

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Speaker 1: But then more recent research has shown him if you

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Speaker 1: take a big chunk of protein in the evening, that

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Speaker 1: muscle protein synthesis can persist for twelve or so ours.

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Speaker 3: Right. So I've been toying in my head with.

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Speaker 1: The idea of waking up in the morning and taking

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Speaker 1: a ketone ester like be the hydroxy buttoryate, right yep,

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Speaker 1: just too fast forward that move into ketosis to get

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Speaker 1: all of those benefits.

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Speaker 3: And then break the fast.

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Speaker 1: Have you ever thought about taking a ketone est or

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Speaker 1: have you ever played with taking a keyton ester if you're.

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Speaker 3: Doing a bit of fasting.

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Speaker 2: I've been interested in them, and I haven't. You know,

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Speaker 2: It's part of the turn off is they're so expensive. Right,

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Speaker 2: If you want a large amount of ketone a lot

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Speaker 2: of those supplements, you know, they would be like ten

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Speaker 2: dollars a day or something.

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Speaker 1: So's that expect because I only just looked at it yesterday.

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Speaker 1: I looked at beta hydroxy beuty yesterday. So this is

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Speaker 1: very hot off the press in my mind.

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Speaker 2: Yeah, it's well, I mean some of them are. There's

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Speaker 2: different forms. I It's been a while since I've dove

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Speaker 2: into this one, but I have been interested in them,

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Speaker 2: and I think that there's there's a lot of good

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Speaker 2: data to show that taking a key tone supplement immediately

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Speaker 2: improves brain function, like the of the There are imaging

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Speaker 2: studies that show this that if you look at aging

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Speaker 2: people who are exhibiting some of the signatures of brain

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Speaker 2: aging on brain scans, you give them a key tone

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Speaker 2: supplement and you recover that function. Like it seems to

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Speaker 2: do something very positive because the brain loves keytones as

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Speaker 2: a fuel source. Yes, so that's kind of where my

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Speaker 2: interest came from. And I have looked at them, but yeah,

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Speaker 2: I haven't haven't experimented with it myself. Yeah, yeah, okay.

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Speaker 1: And then on the topic of fasting, what what's your

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Speaker 1: view on fasting, whether it be short term, intimittent fast

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Speaker 1: periods of longer fasting, what's your what's your.

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Speaker 3: View on that? And do you have a you on

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Speaker 3: what sort of age group that it would benefit more.

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Speaker 2: Yeah, that's a that's a good question. Well, so, so

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Speaker 2: first I would say I think it would benefit people

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Speaker 2: that aren't at risk of frailty or of.

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Speaker 4: Number one number one ye, yeah, and that's not just

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Speaker 4: elderly people that can also be endurance athletes that can

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Speaker 4: be you know a lot of people, fasting might tip

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Speaker 4: them too far into that catabolic state versus where.

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Speaker 2: They're already at. So I don't think it's for everyone.

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Speaker 2: If you're more in the over nutrition camp, you know,

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Speaker 2: you you have some some weight to lose, You're you're

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Speaker 2: getting in shape, you you have enough muscle mass. If

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Speaker 2: you were to lose a little bit of it, it's

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Speaker 2: not going to be the end of the world. I

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Speaker 2: think fasting can be excellent, and there's lots of excellent

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Speaker 2: clinical studies showing benefits. The tough thing is there aren't.

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Speaker 2: I mean, okay, So backing up a little bit. The

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Speaker 2: goal of fasting, as we've been talking about it is

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Speaker 2: to activate autopogy, right, to sort of kick off that

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Speaker 2: cellular recycling mechanism and get all the benefits that we

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Speaker 2: know that that has. The trouble is we don't have

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Speaker 2: great data in humans to know how long that takes. Yes, correct,

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Speaker 2: it's been very tooallenging to measure autoplogy and humans in

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Speaker 2: real time, and there's just recently, in the last couple

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Speaker 2: of years, the first studies have been able to do it,

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Speaker 2: and they've shown that I don't remember exactly how long

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Speaker 2: it was, it was an intermittent fasting protocol does indeed

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Speaker 2: activate autology in humans on an average, But you know,

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Speaker 2: that's not the same as saying that we know what

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Speaker 2: the optimal time is, how that rereads from person to person.

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Speaker 2: So I don't know. I mean, I don't know how

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Speaker 2: long it takes to start autology and how much it

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Speaker 2: ramps up if you continue, And so it's kind of

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Speaker 2: hard to make data based decisions on what to do

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Speaker 2: with fasting, which is why I think it's really for

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Speaker 2: most people, it's going to be how do you feel?

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Speaker 2: You know, are you recovering from exercise still, are you

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Speaker 2: feeling energetic? Do you feel like your your brain function

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Speaker 2: is good? I think, unfortunately, that's the best we can

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Speaker 2: do right now.

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Speaker 1: Yeah, I think anybody who tells you that fasting for

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Speaker 1: this amount of time and just just autophogy is just

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Speaker 1: the foot of ship, right.

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Speaker 2: There's no way to even measure that until very recently.

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Speaker 2: So yeah, it's not that simple. I wish it was.

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Speaker 1: And there does seem to be some research from from

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Speaker 1: and again mostly animal models that that muscle autophogy and

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Speaker 1: we can potentially accelerate the autoplogy and muscle sales from

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Speaker 1: exercising in a fasted state. Right, that's one potential, But

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Speaker 1: again I don't think we know. My view on this

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Speaker 1: is very similar to yours, is what is your mediator.

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Speaker 3: Health go right now?

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Speaker 1: Like if your metabolism is a problem, right, if you

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Speaker 1: have problems with your your glucose, if you're overweight, particularly

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Speaker 1: central obesity. I say that people you know the I

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Speaker 1: think the benefits of fasting outweigh the negatives in terms

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Speaker 1: of any loss of muscle mass.

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Speaker 3: Right.

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Speaker 1: But and particularly if you're like me in your fifties

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Speaker 1: and your major goal is to or one of your

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Speaker 1: major goals is from a health boance perspective, is maintaining

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Speaker 1: your muscle function.

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Speaker 3: I trade a little bit more carefully.

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Speaker 1: Where I've kind of landed is probably cycling through a

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Speaker 1: little bit of intermittent fasting just on a daily basis,

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Speaker 1: And then I think it's probably a good idea for

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Speaker 1: me to do once a year, a four day water

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Speaker 1: fast to get that sort of system right wide reset

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Speaker 1: and and just know that I'm to some resistance training

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Speaker 1: during it and minimize them the loss of muscle. That's

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Speaker 1: kind of where I've landed. Are you in a similar spot?

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Speaker 1: It sounds like you're in a similar spot.

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Speaker 3: Yeah.

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Speaker 2: I think the resistance training while you're doing it is key.

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Speaker 2: I mean, if if you're if you're resistance training enough

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Speaker 2: that you know how strong you are, then you know,

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Speaker 2: you know, for a given exercise at a given way,

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Speaker 2: how many reps you should be able to get. Sort

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Speaker 2: of doing low volume resistance training where you're making sure

400
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Speaker 2: you're not losing reps or losing weight while you're doing it.

401
00:22:26,960 --> 00:22:29,280
Speaker 2: If that's the case, you're not losing muscle, right, You're

402
00:22:29,320 --> 00:22:31,040
Speaker 2: not going to keep your lips where they are if

403
00:22:31,880 --> 00:22:34,679
Speaker 2: if you're losing a bunch of muscles. So I think

404
00:22:34,960 --> 00:22:37,600
Speaker 2: I think that's a very sensible way to go about it. Absolutely.

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Speaker 3: Yeah.

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00:22:38,200 --> 00:22:43,040
Speaker 1: Cool, And so let's not talk about a couple of

407
00:22:43,080 --> 00:22:46,280
Speaker 1: other things that that might be interesting.

408
00:22:47,520 --> 00:22:50,680
Speaker 3: So glysing, I think was something.

409
00:22:50,440 --> 00:22:54,840
Speaker 1: That came up in the intervention testing program as potential,

410
00:22:55,400 --> 00:22:58,560
Speaker 1: and then I saw a series of research papers upbut

411
00:22:58,680 --> 00:23:05,919
Speaker 1: kalinak so glycine and an acetyl cysting. And the reason

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00:23:06,000 --> 00:23:09,760
Speaker 1: I found these research papers interesting was they done and

413
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Speaker 1: I'm not sure if you're familiar with these studies, but

414
00:23:11,560 --> 00:23:14,879
Speaker 1: they've done and studies in mice and showed that glinac

415
00:23:15,240 --> 00:23:17,560
Speaker 1: enhanced their health span.

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00:23:17,680 --> 00:23:19,080
Speaker 3: But it did it through.

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00:23:19,080 --> 00:23:25,160
Speaker 1: Reducing oxidative stress, reducing inflammation, reducing mitochondrial dysfunction. Right, And

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00:23:25,320 --> 00:23:29,159
Speaker 1: the same research group then showed that in humans, in

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00:23:29,320 --> 00:23:37,800
Speaker 1: older adults, this is taking glinac reduced mitochondrial dysfunction, reduced

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00:23:37,800 --> 00:23:43,120
Speaker 1: oxidative stress, reduced inflammation. And I thought, oh, that that's interesting.

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00:23:43,200 --> 00:23:47,280
Speaker 1: And the fact that glycine independently seems to be interesting

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00:23:47,760 --> 00:23:52,600
Speaker 1: and an acetyl cysting independently would seem to have significant

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00:23:52,680 --> 00:23:59,000
Speaker 1: benefits for me, that's one that has got quite good

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00:23:59,119 --> 00:24:03,879
Speaker 1: potential in terms of an intervention, although glenac itself hasn't

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Speaker 1: been tested.

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00:24:04,280 --> 00:24:06,200
Speaker 3: What's your thoughts any thoughts on ginac?

427
00:24:06,960 --> 00:24:08,960
Speaker 2: That's yeah, no, you're you're giving me a new one.

428
00:24:09,119 --> 00:24:11,720
Speaker 2: I have heard of it. I'm not familiar with the research,

429
00:24:11,800 --> 00:24:15,200
Speaker 2: so I need to check it out, but I guess yeah.

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00:24:15,240 --> 00:24:19,840
Speaker 2: My question would be with presumably anecetyl systeine is the

431
00:24:19,920 --> 00:24:23,040
Speaker 2: active agent because that has all sorts of biological activity

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00:24:23,080 --> 00:24:26,080
Speaker 2: for reducing oxidative stress. And yeah, there's very good data

433
00:24:26,080 --> 00:24:29,000
Speaker 2: for that supplement on its own for all sorts of things. Yes,

434
00:24:29,520 --> 00:24:31,800
Speaker 2: So when you conjugate it to glycine, Yeah, what's that doing?

435
00:24:31,920 --> 00:24:32,240
Speaker 3: Is it?

436
00:24:32,280 --> 00:24:37,880
Speaker 2: Is it changing the biodistribution of anacetyl systeine. Presumably it's

437
00:24:37,920 --> 00:24:41,120
Speaker 2: doing something like that. So I would need to read

438
00:24:41,200 --> 00:24:42,000
Speaker 2: up on that one a little.

439
00:24:42,119 --> 00:24:44,080
Speaker 1: So I want to flick you some research papers and

440
00:24:44,080 --> 00:24:48,840
Speaker 1: I look forward to a blog post from you on it. Yeah. Yeah,

441
00:24:48,960 --> 00:24:53,240
Speaker 1: let's we're over an r into this, but let's get

442
00:24:53,320 --> 00:24:56,240
Speaker 1: into the topic that I got to you on.

443
00:24:56,280 --> 00:24:59,240
Speaker 3: Into the show. Yeah, yeah, it's sure, you're right, which

444
00:24:59,400 --> 00:25:00,720
Speaker 3: was your wrote.

445
00:25:00,480 --> 00:25:07,280
Speaker 1: This fascinating article about microplastics and and an intervention that

446
00:25:07,280 --> 00:25:10,120
Speaker 1: that you had done on yourself. And I love self experimentation.

447
00:25:10,320 --> 00:25:13,320
Speaker 1: I'm actually you know, given all that we have talked

448
00:25:13,320 --> 00:25:18,440
Speaker 1: about here and individual differences, I think everybody should be

449
00:25:18,520 --> 00:25:21,919
Speaker 1: self experimenting. An equals one is not a great science

450
00:25:21,960 --> 00:25:28,640
Speaker 1: experiment unless it's done on you. Yeah, right, for you, yeah, exactly,

451
00:25:28,760 --> 00:25:30,400
Speaker 1: as long as you kind of know what you've got

452
00:25:30,440 --> 00:25:32,800
Speaker 1: to know what you're doing. That's that's the key thing,

453
00:25:34,160 --> 00:25:37,360
Speaker 1: so to talk to us about because I'd be more

454
00:25:37,400 --> 00:25:41,720
Speaker 1: and more concerned about the research coming out about plastics,

455
00:25:41,720 --> 00:25:43,879
Speaker 1: and I think most of my listeners would be familiar

456
00:25:43,920 --> 00:25:45,720
Speaker 1: with that. I've done a couple of podcasts on it,

457
00:25:45,800 --> 00:25:48,919
Speaker 1: not not at a deep level, but just the fact

458
00:25:48,960 --> 00:25:51,760
Speaker 1: that they are ubiquitous in the environment, and they found

459
00:25:51,760 --> 00:25:55,960
Speaker 1: it in pretty much every human tissue in placentas. I

460
00:25:55,960 --> 00:25:58,960
Speaker 1: think it was one hundred percent strike rate in US women.

461
00:25:59,080 --> 00:26:01,959
Speaker 1: When they look, they're not finding it. When they're all

462
00:26:02,040 --> 00:26:05,280
Speaker 1: top seeing human brein, they're finding microplastics in there.

463
00:26:05,440 --> 00:26:10,720
Speaker 3: So this ship is insidious. It's clearly not doing good.

464
00:26:11,440 --> 00:26:16,440
Speaker 5: And so give us your view on just on why

465
00:26:16,440 --> 00:26:20,399
Speaker 5: they're bad and then the intervention you did and what

466
00:26:20,600 --> 00:26:22,280
Speaker 5: some people could potentially do.

467
00:26:23,320 --> 00:26:28,040
Speaker 2: Yeah, I'll do my best. So So, the microplastic situation

468
00:26:29,600 --> 00:26:31,920
Speaker 2: is something that I only learned about recently in the

469
00:26:32,000 --> 00:26:34,520
Speaker 2: last year or two, and as I learned more about it,

470
00:26:34,680 --> 00:26:40,600
Speaker 2: I was just like, holy shit, this is terrible. Yeah, yeah,

471
00:26:40,720 --> 00:26:44,560
Speaker 2: it's And I also wondered, like, why aren't we talking

472
00:26:44,560 --> 00:26:48,600
Speaker 2: about this? You know, this is this is this is

473
00:26:48,640 --> 00:26:52,919
Speaker 2: absolutely devastating that that we're we're all facing this exposure

474
00:26:53,000 --> 00:26:55,080
Speaker 2: and that it's in all of our tissues, and it's

475
00:26:55,119 --> 00:26:58,439
Speaker 2: increasing over time, and it's associated with a number of

476
00:26:58,440 --> 00:27:01,439
Speaker 2: really terrible health outcomes. It's it's it's really scary, and

477
00:27:01,480 --> 00:27:04,680
Speaker 2: it is not getting any attention at all. We'll see

478
00:27:04,680 --> 00:27:06,800
Speaker 2: a pop press article once in a while, you know,

479
00:27:06,880 --> 00:27:10,919
Speaker 2: saying they found new microplastic levels in something worse than

480
00:27:10,960 --> 00:27:13,320
Speaker 2: we thought, and it's you know, it's it's getting some attention,

481
00:27:13,400 --> 00:27:16,520
Speaker 2: but people just don't care the way they should. But

482
00:27:16,600 --> 00:27:19,760
Speaker 2: when I learned about this, I was very scared. When

483
00:27:19,800 --> 00:27:21,920
Speaker 2: I when I learned it was the brain paper was

484
00:27:21,920 --> 00:27:24,520
Speaker 2: the one that really got me. This was from Matthew

485
00:27:24,560 --> 00:27:29,760
Speaker 2: Campin's Groove. They looked at brain samples from deceased people

486
00:27:30,280 --> 00:27:34,360
Speaker 2: with a new very sensitive technique that can detect microplastics.

487
00:27:34,359 --> 00:27:37,560
Speaker 2: They used a number of techniques, they detected them multiple ways,

488
00:27:38,240 --> 00:27:40,800
Speaker 2: and what they found was that our brains just have

489
00:27:41,000 --> 00:27:45,600
Speaker 2: an absurd amount of plastic accumulating in them in the

490
00:27:45,920 --> 00:27:50,160
Speaker 2: form of these really tiny micro and nanoparticles. It's higher

491
00:27:50,160 --> 00:27:53,760
Speaker 2: than other tissues in the body. It's you know, you

492
00:27:53,840 --> 00:27:58,200
Speaker 2: can detect them biochemically with mass spec you can detect

493
00:27:58,200 --> 00:28:01,679
Speaker 2: them microscopically. If you stain and look for this the

494
00:28:01,720 --> 00:28:04,920
Speaker 2: plastic particles in the brain, it's it's a very clear finding.

495
00:28:05,359 --> 00:28:08,440
Speaker 2: And of course, you know, the plastic industry is pushing

496
00:28:08,480 --> 00:28:10,720
Speaker 2: back very hard, trying to discredit the science. But it's

497
00:28:10,840 --> 00:28:13,359
Speaker 2: very solid science published in one of the mist journals

498
00:28:13,359 --> 00:28:15,320
Speaker 2: in the world. So if anyone has doubts on the science,

499
00:28:15,760 --> 00:28:19,560
Speaker 2: don't believe it. This is excellent science. But they show

500
00:28:19,600 --> 00:28:22,160
Speaker 2: that it's accumulating to these massive levels in the brain

501
00:28:22,920 --> 00:28:25,320
Speaker 2: and in other tissues. And if you look at brains

502
00:28:25,320 --> 00:28:28,960
Speaker 2: of people with dementia, it's it's quite a bit higher

503
00:28:28,960 --> 00:28:31,040
Speaker 2: than in people without dementia. That doesn't mean that the

504
00:28:31,040 --> 00:28:33,600
Speaker 2: plastic cause the dementia. We don't know what the relationship

505
00:28:33,640 --> 00:28:35,760
Speaker 2: is yet, but it's it's concerning.

506
00:28:35,680 --> 00:28:39,200
Speaker 3: Yeah, probably not doing good. Let's put it out well.

507
00:28:39,160 --> 00:28:42,520
Speaker 2: It's not doing anything good, and so it's you know,

508
00:28:42,600 --> 00:28:45,960
Speaker 2: that's one study in humans. There have been many, many

509
00:28:46,040 --> 00:28:48,680
Speaker 2: other mechanistic studies in mice where they inject mice with

510
00:28:48,720 --> 00:28:51,440
Speaker 2: microplastics and look at what happens. There are cell studies,

511
00:28:52,000 --> 00:28:57,320
Speaker 2: and what we're learning is that these really tiny plastic

512
00:28:57,360 --> 00:28:59,600
Speaker 2: particles they do a lot of really bad stuff in

513
00:28:59,640 --> 00:29:03,600
Speaker 2: the body. But I think at the core what's happening

514
00:29:03,680 --> 00:29:08,440
Speaker 2: is one of the worst things is that your immune cells,

515
00:29:08,480 --> 00:29:11,880
Speaker 2: of course recognize this foreign object in your circulation or

516
00:29:11,880 --> 00:29:14,120
Speaker 2: in your tissue, and they try to eliminate it, and

517
00:29:14,120 --> 00:29:17,080
Speaker 2: that's what their job is, so they'll actually engulf this

518
00:29:17,200 --> 00:29:20,760
Speaker 2: microplastic This little tiny plastic particle goes into the cell.

519
00:29:21,360 --> 00:29:23,240
Speaker 2: But the cells are also little and tiny, so the

520
00:29:23,240 --> 00:29:26,760
Speaker 2: plastic particle is like almost as big as the cell itself. Wow,

521
00:29:27,520 --> 00:29:31,360
Speaker 2: it gets stuck in its lycisme. That cell goes crazy

522
00:29:31,360 --> 00:29:33,840
Speaker 2: and does all sorts of bad things. It starts releasing

523
00:29:33,880 --> 00:29:38,800
Speaker 2: inflammatory cytokinds in the brain. These immune cells get stuck

524
00:29:39,000 --> 00:29:44,760
Speaker 2: and cause little coagulation issues and little thrombotic issues in

525
00:29:44,800 --> 00:29:51,000
Speaker 2: the brain. They drive inflammation. Like, the collective take of

526
00:29:51,040 --> 00:29:53,760
Speaker 2: the studies is that these are not anything we want

527
00:29:53,800 --> 00:29:56,760
Speaker 2: in our bodies. We should all be very concerned that

528
00:29:57,120 --> 00:29:59,719
Speaker 2: you can detect them and most of our tissues and

529
00:30:00,080 --> 00:30:05,680
Speaker 2: they're likely driving persistent chronic inflammation. And yeah, I mean,

530
00:30:05,720 --> 00:30:06,680
Speaker 2: I could go on and.

531
00:30:06,600 --> 00:30:09,640
Speaker 1: On, but I think we could summarize this John microplastics

532
00:30:09,680 --> 00:30:13,240
Speaker 1: equal a cellular shit storm.

533
00:30:13,640 --> 00:30:16,280
Speaker 2: It is a shit storm. It's a whole body wide

534
00:30:16,280 --> 00:30:20,479
Speaker 2: shit storm. It's one study I should also menage. There

535
00:30:20,520 --> 00:30:24,800
Speaker 2: was a study that looked at I believe it was

536
00:30:24,840 --> 00:30:26,040
Speaker 2: carotid artery plaques.

537
00:30:26,360 --> 00:30:26,520
Speaker 3: Right.

538
00:30:26,600 --> 00:30:28,880
Speaker 2: They had patients coming in to get these plaques taken out.

539
00:30:28,880 --> 00:30:31,720
Speaker 2: They were going to have it happen anyways, So they

540
00:30:31,720 --> 00:30:34,360
Speaker 2: consented to patients and asked, can we look and see

541
00:30:34,360 --> 00:30:37,000
Speaker 2: if your plack has microplastics, and then can we follow

542
00:30:37,040 --> 00:30:39,960
Speaker 2: you for a period of time afterwards and see what happens.

543
00:30:41,040 --> 00:30:42,880
Speaker 2: So they did this. They had it was a well

544
00:30:42,920 --> 00:30:45,520
Speaker 2: powered study. They had a large number of patients. They

545
00:30:46,560 --> 00:30:49,840
Speaker 2: they bucketed the patients into two groups. There were patients

546
00:30:49,840 --> 00:30:52,479
Speaker 2: that had microplastics in their plaques and then there were

547
00:30:52,560 --> 00:30:54,560
Speaker 2: patients that had plaques without microplastics.

548
00:30:54,640 --> 00:30:54,800
Speaker 3: Right.

549
00:30:56,680 --> 00:30:58,920
Speaker 2: The patients, they then they followed them for a number

550
00:30:58,960 --> 00:31:00,920
Speaker 2: of years. I wish I remember the exact number, but

551
00:31:00,960 --> 00:31:04,360
Speaker 2: I don't. They followed the patients and the ones that

552
00:31:04,440 --> 00:31:08,960
Speaker 2: had the microplastics in their in their plaques had dramatically

553
00:31:09,040 --> 00:31:14,240
Speaker 2: worse health outcomes in terms of fatality, stroke, heart attack.

554
00:31:14,760 --> 00:31:17,680
Speaker 2: It was it was a very clear difference. And it's

555
00:31:17,720 --> 00:31:19,960
Speaker 2: They also had a lot of beautiful mechanistic data in

556
00:31:20,000 --> 00:31:22,320
Speaker 2: the study where they looked at markers of inflammation in

557
00:31:22,360 --> 00:31:25,520
Speaker 2: the plaques much much higher when the microplastics are present.

558
00:31:25,920 --> 00:31:29,360
Speaker 2: So it's it's it's observational data. People will always push

559
00:31:29,400 --> 00:31:31,480
Speaker 2: back and they it's not a randomized controlled trial, but

560
00:31:31,840 --> 00:31:33,400
Speaker 2: we're never going to have that where I can inject

561
00:31:33,440 --> 00:31:36,479
Speaker 2: people with microplastics. So this is the best we can do.

562
00:31:36,880 --> 00:31:40,080
Speaker 2: And it says that it's very very bad and and

563
00:31:40,080 --> 00:31:44,480
Speaker 2: and yeah, it's a signal is consistent across multiple studies.

564
00:31:45,080 --> 00:31:47,120
Speaker 1: You need to take set up and take notice and

565
00:31:47,120 --> 00:31:50,960
Speaker 1: forget about a bloody randomized control draw right. So yeah, yeah,

566
00:31:51,240 --> 00:31:54,240
Speaker 1: so what I be you done then as a result

567
00:31:54,280 --> 00:31:56,320
Speaker 1: of this, tell us about this experiment?

568
00:31:56,560 --> 00:32:00,640
Speaker 2: Okay, Well, so, as I kind of went down the

569
00:32:00,680 --> 00:32:04,320
Speaker 2: rabbit hole and learned more about microplastics, one of the

570
00:32:04,320 --> 00:32:07,720
Speaker 2: things that was frustrating was that nobody is publishing trials

571
00:32:07,800 --> 00:32:10,680
Speaker 2: yet in mice or in cell models on how to

572
00:32:10,720 --> 00:32:13,840
Speaker 2: get these things out of ourselves. You know, it's I'm

573
00:32:13,880 --> 00:32:15,680
Speaker 2: sure there are people working on it. The field is

574
00:32:15,760 --> 00:32:19,000
Speaker 2: moving very rapidly. I'm sure there's all sorts of new

575
00:32:19,080 --> 00:32:20,880
Speaker 2: labs that are just starting to work on this, But

576
00:32:20,920 --> 00:32:24,440
Speaker 2: the the interventional stuff just really isn't out there yet.

577
00:32:25,160 --> 00:32:27,200
Speaker 2: There's a couple of groups that have shown that if

578
00:32:27,200 --> 00:32:31,000
Speaker 2: you ingest certain certain supplements you can kind of bind

579
00:32:31,080 --> 00:32:33,440
Speaker 2: up microplastics in the gut because most of it's coming

580
00:32:33,440 --> 00:32:36,320
Speaker 2: from dietary intake, and you can help prevent the gut

581
00:32:36,360 --> 00:32:38,360
Speaker 2: from absorbing them. So that's that's one positive.

582
00:32:39,000 --> 00:32:40,960
Speaker 1: But as far as what were those things that you

583
00:32:41,000 --> 00:32:43,200
Speaker 1: could take to bind them? Jones, can you remember off

584
00:32:43,200 --> 00:32:43,760
Speaker 1: the time.

585
00:32:43,600 --> 00:32:45,400
Speaker 2: Yeah, there's a couple. I think one of them was

586
00:32:46,120 --> 00:32:52,040
Speaker 2: Kaido sand, which is yeah, I know back when I

587
00:32:52,120 --> 00:32:55,040
Speaker 2: used to brew beer. It's an additive that people use there,

588
00:32:55,040 --> 00:32:58,280
Speaker 2: so I was familiar with it from but it's and

589
00:32:58,280 --> 00:33:00,760
Speaker 2: then there were I think some fibers supplements that could

590
00:33:00,800 --> 00:33:04,280
Speaker 2: also be basically binding agents. It's physical binding agents that

591
00:33:04,400 --> 00:33:06,480
Speaker 2: sequester it in the gut and prevent your gut from

592
00:33:06,520 --> 00:33:10,120
Speaker 2: absorbing it. And there are some supplements that I think

593
00:33:10,120 --> 00:33:11,880
Speaker 2: are going to be on the market soon that include

594
00:33:11,880 --> 00:33:15,800
Speaker 2: those ingredients with the goal the stated goal of reducing microplastics.

595
00:33:15,960 --> 00:33:20,640
Speaker 2: We won't know how well work in humans, so that's encouraging,

596
00:33:20,720 --> 00:33:23,720
Speaker 2: But once they're in our bodies and we know that,

597
00:33:24,080 --> 00:33:25,920
Speaker 2: you know they are in our bodies, most of them,

598
00:33:26,160 --> 00:33:28,160
Speaker 2: most of us probably have absurd amounts of these in

599
00:33:28,200 --> 00:33:31,560
Speaker 2: our bodies. We don't have a clue how to get

600
00:33:31,560 --> 00:33:35,640
Speaker 2: them out sort of reverse that process because I don't

601
00:33:35,680 --> 00:33:38,440
Speaker 2: want microplastics in my cells driving inflammation. I don't know

602
00:33:38,440 --> 00:33:40,880
Speaker 2: about you, but when I get rid of it, I

603
00:33:40,880 --> 00:33:42,720
Speaker 2: immediately think, like, how do I get rid of this?

604
00:33:43,360 --> 00:33:46,600
Speaker 1: Particularly because you're so into lysisomes and you know that

605
00:33:46,680 --> 00:33:52,840
Speaker 1: they bunk up the lysisomes. So she's almost an existential crisis.

606
00:33:53,440 --> 00:33:56,200
Speaker 2: Is it's like, oh my god, like I have this

607
00:33:56,320 --> 00:33:58,880
Speaker 2: crap clogging up my lysisomes. I know what happens when

608
00:33:58,920 --> 00:34:00,880
Speaker 2: your lycismes get sick. I don't want anything to do

609
00:34:00,960 --> 00:34:01,120
Speaker 2: with that.

610
00:34:01,400 --> 00:34:03,720
Speaker 3: Yeah, yeah, So yeah, it was on a.

611
00:34:03,680 --> 00:34:08,040
Speaker 2: Personal level, it was scary, and so being a lysosome

612
00:34:08,080 --> 00:34:11,719
Speaker 2: biologist and someone who's worked in this space, I it

613
00:34:11,800 --> 00:34:14,640
Speaker 2: was I had one idea. I was like, well, if

614
00:34:14,719 --> 00:34:17,560
Speaker 2: other stuff accumulates in lysosomes, we know how to get

615
00:34:17,600 --> 00:34:19,760
Speaker 2: that out. I mean, we know how to get extra

616
00:34:19,880 --> 00:34:22,680
Speaker 2: cholesterol out of lysisomes. We know how to get other

617
00:34:22,719 --> 00:34:24,840
Speaker 2: substrates that build up out of lycismes. There are a

618
00:34:24,920 --> 00:34:27,640
Speaker 2: number of drugs that can do this in mice and

619
00:34:27,719 --> 00:34:31,359
Speaker 2: in humans, and one of them that had just been

620
00:34:31,400 --> 00:34:34,879
Speaker 2: published in a really interesting paper on a disease called

621
00:34:34,920 --> 00:34:37,480
Speaker 2: Nieman Pick disease, which is a disease where your lysisome

622
00:34:37,520 --> 00:34:41,880
Speaker 2: to accumulate cholesterol. This paper had used a compound called sulforophane,

623
00:34:42,360 --> 00:34:46,839
Speaker 2: and they treated the mice with sulforophane. They showed very

624
00:34:47,320 --> 00:34:50,920
Speaker 2: convincingly that that caused the lysosomes to basically dump their

625
00:34:50,920 --> 00:34:53,719
Speaker 2: contents outside of the cell so they could get rid

626
00:34:53,719 --> 00:34:56,880
Speaker 2: of all this extra cholesterol. And then once they did that,

627
00:34:57,000 --> 00:34:59,520
Speaker 2: the lysismes were much healthier and the cells were much healthier,

628
00:34:59,520 --> 00:35:01,560
Speaker 2: and so were the and have had a very positive

629
00:35:01,600 --> 00:35:06,439
Speaker 2: outcome in that study. So you know, I yeah, I thought, well,

630
00:35:06,480 --> 00:35:10,239
Speaker 2: it'd be really interesting if someone would test sulforofane in

631
00:35:10,320 --> 00:35:14,560
Speaker 2: a mouse study to see if it could reduce microplastics

632
00:35:14,600 --> 00:35:17,680
Speaker 2: accumulation and mysosomes because they're you know, they're accumulating just

633
00:35:17,719 --> 00:35:22,000
Speaker 2: like these other things do. To get that study done

634
00:35:22,040 --> 00:35:25,640
Speaker 2: would take years. Who's very slow. Someone probably is trying that,

635
00:35:26,200 --> 00:35:28,960
Speaker 2: but I didn't want to wait for that. I thought, well, sulforaphane,

636
00:35:29,000 --> 00:35:30,640
Speaker 2: this is something people take this all the time. There

637
00:35:30,680 --> 00:35:33,959
Speaker 2: are tons of clinical studies showing good things from taking sulforaphane.

638
00:35:34,840 --> 00:35:36,920
Speaker 2: I wonder if it's already doing this in people. I

639
00:35:36,920 --> 00:35:39,520
Speaker 2: wonder if people who are taking this or rejecting microplastics

640
00:35:39,560 --> 00:35:42,799
Speaker 2: out of their cells. So that was the basis for

641
00:35:42,840 --> 00:35:44,560
Speaker 2: this self experiment. I said, I'm going to do it.

642
00:35:44,680 --> 00:35:46,160
Speaker 2: I have a way to measure this. Now there's a

643
00:35:46,239 --> 00:35:49,920
Speaker 2: nice test that is commercially available, and I can see

644
00:35:49,960 --> 00:35:52,400
Speaker 2: exactly what happens in my blood before and after taking

645
00:35:52,400 --> 00:35:56,240
Speaker 2: the supplement and measure what's happening to my microplastic levels.

646
00:35:56,360 --> 00:35:59,800
Speaker 2: And sure enough, after I took a big dose of sulforafane,

647
00:36:00,600 --> 00:36:04,000
Speaker 2: it released many, many millions of microplastic particles from my

648
00:36:04,120 --> 00:36:09,359
Speaker 2: cell wow, and dumped them into my blood. Which that's

649
00:36:09,719 --> 00:36:12,759
Speaker 2: a nice result. Scientifically, it does Okay, it worked, you know,

650
00:36:12,800 --> 00:36:16,799
Speaker 2: the hypothesis is supported by the data. The sulforafane did

651
00:36:16,840 --> 00:36:20,400
Speaker 2: something that liberated the microplastics out of the spells. But

652
00:36:20,480 --> 00:36:22,919
Speaker 2: the other side of that is what happened next? Where

653
00:36:22,960 --> 00:36:25,640
Speaker 2: did they go? And I don't know, I can't answer

654
00:36:25,640 --> 00:36:28,759
Speaker 2: that question for you. I don't know if they went

655
00:36:28,880 --> 00:36:31,840
Speaker 2: back into the same or different cells and just caused

656
00:36:31,960 --> 00:36:35,719
Speaker 2: you know, caused more problems. My hope is that if

657
00:36:35,760 --> 00:36:38,080
Speaker 2: you do something like this, maybe your body has another

658
00:36:38,160 --> 00:36:40,879
Speaker 2: chance to eliminate them. Yes, maybe some of them can

659
00:36:40,960 --> 00:36:43,360
Speaker 2: end up in your urine. We know microplastic particles do

660
00:36:43,480 --> 00:36:46,280
Speaker 2: end up in urine, so is the reason that could happened.

661
00:36:47,160 --> 00:36:50,359
Speaker 2: They also end up in bile, which is a way

662
00:36:50,400 --> 00:36:53,560
Speaker 2: of excreting them through your gut. So it's possible that

663
00:36:53,560 --> 00:36:57,680
Speaker 2: that's happening. But in the absence of a test that

664
00:36:57,719 --> 00:37:01,080
Speaker 2: can test those fluids, I don't have a way to

665
00:37:01,120 --> 00:37:03,880
Speaker 2: answer that question, which I think is an important next

666
00:37:03,920 --> 00:37:06,480
Speaker 2: step for someone to figure out, is if you liberate

667
00:37:06,480 --> 00:37:08,960
Speaker 2: a whole bunch of microplastics like this, where do they go?

668
00:37:09,320 --> 00:37:13,120
Speaker 1: Yeah, yeah, yeah, yeah, and hopefully it's out of the body,

669
00:37:13,280 --> 00:37:19,399
Speaker 1: and the our detoxification process is peas one and feast two.

670
00:37:19,520 --> 00:37:22,400
Speaker 3: Would they have potential to excrete microplastics?

671
00:37:23,200 --> 00:37:26,000
Speaker 2: Yeah, So that's that's one. That's why most people are

672
00:37:26,040 --> 00:37:30,280
Speaker 2: familiar with sulfur or fane is that it's activating these

673
00:37:30,360 --> 00:37:34,200
Speaker 2: metabolic pathways. That's a good thing. What that probably helps

674
00:37:34,200 --> 00:37:38,760
Speaker 2: more with than the plastic particles themselves, are these plasticizers,

675
00:37:38,800 --> 00:37:41,560
Speaker 2: these chemicals that are bound up in the microplastic particles

676
00:37:42,080 --> 00:37:44,600
Speaker 2: things make like this phenol A b p A. People

677
00:37:44,600 --> 00:37:49,160
Speaker 2: are familiar with one. Right, It's probably very helpful for

678
00:37:49,200 --> 00:37:53,440
Speaker 2: eliminating those toxins, probably less helpful for the particles themselves,

679
00:37:53,480 --> 00:37:57,120
Speaker 2: just because our bodies are we have no evolutionary mechanism

680
00:37:57,200 --> 00:37:58,080
Speaker 2: to deal with something like.

681
00:37:58,120 --> 00:38:01,120
Speaker 1: Yeah, we don't even recognize it, right, well, probably probably

682
00:38:01,239 --> 00:38:03,000
Speaker 1: nice of it's bad, but don't know what to do

683
00:38:03,080 --> 00:38:03,600
Speaker 1: with it yet.

684
00:38:04,000 --> 00:38:04,440
Speaker 3: Interesting.

685
00:38:04,480 --> 00:38:08,560
Speaker 2: Yeah, I mean we probably have enzymes in our bodies

686
00:38:08,600 --> 00:38:12,280
Speaker 2: that recognize it as the wrong thing. You know, ourselves

687
00:38:12,280 --> 00:38:14,719
Speaker 2: probably think these are fats or something, because that's what

688
00:38:14,760 --> 00:38:17,720
Speaker 2: they look like. On a molecular level, they look like lipids,

689
00:38:18,880 --> 00:38:22,000
Speaker 2: So it's probably screwing up all sort of lipid metabolism machinery.

690
00:38:22,160 --> 00:38:25,919
Speaker 2: And it's we certainly have no way of naturally eliminating them.

691
00:38:26,000 --> 00:38:27,800
Speaker 2: It's it's it's going to be a push in the

692
00:38:27,880 --> 00:38:28,400
Speaker 2: right direction.

693
00:38:28,960 --> 00:38:32,440
Speaker 1: Yeah, that's a That's an interesting watch this space, isn't it?

694
00:38:33,040 --> 00:38:33,320
Speaker 3: John?

695
00:38:33,440 --> 00:38:38,919
Speaker 1: This has been absolutely fantastic, And I'm completely unscripted as well,

696
00:38:38,960 --> 00:38:42,479
Speaker 1: which is more more impressive that I can just wing

697
00:38:42,640 --> 00:38:45,799
Speaker 1: questions that you with no preparation and you just talk

698
00:38:46,000 --> 00:38:49,280
Speaker 1: off the hip with all of this stuff. So where

699
00:38:49,320 --> 00:38:54,520
Speaker 1: can people go to find out more about you? I

700
00:38:55,280 --> 00:38:57,440
Speaker 1: know you're on LinkedIn, That's where I found you, so,

701
00:38:57,680 --> 00:39:01,280
Speaker 1: but also you write quite a lot. You're on substack,

702
00:39:01,360 --> 00:39:01,680
Speaker 1: don't you.

703
00:39:02,480 --> 00:39:05,839
Speaker 2: Yeah, that's kind of a new platform for me. Yeah.

704
00:39:05,840 --> 00:39:08,520
Speaker 2: My subseac newsletter is called Translation and you can also

705
00:39:08,560 --> 00:39:11,400
Speaker 2: find it by searching my name, and that's you know.

706
00:39:11,640 --> 00:39:13,759
Speaker 2: The plan is for that to become sort of my

707
00:39:13,800 --> 00:39:17,880
Speaker 2: primary channel for articles and maybe some interviews in the

708
00:39:17,880 --> 00:39:19,680
Speaker 2: future and that sort of thing. And I'm a still

709
00:39:19,719 --> 00:39:22,800
Speaker 2: working on a book. Substack will be where I communicate

710
00:39:22,880 --> 00:39:25,600
Speaker 2: updates on that. So they tuned there.

711
00:39:25,680 --> 00:39:30,400
Speaker 1: Yes, how long do you think you are away from publishing?

712
00:39:31,680 --> 00:39:33,319
Speaker 2: Are you early or.

713
00:39:33,280 --> 00:39:34,759
Speaker 1: Have you got a for a bit of You've got

714
00:39:34,880 --> 00:39:36,520
Speaker 1: for a bit of progress made on it.

715
00:39:37,320 --> 00:39:40,760
Speaker 2: I've made some progress. It's going to be heavily depended

716
00:39:40,840 --> 00:39:43,440
Speaker 2: on some contributions from other people too. I'm interviewing a

717
00:39:43,520 --> 00:39:46,239
Speaker 2: number of people to sort of gather content and and

718
00:39:46,360 --> 00:39:48,440
Speaker 2: build out the framework that I'm going to present in

719
00:39:48,480 --> 00:39:50,680
Speaker 2: the book. So it's it's a little ways off still,

720
00:39:50,719 --> 00:39:54,120
Speaker 2: I'd say about a year, but we're getting there. I'd

721
00:39:54,160 --> 00:39:55,759
Speaker 2: love to chat with you sometimes about that. It sounds

722
00:39:55,760 --> 00:39:57,400
Speaker 2: like you have a lot of experience in that space.

723
00:39:57,560 --> 00:39:58,880
Speaker 2: I'm sure I can learn a lot from you.

724
00:39:59,000 --> 00:40:01,440
Speaker 1: So, well, yeah, I've written a couple and I think

725
00:40:01,520 --> 00:40:03,680
Speaker 1: I think the thing I would say is that you're

726
00:40:03,760 --> 00:40:07,919
Speaker 1: never going to get it perfect, that you just keep going,

727
00:40:07,960 --> 00:40:09,640
Speaker 1: oh and there's a little bit now, there's a new

728
00:40:09,680 --> 00:40:12,840
Speaker 1: research studies, like, just just just get it out and

729
00:40:12,920 --> 00:40:16,160
Speaker 1: you can always do an update later on. Because yeah,

730
00:40:16,160 --> 00:40:20,080
Speaker 1: when I've reread my my, my book, my first book,

731
00:40:20,080 --> 00:40:21,719
Speaker 1: I went shit, I'd like to put that and that

732
00:40:21,800 --> 00:40:24,000
Speaker 1: I'm probably going to do a revised edition, and in

733
00:40:24,120 --> 00:40:28,560
Speaker 1: this one, even sending it off to so you go

734
00:40:28,640 --> 00:40:30,920
Speaker 1: through the editing process and then get it back and

735
00:40:30,960 --> 00:40:33,399
Speaker 1: in its final edits, and then they sent me through

736
00:40:33,400 --> 00:40:34,720
Speaker 1: in here's now the layout.

737
00:40:34,760 --> 00:40:36,360
Speaker 3: I want you to check the layout.

738
00:40:36,480 --> 00:40:39,440
Speaker 1: And I'm still wanting to tweak it and add a

739
00:40:39,480 --> 00:40:41,439
Speaker 1: new study that I just read the other day.

740
00:40:41,600 --> 00:40:44,239
Speaker 3: So so don't let perfect be the enemy of grit.

741
00:40:44,600 --> 00:40:46,520
Speaker 2: That good advice. I'll try to remember that.

742
00:40:46,520 --> 00:40:49,360
Speaker 1: That would be definitely my my t But but me

743
00:40:49,560 --> 00:40:51,799
Speaker 1: I I'm certainly going to be following you on on

744
00:40:51,920 --> 00:40:54,440
Speaker 1: sub stacks, So we will put that link into the

745
00:40:54,440 --> 00:40:57,160
Speaker 1: show notes. I'll also put the link into your LinkedIn

746
00:40:57,200 --> 00:41:00,280
Speaker 1: because you've got a lot of interesting articles for anybody

747
00:41:00,320 --> 00:41:02,839
Speaker 1: who's interested in this space. And you know, the thing

748
00:41:02,960 --> 00:41:05,480
Speaker 1: I like about you is that you're not You're not

749
00:41:05,520 --> 00:41:08,880
Speaker 1: out pushing supplements, you're not pushing a product. You're just

750
00:41:09,080 --> 00:41:13,839
Speaker 1: somebody who is a hardcore scientist who's interested in this

751
00:41:13,960 --> 00:41:17,319
Speaker 1: area and has quite a lot of smarts. So it's

752
00:41:17,320 --> 00:41:21,880
Speaker 1: people like you that listeners should be following, not whinkers

753
00:41:21,960 --> 00:41:23,959
Speaker 1: like David Sinclair on.

754
00:41:25,440 --> 00:41:29,680
Speaker 2: So I appreciate that you don't bucking me with the wankers.

755
00:41:31,200 --> 00:41:33,520
Speaker 3: Definitely not. This has been awesome.

756
00:41:33,920 --> 00:41:36,160
Speaker 1: So we'll get those links, we'll put them in the

757
00:41:36,160 --> 00:41:38,839
Speaker 1: show notes, and yeah, good luck on your book, and

758
00:41:38,880 --> 00:41:41,799
Speaker 1: i'd certainly love to have you back on whenever you're

759
00:41:41,800 --> 00:41:44,879
Speaker 1: doing your book, and we'll get it promoted to our listeners.

760
00:41:45,440 --> 00:41:47,879
Speaker 2: Awesome, let's do it. Thanks Paul, it's been great, really,