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Unpacking Longevity and Cellular Health: A Conversation with Dr. Jon Brudvig - Part Two · Hardiness with Dr Paul Taylor

• 0:08
  Speaker 1: Yeah, So mixing it up a little bit, I think
• 0:11
  Speaker 1: is really important. Let's die, Let's get back to the
• 0:15
  Speaker 1: SGL two inhibitors now. Is interesting to hear you say that.
• 0:20
  Speaker 1: I'll give you a little bit of background. So January
• 0:23
  Speaker 1: this year, I had open heart surgery for a dodgy
• 0:27
  Speaker 1: valve that I was born with. I was born with
• 0:28
  Speaker 1: a bi cuspan aortic valve. But it's all good. But
• 0:31
  Speaker 1: the upshot of this is the one drug that they've
• 0:36
  Speaker 1: put me on is an SGL two inhibitor. And actually,
• 0:41
  Speaker 1: when I dug into it, I went, you know what,
• 0:43
  Speaker 1: that's a drug. I'm not basically a big fan of
• 0:46
  Speaker 1: taking drugs, but I'm like, I'm actually happy that they
• 0:50
  Speaker 1: put me on an SGL two inhibitor. It's essentially a
• 0:53
  Speaker 1: diabetes drug or our drug for managing your blood sugar
• 0:57
  Speaker 1: slice insulin, but it also has benefits for heart and
• 1:01
  Speaker 1: so I'm actually pretty happy to be on an SGL
• 1:05
  Speaker 1: to inhibitor. That's a nice unintended consequence of my being
• 1:11
  Speaker 1: born with the doachi for help, So tell our listeners
• 1:15
  Speaker 1: what and because actually, out of the interventional's testing program,
• 1:19
  Speaker 1: a lot of them, the drugs that were successful controlled
• 1:23
  Speaker 1: inchilin our and or glucose, which is an interesting thread, right,
• 1:29
  Speaker 1: But one of them, and canaga flows in and is
• 1:33
  Speaker 1: an sgl TO inhibitor. So talk to our listeners about
• 1:38
  Speaker 1: what an sgl TO inhibitor is and why you think
• 1:42
  Speaker 1: it's interesting from a longevity slice health span perspective.
• 1:47
  Speaker 2: Yeah, well, so the reason I'm excited about these is
• 1:50
  Speaker 2: just the abundance of data that we have suggesting that
• 1:53
  Speaker 2: they can be beneficial. And it's We've talked about the
• 1:56
  Speaker 2: issues with mouse studies. They do extend lifespan in my
• 2:00
  Speaker 2: least in mail lice, yes, but you know that's just
• 2:03
  Speaker 2: the beginning of the data. We have tons of data
• 2:06
  Speaker 2: for many, many thousands of patients taking these drugs in
• 2:09
  Speaker 2: the real world showing that it generates positive health outcomes
• 2:13
  Speaker 2: and reduces the incidents of negative health outcomes. They appear
• 2:17
  Speaker 2: to be very protective for the heart, like you mentioned,
• 2:20
  Speaker 2: also the kidneys. There's also a lot of data emerging
• 2:24
  Speaker 2: to suggest that they're very good for the brain. So
• 2:28
  Speaker 2: we have that piece of data saying, you know, patients
• 2:30
  Speaker 2: that are on these for diabetes tend to exhibit better
• 2:35
  Speaker 2: health outcomes over time, even outcomes unrelated to diabetes. Yes,
• 2:39
  Speaker 2: and then there's this other piece that you don't often
• 2:42
  Speaker 2: get for a longevity intervention, and this comes from studies,
• 2:46
  Speaker 2: these Mendelian randomization studies, which can you take me.
• 2:51
  Speaker 1: Take a step back and explain what those are and
• 2:55
  Speaker 1: why they're actually useful.
• 2:57
  Speaker 2: Yeah, so these are sort of a clever way of
• 3:03
  Speaker 2: modeling the impact of different interventions, in this case the
• 3:06
  Speaker 2: drug intervection and intervention by looking at sort of a
• 3:09
  Speaker 2: natural experiment that genetics have given us. So we all
• 3:14
  Speaker 2: have this protein called SGLT two that's the target of
• 3:19
  Speaker 2: this drug, right, and it's a channel. It's a channel
• 3:22
  Speaker 2: that recovers glucose in your kidney so that you don't
• 3:26
  Speaker 2: have glucose in your urine and we're keeping it in
• 3:28
  Speaker 2: the body where we need it because glucose is a
• 3:31
  Speaker 2: nutrient that we need. It's important for energy production. But
• 3:36
  Speaker 2: we have different genetic variants in SGLT two. So you know,
• 3:40
  Speaker 2: most of us have a fully functional version, but there
• 3:43
  Speaker 2: are rare genetic variants where you have a dysfunctional SGLT
• 3:48
  Speaker 2: two protein that doesn't come glucose as efficiently. So that's
• 3:53
  Speaker 2: very similar to what the drugs doing.
• 3:54
  Speaker 3: Right.
• 3:54
  Speaker 2: If the drug inhibits. And then there are some people
• 3:57
  Speaker 2: that have just been operating this way their whole lives,
• 3:59
  Speaker 2: their SGLT two never worked efficiently. You can look at
• 4:03
  Speaker 2: what happens to those people have a pretty good idea
• 4:06
  Speaker 2: of what the drug's gonna do. Right, Have I blamed
• 4:09
  Speaker 2: this in.
• 4:09
  Speaker 3: A way in a minute you have? Yeah, you've explained
• 4:11
  Speaker 3: really well.
• 4:13
  Speaker 2: So, yeah, that's that's an Ndelian randomization. And when you
• 4:16
  Speaker 2: look at it for SGLT two and you look at
• 4:20
  Speaker 2: studies sort of modeling the impact of these drugs, you
• 4:23
  Speaker 2: see really cool stuff. You see longer life span in
• 4:27
  Speaker 2: males just like the ip saw and mail mice. You
• 4:31
  Speaker 2: see increased intelligence, which is kind of a surprising one, right,
• 4:34
  Speaker 2: like why would having h this dysfunctional glucose channel increase
• 4:39
  Speaker 2: or intelligence? But it's probably doing really good things for
• 4:41
  Speaker 2: brain health and that's probably why.
• 4:43
  Speaker 3: Yeah.
• 4:45
  Speaker 2: But so we sort of have this natural experiment that
• 4:48
  Speaker 2: tells us, hey, you know, if you're worried about taking
• 4:51
  Speaker 2: this drug and inhibiting this protein, there are many people
• 4:54
  Speaker 2: walking around their whole lives with the equivalent of the
• 4:58
  Speaker 2: impact of this drug. It may have very good health outcomes.
• 5:00
  Speaker 2: So for me personally, that just sort of gives me
• 5:03
  Speaker 2: more reassurance that this could be a really good thing.
• 5:06
  Speaker 3: Yeah, uh, I think it's a.
• 5:09
  Speaker 1: I think it's a it's a it's a pretty deep
• 5:12
  Speaker 1: level of reassurance whenever you see real humans with a
• 5:19
  Speaker 1: genetic change that that seems to then have good outcomes,
• 5:24
  Speaker 1: and then we understand the process by which it happens
• 5:28
  Speaker 1: as well, and then we have a drug that that
• 5:30
  Speaker 1: mimics that process, that has a low side effect profile.
• 5:34
  Speaker 1: You're starting to get towards slam dunk interventions, right, Yeah.
• 5:40
  Speaker 2: I mean it's it's a lot of data. You don't
• 5:42
  Speaker 2: you don't have that for any other longevity drug. Yeah,
• 5:46
  Speaker 2: the Mendelian randomization. You have to get lucky. There has
• 5:48
  Speaker 2: to be a gene that can model the impact of
• 5:50
  Speaker 2: the drug that in the human population. Most of the
• 5:52
  Speaker 2: time there isn't one, but we got lucky. That's JILT too,
• 5:57
  Speaker 2: But yeah, that I think the strongest data really is
• 5:59
  Speaker 2: just what's see seeing what's happening to the patients who
• 6:02
  Speaker 2: are taking it, how how they go on after many
• 6:06
  Speaker 2: years of taking this drug, and they have lower incidences
• 6:09
  Speaker 2: of heart failure, of a chronic kidney disease. It they're
• 6:15
  Speaker 2: really really impactful drugs, and it seems to be occurring
• 6:19
  Speaker 2: through the mechanism that makes them useful diabetes drugs. It's
• 6:23
  Speaker 2: decreasing blood ghos. We haven't talked about how these drugs work.
• 6:26
  Speaker 2: We kind of hinted at it with the function of
• 6:29
  Speaker 2: the protein. But at the most basic way to explain
• 6:32
  Speaker 2: how these work is they make you pee out some sugar.
• 6:34
  Speaker 2: Not what they do, because two different.
• 6:37
  Speaker 1: Diabetes strugs have different effects and will probably come on
• 6:40
  Speaker 1: the Tall Apartment form and as well. So, but to
• 6:42
  Speaker 1: think this is important, right, is that that that process.
• 6:46
  Speaker 3: By which they work.
• 6:48
  Speaker 2: Yep, absolutely, yeah, they in this case. I mean, there's
• 6:53
  Speaker 2: different ways you can decrease blood sugar, right. One way
• 6:56
  Speaker 2: is to let more of it out in the urine
• 6:58
  Speaker 2: and with sglt too. And it's a substantial amount. I'm
• 7:03
  Speaker 2: not the best with numbers all the time. I can't
• 7:05
  Speaker 2: remember how many grams of sugar it is that you
• 7:08
  Speaker 2: lose per day, but it's substantial. It's something like I
• 7:10
  Speaker 2: want to say it's fifty grams that don't quote me
• 7:12
  Speaker 2: on that, but you're losing a substantial amount of sugar
• 7:15
  Speaker 2: in your urine. It's higher in a diabetic that has
• 7:17
  Speaker 2: high blood sugar to begin with, but it happens in
• 7:19
  Speaker 2: healthy individuals too, So you're basically taking taking your blood
• 7:23
  Speaker 2: sugar level, which you know you have your stable zones
• 7:26
  Speaker 2: and your spikes, and you're just shifting all of it down.
• 7:29
  Speaker 2: You're just decreasing the basal tone in that blood sugar level.
• 7:32
  Speaker 2: You're making the blood sugar spikes less spiky, so it's
• 7:38
  Speaker 2: I'm presumably john then less inchillin exactly, then you get
• 7:43
  Speaker 2: less insulin signaling. So in some ways it's sort of
• 7:45
  Speaker 2: mimicking what happens with chloric restriction, which is sort of
• 7:49
  Speaker 2: a gold standard intervention for lifespan extension, right, So at
• 7:54
  Speaker 2: a fundamental level, that's at least one of the things
• 7:57
  Speaker 2: they're doing is decreasing blood sugar, which has onstream benefits
• 8:01
  Speaker 2: throughout the body. In the kidney I mentioned, they have
• 8:04
  Speaker 2: sort of a protective effect on the kidney. One of
• 8:07
  Speaker 2: the by products of inhibiting that sodia well glucose and
• 8:12
  Speaker 2: also it inhibits sodium re uptake in the kidney is
• 8:15
  Speaker 2: that you decrease the pressure in your kidney, so you're
• 8:18
  Speaker 2: just putting less stress on it over time. So people
• 8:20
  Speaker 2: don't think about kidneys in terms of longevity so often,
• 8:24
  Speaker 2: but it's important to realize as we get older, all
• 8:26
  Speaker 2: of our kidneys are starting to fail. Your kidney function
• 8:29
  Speaker 2: is never going up, it's always going down. So if
• 8:32
  Speaker 2: you have a drug that can stop that, and that's
• 8:34
  Speaker 2: exactly what these do, They stop the decline of kidney function,
• 8:37
  Speaker 2: that's that's potentially a very good thing.
• 8:39
  Speaker 3: Kidneys are really interesting.
• 8:40
  Speaker 1: I remember I went to the Ukena was sitting beside
• 8:43
  Speaker 1: an nephrologist and we had a long chat about kidneys
• 8:48
  Speaker 1: and kidney health and basically they're a window into your
• 8:52
  Speaker 1: cardiovascular system, which I'd never thought about because he said
• 8:56
  Speaker 1: that the amount of blood vessels concentrated in the kidney,
• 9:00
  Speaker 1: so he said, in nerve research, they see a lot
• 9:03
  Speaker 1: of cardiovascular issues appearing in the kidney first.
• 9:07
  Speaker 3: That's the place that they can look for them.
• 9:10
  Speaker 2: That makes sense. I mean, kidneys they're not a regenerative organ.
• 9:14
  Speaker 2: So you knows, as you lose the filtering units in
• 9:17
  Speaker 2: your kidneys as you get older, you're never getting them
• 9:19
  Speaker 2: aer back. And they're also very susceptible to stress. You know,
• 9:22
  Speaker 2: things like high blood pressure, high blood sugar. It stresses
• 9:26
  Speaker 2: the kidney and you start to lose more of that function.
• 9:28
  Speaker 2: So yeah, I mean it makes sense that you could
• 9:30
  Speaker 2: free it that way.
• 9:31
  Speaker 1: Yeah. Okay, So we've talked about SGL two inhibitors and
• 9:36
  Speaker 1: and that that they and I completely agree with you
• 9:40
  Speaker 1: that they seem to be the one drug. I think
• 9:44
  Speaker 1: that data is much clearer for humans than wrappamacin. Let's
• 9:49
  Speaker 1: then talk about mett Foreman, right, because it's it's interesting
• 9:53
  Speaker 1: when as I've talked about longevity before in topics, and
• 9:57
  Speaker 1: I've had you know, molecules that or drugs that are
• 10:01
  Speaker 1: really interesting, and then I had a category of yen nah.
• 10:08
  Speaker 3: It's a it's a kind of an Australian thing.
• 10:10
  Speaker 1: Yeah nah, yeah, the same, right, And so I had
• 10:15
  Speaker 1: put met forman in the yen nah and now it's
• 10:18
  Speaker 1: in the yen na maybe camp for me, right and
• 10:22
  Speaker 1: reason So the reason I'll give you for that was
• 10:26
  Speaker 1: you you'll probably be more over this than me. But
• 10:28
  Speaker 1: there was that early experiment that showed and correct me
• 10:31
  Speaker 1: if I'm I get the details wrong here, John, but
• 10:33
  Speaker 1: people who were at diabetics who were taking met Foreman
• 10:38
  Speaker 1: and appeared to live longer, and then people who were
• 10:42
  Speaker 1: non diabetics and not on met forman right in this
• 10:46
  Speaker 1: one particular study, and then there was all of this
• 10:49
  Speaker 1: creas about met forman being a longevity molecular longevity drug.
• 10:53
  Speaker 1: And then another study came out which actually criticized some
• 10:58
  Speaker 1: of the methodology in the first study and that that
• 11:01
  Speaker 1: some of the people who were excluded were because they
• 11:06
  Speaker 1: had disease, and it was like, well, you can't really
• 11:08
  Speaker 1: do that. And this intervention where they included everybody and
• 11:14
  Speaker 1: showed that there was no longevity benefit to the people
• 11:18
  Speaker 1: who were diabetic taking met forms So there was a
• 11:20
  Speaker 1: bit of a ooh dob squid, but they and some
• 11:23
  Speaker 1: interesting stuff has come out about met forming recently in
• 11:27
  Speaker 1: terms of other health benefits, which I'm sure you're more
• 11:31
  Speaker 1: over than me, and and lots of animal So talk
• 11:35
  Speaker 1: us through met forming and your take on met forming
• 11:39
  Speaker 1: and and.
• 11:40
  Speaker 3: It's yeah, is it a year na? Is it a yeah?
• 11:43
  Speaker 1: Nah?
• 11:43
  Speaker 3: Yeah, yeah, work.
• 11:45
  Speaker 2: I'm kind of gonna eat I guess it's a yeah.
• 11:48
  Speaker 1: No.
• 11:48
  Speaker 2: I think I think there's reason to believe that could
• 11:51
  Speaker 2: be beneficial, but we don't have, you know, the rock
• 11:54
  Speaker 2: solid data that I think we have for SGLT too inhibitors.
• 12:00
  Speaker 2: So yeah, met foreman, I've I've tried met Foreman as
• 12:03
  Speaker 2: a longevity intervention myself.
• 12:06
  Speaker 3: I think, how did you how did you find that?
• 12:08
  Speaker 3: What would they also that any positive SETI negatives that
• 12:12
  Speaker 3: you noticed.
• 12:13
  Speaker 1: You're running reasonably tightly controlled experiments as much as you
• 12:16
  Speaker 1: can in a free living human.
• 12:18
  Speaker 2: Yeah, I'd try to change a million things at once,
• 12:21
  Speaker 2: and you know, take good notes on my biomarkers and
• 12:24
  Speaker 2: how I feel and that sort of thing. Met Foreman,
• 12:27
  Speaker 2: It's one of those that. So there there are some
• 12:30
  Speaker 2: drugs that I've noticed when I've taken, like an SGLT
• 12:34
  Speaker 2: two inhibitor. I feel fantastic when I when I take
• 12:37
  Speaker 2: an SGLT two inhibitor, and I think it's probably because
• 12:41
  Speaker 2: I wake up in ketosis. I have these keytnes going
• 12:44
  Speaker 2: into my brain in the morning, and I just feel
• 12:46
  Speaker 2: crystal clear and energetic. And I notice when I'm taking
• 12:50
  Speaker 2: one of those drugs and it feels very good. Met Foreman.
• 12:53
  Speaker 2: Kind of is the other way. I don't feel the
• 12:56
  Speaker 2: greatest met Foreman, I feel kind of sleepy and then
• 13:01
  Speaker 2: like I have a little bit less energy. So that's
• 13:05
  Speaker 2: that's a turn off, right. I don't like to feel
• 13:07
  Speaker 2: that way. Yeah, And I've tried to you know, tweaking
• 13:10
  Speaker 2: the dose a little bit, seeing if I can find
• 13:13
  Speaker 2: a low enough dose where it's doing something. But I
• 13:15
  Speaker 2: don't have those side effects and that that does help.
• 13:19
  Speaker 2: But you know, everybody's different. That's probably just a me thing.
• 13:22
  Speaker 2: I don't think everybody's going to be leepy if they
• 13:25
  Speaker 2: take a low dose in that form, and I think
• 13:27
  Speaker 2: maybe I'm just kind of sensitive to some of the
• 13:29
  Speaker 2: downstream effects of that one. But for that reason, it's
• 13:32
  Speaker 2: not my favorite. But I do think there's good data
• 13:36
  Speaker 2: to support that it's doing positive things for health, absolutely, but.
• 13:41
  Speaker 1: It's in exercise interference. Yeah, do you do you think
• 13:46
  Speaker 1: that's real?
• 13:49
  Speaker 2: I think it's real if you are the type of
• 13:51
  Speaker 2: subject that that study was run on, if you're if
• 13:54
  Speaker 2: you're an elderly person who is at risk of frailty
• 13:58
  Speaker 2: and you're not resistance training. Yeah, I mean, I think
• 14:01
  Speaker 2: there's a risk that then you take a drug like
• 14:04
  Speaker 2: Matt Foreman that is going to decrease your blood sugar
• 14:06
  Speaker 2: levels and lead to some muscle atrophy.
• 14:09
  Speaker 3: Yeah.
• 14:10
  Speaker 2: I think that's a real risk For someone who is
• 14:13
  Speaker 2: regularly in the gym, they're you know, eating enough protein
• 14:17
  Speaker 2: to build some muscle. Maybe they've already built some muscle.
• 14:20
  Speaker 2: I think it's, you know, probably not a concern. I
• 14:23
  Speaker 2: think the benefits of that resistance training are going to
• 14:26
  Speaker 2: outweigh any any slight negative exercise adaptation effects of a
• 14:31
  Speaker 2: drug like that.
• 14:33
  Speaker 1: Okay, interesting, and now I interesting you mentioned with the
• 14:37
  Speaker 1: SGL two inhibitor you wake up in kontosis. I've been
• 14:43
  Speaker 1: recently thinking about intermittent fasting, right, So I used to
• 14:48
  Speaker 1: do intimittent fasting. Used to do sometimes sixteen it's sometimes
• 14:52
  Speaker 1: fourteen ten whatever, But I would just push.
• 14:55
  Speaker 3: My breakfast out.
• 14:57
  Speaker 1: And then I stopped doing it because I was having
• 15:01
  Speaker 1: DEXA scans every sort of six months to a year
• 15:05
  Speaker 1: and I had lost with it. But I'd lost significant
• 15:08
  Speaker 1: amounts of muscle, right, and so I stopped intermittent fasting.
• 15:13
  Speaker 1: And then I find out that I had a bicusp
• 15:17
  Speaker 1: of iotic valve and significant regurgitation, which probably explained my
• 15:24
  Speaker 1: muscle loss right over and above the intermittent fasting. So
• 15:30
  Speaker 1: I'm not like, ah shit, maybe that was any you know,
• 15:33
  Speaker 1: you have seen some of the data coming out. Some
• 15:35
  Speaker 1: of the concern about the intermittent fasting is obviously that
• 15:39
  Speaker 1: you fast overnight, that you've only you don't have a
• 15:43
  Speaker 1: big amino acid storage pull in your body. So if
• 15:46
  Speaker 1: you're fasting twelve, thirteen, fourteen hours, your body is going
• 15:49
  Speaker 1: to be breaking down muscle to get those amino acids
• 15:52
  Speaker 1: that are very critical for cellular function.
• 15:54
  Speaker 3: Right.
• 15:55
  Speaker 1: But then more recent research has shown him if you
• 15:57
  Speaker 1: take a big chunk of protein in the evening, that
• 16:01
  Speaker 1: muscle protein synthesis can persist for twelve or so ours.
• 16:06
  Speaker 3: Right. So I've been toying in my head with.
• 16:09
  Speaker 1: The idea of waking up in the morning and taking
• 16:14
  Speaker 1: a ketone ester like be the hydroxy buttoryate, right yep,
• 16:18
  Speaker 1: just too fast forward that move into ketosis to get
• 16:24
  Speaker 1: all of those benefits.
• 16:26
  Speaker 3: And then break the fast.
• 16:29
  Speaker 1: Have you ever thought about taking a ketone est or
• 16:33
  Speaker 1: have you ever played with taking a keyton ester if you're.
• 16:35
  Speaker 3: Doing a bit of fasting.
• 16:37
  Speaker 2: I've been interested in them, and I haven't. You know,
• 16:41
  Speaker 2: It's part of the turn off is they're so expensive. Right,
• 16:43
  Speaker 2: If you want a large amount of ketone a lot
• 16:48
  Speaker 2: of those supplements, you know, they would be like ten
• 16:51
  Speaker 2: dollars a day or something.
• 16:52
  Speaker 1: So's that expect because I only just looked at it yesterday.
• 16:56
  Speaker 1: I looked at beta hydroxy beuty yesterday. So this is
• 16:59
  Speaker 1: very hot off the press in my mind.
• 17:01
  Speaker 2: Yeah, it's well, I mean some of them are. There's
• 17:03
  Speaker 2: different forms. I It's been a while since I've dove
• 17:06
  Speaker 2: into this one, but I have been interested in them,
• 17:09
  Speaker 2: and I think that there's there's a lot of good
• 17:11
  Speaker 2: data to show that taking a key tone supplement immediately
• 17:16
  Speaker 2: improves brain function, like the of the There are imaging
• 17:20
  Speaker 2: studies that show this that if you look at aging
• 17:24
  Speaker 2: people who are exhibiting some of the signatures of brain
• 17:28
  Speaker 2: aging on brain scans, you give them a key tone
• 17:31
  Speaker 2: supplement and you recover that function. Like it seems to
• 17:35
  Speaker 2: do something very positive because the brain loves keytones as
• 17:37
  Speaker 2: a fuel source. Yes, so that's kind of where my
• 17:39
  Speaker 2: interest came from. And I have looked at them, but yeah,
• 17:41
  Speaker 2: I haven't haven't experimented with it myself. Yeah, yeah, okay.
• 17:46
  Speaker 1: And then on the topic of fasting, what what's your
• 17:50
  Speaker 1: view on fasting, whether it be short term, intimittent fast
• 17:55
  Speaker 1: periods of longer fasting, what's your what's your.
• 17:58
  Speaker 3: View on that? And do you have a you on
• 18:01
  Speaker 3: what sort of age group that it would benefit more.
• 18:06
  Speaker 2: Yeah, that's a that's a good question. Well, so, so
• 18:09
  Speaker 2: first I would say I think it would benefit people
• 18:13
  Speaker 2: that aren't at risk of frailty or of.
• 18:16
  Speaker 4: Number one number one ye, yeah, and that's not just
• 18:21
  Speaker 4: elderly people that can also be endurance athletes that can
• 18:24
  Speaker 4: be you know a lot of people, fasting might tip
• 18:30
  Speaker 4: them too far into that catabolic state versus where.
• 18:34
  Speaker 2: They're already at. So I don't think it's for everyone.
• 18:38
  Speaker 2: If you're more in the over nutrition camp, you know,
• 18:40
  Speaker 2: you you have some some weight to lose, You're you're
• 18:44
  Speaker 2: getting in shape, you you have enough muscle mass. If
• 18:50
  Speaker 2: you were to lose a little bit of it, it's
• 18:51
  Speaker 2: not going to be the end of the world. I
• 18:53
  Speaker 2: think fasting can be excellent, and there's lots of excellent
• 18:57
  Speaker 2: clinical studies showing benefits. The tough thing is there aren't.
• 19:01
  Speaker 2: I mean, okay, So backing up a little bit. The
• 19:04
  Speaker 2: goal of fasting, as we've been talking about it is
• 19:06
  Speaker 2: to activate autopogy, right, to sort of kick off that
• 19:08
  Speaker 2: cellular recycling mechanism and get all the benefits that we
• 19:13
  Speaker 2: know that that has. The trouble is we don't have
• 19:16
  Speaker 2: great data in humans to know how long that takes. Yes, correct,
• 19:20
  Speaker 2: it's been very tooallenging to measure autoplogy and humans in
• 19:24
  Speaker 2: real time, and there's just recently, in the last couple
• 19:27
  Speaker 2: of years, the first studies have been able to do it,
• 19:29
  Speaker 2: and they've shown that I don't remember exactly how long
• 19:32
  Speaker 2: it was, it was an intermittent fasting protocol does indeed
• 19:36
  Speaker 2: activate autology in humans on an average, But you know,
• 19:42
  Speaker 2: that's not the same as saying that we know what
• 19:44
  Speaker 2: the optimal time is, how that rereads from person to person.
• 19:47
  Speaker 2: So I don't know. I mean, I don't know how
• 19:49
  Speaker 2: long it takes to start autology and how much it
• 19:53
  Speaker 2: ramps up if you continue, And so it's kind of
• 19:55
  Speaker 2: hard to make data based decisions on what to do
• 19:58
  Speaker 2: with fasting, which is why I think it's really for
• 20:02
  Speaker 2: most people, it's going to be how do you feel?
• 20:04
  Speaker 2: You know, are you recovering from exercise still, are you
• 20:08
  Speaker 2: feeling energetic? Do you feel like your your brain function
• 20:11
  Speaker 2: is good? I think, unfortunately, that's the best we can
• 20:14
  Speaker 2: do right now.
• 20:15
  Speaker 1: Yeah, I think anybody who tells you that fasting for
• 20:19
  Speaker 1: this amount of time and just just autophogy is just
• 20:23
  Speaker 1: the foot of ship, right.
• 20:25
  Speaker 2: There's no way to even measure that until very recently.
• 20:27
  Speaker 2: So yeah, it's not that simple. I wish it was.
• 20:31
  Speaker 1: And there does seem to be some research from from
• 20:34
  Speaker 1: and again mostly animal models that that muscle autophogy and
• 20:40
  Speaker 1: we can potentially accelerate the autoplogy and muscle sales from
• 20:45
  Speaker 1: exercising in a fasted state. Right, that's one potential, But
• 20:50
  Speaker 1: again I don't think we know. My view on this
• 20:54
  Speaker 1: is very similar to yours, is what is your mediator.
• 20:58
  Speaker 3: Health go right now?
• 20:59
  Speaker 1: Like if your metabolism is a problem, right, if you
• 21:04
  Speaker 1: have problems with your your glucose, if you're overweight, particularly
• 21:09
  Speaker 1: central obesity. I say that people you know the I
• 21:13
  Speaker 1: think the benefits of fasting outweigh the negatives in terms
• 21:16
  Speaker 1: of any loss of muscle mass.
• 21:18
  Speaker 3: Right.
• 21:18
  Speaker 1: But and particularly if you're like me in your fifties
• 21:22
  Speaker 1: and your major goal is to or one of your
• 21:26
  Speaker 1: major goals is from a health boance perspective, is maintaining
• 21:30
  Speaker 1: your muscle function.
• 21:32
  Speaker 3: I trade a little bit more carefully.
• 21:35
  Speaker 1: Where I've kind of landed is probably cycling through a
• 21:39
  Speaker 1: little bit of intermittent fasting just on a daily basis,
• 21:42
  Speaker 1: And then I think it's probably a good idea for
• 21:45
  Speaker 1: me to do once a year, a four day water
• 21:48
  Speaker 1: fast to get that sort of system right wide reset
• 21:53
  Speaker 1: and and just know that I'm to some resistance training
• 21:57
  Speaker 1: during it and minimize them the loss of muscle. That's
• 22:00
  Speaker 1: kind of where I've landed. Are you in a similar spot?
• 22:04
  Speaker 1: It sounds like you're in a similar spot.
• 22:06
  Speaker 3: Yeah.
• 22:07
  Speaker 2: I think the resistance training while you're doing it is key.
• 22:10
  Speaker 2: I mean, if if you're if you're resistance training enough
• 22:13
  Speaker 2: that you know how strong you are, then you know,
• 22:16
  Speaker 2: you know, for a given exercise at a given way,
• 22:18
  Speaker 2: how many reps you should be able to get. Sort
• 22:21
  Speaker 2: of doing low volume resistance training where you're making sure
• 22:24
  Speaker 2: you're not losing reps or losing weight while you're doing it.
• 22:26
  Speaker 2: If that's the case, you're not losing muscle, right, You're
• 22:29
  Speaker 2: not going to keep your lips where they are if
• 22:31
  Speaker 2: if you're losing a bunch of muscles. So I think
• 22:34
  Speaker 2: I think that's a very sensible way to go about it. Absolutely.
• 22:37
  Speaker 3: Yeah.
• 22:38
  Speaker 1: Cool, And so let's not talk about a couple of
• 22:43
  Speaker 1: other things that that might be interesting.
• 22:47
  Speaker 3: So glysing, I think was something.
• 22:50
  Speaker 1: That came up in the intervention testing program as potential,
• 22:55
  Speaker 1: and then I saw a series of research papers upbut
• 22:58
  Speaker 1: kalinak so glycine and an acetyl cysting. And the reason
• 23:06
  Speaker 1: I found these research papers interesting was they done and
• 23:09
  Speaker 1: I'm not sure if you're familiar with these studies, but
• 23:11
  Speaker 1: they've done and studies in mice and showed that glinac
• 23:15
  Speaker 1: enhanced their health span.
• 23:17
  Speaker 3: But it did it through.
• 23:19
  Speaker 1: Reducing oxidative stress, reducing inflammation, reducing mitochondrial dysfunction. Right, And
• 23:25
  Speaker 1: the same research group then showed that in humans, in
• 23:29
  Speaker 1: older adults, this is taking glinac reduced mitochondrial dysfunction, reduced
• 23:37
  Speaker 1: oxidative stress, reduced inflammation. And I thought, oh, that that's interesting.
• 23:43
  Speaker 1: And the fact that glycine independently seems to be interesting
• 23:47
  Speaker 1: and an acetyl cysting independently would seem to have significant
• 23:52
  Speaker 1: benefits for me, that's one that has got quite good
• 23:59
  Speaker 1: potential in terms of an intervention, although glenac itself hasn't
• 24:03
  Speaker 1: been tested.
• 24:04
  Speaker 3: What's your thoughts any thoughts on ginac?
• 24:06
  Speaker 2: That's yeah, no, you're you're giving me a new one.
• 24:09
  Speaker 2: I have heard of it. I'm not familiar with the research,
• 24:11
  Speaker 2: so I need to check it out, but I guess yeah.
• 24:15
  Speaker 2: My question would be with presumably anecetyl systeine is the
• 24:19
  Speaker 2: active agent because that has all sorts of biological activity
• 24:23
  Speaker 2: for reducing oxidative stress. And yeah, there's very good data
• 24:26
  Speaker 2: for that supplement on its own for all sorts of things. Yes,
• 24:29
  Speaker 2: So when you conjugate it to glycine, Yeah, what's that doing?
• 24:31
  Speaker 3: Is it?
• 24:32
  Speaker 2: Is it changing the biodistribution of anacetyl systeine. Presumably it's
• 24:37
  Speaker 2: doing something like that. So I would need to read
• 24:41
  Speaker 2: up on that one a little.
• 24:42
  Speaker 1: So I want to flick you some research papers and
• 24:44
  Speaker 1: I look forward to a blog post from you on it. Yeah. Yeah,
• 24:48
  Speaker 1: let's we're over an r into this, but let's get
• 24:53
  Speaker 1: into the topic that I got to you on.
• 24:56
  Speaker 3: Into the show. Yeah, yeah, it's sure, you're right, which
• 24:59
  Speaker 3: was your wrote.
• 25:00
  Speaker 1: This fascinating article about microplastics and and an intervention that
• 25:07
  Speaker 1: that you had done on yourself. And I love self experimentation.
• 25:10
  Speaker 1: I'm actually you know, given all that we have talked
• 25:13
  Speaker 1: about here and individual differences, I think everybody should be
• 25:18
  Speaker 1: self experimenting. An equals one is not a great science
• 25:21
  Speaker 1: experiment unless it's done on you. Yeah, right, for you, yeah, exactly,
• 25:28
  Speaker 1: as long as you kind of know what you've got
• 25:30
  Speaker 1: to know what you're doing. That's that's the key thing,
• 25:34
  Speaker 1: so to talk to us about because I'd be more
• 25:37
  Speaker 1: and more concerned about the research coming out about plastics,
• 25:41
  Speaker 1: and I think most of my listeners would be familiar
• 25:43
  Speaker 1: with that. I've done a couple of podcasts on it,
• 25:45
  Speaker 1: not not at a deep level, but just the fact
• 25:48
  Speaker 1: that they are ubiquitous in the environment, and they found
• 25:51
  Speaker 1: it in pretty much every human tissue in placentas. I
• 25:55
  Speaker 1: think it was one hundred percent strike rate in US women.
• 25:59
  Speaker 1: When they look, they're not finding it. When they're all
• 26:02
  Speaker 1: top seeing human brein, they're finding microplastics in there.
• 26:05
  Speaker 3: So this ship is insidious. It's clearly not doing good.
• 26:11
  Speaker 5: And so give us your view on just on why
• 26:16
  Speaker 5: they're bad and then the intervention you did and what
• 26:20
  Speaker 5: some people could potentially do.
• 26:23
  Speaker 2: Yeah, I'll do my best. So So, the microplastic situation
• 26:29
  Speaker 2: is something that I only learned about recently in the
• 26:32
  Speaker 2: last year or two, and as I learned more about it,
• 26:34
  Speaker 2: I was just like, holy shit, this is terrible. Yeah, yeah,
• 26:40
  Speaker 2: it's And I also wondered, like, why aren't we talking
• 26:44
  Speaker 2: about this? You know, this is this is this is
• 26:48
  Speaker 2: absolutely devastating that that we're we're all facing this exposure
• 26:53
  Speaker 2: and that it's in all of our tissues, and it's
• 26:55
  Speaker 2: increasing over time, and it's associated with a number of
• 26:58
  Speaker 2: really terrible health outcomes. It's it's it's really scary, and
• 27:01
  Speaker 2: it is not getting any attention at all. We'll see
• 27:04
  Speaker 2: a pop press article once in a while, you know,
• 27:06
  Speaker 2: saying they found new microplastic levels in something worse than
• 27:10
  Speaker 2: we thought, and it's you know, it's it's getting some attention,
• 27:13
  Speaker 2: but people just don't care the way they should. But
• 27:16
  Speaker 2: when I learned about this, I was very scared. When
• 27:19
  Speaker 2: I when I learned it was the brain paper was
• 27:21
  Speaker 2: the one that really got me. This was from Matthew
• 27:24
  Speaker 2: Campin's Groove. They looked at brain samples from deceased people
• 27:30
  Speaker 2: with a new very sensitive technique that can detect microplastics.
• 27:34
  Speaker 2: They used a number of techniques, they detected them multiple ways,
• 27:38
  Speaker 2: and what they found was that our brains just have
• 27:41
  Speaker 2: an absurd amount of plastic accumulating in them in the
• 27:45
  Speaker 2: form of these really tiny micro and nanoparticles. It's higher
• 27:50
  Speaker 2: than other tissues in the body. It's you know, you
• 27:53
  Speaker 2: can detect them biochemically with mass spec you can detect
• 27:58
  Speaker 2: them microscopically. If you stain and look for this the
• 28:01
  Speaker 2: plastic particles in the brain, it's it's a very clear finding.
• 28:05
  Speaker 2: And of course, you know, the plastic industry is pushing
• 28:08
  Speaker 2: back very hard, trying to discredit the science. But it's
• 28:10
  Speaker 2: very solid science published in one of the mist journals
• 28:13
  Speaker 2: in the world. So if anyone has doubts on the science,
• 28:15
  Speaker 2: don't believe it. This is excellent science. But they show
• 28:19
  Speaker 2: that it's accumulating to these massive levels in the brain
• 28:22
  Speaker 2: and in other tissues. And if you look at brains
• 28:25
  Speaker 2: of people with dementia, it's it's quite a bit higher
• 28:28
  Speaker 2: than in people without dementia. That doesn't mean that the
• 28:31
  Speaker 2: plastic cause the dementia. We don't know what the relationship
• 28:33
  Speaker 2: is yet, but it's it's concerning.
• 28:35
  Speaker 3: Yeah, probably not doing good. Let's put it out well.
• 28:39
  Speaker 2: It's not doing anything good, and so it's you know,
• 28:42
  Speaker 2: that's one study in humans. There have been many, many
• 28:46
  Speaker 2: other mechanistic studies in mice where they inject mice with
• 28:48
  Speaker 2: microplastics and look at what happens. There are cell studies,
• 28:52
  Speaker 2: and what we're learning is that these really tiny plastic
• 28:57
  Speaker 2: particles they do a lot of really bad stuff in
• 28:59
  Speaker 2: the body. But I think at the core what's happening
• 29:03
  Speaker 2: is one of the worst things is that your immune cells,
• 29:08
  Speaker 2: of course recognize this foreign object in your circulation or
• 29:11
  Speaker 2: in your tissue, and they try to eliminate it, and
• 29:14
  Speaker 2: that's what their job is, so they'll actually engulf this
• 29:17
  Speaker 2: microplastic This little tiny plastic particle goes into the cell.
• 29:21
  Speaker 2: But the cells are also little and tiny, so the
• 29:23
  Speaker 2: plastic particle is like almost as big as the cell itself. Wow,
• 29:27
  Speaker 2: it gets stuck in its lycisme. That cell goes crazy
• 29:31
  Speaker 2: and does all sorts of bad things. It starts releasing
• 29:33
  Speaker 2: inflammatory cytokinds in the brain. These immune cells get stuck
• 29:39
  Speaker 2: and cause little coagulation issues and little thrombotic issues in
• 29:44
  Speaker 2: the brain. They drive inflammation. Like, the collective take of
• 29:51
  Speaker 2: the studies is that these are not anything we want
• 29:53
  Speaker 2: in our bodies. We should all be very concerned that
• 29:57
  Speaker 2: you can detect them and most of our tissues and
• 30:00
  Speaker 2: they're likely driving persistent chronic inflammation. And yeah, I mean,
• 30:05
  Speaker 2: I could go on and.
• 30:06
  Speaker 1: On, but I think we could summarize this John microplastics
• 30:09
  Speaker 1: equal a cellular shit storm.
• 30:13
  Speaker 2: It is a shit storm. It's a whole body wide
• 30:16
  Speaker 2: shit storm. It's one study I should also menage. There
• 30:20
  Speaker 2: was a study that looked at I believe it was
• 30:24
  Speaker 2: carotid artery plaques.
• 30:26
  Speaker 3: Right.
• 30:26
  Speaker 2: They had patients coming in to get these plaques taken out.
• 30:28
  Speaker 2: They were going to have it happen anyways, So they
• 30:31
  Speaker 2: consented to patients and asked, can we look and see
• 30:34
  Speaker 2: if your plack has microplastics, and then can we follow
• 30:37
  Speaker 2: you for a period of time afterwards and see what happens.
• 30:41
  Speaker 2: So they did this. They had it was a well
• 30:42
  Speaker 2: powered study. They had a large number of patients. They
• 30:46
  Speaker 2: they bucketed the patients into two groups. There were patients
• 30:49
  Speaker 2: that had microplastics in their plaques and then there were
• 30:52
  Speaker 2: patients that had plaques without microplastics.
• 30:54
  Speaker 3: Right.
• 30:56
  Speaker 2: The patients, they then they followed them for a number
• 30:58
  Speaker 2: of years. I wish I remember the exact number, but
• 31:00
  Speaker 2: I don't. They followed the patients and the ones that
• 31:04
  Speaker 2: had the microplastics in their in their plaques had dramatically
• 31:09
  Speaker 2: worse health outcomes in terms of fatality, stroke, heart attack.
• 31:14
  Speaker 2: It was it was a very clear difference. And it's
• 31:17
  Speaker 2: They also had a lot of beautiful mechanistic data in
• 31:20
  Speaker 2: the study where they looked at markers of inflammation in
• 31:22
  Speaker 2: the plaques much much higher when the microplastics are present.
• 31:25
  Speaker 2: So it's it's it's observational data. People will always push
• 31:29
  Speaker 2: back and they it's not a randomized controlled trial, but
• 31:31
  Speaker 2: we're never going to have that where I can inject
• 31:33
  Speaker 2: people with microplastics. So this is the best we can do.
• 31:36
  Speaker 2: And it says that it's very very bad and and
• 31:40
  Speaker 2: and yeah, it's a signal is consistent across multiple studies.
• 31:45
  Speaker 1: You need to take set up and take notice and
• 31:47
  Speaker 1: forget about a bloody randomized control draw right. So yeah, yeah,
• 31:51
  Speaker 1: so what I be you done then as a result
• 31:54
  Speaker 1: of this, tell us about this experiment?
• 31:56
  Speaker 2: Okay, Well, so, as I kind of went down the
• 32:00
  Speaker 2: rabbit hole and learned more about microplastics, one of the
• 32:04
  Speaker 2: things that was frustrating was that nobody is publishing trials
• 32:07
  Speaker 2: yet in mice or in cell models on how to
• 32:10
  Speaker 2: get these things out of ourselves. You know, it's I'm
• 32:13
  Speaker 2: sure there are people working on it. The field is
• 32:15
  Speaker 2: moving very rapidly. I'm sure there's all sorts of new
• 32:19
  Speaker 2: labs that are just starting to work on this, But
• 32:20
  Speaker 2: the the interventional stuff just really isn't out there yet.
• 32:25
  Speaker 2: There's a couple of groups that have shown that if
• 32:27
  Speaker 2: you ingest certain certain supplements you can kind of bind
• 32:31
  Speaker 2: up microplastics in the gut because most of it's coming
• 32:33
  Speaker 2: from dietary intake, and you can help prevent the gut
• 32:36
  Speaker 2: from absorbing them. So that's that's one positive.
• 32:39
  Speaker 1: But as far as what were those things that you
• 32:41
  Speaker 1: could take to bind them? Jones, can you remember off
• 32:43
  Speaker 1: the time.
• 32:43
  Speaker 2: Yeah, there's a couple. I think one of them was
• 32:46
  Speaker 2: Kaido sand, which is yeah, I know back when I
• 32:52
  Speaker 2: used to brew beer. It's an additive that people use there,
• 32:55
  Speaker 2: so I was familiar with it from but it's and
• 32:58
  Speaker 2: then there were I think some fibers supplements that could
• 33:00
  Speaker 2: also be basically binding agents. It's physical binding agents that
• 33:04
  Speaker 2: sequester it in the gut and prevent your gut from
• 33:06
  Speaker 2: absorbing it. And there are some supplements that I think
• 33:10
  Speaker 2: are going to be on the market soon that include
• 33:11
  Speaker 2: those ingredients with the goal the stated goal of reducing microplastics.
• 33:15
  Speaker 2: We won't know how well work in humans, so that's encouraging,
• 33:20
  Speaker 2: But once they're in our bodies and we know that,
• 33:24
  Speaker 2: you know they are in our bodies, most of them,
• 33:26
  Speaker 2: most of us probably have absurd amounts of these in
• 33:28
  Speaker 2: our bodies. We don't have a clue how to get
• 33:31
  Speaker 2: them out sort of reverse that process because I don't
• 33:35
  Speaker 2: want microplastics in my cells driving inflammation. I don't know
• 33:38
  Speaker 2: about you, but when I get rid of it, I
• 33:40
  Speaker 2: immediately think, like, how do I get rid of this?
• 33:43
  Speaker 1: Particularly because you're so into lysisomes and you know that
• 33:46
  Speaker 1: they bunk up the lysisomes. So she's almost an existential crisis.
• 33:53
  Speaker 2: Is it's like, oh my god, like I have this
• 33:56
  Speaker 2: crap clogging up my lysisomes. I know what happens when
• 33:58
  Speaker 2: your lycismes get sick. I don't want anything to do
• 34:00
  Speaker 2: with that.
• 34:01
  Speaker 3: Yeah, yeah, So yeah, it was on a.
• 34:03
  Speaker 2: Personal level, it was scary, and so being a lysosome
• 34:08
  Speaker 2: biologist and someone who's worked in this space, I it
• 34:11
  Speaker 2: was I had one idea. I was like, well, if
• 34:14
  Speaker 2: other stuff accumulates in lysosomes, we know how to get
• 34:17
  Speaker 2: that out. I mean, we know how to get extra
• 34:19
  Speaker 2: cholesterol out of lysisomes. We know how to get other
• 34:22
  Speaker 2: substrates that build up out of lycismes. There are a
• 34:24
  Speaker 2: number of drugs that can do this in mice and
• 34:27
  Speaker 2: in humans, and one of them that had just been
• 34:31
  Speaker 2: published in a really interesting paper on a disease called
• 34:34
  Speaker 2: Nieman Pick disease, which is a disease where your lysisome
• 34:37
  Speaker 2: to accumulate cholesterol. This paper had used a compound called sulforophane,
• 34:42
  Speaker 2: and they treated the mice with sulforophane. They showed very
• 34:47
  Speaker 2: convincingly that that caused the lysosomes to basically dump their
• 34:50
  Speaker 2: contents outside of the cell so they could get rid
• 34:53
  Speaker 2: of all this extra cholesterol. And then once they did that,
• 34:57
  Speaker 2: the lysismes were much healthier and the cells were much healthier,
• 34:59
  Speaker 2: and so were the and have had a very positive
• 35:01
  Speaker 2: outcome in that study. So you know, I yeah, I thought, well,
• 35:06
  Speaker 2: it'd be really interesting if someone would test sulforofane in
• 35:10
  Speaker 2: a mouse study to see if it could reduce microplastics
• 35:14
  Speaker 2: accumulation and mysosomes because they're you know, they're accumulating just
• 35:17
  Speaker 2: like these other things do. To get that study done
• 35:22
  Speaker 2: would take years. Who's very slow. Someone probably is trying that,
• 35:26
  Speaker 2: but I didn't want to wait for that. I thought, well, sulforaphane,
• 35:29
  Speaker 2: this is something people take this all the time. There
• 35:30
  Speaker 2: are tons of clinical studies showing good things from taking sulforaphane.
• 35:34
  Speaker 2: I wonder if it's already doing this in people. I
• 35:36
  Speaker 2: wonder if people who are taking this or rejecting microplastics
• 35:39
  Speaker 2: out of their cells. So that was the basis for
• 35:42
  Speaker 2: this self experiment. I said, I'm going to do it.
• 35:44
  Speaker 2: I have a way to measure this. Now there's a
• 35:46
  Speaker 2: nice test that is commercially available, and I can see
• 35:49
  Speaker 2: exactly what happens in my blood before and after taking
• 35:52
  Speaker 2: the supplement and measure what's happening to my microplastic levels.
• 35:56
  Speaker 2: And sure enough, after I took a big dose of sulforafane,
• 36:00
  Speaker 2: it released many, many millions of microplastic particles from my
• 36:04
  Speaker 2: cell wow, and dumped them into my blood. Which that's
• 36:09
  Speaker 2: a nice result. Scientifically, it does Okay, it worked, you know,
• 36:12
  Speaker 2: the hypothesis is supported by the data. The sulforafane did
• 36:16
  Speaker 2: something that liberated the microplastics out of the spells. But
• 36:20
  Speaker 2: the other side of that is what happened next? Where
• 36:22
  Speaker 2: did they go? And I don't know, I can't answer
• 36:25
  Speaker 2: that question for you. I don't know if they went
• 36:28
  Speaker 2: back into the same or different cells and just caused
• 36:31
  Speaker 2: you know, caused more problems. My hope is that if
• 36:35
  Speaker 2: you do something like this, maybe your body has another
• 36:38
  Speaker 2: chance to eliminate them. Yes, maybe some of them can
• 36:40
  Speaker 2: end up in your urine. We know microplastic particles do
• 36:43
  Speaker 2: end up in urine, so is the reason that could happened.
• 36:47
  Speaker 2: They also end up in bile, which is a way
• 36:50
  Speaker 2: of excreting them through your gut. So it's possible that
• 36:53
  Speaker 2: that's happening. But in the absence of a test that
• 36:57
  Speaker 2: can test those fluids, I don't have a way to
• 37:01
  Speaker 2: answer that question, which I think is an important next
• 37:03
  Speaker 2: step for someone to figure out, is if you liberate
• 37:06
  Speaker 2: a whole bunch of microplastics like this, where do they go?
• 37:09
  Speaker 1: Yeah, yeah, yeah, yeah, and hopefully it's out of the body,
• 37:13
  Speaker 1: and the our detoxification process is peas one and feast two.
• 37:19
  Speaker 3: Would they have potential to excrete microplastics?
• 37:23
  Speaker 2: Yeah, So that's that's one. That's why most people are
• 37:26
  Speaker 2: familiar with sulfur or fane is that it's activating these
• 37:30
  Speaker 2: metabolic pathways. That's a good thing. What that probably helps
• 37:34
  Speaker 2: more with than the plastic particles themselves, are these plasticizers,
• 37:38
  Speaker 2: these chemicals that are bound up in the microplastic particles
• 37:42
  Speaker 2: things make like this phenol A b p A. People
• 37:44
  Speaker 2: are familiar with one. Right, It's probably very helpful for
• 37:49
  Speaker 2: eliminating those toxins, probably less helpful for the particles themselves,
• 37:53
  Speaker 2: just because our bodies are we have no evolutionary mechanism
• 37:57
  Speaker 2: to deal with something like.
• 37:58
  Speaker 1: Yeah, we don't even recognize it, right, well, probably probably
• 38:01
  Speaker 1: nice of it's bad, but don't know what to do
• 38:03
  Speaker 1: with it yet.
• 38:04
  Speaker 3: Interesting.
• 38:04
  Speaker 2: Yeah, I mean we probably have enzymes in our bodies
• 38:08
  Speaker 2: that recognize it as the wrong thing. You know, ourselves
• 38:12
  Speaker 2: probably think these are fats or something, because that's what
• 38:14
  Speaker 2: they look like. On a molecular level, they look like lipids,
• 38:18
  Speaker 2: So it's probably screwing up all sort of lipid metabolism machinery.
• 38:22
  Speaker 2: And it's we certainly have no way of naturally eliminating them.
• 38:26
  Speaker 2: It's it's it's going to be a push in the
• 38:27
  Speaker 2: right direction.
• 38:28
  Speaker 1: Yeah, that's a That's an interesting watch this space, isn't it?
• 38:33
  Speaker 3: John?
• 38:33
  Speaker 1: This has been absolutely fantastic, And I'm completely unscripted as well,
• 38:38
  Speaker 1: which is more more impressive that I can just wing
• 38:42
  Speaker 1: questions that you with no preparation and you just talk
• 38:46
  Speaker 1: off the hip with all of this stuff. So where
• 38:49
  Speaker 1: can people go to find out more about you? I
• 38:55
  Speaker 1: know you're on LinkedIn, That's where I found you, so,
• 38:57
  Speaker 1: but also you write quite a lot. You're on substack,
• 39:01
  Speaker 1: don't you.
• 39:02
  Speaker 2: Yeah, that's kind of a new platform for me. Yeah.
• 39:05
  Speaker 2: My subseac newsletter is called Translation and you can also
• 39:08
  Speaker 2: find it by searching my name, and that's you know.
• 39:11
  Speaker 2: The plan is for that to become sort of my
• 39:13
  Speaker 2: primary channel for articles and maybe some interviews in the
• 39:17
  Speaker 2: future and that sort of thing. And I'm a still
• 39:19
  Speaker 2: working on a book. Substack will be where I communicate
• 39:22
  Speaker 2: updates on that. So they tuned there.
• 39:25
  Speaker 1: Yes, how long do you think you are away from publishing?
• 39:31
  Speaker 2: Are you early or.
• 39:33
  Speaker 1: Have you got a for a bit of You've got
• 39:34
  Speaker 1: for a bit of progress made on it.
• 39:37
  Speaker 2: I've made some progress. It's going to be heavily depended
• 39:40
  Speaker 2: on some contributions from other people too. I'm interviewing a
• 39:43
  Speaker 2: number of people to sort of gather content and and
• 39:46
  Speaker 2: build out the framework that I'm going to present in
• 39:48
  Speaker 2: the book. So it's it's a little ways off still,
• 39:50
  Speaker 2: I'd say about a year, but we're getting there. I'd
• 39:54
  Speaker 2: love to chat with you sometimes about that. It sounds
• 39:55
  Speaker 2: like you have a lot of experience in that space.
• 39:57
  Speaker 2: I'm sure I can learn a lot from you.
• 39:59
  Speaker 1: So, well, yeah, I've written a couple and I think
• 40:01
  Speaker 1: I think the thing I would say is that you're
• 40:03
  Speaker 1: never going to get it perfect, that you just keep going,
• 40:07
  Speaker 1: oh and there's a little bit now, there's a new
• 40:09
  Speaker 1: research studies, like, just just just get it out and
• 40:12
  Speaker 1: you can always do an update later on. Because yeah,
• 40:16
  Speaker 1: when I've reread my my, my book, my first book,
• 40:20
  Speaker 1: I went shit, I'd like to put that and that
• 40:21
  Speaker 1: I'm probably going to do a revised edition, and in
• 40:24
  Speaker 1: this one, even sending it off to so you go
• 40:28
  Speaker 1: through the editing process and then get it back and
• 40:30
  Speaker 1: in its final edits, and then they sent me through
• 40:33
  Speaker 1: in here's now the layout.
• 40:34
  Speaker 3: I want you to check the layout.
• 40:36
  Speaker 1: And I'm still wanting to tweak it and add a
• 40:39
  Speaker 1: new study that I just read the other day.
• 40:41
  Speaker 3: So so don't let perfect be the enemy of grit.
• 40:44
  Speaker 2: That good advice. I'll try to remember that.
• 40:46
  Speaker 1: That would be definitely my my t But but me
• 40:49
  Speaker 1: I I'm certainly going to be following you on on
• 40:51
  Speaker 1: sub stacks, So we will put that link into the
• 40:54
  Speaker 1: show notes. I'll also put the link into your LinkedIn
• 40:57
  Speaker 1: because you've got a lot of interesting articles for anybody
• 41:00
  Speaker 1: who's interested in this space. And you know, the thing
• 41:02
  Speaker 1: I like about you is that you're not You're not
• 41:05
  Speaker 1: out pushing supplements, you're not pushing a product. You're just
• 41:09
  Speaker 1: somebody who is a hardcore scientist who's interested in this
• 41:13
  Speaker 1: area and has quite a lot of smarts. So it's
• 41:17
  Speaker 1: people like you that listeners should be following, not whinkers
• 41:21
  Speaker 1: like David Sinclair on.
• 41:25
  Speaker 2: So I appreciate that you don't bucking me with the wankers.
• 41:31
  Speaker 3: Definitely not. This has been awesome.
• 41:33
  Speaker 1: So we'll get those links, we'll put them in the
• 41:36
  Speaker 1: show notes, and yeah, good luck on your book, and
• 41:38
  Speaker 1: i'd certainly love to have you back on whenever you're
• 41:41
  Speaker 1: doing your book, and we'll get it promoted to our listeners.
• 41:45
  Speaker 2: Awesome, let's do it. Thanks Paul, it's been great, really,