September 12, 2025 • 41 mins
Here is the second part of my conversation with biochemist Jon Brudvig to delve into the fascinating world of longevity and contemporary health interventions. We tackle topics ranging from SGLT2 inhibitors and their unexpected benefits to the controversial nature of microplastics in our environment. This dialogue is a treasure trove for anyone interested in the intersections of health, science, and longevity.
What You'll Learn:
Exploring SGLT2 Inhibitors: Discover the multifaceted benefits of SGLT2 inhibitors, originally diabetes drugs, for heart, kidney, and possibly cognitive health.
Metformin: A Mixed Bag: Get an overview of the metformin debate, examining its potential benefits and the contentious nature of the research.
Fasting Fundamentals: Gain insights into intermittent fasting, its impact on metabolism, potential benefits, and the critical role of resistance training to mitigate muscle loss.
Microplastics: An Underestimated Threat: Learn about the insidious presence of microplastics in human tissues and their potential health repercussions.
Potential Interventions: Hear about experimental approaches to reducing microplastics in the body, including the potential role of sulforaphane.
Key Takeaways:
- SGLT2 inhibitors: These drugs have shown promising longevity benefits beyond their initial purpose for diabetes management.
- Metformin's Controversy: While some data suggests potential longevity benefits, criticism exists regarding its exercise interference and study methodologies.
- The Role of Fasting: Intermittent fasting can be beneficial, particularly for metabolic health, but must be carefully balanced with nutritional needs and physical activity.
- Microplastics Concern: Ubiquitous in the environment, microplastics are potentially linked to inflammation and adverse health outcomes, necessitating further research and interventions.
- Self-Experimentation: Personal health experiments, like those done by Jon Brudvig, highlight the importance of understanding one’s own biology in response to health interventions.
Resources:
Connect with Dr. Jon Brudvig for more insights into longevity and health:
LinkedIn: Jon Brudvig
Substack: https://jonbrudvig.substack.com/
Support the Podcast:
If you found this episode valuable, please consider subscribing to our podcast and leaving a review. Your feedback helps us continue bringing important conversations like these to a wider audience.
Whether you're driven by personal health challenges or broader scientific curiosity, this conversation provides a unique peek into the current and future possibilities of living healthier, longer lives. Share this with individuals passionate about health and longevity, and join the ongoing dialogue to advance our understanding and well-being.
00:12 Understanding SGLT2 Inhibitors
02:51 Mendelian Randomization and SGLT2 Inhibitors
06:24 Benefits and Mechanisms of SGLT2 Inhibitors
09:47 Discussion on Metformin
14:36 Intermittent Fasting and Ketone Supplements
17:46 Fasting, Autophagy, and Muscle Health
22:38 Exploring Glycine and N-Acetyl Cysteine
24:48 Microplastics: A Growing Concern
26:25 The Impact of Microplastics on Health
31:54 Self-Experimentation with Sulforaphane
38:33 Final Thoughts and Future Work
See omnystudio.com/listener for privacy information.
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:08):
Yeah, So mixing it up a little bit, I think
is really important. Let's die, Let's get back to the
SGL two inhibitors now. Is interesting to hear you say that.
I'll give you a little bit of background. So January
this year, I had open heart surgery for a dodgy
valve that I was born with. I was born with
(00:28):
a bi cuspan aortic valve. But it's all good. But
the upshot of this is the one drug that they've
put me on is an SGL two inhibitor. And actually,
when I dug into it, I went, you know what,
that's a drug. I'm not basically a big fan of
taking drugs, but I'm like, I'm actually happy that they
(00:50):
put me on an SGL two inhibitor. It's essentially a
diabetes drug or our drug for managing your blood sugar
slice insulin, but it also has benefits for heart and
so I'm actually pretty happy to be on an SGL
to inhibitor. That's a nice unintended consequence of my being
(01:11):
born with the doachi for help, So tell our listeners
what and because actually, out of the interventional's testing program,
a lot of them, the drugs that were successful controlled
inchilin our and or glucose, which is an interesting thread, right,
But one of them, and canaga flows in and is
(01:33):
an sgl TO inhibitor. So talk to our listeners about
what an sgl TO inhibitor is and why you think
it's interesting from a longevity slice health span perspective.
Speaker 2 (01:47):
Yeah, well, so the reason I'm excited about these is
just the abundance of data that we have suggesting that
they can be beneficial. And it's We've talked about the
issues with mouse studies. They do extend lifespan in my
least in mail lice, yes, but you know that's just
the beginning of the data. We have tons of data
for many, many thousands of patients taking these drugs in
(02:09):
the real world showing that it generates positive health outcomes
and reduces the incidents of negative health outcomes. They appear
to be very protective for the heart, like you mentioned,
also the kidneys. There's also a lot of data emerging
to suggest that they're very good for the brain. So
we have that piece of data saying, you know, patients
(02:30):
that are on these for diabetes tend to exhibit better
health outcomes over time, even outcomes unrelated to diabetes. Yes,
and then there's this other piece that you don't often
get for a longevity intervention, and this comes from studies,
these Mendelian randomization studies, which can you take me.
Speaker 1 (02:51):
Take a step back and explain what those are and
why they're actually useful.
Speaker 2 (02:57):
Yeah, so these are sort of a clever way of
modeling the impact of different interventions, in this case the
drug intervection and intervention by looking at sort of a
natural experiment that genetics have given us. So we all
have this protein called SGLT two that's the target of
(03:19):
this drug, right, and it's a channel. It's a channel
that recovers glucose in your kidney so that you don't
have glucose in your urine and we're keeping it in
the body where we need it because glucose is a
nutrient that we need. It's important for energy production. But
we have different genetic variants in SGLT two. So you know,
(03:40):
most of us have a fully functional version, but there
are rare genetic variants where you have a dysfunctional SGLT
two protein that doesn't come glucose as efficiently. So that's
very similar to what the drugs doing.
Speaker 3 (03:54):
Right.
Speaker 2 (03:54):
If the drug inhibits. And then there are some people
that have just been operating this way their whole lives,
their SGLT two never worked efficiently. You can look at
what happens to those people have a pretty good idea
of what the drug's gonna do. Right, Have I blamed
this in.
Speaker 3 (04:09):
A way in a minute you have? Yeah, you've explained
really well.
Speaker 2 (04:13):
So, yeah, that's that's an Ndelian randomization. And when you
look at it for SGLT two and you look at
studies sort of modeling the impact of these drugs, you
see really cool stuff. You see longer life span in
males just like the ip saw and mail mice. You
see increased intelligence, which is kind of a surprising one, right,
(04:34):
like why would having h this dysfunctional glucose channel increase
or intelligence? But it's probably doing really good things for
brain health and that's probably why.
Speaker 3 (04:43):
Yeah.
Speaker 2 (04:45):
But so we sort of have this natural experiment that
tells us, hey, you know, if you're worried about taking
this drug and inhibiting this protein, there are many people
walking around their whole lives with the equivalent of the
impact of this drug. It may have very good health outcomes.
So for me personally, that just sort of gives me
more reassurance that this could be a really good thing.
Speaker 3 (05:06):
Yeah, uh, I think it's a.
Speaker 1 (05:09):
I think it's a it's a it's a pretty deep
level of reassurance whenever you see real humans with a
genetic change that that seems to then have good outcomes,
and then we understand the process by which it happens
as well, and then we have a drug that that
(05:30):
mimics that process, that has a low side effect profile.
You're starting to get towards slam dunk interventions, right, Yeah.
Speaker 2 (05:40):
I mean it's it's a lot of data. You don't
you don't have that for any other longevity drug. Yeah,
the Mendelian randomization. You have to get lucky. There has
to be a gene that can model the impact of
the drug that in the human population. Most of the
time there isn't one, but we got lucky. That's JILT too,
But yeah, that I think the strongest data really is
just what's see seeing what's happening to the patients who
(06:02):
are taking it, how how they go on after many
years of taking this drug, and they have lower incidences
of heart failure, of a chronic kidney disease. It they're
really really impactful drugs, and it seems to be occurring
through the mechanism that makes them useful diabetes drugs. It's
(06:23):
decreasing blood ghos. We haven't talked about how these drugs work.
We kind of hinted at it with the function of
the protein. But at the most basic way to explain
how these work is they make you pee out some sugar.
Not what they do, because two different.
Speaker 1 (06:37):
Diabetes strugs have different effects and will probably come on
the Tall Apartment form and as well. So, but to
think this is important, right, is that that that process.
Speaker 3 (06:46):
By which they work.
Speaker 2 (06:48):
Yep, absolutely, yeah, they in this case. I mean, there's
different ways you can decrease blood sugar, right. One way
is to let more of it out in the urine
and with sglt too. And it's a substantial amount. I'm
not the best with numbers all the time. I can't
remember how many grams of sugar it is that you
lose per day, but it's substantial. It's something like I
(07:10):
want to say it's fifty grams that don't quote me
on that, but you're losing a substantial amount of sugar
in your urine. It's higher in a diabetic that has
high blood sugar to begin with, but it happens in
healthy individuals too, So you're basically taking taking your blood
sugar level, which you know you have your stable zones
and your spikes, and you're just shifting all of it down.
You're just decreasing the basal tone in that blood sugar level.
(07:32):
You're making the blood sugar spikes less spiky, so it's
I'm presumably john then less inchillin exactly, then you get
less insulin signaling. So in some ways it's sort of
mimicking what happens with chloric restriction, which is sort of
a gold standard intervention for lifespan extension, right, So at
(07:54):
a fundamental level, that's at least one of the things
they're doing is decreasing blood sugar, which has onstream benefits
throughout the body. In the kidney I mentioned, they have
sort of a protective effect on the kidney. One of
the by products of inhibiting that sodia well glucose and
also it inhibits sodium re uptake in the kidney is
(08:15):
that you decrease the pressure in your kidney, so you're
just putting less stress on it over time. So people
don't think about kidneys in terms of longevity so often,
but it's important to realize as we get older, all
of our kidneys are starting to fail. Your kidney function
is never going up, it's always going down. So if
you have a drug that can stop that, and that's
exactly what these do, They stop the decline of kidney function,
(08:37):
that's that's potentially a very good thing.
Speaker 3 (08:39):
Kidneys are really interesting.
Speaker 1 (08:40):
I remember I went to the Ukena was sitting beside
an nephrologist and we had a long chat about kidneys
and kidney health and basically they're a window into your
cardiovascular system, which I'd never thought about because he said
that the amount of blood vessels concentrated in the kidney,
so he said, in nerve research, they see a lot
(09:03):
of cardiovascular issues appearing in the kidney first.
Speaker 3 (09:07):
That's the place that they can look for them.
Speaker 2 (09:10):
That makes sense. I mean, kidneys they're not a regenerative organ.
So you knows, as you lose the filtering units in
your kidneys as you get older, you're never getting them
aer back. And they're also very susceptible to stress. You know,
things like high blood pressure, high blood sugar. It stresses
the kidney and you start to lose more of that function.
So yeah, I mean it makes sense that you could
free it that way.
Speaker 1 (09:31):
Yeah. Okay, So we've talked about SGL two inhibitors and
and that that they and I completely agree with you
that they seem to be the one drug. I think
that data is much clearer for humans than wrappamacin. Let's
then talk about mett Foreman, right, because it's it's interesting
(09:53):
when as I've talked about longevity before in topics, and
I've had you know, molecules that or drugs that are
really interesting, and then I had a category of yen nah.
Speaker 3 (10:08):
It's a it's a kind of an Australian thing.
Speaker 1 (10:10):
Yeah nah, yeah, the same, right, And so I had
put met forman in the yen nah and now it's
in the yen na maybe camp for me, right and
reason So the reason I'll give you for that was
you you'll probably be more over this than me. But
there was that early experiment that showed and correct me
(10:31):
if I'm I get the details wrong here, John, but
people who were at diabetics who were taking met Foreman
and appeared to live longer, and then people who were
non diabetics and not on met forman right in this
one particular study, and then there was all of this
creas about met forman being a longevity molecular longevity drug.
(10:53):
And then another study came out which actually criticized some
of the methodology in the first study and that that
some of the people who were excluded were because they
had disease, and it was like, well, you can't really
do that. And this intervention where they included everybody and
(11:14):
showed that there was no longevity benefit to the people
who were diabetic taking met forms So there was a
bit of a ooh dob squid, but they and some
interesting stuff has come out about met forming recently in
terms of other health benefits, which I'm sure you're more
over than me, and and lots of animal So talk
(11:35):
us through met forming and your take on met forming
and and.
Speaker 3 (11:40):
It's yeah, is it a year na? Is it a yeah?
Speaker 1 (11:43):
Nah?
Speaker 3 (11:43):
Yeah, yeah, work.
Speaker 2 (11:45):
I'm kind of gonna eat I guess it's a yeah.
Speaker 1 (11:48):
No.
Speaker 2 (11:48):
I think I think there's reason to believe that could
be beneficial, but we don't have, you know, the rock
solid data that I think we have for SGLT too inhibitors.
So yeah, met foreman, I've I've tried met Foreman as
a longevity intervention myself.
Speaker 3 (12:06):
I think, how did you how did you find that?
What would they also that any positive SETI negatives that
you noticed.
Speaker 1 (12:13):
You're running reasonably tightly controlled experiments as much as you
can in a free living human.
Speaker 2 (12:18):
Yeah, I'd try to change a million things at once,
and you know, take good notes on my biomarkers and
how I feel and that sort of thing. Met Foreman,
It's one of those that. So there there are some
drugs that I've noticed when I've taken, like an SGLT
two inhibitor. I feel fantastic when I when I take
an SGLT two inhibitor, and I think it's probably because
(12:41):
I wake up in ketosis. I have these keytnes going
into my brain in the morning, and I just feel
crystal clear and energetic. And I notice when I'm taking
one of those drugs and it feels very good. Met Foreman.
Kind of is the other way. I don't feel the
greatest met Foreman, I feel kind of sleepy and then
like I have a little bit less energy. So that's
(13:05):
that's a turn off, right. I don't like to feel
that way. Yeah, And I've tried to you know, tweaking
the dose a little bit, seeing if I can find
a low enough dose where it's doing something. But I
don't have those side effects and that that does help.
But you know, everybody's different. That's probably just a me thing.
I don't think everybody's going to be leepy if they
(13:25):
take a low dose in that form, and I think
maybe I'm just kind of sensitive to some of the
downstream effects of that one. But for that reason, it's
not my favorite. But I do think there's good data
to support that it's doing positive things for health, absolutely, but.
Speaker 1 (13:41):
It's in exercise interference. Yeah, do you do you think
that's real?
Speaker 2 (13:49):
I think it's real if you are the type of
subject that that study was run on, if you're if
you're an elderly person who is at risk of frailty
and you're not resistance training. Yeah, I mean, I think
there's a risk that then you take a drug like
Matt Foreman that is going to decrease your blood sugar
levels and lead to some muscle atrophy.
Speaker 3 (14:09):
Yeah.
Speaker 2 (14:10):
I think that's a real risk For someone who is
regularly in the gym, they're you know, eating enough protein
to build some muscle. Maybe they've already built some muscle.
I think it's, you know, probably not a concern. I
think the benefits of that resistance training are going to
outweigh any any slight negative exercise adaptation effects of a
(14:31):
drug like that.
Speaker 1 (14:33):
Okay, interesting, and now I interesting you mentioned with the
SGL two inhibitor you wake up in kontosis. I've been
recently thinking about intermittent fasting, right, So I used to
do intimittent fasting. Used to do sometimes sixteen it's sometimes
fourteen ten whatever, But I would just push.
Speaker 3 (14:55):
My breakfast out.
Speaker 1 (14:57):
And then I stopped doing it because I was having
DEXA scans every sort of six months to a year
and I had lost with it. But I'd lost significant
amounts of muscle, right, and so I stopped intermittent fasting.
And then I find out that I had a bicusp
(15:17):
of iotic valve and significant regurgitation, which probably explained my
muscle loss right over and above the intermittent fasting. So
I'm not like, ah shit, maybe that was any you know,
you have seen some of the data coming out. Some
of the concern about the intermittent fasting is obviously that
(15:39):
you fast overnight, that you've only you don't have a
big amino acid storage pull in your body. So if
you're fasting twelve, thirteen, fourteen hours, your body is going
to be breaking down muscle to get those amino acids
that are very critical for cellular function.
Speaker 3 (15:54):
Right.
Speaker 1 (15:55):
But then more recent research has shown him if you
take a big chunk of protein in the evening, that
muscle protein synthesis can persist for twelve or so ours.
Speaker 3 (16:06):
Right. So I've been toying in my head with.
Speaker 1 (16:09):
The idea of waking up in the morning and taking
a ketone ester like be the hydroxy buttoryate, right yep,
just too fast forward that move into ketosis to get
all of those benefits.
Speaker 3 (16:26):
And then break the fast.
Speaker 1 (16:29):
Have you ever thought about taking a ketone est or
have you ever played with taking a keyton ester if you're.
Speaker 3 (16:35):
Doing a bit of fasting.
Speaker 2 (16:37):
I've been interested in them, and I haven't. You know,
It's part of the turn off is they're so expensive. Right,
If you want a large amount of ketone a lot
of those supplements, you know, they would be like ten
dollars a day or something.
Speaker 1 (16:52):
So's that expect because I only just looked at it yesterday.
I looked at beta hydroxy beuty yesterday. So this is
very hot off the press in my mind.
Speaker 2 (17:01):
Yeah, it's well, I mean some of them are. There's
different forms. I It's been a while since I've dove
into this one, but I have been interested in them,
and I think that there's there's a lot of good
data to show that taking a key tone supplement immediately
improves brain function, like the of the There are imaging
studies that show this that if you look at aging
(17:24):
people who are exhibiting some of the signatures of brain
aging on brain scans, you give them a key tone
supplement and you recover that function. Like it seems to
do something very positive because the brain loves keytones as
a fuel source. Yes, so that's kind of where my
interest came from. And I have looked at them, but yeah,
I haven't haven't experimented with it myself. Yeah, yeah, okay.
Speaker 1 (17:46):
And then on the topic of fasting, what what's your
view on fasting, whether it be short term, intimittent fast
periods of longer fasting, what's your what's your.
Speaker 3 (17:58):
View on that? And do you have a you on
what sort of age group that it would benefit more.
Speaker 2 (18:06):
Yeah, that's a that's a good question. Well, so, so
first I would say I think it would benefit people
that aren't at risk of frailty or of.
Speaker 4 (18:16):
Number one number one ye, yeah, and that's not just
elderly people that can also be endurance athletes that can
be you know a lot of people, fasting might tip
them too far into that catabolic state versus where.
Speaker 2 (18:34):
They're already at. So I don't think it's for everyone.
If you're more in the over nutrition camp, you know,
you you have some some weight to lose, You're you're
getting in shape, you you have enough muscle mass. If
you were to lose a little bit of it, it's
not going to be the end of the world. I
think fasting can be excellent, and there's lots of excellent
(18:57):
clinical studies showing benefits. The tough thing is there aren't.
I mean, okay, So backing up a little bit. The
goal of fasting, as we've been talking about it is
to activate autopogy, right, to sort of kick off that
cellular recycling mechanism and get all the benefits that we
know that that has. The trouble is we don't have
great data in humans to know how long that takes. Yes, correct,
(19:20):
it's been very tooallenging to measure autoplogy and humans in
real time, and there's just recently, in the last couple
of years, the first studies have been able to do it,
and they've shown that I don't remember exactly how long
it was, it was an intermittent fasting protocol does indeed
activate autology in humans on an average, But you know,
(19:42):
that's not the same as saying that we know what
the optimal time is, how that rereads from person to person.
So I don't know. I mean, I don't know how
long it takes to start autology and how much it
ramps up if you continue, And so it's kind of
hard to make data based decisions on what to do
with fasting, which is why I think it's really for
most people, it's going to be how do you feel?
(20:04):
You know, are you recovering from exercise still, are you
feeling energetic? Do you feel like your your brain function
is good? I think, unfortunately, that's the best we can
do right now.
Speaker 1 (20:15):
Yeah, I think anybody who tells you that fasting for
this amount of time and just just autophogy is just
the foot of ship, right.
Speaker 2 (20:25):
There's no way to even measure that until very recently.
So yeah, it's not that simple. I wish it was.
Speaker 1 (20:31):
And there does seem to be some research from from
and again mostly animal models that that muscle autophogy and
we can potentially accelerate the autoplogy and muscle sales from
exercising in a fasted state. Right, that's one potential, But
again I don't think we know. My view on this
(20:54):
is very similar to yours, is what is your mediator.
Speaker 3 (20:58):
Health go right now?
Speaker 1 (20:59):
Like if your metabolism is a problem, right, if you
have problems with your your glucose, if you're overweight, particularly
central obesity. I say that people you know the I
think the benefits of fasting outweigh the negatives in terms
of any loss of muscle mass.
Speaker 3 (21:18):
Right.
Speaker 1 (21:18):
But and particularly if you're like me in your fifties
and your major goal is to or one of your
major goals is from a health boance perspective, is maintaining
your muscle function.
Speaker 3 (21:32):
I trade a little bit more carefully.
Speaker 1 (21:35):
Where I've kind of landed is probably cycling through a
little bit of intermittent fasting just on a daily basis,
And then I think it's probably a good idea for
me to do once a year, a four day water
fast to get that sort of system right wide reset
and and just know that I'm to some resistance training
(21:57):
during it and minimize them the loss of muscle. That's
kind of where I've landed. Are you in a similar spot?
It sounds like you're in a similar spot.
Speaker 3 (22:06):
Yeah.
Speaker 2 (22:07):
I think the resistance training while you're doing it is key.
I mean, if if you're if you're resistance training enough
that you know how strong you are, then you know,
you know, for a given exercise at a given way,
how many reps you should be able to get. Sort
of doing low volume resistance training where you're making sure
you're not losing reps or losing weight while you're doing it.
If that's the case, you're not losing muscle, right, You're
(22:29):
not going to keep your lips where they are if
if you're losing a bunch of muscles. So I think
I think that's a very sensible way to go about it. Absolutely.
Speaker 3 (22:37):
Yeah.
Speaker 1 (22:38):
Cool, And so let's not talk about a couple of
other things that that might be interesting.
Speaker 3 (22:47):
So glysing, I think was something.
Speaker 1 (22:50):
That came up in the intervention testing program as potential,
and then I saw a series of research papers upbut
kalinak so glycine and an acetyl cysting. And the reason
I found these research papers interesting was they done and
I'm not sure if you're familiar with these studies, but
(23:11):
they've done and studies in mice and showed that glinac
enhanced their health span.
Speaker 3 (23:17):
But it did it through.
Speaker 1 (23:19):
Reducing oxidative stress, reducing inflammation, reducing mitochondrial dysfunction. Right, And
the same research group then showed that in humans, in
older adults, this is taking glinac reduced mitochondrial dysfunction, reduced
oxidative stress, reduced inflammation. And I thought, oh, that that's interesting.
(23:43):
And the fact that glycine independently seems to be interesting
and an acetyl cysting independently would seem to have significant
benefits for me, that's one that has got quite good
potential in terms of an intervention, although glenac itself hasn't
(24:03):
been tested.
Speaker 3 (24:04):
What's your thoughts any thoughts on ginac?
Speaker 2 (24:06):
That's yeah, no, you're you're giving me a new one.
I have heard of it. I'm not familiar with the research,
so I need to check it out, but I guess yeah.
My question would be with presumably anecetyl systeine is the
active agent because that has all sorts of biological activity
for reducing oxidative stress. And yeah, there's very good data
for that supplement on its own for all sorts of things. Yes,
(24:29):
So when you conjugate it to glycine, Yeah, what's that doing?
Speaker 3 (24:31):
Is it?
Speaker 2 (24:32):
Is it changing the biodistribution of anacetyl systeine. Presumably it's
doing something like that. So I would need to read
up on that one a little.
Speaker 1 (24:42):
So I want to flick you some research papers and
I look forward to a blog post from you on it. Yeah. Yeah,
let's we're over an r into this, but let's get
into the topic that I got to you on.
Speaker 3 (24:56):
Into the show. Yeah, yeah, it's sure, you're right, which
was your wrote.
Speaker 1 (25:00):
This fascinating article about microplastics and and an intervention that
that you had done on yourself. And I love self experimentation.
I'm actually you know, given all that we have talked
about here and individual differences, I think everybody should be
self experimenting. An equals one is not a great science
(25:21):
experiment unless it's done on you. Yeah, right, for you, yeah, exactly,
as long as you kind of know what you've got
to know what you're doing. That's that's the key thing,
so to talk to us about because I'd be more
and more concerned about the research coming out about plastics,
and I think most of my listeners would be familiar
(25:43):
with that. I've done a couple of podcasts on it,
not not at a deep level, but just the fact
that they are ubiquitous in the environment, and they found
it in pretty much every human tissue in placentas. I
think it was one hundred percent strike rate in US women.
When they look, they're not finding it. When they're all
top seeing human brein, they're finding microplastics in there.
Speaker 3 (26:05):
So this ship is insidious. It's clearly not doing good.
Speaker 5 (26:11):
And so give us your view on just on why
they're bad and then the intervention you did and what
some people could potentially do.
Speaker 2 (26:23):
Yeah, I'll do my best. So So, the microplastic situation
is something that I only learned about recently in the
last year or two, and as I learned more about it,
I was just like, holy shit, this is terrible. Yeah, yeah,
it's And I also wondered, like, why aren't we talking
(26:44):
about this? You know, this is this is this is
absolutely devastating that that we're we're all facing this exposure
and that it's in all of our tissues, and it's
increasing over time, and it's associated with a number of
really terrible health outcomes. It's it's it's really scary, and
it is not getting any attention at all. We'll see
(27:04):
a pop press article once in a while, you know,
saying they found new microplastic levels in something worse than
we thought, and it's you know, it's it's getting some attention,
but people just don't care the way they should. But
when I learned about this, I was very scared. When
I when I learned it was the brain paper was
the one that really got me. This was from Matthew
Campin's Groove. They looked at brain samples from deceased people
(27:30):
with a new very sensitive technique that can detect microplastics.
They used a number of techniques, they detected them multiple ways,
and what they found was that our brains just have
an absurd amount of plastic accumulating in them in the
form of these really tiny micro and nanoparticles. It's higher
than other tissues in the body. It's you know, you
(27:53):
can detect them biochemically with mass spec you can detect
them microscopically. If you stain and look for this the
plastic particles in the brain, it's it's a very clear finding.
And of course, you know, the plastic industry is pushing
back very hard, trying to discredit the science. But it's
very solid science published in one of the mist journals
in the world. So if anyone has doubts on the science,
(28:15):
don't believe it. This is excellent science. But they show
that it's accumulating to these massive levels in the brain
and in other tissues. And if you look at brains
of people with dementia, it's it's quite a bit higher
than in people without dementia. That doesn't mean that the
plastic cause the dementia. We don't know what the relationship
is yet, but it's it's concerning.
Speaker 3 (28:35):
Yeah, probably not doing good. Let's put it out well.
Speaker 2 (28:39):
It's not doing anything good, and so it's you know,
that's one study in humans. There have been many, many
other mechanistic studies in mice where they inject mice with
microplastics and look at what happens. There are cell studies,
and what we're learning is that these really tiny plastic
particles they do a lot of really bad stuff in
(28:59):
the body. But I think at the core what's happening
is one of the worst things is that your immune cells,
of course recognize this foreign object in your circulation or
in your tissue, and they try to eliminate it, and
that's what their job is, so they'll actually engulf this
microplastic This little tiny plastic particle goes into the cell.
(29:21):
But the cells are also little and tiny, so the
plastic particle is like almost as big as the cell itself. Wow,
it gets stuck in its lycisme. That cell goes crazy
and does all sorts of bad things. It starts releasing
inflammatory cytokinds in the brain. These immune cells get stuck
and cause little coagulation issues and little thrombotic issues in
(29:44):
the brain. They drive inflammation. Like, the collective take of
the studies is that these are not anything we want
in our bodies. We should all be very concerned that
you can detect them and most of our tissues and
they're likely driving persistent chronic inflammation. And yeah, I mean,
(30:05):
I could go on and.
Speaker 1 (30:06):
On, but I think we could summarize this John microplastics
equal a cellular shit storm.
Speaker 2 (30:13):
It is a shit storm. It's a whole body wide
shit storm. It's one study I should also menage. There
was a study that looked at I believe it was
carotid artery plaques.
Speaker 3 (30:26):
Right.
Speaker 2 (30:26):
They had patients coming in to get these plaques taken out.
They were going to have it happen anyways, So they
consented to patients and asked, can we look and see
if your plack has microplastics, and then can we follow
you for a period of time afterwards and see what happens.
So they did this. They had it was a well
powered study. They had a large number of patients. They
they bucketed the patients into two groups. There were patients
(30:49):
that had microplastics in their plaques and then there were
patients that had plaques without microplastics.
Speaker 3 (30:54):
Right.
Speaker 2 (30:56):
The patients, they then they followed them for a number
of years. I wish I remember the exact number, but
I don't. They followed the patients and the ones that
had the microplastics in their in their plaques had dramatically
worse health outcomes in terms of fatality, stroke, heart attack.
It was it was a very clear difference. And it's
(31:17):
They also had a lot of beautiful mechanistic data in
the study where they looked at markers of inflammation in
the plaques much much higher when the microplastics are present.
So it's it's it's observational data. People will always push
back and they it's not a randomized controlled trial, but
we're never going to have that where I can inject
people with microplastics. So this is the best we can do.
And it says that it's very very bad and and
(31:40):
and yeah, it's a signal is consistent across multiple studies.
Speaker 1 (31:45):
You need to take set up and take notice and
forget about a bloody randomized control draw right. So yeah, yeah,
so what I be you done then as a result
of this, tell us about this experiment?
Speaker 2 (31:56):
Okay, Well, so, as I kind of went down the
rabbit hole and learned more about microplastics, one of the
things that was frustrating was that nobody is publishing trials
yet in mice or in cell models on how to
get these things out of ourselves. You know, it's I'm
sure there are people working on it. The field is
moving very rapidly. I'm sure there's all sorts of new
(32:19):
labs that are just starting to work on this, But
the the interventional stuff just really isn't out there yet.
There's a couple of groups that have shown that if
you ingest certain certain supplements you can kind of bind
up microplastics in the gut because most of it's coming
from dietary intake, and you can help prevent the gut
from absorbing them. So that's that's one positive.
Speaker 1 (32:39):
But as far as what were those things that you
could take to bind them? Jones, can you remember off
the time.
Speaker 2 (32:43):
Yeah, there's a couple. I think one of them was
Kaido sand, which is yeah, I know back when I
used to brew beer. It's an additive that people use there,
so I was familiar with it from but it's and
then there were I think some fibers supplements that could
also be basically binding agents. It's physical binding agents that
(33:04):
sequester it in the gut and prevent your gut from
absorbing it. And there are some supplements that I think
are going to be on the market soon that include
those ingredients with the goal the stated goal of reducing microplastics.
We won't know how well work in humans, so that's encouraging,
But once they're in our bodies and we know that,
you know they are in our bodies, most of them,
(33:26):
most of us probably have absurd amounts of these in
our bodies. We don't have a clue how to get
them out sort of reverse that process because I don't
want microplastics in my cells driving inflammation. I don't know
about you, but when I get rid of it, I
immediately think, like, how do I get rid of this?
Speaker 1 (33:43):
Particularly because you're so into lysisomes and you know that
they bunk up the lysisomes. So she's almost an existential crisis.
Speaker 2 (33:53):
Is it's like, oh my god, like I have this
crap clogging up my lysisomes. I know what happens when
your lycismes get sick. I don't want anything to do
with that.
Speaker 3 (34:01):
Yeah, yeah, So yeah, it was on a.
Speaker 2 (34:03):
Personal level, it was scary, and so being a lysosome
biologist and someone who's worked in this space, I it
was I had one idea. I was like, well, if
other stuff accumulates in lysosomes, we know how to get
that out. I mean, we know how to get extra
cholesterol out of lysisomes. We know how to get other
substrates that build up out of lycismes. There are a
(34:24):
number of drugs that can do this in mice and
in humans, and one of them that had just been
published in a really interesting paper on a disease called
Nieman Pick disease, which is a disease where your lysisome
to accumulate cholesterol. This paper had used a compound called sulforophane,
and they treated the mice with sulforophane. They showed very
(34:47):
convincingly that that caused the lysosomes to basically dump their
contents outside of the cell so they could get rid
of all this extra cholesterol. And then once they did that,
the lysismes were much healthier and the cells were much healthier,
and so were the and have had a very positive
outcome in that study. So you know, I yeah, I thought, well,
it'd be really interesting if someone would test sulforofane in
(35:10):
a mouse study to see if it could reduce microplastics
accumulation and mysosomes because they're you know, they're accumulating just
like these other things do. To get that study done
would take years. Who's very slow. Someone probably is trying that,
but I didn't want to wait for that. I thought, well, sulforaphane,
this is something people take this all the time. There
(35:30):
are tons of clinical studies showing good things from taking sulforaphane.
I wonder if it's already doing this in people. I
wonder if people who are taking this or rejecting microplastics
out of their cells. So that was the basis for
this self experiment. I said, I'm going to do it.
I have a way to measure this. Now there's a
nice test that is commercially available, and I can see
exactly what happens in my blood before and after taking
(35:52):
the supplement and measure what's happening to my microplastic levels.
And sure enough, after I took a big dose of sulforafane,
it released many, many millions of microplastic particles from my
cell wow, and dumped them into my blood. Which that's
a nice result. Scientifically, it does Okay, it worked, you know,
(36:12):
the hypothesis is supported by the data. The sulforafane did
something that liberated the microplastics out of the spells. But
the other side of that is what happened next? Where
did they go? And I don't know, I can't answer
that question for you. I don't know if they went
back into the same or different cells and just caused
you know, caused more problems. My hope is that if
(36:35):
you do something like this, maybe your body has another
chance to eliminate them. Yes, maybe some of them can
end up in your urine. We know microplastic particles do
end up in urine, so is the reason that could happened.
They also end up in bile, which is a way
of excreting them through your gut. So it's possible that
that's happening. But in the absence of a test that
(36:57):
can test those fluids, I don't have a way to
answer that question, which I think is an important next
step for someone to figure out, is if you liberate
a whole bunch of microplastics like this, where do they go?
Speaker 1 (37:09):
Yeah, yeah, yeah, yeah, and hopefully it's out of the body,
and the our detoxification process is peas one and feast two.
Speaker 3 (37:19):
Would they have potential to excrete microplastics?
Speaker 2 (37:23):
Yeah, So that's that's one. That's why most people are
familiar with sulfur or fane is that it's activating these
metabolic pathways. That's a good thing. What that probably helps
more with than the plastic particles themselves, are these plasticizers,
these chemicals that are bound up in the microplastic particles
things make like this phenol A b p A. People
(37:44):
are familiar with one. Right, It's probably very helpful for
eliminating those toxins, probably less helpful for the particles themselves,
just because our bodies are we have no evolutionary mechanism
to deal with something like.
Speaker 1 (37:58):
Yeah, we don't even recognize it, right, well, probably probably
nice of it's bad, but don't know what to do
with it yet.
Speaker 3 (38:04):
Interesting.
Speaker 2 (38:04):
Yeah, I mean we probably have enzymes in our bodies
that recognize it as the wrong thing. You know, ourselves
probably think these are fats or something, because that's what
they look like. On a molecular level, they look like lipids,
So it's probably screwing up all sort of lipid metabolism machinery.
And it's we certainly have no way of naturally eliminating them.
(38:26):
It's it's it's going to be a push in the
right direction.
Speaker 1 (38:28):
Yeah, that's a That's an interesting watch this space, isn't it?
Speaker 3 (38:33):
John?
Speaker 1 (38:33):
This has been absolutely fantastic, And I'm completely unscripted as well,
which is more more impressive that I can just wing
questions that you with no preparation and you just talk
off the hip with all of this stuff. So where
can people go to find out more about you? I
(38:55):
know you're on LinkedIn, That's where I found you, so,
but also you write quite a lot. You're on substack,
don't you.
Speaker 2 (39:02):
Yeah, that's kind of a new platform for me. Yeah.
My subseac newsletter is called Translation and you can also
find it by searching my name, and that's you know.
The plan is for that to become sort of my
primary channel for articles and maybe some interviews in the
future and that sort of thing. And I'm a still
working on a book. Substack will be where I communicate
(39:22):
updates on that. So they tuned there.
Speaker 1 (39:25):
Yes, how long do you think you are away from publishing?
Speaker 2 (39:31):
Are you early or.
Speaker 1 (39:33):
Have you got a for a bit of You've got
for a bit of progress made on it.
Speaker 2 (39:37):
I've made some progress. It's going to be heavily depended
on some contributions from other people too. I'm interviewing a
number of people to sort of gather content and and
build out the framework that I'm going to present in
the book. So it's it's a little ways off still,
I'd say about a year, but we're getting there. I'd
love to chat with you sometimes about that. It sounds
like you have a lot of experience in that space.
(39:57):
I'm sure I can learn a lot from you.
Speaker 1 (39:59):
So, well, yeah, I've written a couple and I think
I think the thing I would say is that you're
never going to get it perfect, that you just keep going,
oh and there's a little bit now, there's a new
research studies, like, just just just get it out and
you can always do an update later on. Because yeah,
when I've reread my my, my book, my first book,
(40:20):
I went shit, I'd like to put that and that
I'm probably going to do a revised edition, and in
this one, even sending it off to so you go
through the editing process and then get it back and
in its final edits, and then they sent me through
in here's now the layout.
Speaker 3 (40:34):
I want you to check the layout.
Speaker 1 (40:36):
And I'm still wanting to tweak it and add a
new study that I just read the other day.
Speaker 3 (40:41):
So so don't let perfect be the enemy of grit.
Speaker 2 (40:44):
That good advice. I'll try to remember that.
Speaker 1 (40:46):
That would be definitely my my t But but me
I I'm certainly going to be following you on on
sub stacks, So we will put that link into the
show notes. I'll also put the link into your LinkedIn
because you've got a lot of interesting articles for anybody
who's interested in this space. And you know, the thing
I like about you is that you're not You're not
out pushing supplements, you're not pushing a product. You're just
(41:09):
somebody who is a hardcore scientist who's interested in this
area and has quite a lot of smarts. So it's
people like you that listeners should be following, not whinkers
like David Sinclair on.
Speaker 2 (41:25):
So I appreciate that you don't bucking me with the wankers.
Speaker 3 (41:31):
Definitely not. This has been awesome.
Speaker 1 (41:33):
So we'll get those links, we'll put them in the
show notes, and yeah, good luck on your book, and
i'd certainly love to have you back on whenever you're
doing your book, and we'll get it promoted to our listeners.
Speaker 2 (41:45):
Awesome, let's do it. Thanks Paul, it's been great, really,
Yeah, So mixing it up a little bit, I think
is really important. Let's die, Let's get back to the
SGL two inhibitors now. Is interesting to hear you say that.
I'll give you a little bit of background. So January
this year, I had open heart surgery for a dodgy
valve that I was born with. I was born with
(00:28):
a bi cuspan aortic valve. But it's all good. But
the upshot of this is the one drug that they've
put me on is an SGL two inhibitor. And actually,
when I dug into it, I went, you know what,
that's a drug. I'm not basically a big fan of
taking drugs, but I'm like, I'm actually happy that they
(00:50):
put me on an SGL two inhibitor. It's essentially a
diabetes drug or our drug for managing your blood sugar
slice insulin, but it also has benefits for heart and
so I'm actually pretty happy to be on an SGL
to inhibitor. That's a nice unintended consequence of my being
(01:11):
born with the doachi for help, So tell our listeners
what and because actually, out of the interventional's testing program,
a lot of them, the drugs that were successful controlled
inchilin our and or glucose, which is an interesting thread, right,
But one of them, and canaga flows in and is
(01:33):
an sgl TO inhibitor. So talk to our listeners about
what an sgl TO inhibitor is and why you think
it's interesting from a longevity slice health span perspective.
Speaker 2 (01:47):
Yeah, well, so the reason I'm excited about these is
just the abundance of data that we have suggesting that
they can be beneficial. And it's We've talked about the
issues with mouse studies. They do extend lifespan in my
least in mail lice, yes, but you know that's just
the beginning of the data. We have tons of data
for many, many thousands of patients taking these drugs in
(02:09):
the real world showing that it generates positive health outcomes
and reduces the incidents of negative health outcomes. They appear
to be very protective for the heart, like you mentioned,
also the kidneys. There's also a lot of data emerging
to suggest that they're very good for the brain. So
we have that piece of data saying, you know, patients
(02:30):
that are on these for diabetes tend to exhibit better
health outcomes over time, even outcomes unrelated to diabetes. Yes,
and then there's this other piece that you don't often
get for a longevity intervention, and this comes from studies,
these Mendelian randomization studies, which can you take me.
Speaker 1 (02:51):
Take a step back and explain what those are and
why they're actually useful.
Speaker 2 (02:57):
Yeah, so these are sort of a clever way of
modeling the impact of different interventions, in this case the
drug intervection and intervention by looking at sort of a
natural experiment that genetics have given us. So we all
have this protein called SGLT two that's the target of
(03:19):
this drug, right, and it's a channel. It's a channel
that recovers glucose in your kidney so that you don't
have glucose in your urine and we're keeping it in
the body where we need it because glucose is a
nutrient that we need. It's important for energy production. But
we have different genetic variants in SGLT two. So you know,
(03:40):
most of us have a fully functional version, but there
are rare genetic variants where you have a dysfunctional SGLT
two protein that doesn't come glucose as efficiently. So that's
very similar to what the drugs doing.
Speaker 3 (03:54):
Right.
Speaker 2 (03:54):
If the drug inhibits. And then there are some people
that have just been operating this way their whole lives,
their SGLT two never worked efficiently. You can look at
what happens to those people have a pretty good idea
of what the drug's gonna do. Right, Have I blamed
this in.
Speaker 3 (04:09):
A way in a minute you have? Yeah, you've explained
really well.
Speaker 2 (04:13):
So, yeah, that's that's an Ndelian randomization. And when you
look at it for SGLT two and you look at
studies sort of modeling the impact of these drugs, you
see really cool stuff. You see longer life span in
males just like the ip saw and mail mice. You
see increased intelligence, which is kind of a surprising one, right,
(04:34):
like why would having h this dysfunctional glucose channel increase
or intelligence? But it's probably doing really good things for
brain health and that's probably why.
Speaker 3 (04:43):
Yeah.
Speaker 2 (04:45):
But so we sort of have this natural experiment that
tells us, hey, you know, if you're worried about taking
this drug and inhibiting this protein, there are many people
walking around their whole lives with the equivalent of the
impact of this drug. It may have very good health outcomes.
So for me personally, that just sort of gives me
more reassurance that this could be a really good thing.
Speaker 3 (05:06):
Yeah, uh, I think it's a.
Speaker 1 (05:09):
I think it's a it's a it's a pretty deep
level of reassurance whenever you see real humans with a
genetic change that that seems to then have good outcomes,
and then we understand the process by which it happens
as well, and then we have a drug that that
(05:30):
mimics that process, that has a low side effect profile.
You're starting to get towards slam dunk interventions, right, Yeah.
Speaker 2 (05:40):
I mean it's it's a lot of data. You don't
you don't have that for any other longevity drug. Yeah,
the Mendelian randomization. You have to get lucky. There has
to be a gene that can model the impact of
the drug that in the human population. Most of the
time there isn't one, but we got lucky. That's JILT too,
But yeah, that I think the strongest data really is
just what's see seeing what's happening to the patients who
(06:02):
are taking it, how how they go on after many
years of taking this drug, and they have lower incidences
of heart failure, of a chronic kidney disease. It they're
really really impactful drugs, and it seems to be occurring
through the mechanism that makes them useful diabetes drugs. It's
(06:23):
decreasing blood ghos. We haven't talked about how these drugs work.
We kind of hinted at it with the function of
the protein. But at the most basic way to explain
how these work is they make you pee out some sugar.
Not what they do, because two different.
Speaker 1 (06:37):
Diabetes strugs have different effects and will probably come on
the Tall Apartment form and as well. So, but to
think this is important, right, is that that that process.
Speaker 3 (06:46):
By which they work.
Speaker 2 (06:48):
Yep, absolutely, yeah, they in this case. I mean, there's
different ways you can decrease blood sugar, right. One way
is to let more of it out in the urine
and with sglt too. And it's a substantial amount. I'm
not the best with numbers all the time. I can't
remember how many grams of sugar it is that you
lose per day, but it's substantial. It's something like I
(07:10):
want to say it's fifty grams that don't quote me
on that, but you're losing a substantial amount of sugar
in your urine. It's higher in a diabetic that has
high blood sugar to begin with, but it happens in
healthy individuals too, So you're basically taking taking your blood
sugar level, which you know you have your stable zones
and your spikes, and you're just shifting all of it down.
You're just decreasing the basal tone in that blood sugar level.
(07:32):
You're making the blood sugar spikes less spiky, so it's
I'm presumably john then less inchillin exactly, then you get
less insulin signaling. So in some ways it's sort of
mimicking what happens with chloric restriction, which is sort of
a gold standard intervention for lifespan extension, right, So at
(07:54):
a fundamental level, that's at least one of the things
they're doing is decreasing blood sugar, which has onstream benefits
throughout the body. In the kidney I mentioned, they have
sort of a protective effect on the kidney. One of
the by products of inhibiting that sodia well glucose and
also it inhibits sodium re uptake in the kidney is
(08:15):
that you decrease the pressure in your kidney, so you're
just putting less stress on it over time. So people
don't think about kidneys in terms of longevity so often,
but it's important to realize as we get older, all
of our kidneys are starting to fail. Your kidney function
is never going up, it's always going down. So if
you have a drug that can stop that, and that's
exactly what these do, They stop the decline of kidney function,
(08:37):
that's that's potentially a very good thing.
Speaker 3 (08:39):
Kidneys are really interesting.
Speaker 1 (08:40):
I remember I went to the Ukena was sitting beside
an nephrologist and we had a long chat about kidneys
and kidney health and basically they're a window into your
cardiovascular system, which I'd never thought about because he said
that the amount of blood vessels concentrated in the kidney,
so he said, in nerve research, they see a lot
(09:03):
of cardiovascular issues appearing in the kidney first.
Speaker 3 (09:07):
That's the place that they can look for them.
Speaker 2 (09:10):
That makes sense. I mean, kidneys they're not a regenerative organ.
So you knows, as you lose the filtering units in
your kidneys as you get older, you're never getting them
aer back. And they're also very susceptible to stress. You know,
things like high blood pressure, high blood sugar. It stresses
the kidney and you start to lose more of that function.
So yeah, I mean it makes sense that you could
free it that way.
Speaker 1 (09:31):
Yeah. Okay, So we've talked about SGL two inhibitors and
and that that they and I completely agree with you
that they seem to be the one drug. I think
that data is much clearer for humans than wrappamacin. Let's
then talk about mett Foreman, right, because it's it's interesting
(09:53):
when as I've talked about longevity before in topics, and
I've had you know, molecules that or drugs that are
really interesting, and then I had a category of yen nah.
Speaker 3 (10:08):
It's a it's a kind of an Australian thing.
Speaker 1 (10:10):
Yeah nah, yeah, the same, right, And so I had
put met forman in the yen nah and now it's
in the yen na maybe camp for me, right and
reason So the reason I'll give you for that was
you you'll probably be more over this than me. But
there was that early experiment that showed and correct me
(10:31):
if I'm I get the details wrong here, John, but
people who were at diabetics who were taking met Foreman
and appeared to live longer, and then people who were
non diabetics and not on met forman right in this
one particular study, and then there was all of this
creas about met forman being a longevity molecular longevity drug.
(10:53):
And then another study came out which actually criticized some
of the methodology in the first study and that that
some of the people who were excluded were because they
had disease, and it was like, well, you can't really
do that. And this intervention where they included everybody and
(11:14):
showed that there was no longevity benefit to the people
who were diabetic taking met forms So there was a
bit of a ooh dob squid, but they and some
interesting stuff has come out about met forming recently in
terms of other health benefits, which I'm sure you're more
over than me, and and lots of animal So talk
(11:35):
us through met forming and your take on met forming
and and.
Speaker 3 (11:40):
It's yeah, is it a year na? Is it a yeah?
Speaker 1 (11:43):
Nah?
Speaker 3 (11:43):
Yeah, yeah, work.
Speaker 2 (11:45):
I'm kind of gonna eat I guess it's a yeah.
Speaker 1 (11:48):
No.
Speaker 2 (11:48):
I think I think there's reason to believe that could
be beneficial, but we don't have, you know, the rock
solid data that I think we have for SGLT too inhibitors.
So yeah, met foreman, I've I've tried met Foreman as
a longevity intervention myself.
Speaker 3 (12:06):
I think, how did you how did you find that?
What would they also that any positive SETI negatives that
you noticed.
Speaker 1 (12:13):
You're running reasonably tightly controlled experiments as much as you
can in a free living human.
Speaker 2 (12:18):
Yeah, I'd try to change a million things at once,
and you know, take good notes on my biomarkers and
how I feel and that sort of thing. Met Foreman,
It's one of those that. So there there are some
drugs that I've noticed when I've taken, like an SGLT
two inhibitor. I feel fantastic when I when I take
an SGLT two inhibitor, and I think it's probably because
(12:41):
I wake up in ketosis. I have these keytnes going
into my brain in the morning, and I just feel
crystal clear and energetic. And I notice when I'm taking
one of those drugs and it feels very good. Met Foreman.
Kind of is the other way. I don't feel the
greatest met Foreman, I feel kind of sleepy and then
like I have a little bit less energy. So that's
(13:05):
that's a turn off, right. I don't like to feel
that way. Yeah, And I've tried to you know, tweaking
the dose a little bit, seeing if I can find
a low enough dose where it's doing something. But I
don't have those side effects and that that does help.
But you know, everybody's different. That's probably just a me thing.
I don't think everybody's going to be leepy if they
(13:25):
take a low dose in that form, and I think
maybe I'm just kind of sensitive to some of the
downstream effects of that one. But for that reason, it's
not my favorite. But I do think there's good data
to support that it's doing positive things for health, absolutely, but.
Speaker 1 (13:41):
It's in exercise interference. Yeah, do you do you think
that's real?
Speaker 2 (13:49):
I think it's real if you are the type of
subject that that study was run on, if you're if
you're an elderly person who is at risk of frailty
and you're not resistance training. Yeah, I mean, I think
there's a risk that then you take a drug like
Matt Foreman that is going to decrease your blood sugar
levels and lead to some muscle atrophy.
Speaker 3 (14:09):
Yeah.
Speaker 2 (14:10):
I think that's a real risk For someone who is
regularly in the gym, they're you know, eating enough protein
to build some muscle. Maybe they've already built some muscle.
I think it's, you know, probably not a concern. I
think the benefits of that resistance training are going to
outweigh any any slight negative exercise adaptation effects of a
(14:31):
drug like that.
Speaker 1 (14:33):
Okay, interesting, and now I interesting you mentioned with the
SGL two inhibitor you wake up in kontosis. I've been
recently thinking about intermittent fasting, right, So I used to
do intimittent fasting. Used to do sometimes sixteen it's sometimes
fourteen ten whatever, But I would just push.
Speaker 3 (14:55):
My breakfast out.
Speaker 1 (14:57):
And then I stopped doing it because I was having
DEXA scans every sort of six months to a year
and I had lost with it. But I'd lost significant
amounts of muscle, right, and so I stopped intermittent fasting.
And then I find out that I had a bicusp
(15:17):
of iotic valve and significant regurgitation, which probably explained my
muscle loss right over and above the intermittent fasting. So
I'm not like, ah shit, maybe that was any you know,
you have seen some of the data coming out. Some
of the concern about the intermittent fasting is obviously that
(15:39):
you fast overnight, that you've only you don't have a
big amino acid storage pull in your body. So if
you're fasting twelve, thirteen, fourteen hours, your body is going
to be breaking down muscle to get those amino acids
that are very critical for cellular function.
Speaker 3 (15:54):
Right.
Speaker 1 (15:55):
But then more recent research has shown him if you
take a big chunk of protein in the evening, that
muscle protein synthesis can persist for twelve or so ours.
Speaker 3 (16:06):
Right. So I've been toying in my head with.
Speaker 1 (16:09):
The idea of waking up in the morning and taking
a ketone ester like be the hydroxy buttoryate, right yep,
just too fast forward that move into ketosis to get
all of those benefits.
Speaker 3 (16:26):
And then break the fast.
Speaker 1 (16:29):
Have you ever thought about taking a ketone est or
have you ever played with taking a keyton ester if you're.
Speaker 3 (16:35):
Doing a bit of fasting.
Speaker 2 (16:37):
I've been interested in them, and I haven't. You know,
It's part of the turn off is they're so expensive. Right,
If you want a large amount of ketone a lot
of those supplements, you know, they would be like ten
dollars a day or something.
Speaker 1 (16:52):
So's that expect because I only just looked at it yesterday.
I looked at beta hydroxy beuty yesterday. So this is
very hot off the press in my mind.
Speaker 2 (17:01):
Yeah, it's well, I mean some of them are. There's
different forms. I It's been a while since I've dove
into this one, but I have been interested in them,
and I think that there's there's a lot of good
data to show that taking a key tone supplement immediately
improves brain function, like the of the There are imaging
studies that show this that if you look at aging
(17:24):
people who are exhibiting some of the signatures of brain
aging on brain scans, you give them a key tone
supplement and you recover that function. Like it seems to
do something very positive because the brain loves keytones as
a fuel source. Yes, so that's kind of where my
interest came from. And I have looked at them, but yeah,
I haven't haven't experimented with it myself. Yeah, yeah, okay.
Speaker 1 (17:46):
And then on the topic of fasting, what what's your
view on fasting, whether it be short term, intimittent fast
periods of longer fasting, what's your what's your.
Speaker 3 (17:58):
View on that? And do you have a you on
what sort of age group that it would benefit more.
Speaker 2 (18:06):
Yeah, that's a that's a good question. Well, so, so
first I would say I think it would benefit people
that aren't at risk of frailty or of.
Speaker 4 (18:16):
Number one number one ye, yeah, and that's not just
elderly people that can also be endurance athletes that can
be you know a lot of people, fasting might tip
them too far into that catabolic state versus where.
Speaker 2 (18:34):
They're already at. So I don't think it's for everyone.
If you're more in the over nutrition camp, you know,
you you have some some weight to lose, You're you're
getting in shape, you you have enough muscle mass. If
you were to lose a little bit of it, it's
not going to be the end of the world. I
think fasting can be excellent, and there's lots of excellent
(18:57):
clinical studies showing benefits. The tough thing is there aren't.
I mean, okay, So backing up a little bit. The
goal of fasting, as we've been talking about it is
to activate autopogy, right, to sort of kick off that
cellular recycling mechanism and get all the benefits that we
know that that has. The trouble is we don't have
great data in humans to know how long that takes. Yes, correct,
(19:20):
it's been very tooallenging to measure autoplogy and humans in
real time, and there's just recently, in the last couple
of years, the first studies have been able to do it,
and they've shown that I don't remember exactly how long
it was, it was an intermittent fasting protocol does indeed
activate autology in humans on an average, But you know,
(19:42):
that's not the same as saying that we know what
the optimal time is, how that rereads from person to person.
So I don't know. I mean, I don't know how
long it takes to start autology and how much it
ramps up if you continue, And so it's kind of
hard to make data based decisions on what to do
with fasting, which is why I think it's really for
most people, it's going to be how do you feel?
(20:04):
You know, are you recovering from exercise still, are you
feeling energetic? Do you feel like your your brain function
is good? I think, unfortunately, that's the best we can
do right now.
Speaker 1 (20:15):
Yeah, I think anybody who tells you that fasting for
this amount of time and just just autophogy is just
the foot of ship, right.
Speaker 2 (20:25):
There's no way to even measure that until very recently.
So yeah, it's not that simple. I wish it was.
Speaker 1 (20:31):
And there does seem to be some research from from
and again mostly animal models that that muscle autophogy and
we can potentially accelerate the autoplogy and muscle sales from
exercising in a fasted state. Right, that's one potential, But
again I don't think we know. My view on this
(20:54):
is very similar to yours, is what is your mediator.
Speaker 3 (20:58):
Health go right now?
Speaker 1 (20:59):
Like if your metabolism is a problem, right, if you
have problems with your your glucose, if you're overweight, particularly
central obesity. I say that people you know the I
think the benefits of fasting outweigh the negatives in terms
of any loss of muscle mass.
Speaker 3 (21:18):
Right.
Speaker 1 (21:18):
But and particularly if you're like me in your fifties
and your major goal is to or one of your
major goals is from a health boance perspective, is maintaining
your muscle function.
Speaker 3 (21:32):
I trade a little bit more carefully.
Speaker 1 (21:35):
Where I've kind of landed is probably cycling through a
little bit of intermittent fasting just on a daily basis,
And then I think it's probably a good idea for
me to do once a year, a four day water
fast to get that sort of system right wide reset
and and just know that I'm to some resistance training
(21:57):
during it and minimize them the loss of muscle. That's
kind of where I've landed. Are you in a similar spot?
It sounds like you're in a similar spot.
Speaker 3 (22:06):
Yeah.
Speaker 2 (22:07):
I think the resistance training while you're doing it is key.
I mean, if if you're if you're resistance training enough
that you know how strong you are, then you know,
you know, for a given exercise at a given way,
how many reps you should be able to get. Sort
of doing low volume resistance training where you're making sure
you're not losing reps or losing weight while you're doing it.
If that's the case, you're not losing muscle, right, You're
(22:29):
not going to keep your lips where they are if
if you're losing a bunch of muscles. So I think
I think that's a very sensible way to go about it. Absolutely.
Speaker 3 (22:37):
Yeah.
Speaker 1 (22:38):
Cool, And so let's not talk about a couple of
other things that that might be interesting.
Speaker 3 (22:47):
So glysing, I think was something.
Speaker 1 (22:50):
That came up in the intervention testing program as potential,
and then I saw a series of research papers upbut
kalinak so glycine and an acetyl cysting. And the reason
I found these research papers interesting was they done and
I'm not sure if you're familiar with these studies, but
(23:11):
they've done and studies in mice and showed that glinac
enhanced their health span.
Speaker 3 (23:17):
But it did it through.
Speaker 1 (23:19):
Reducing oxidative stress, reducing inflammation, reducing mitochondrial dysfunction. Right, And
the same research group then showed that in humans, in
older adults, this is taking glinac reduced mitochondrial dysfunction, reduced
oxidative stress, reduced inflammation. And I thought, oh, that that's interesting.
(23:43):
And the fact that glycine independently seems to be interesting
and an acetyl cysting independently would seem to have significant
benefits for me, that's one that has got quite good
potential in terms of an intervention, although glenac itself hasn't
(24:03):
been tested.
Speaker 3 (24:04):
What's your thoughts any thoughts on ginac?
Speaker 2 (24:06):
That's yeah, no, you're you're giving me a new one.
I have heard of it. I'm not familiar with the research,
so I need to check it out, but I guess yeah.
My question would be with presumably anecetyl systeine is the
active agent because that has all sorts of biological activity
for reducing oxidative stress. And yeah, there's very good data
for that supplement on its own for all sorts of things. Yes,
(24:29):
So when you conjugate it to glycine, Yeah, what's that doing?
Speaker 3 (24:31):
Is it?
Speaker 2 (24:32):
Is it changing the biodistribution of anacetyl systeine. Presumably it's
doing something like that. So I would need to read
up on that one a little.
Speaker 1 (24:42):
So I want to flick you some research papers and
I look forward to a blog post from you on it. Yeah. Yeah,
let's we're over an r into this, but let's get
into the topic that I got to you on.
Speaker 3 (24:56):
Into the show. Yeah, yeah, it's sure, you're right, which
was your wrote.
Speaker 1 (25:00):
This fascinating article about microplastics and and an intervention that
that you had done on yourself. And I love self experimentation.
I'm actually you know, given all that we have talked
about here and individual differences, I think everybody should be
self experimenting. An equals one is not a great science
(25:21):
experiment unless it's done on you. Yeah, right, for you, yeah, exactly,
as long as you kind of know what you've got
to know what you're doing. That's that's the key thing,
so to talk to us about because I'd be more
and more concerned about the research coming out about plastics,
and I think most of my listeners would be familiar
(25:43):
with that. I've done a couple of podcasts on it,
not not at a deep level, but just the fact
that they are ubiquitous in the environment, and they found
it in pretty much every human tissue in placentas. I
think it was one hundred percent strike rate in US women.
When they look, they're not finding it. When they're all
top seeing human brein, they're finding microplastics in there.
Speaker 3 (26:05):
So this ship is insidious. It's clearly not doing good.
Speaker 5 (26:11):
And so give us your view on just on why
they're bad and then the intervention you did and what
some people could potentially do.
Speaker 2 (26:23):
Yeah, I'll do my best. So So, the microplastic situation
is something that I only learned about recently in the
last year or two, and as I learned more about it,
I was just like, holy shit, this is terrible. Yeah, yeah,
it's And I also wondered, like, why aren't we talking
(26:44):
about this? You know, this is this is this is
absolutely devastating that that we're we're all facing this exposure
and that it's in all of our tissues, and it's
increasing over time, and it's associated with a number of
really terrible health outcomes. It's it's it's really scary, and
it is not getting any attention at all. We'll see
(27:04):
a pop press article once in a while, you know,
saying they found new microplastic levels in something worse than
we thought, and it's you know, it's it's getting some attention,
but people just don't care the way they should. But
when I learned about this, I was very scared. When
I when I learned it was the brain paper was
the one that really got me. This was from Matthew
Campin's Groove. They looked at brain samples from deceased people
(27:30):
with a new very sensitive technique that can detect microplastics.
They used a number of techniques, they detected them multiple ways,
and what they found was that our brains just have
an absurd amount of plastic accumulating in them in the
form of these really tiny micro and nanoparticles. It's higher
than other tissues in the body. It's you know, you
(27:53):
can detect them biochemically with mass spec you can detect
them microscopically. If you stain and look for this the
plastic particles in the brain, it's it's a very clear finding.
And of course, you know, the plastic industry is pushing
back very hard, trying to discredit the science. But it's
very solid science published in one of the mist journals
in the world. So if anyone has doubts on the science,
(28:15):
don't believe it. This is excellent science. But they show
that it's accumulating to these massive levels in the brain
and in other tissues. And if you look at brains
of people with dementia, it's it's quite a bit higher
than in people without dementia. That doesn't mean that the
plastic cause the dementia. We don't know what the relationship
is yet, but it's it's concerning.
Speaker 3 (28:35):
Yeah, probably not doing good. Let's put it out well.
Speaker 2 (28:39):
It's not doing anything good, and so it's you know,
that's one study in humans. There have been many, many
other mechanistic studies in mice where they inject mice with
microplastics and look at what happens. There are cell studies,
and what we're learning is that these really tiny plastic
particles they do a lot of really bad stuff in
(28:59):
the body. But I think at the core what's happening
is one of the worst things is that your immune cells,
of course recognize this foreign object in your circulation or
in your tissue, and they try to eliminate it, and
that's what their job is, so they'll actually engulf this
microplastic This little tiny plastic particle goes into the cell.
(29:21):
But the cells are also little and tiny, so the
plastic particle is like almost as big as the cell itself. Wow,
it gets stuck in its lycisme. That cell goes crazy
and does all sorts of bad things. It starts releasing
inflammatory cytokinds in the brain. These immune cells get stuck
and cause little coagulation issues and little thrombotic issues in
(29:44):
the brain. They drive inflammation. Like, the collective take of
the studies is that these are not anything we want
in our bodies. We should all be very concerned that
you can detect them and most of our tissues and
they're likely driving persistent chronic inflammation. And yeah, I mean,
(30:05):
I could go on and.
Speaker 1 (30:06):
On, but I think we could summarize this John microplastics
equal a cellular shit storm.
Speaker 2 (30:13):
It is a shit storm. It's a whole body wide
shit storm. It's one study I should also menage. There
was a study that looked at I believe it was
carotid artery plaques.
Speaker 3 (30:26):
Right.
Speaker 2 (30:26):
They had patients coming in to get these plaques taken out.
They were going to have it happen anyways, So they
consented to patients and asked, can we look and see
if your plack has microplastics, and then can we follow
you for a period of time afterwards and see what happens.
So they did this. They had it was a well
powered study. They had a large number of patients. They
they bucketed the patients into two groups. There were patients
(30:49):
that had microplastics in their plaques and then there were
patients that had plaques without microplastics.
Speaker 3 (30:54):
Right.
Speaker 2 (30:56):
The patients, they then they followed them for a number
of years. I wish I remember the exact number, but
I don't. They followed the patients and the ones that
had the microplastics in their in their plaques had dramatically
worse health outcomes in terms of fatality, stroke, heart attack.
It was it was a very clear difference. And it's
(31:17):
They also had a lot of beautiful mechanistic data in
the study where they looked at markers of inflammation in
the plaques much much higher when the microplastics are present.
So it's it's it's observational data. People will always push
back and they it's not a randomized controlled trial, but
we're never going to have that where I can inject
people with microplastics. So this is the best we can do.
And it says that it's very very bad and and
(31:40):
and yeah, it's a signal is consistent across multiple studies.
Speaker 1 (31:45):
You need to take set up and take notice and
forget about a bloody randomized control draw right. So yeah, yeah,
so what I be you done then as a result
of this, tell us about this experiment?
Speaker 2 (31:56):
Okay, Well, so, as I kind of went down the
rabbit hole and learned more about microplastics, one of the
things that was frustrating was that nobody is publishing trials
yet in mice or in cell models on how to
get these things out of ourselves. You know, it's I'm
sure there are people working on it. The field is
moving very rapidly. I'm sure there's all sorts of new
(32:19):
labs that are just starting to work on this, But
the the interventional stuff just really isn't out there yet.
There's a couple of groups that have shown that if
you ingest certain certain supplements you can kind of bind
up microplastics in the gut because most of it's coming
from dietary intake, and you can help prevent the gut
from absorbing them. So that's that's one positive.
Speaker 1 (32:39):
But as far as what were those things that you
could take to bind them? Jones, can you remember off
the time.
Speaker 2 (32:43):
Yeah, there's a couple. I think one of them was
Kaido sand, which is yeah, I know back when I
used to brew beer. It's an additive that people use there,
so I was familiar with it from but it's and
then there were I think some fibers supplements that could
also be basically binding agents. It's physical binding agents that
(33:04):
sequester it in the gut and prevent your gut from
absorbing it. And there are some supplements that I think
are going to be on the market soon that include
those ingredients with the goal the stated goal of reducing microplastics.
We won't know how well work in humans, so that's encouraging,
But once they're in our bodies and we know that,
you know they are in our bodies, most of them,
(33:26):
most of us probably have absurd amounts of these in
our bodies. We don't have a clue how to get
them out sort of reverse that process because I don't
want microplastics in my cells driving inflammation. I don't know
about you, but when I get rid of it, I
immediately think, like, how do I get rid of this?
Speaker 1 (33:43):
Particularly because you're so into lysisomes and you know that
they bunk up the lysisomes. So she's almost an existential crisis.
Speaker 2 (33:53):
Is it's like, oh my god, like I have this
crap clogging up my lysisomes. I know what happens when
your lycismes get sick. I don't want anything to do
with that.
Speaker 3 (34:01):
Yeah, yeah, So yeah, it was on a.
Speaker 2 (34:03):
Personal level, it was scary, and so being a lysosome
biologist and someone who's worked in this space, I it
was I had one idea. I was like, well, if
other stuff accumulates in lysosomes, we know how to get
that out. I mean, we know how to get extra
cholesterol out of lysisomes. We know how to get other
substrates that build up out of lycismes. There are a
(34:24):
number of drugs that can do this in mice and
in humans, and one of them that had just been
published in a really interesting paper on a disease called
Nieman Pick disease, which is a disease where your lysisome
to accumulate cholesterol. This paper had used a compound called sulforophane,
and they treated the mice with sulforophane. They showed very
(34:47):
convincingly that that caused the lysosomes to basically dump their
contents outside of the cell so they could get rid
of all this extra cholesterol. And then once they did that,
the lysismes were much healthier and the cells were much healthier,
and so were the and have had a very positive
outcome in that study. So you know, I yeah, I thought, well,
it'd be really interesting if someone would test sulforofane in
(35:10):
a mouse study to see if it could reduce microplastics
accumulation and mysosomes because they're you know, they're accumulating just
like these other things do. To get that study done
would take years. Who's very slow. Someone probably is trying that,
but I didn't want to wait for that. I thought, well, sulforaphane,
this is something people take this all the time. There
(35:30):
are tons of clinical studies showing good things from taking sulforaphane.
I wonder if it's already doing this in people. I
wonder if people who are taking this or rejecting microplastics
out of their cells. So that was the basis for
this self experiment. I said, I'm going to do it.
I have a way to measure this. Now there's a
nice test that is commercially available, and I can see
exactly what happens in my blood before and after taking
(35:52):
the supplement and measure what's happening to my microplastic levels.
And sure enough, after I took a big dose of sulforafane,
it released many, many millions of microplastic particles from my
cell wow, and dumped them into my blood. Which that's
a nice result. Scientifically, it does Okay, it worked, you know,
(36:12):
the hypothesis is supported by the data. The sulforafane did
something that liberated the microplastics out of the spells. But
the other side of that is what happened next? Where
did they go? And I don't know, I can't answer
that question for you. I don't know if they went
back into the same or different cells and just caused
you know, caused more problems. My hope is that if
(36:35):
you do something like this, maybe your body has another
chance to eliminate them. Yes, maybe some of them can
end up in your urine. We know microplastic particles do
end up in urine, so is the reason that could happened.
They also end up in bile, which is a way
of excreting them through your gut. So it's possible that
that's happening. But in the absence of a test that
(36:57):
can test those fluids, I don't have a way to
answer that question, which I think is an important next
step for someone to figure out, is if you liberate
a whole bunch of microplastics like this, where do they go?
Speaker 1 (37:09):
Yeah, yeah, yeah, yeah, and hopefully it's out of the body,
and the our detoxification process is peas one and feast two.
Speaker 3 (37:19):
Would they have potential to excrete microplastics?
Speaker 2 (37:23):
Yeah, So that's that's one. That's why most people are
familiar with sulfur or fane is that it's activating these
metabolic pathways. That's a good thing. What that probably helps
more with than the plastic particles themselves, are these plasticizers,
these chemicals that are bound up in the microplastic particles
things make like this phenol A b p A. People
(37:44):
are familiar with one. Right, It's probably very helpful for
eliminating those toxins, probably less helpful for the particles themselves,
just because our bodies are we have no evolutionary mechanism
to deal with something like.
Speaker 1 (37:58):
Yeah, we don't even recognize it, right, well, probably probably
nice of it's bad, but don't know what to do
with it yet.
Speaker 3 (38:04):
Interesting.
Speaker 2 (38:04):
Yeah, I mean we probably have enzymes in our bodies
that recognize it as the wrong thing. You know, ourselves
probably think these are fats or something, because that's what
they look like. On a molecular level, they look like lipids,
So it's probably screwing up all sort of lipid metabolism machinery.
And it's we certainly have no way of naturally eliminating them.
(38:26):
It's it's it's going to be a push in the
right direction.
Speaker 1 (38:28):
Yeah, that's a That's an interesting watch this space, isn't it?
Speaker 3 (38:33):
John?
Speaker 1 (38:33):
This has been absolutely fantastic, And I'm completely unscripted as well,
which is more more impressive that I can just wing
questions that you with no preparation and you just talk
off the hip with all of this stuff. So where
can people go to find out more about you? I
(38:55):
know you're on LinkedIn, That's where I found you, so,
but also you write quite a lot. You're on substack,
don't you.
Speaker 2 (39:02):
Yeah, that's kind of a new platform for me. Yeah.
My subseac newsletter is called Translation and you can also
find it by searching my name, and that's you know.
The plan is for that to become sort of my
primary channel for articles and maybe some interviews in the
future and that sort of thing. And I'm a still
working on a book. Substack will be where I communicate
(39:22):
updates on that. So they tuned there.
Speaker 1 (39:25):
Yes, how long do you think you are away from publishing?
Speaker 2 (39:31):
Are you early or.
Speaker 1 (39:33):
Have you got a for a bit of You've got
for a bit of progress made on it.
Speaker 2 (39:37):
I've made some progress. It's going to be heavily depended
on some contributions from other people too. I'm interviewing a
number of people to sort of gather content and and
build out the framework that I'm going to present in
the book. So it's it's a little ways off still,
I'd say about a year, but we're getting there. I'd
love to chat with you sometimes about that. It sounds
like you have a lot of experience in that space.
(39:57):
I'm sure I can learn a lot from you.
Speaker 1 (39:59):
So, well, yeah, I've written a couple and I think
I think the thing I would say is that you're
never going to get it perfect, that you just keep going,
oh and there's a little bit now, there's a new
research studies, like, just just just get it out and
you can always do an update later on. Because yeah,
when I've reread my my, my book, my first book,
(40:20):
I went shit, I'd like to put that and that
I'm probably going to do a revised edition, and in
this one, even sending it off to so you go
through the editing process and then get it back and
in its final edits, and then they sent me through
in here's now the layout.
Speaker 3 (40:34):
I want you to check the layout.
Speaker 1 (40:36):
And I'm still wanting to tweak it and add a
new study that I just read the other day.
Speaker 3 (40:41):
So so don't let perfect be the enemy of grit.
Speaker 2 (40:44):
That good advice. I'll try to remember that.
Speaker 1 (40:46):
That would be definitely my my t But but me
I I'm certainly going to be following you on on
sub stacks, So we will put that link into the
show notes. I'll also put the link into your LinkedIn
because you've got a lot of interesting articles for anybody
who's interested in this space. And you know, the thing
I like about you is that you're not You're not
out pushing supplements, you're not pushing a product. You're just
(41:09):
somebody who is a hardcore scientist who's interested in this
area and has quite a lot of smarts. So it's
people like you that listeners should be following, not whinkers
like David Sinclair on.
Speaker 2 (41:25):
So I appreciate that you don't bucking me with the wankers.
Speaker 3 (41:31):
Definitely not. This has been awesome.
Speaker 1 (41:33):
So we'll get those links, we'll put them in the
show notes, and yeah, good luck on your book, and
i'd certainly love to have you back on whenever you're
doing your book, and we'll get it promoted to our listeners.
Speaker 2 (41:45):
Awesome, let's do it. Thanks Paul, it's been great, really,
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