Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:08):
Hey folks.
Speaker 2 (00:09):
Before the podcast, a quick announcement for me. I'm running
a special event called The Hardiness Effect. It's a full
day workshop plus six week app based program designed to
literally rewy your body and brand to thrive under pressure,
whilst helping you optimize your health and live longer.
Speaker 1 (00:28):
Now, this isn't.
Speaker 2 (00:29):
Fluffy self help bullship. This is based on my published research.
The same intervention we tested in a recent randomized control trial.
The results on average people saw a twenty seven percent
improvement in mood, a twenty six percent reduction in perceived stress,
and a twenty six percent jump in gratitude. On top
(00:50):
of that, we also measured enhanced cognitive function.
Speaker 1 (00:54):
So this isn't theory. It works. Here's what you'll get
on the day.
Speaker 2 (00:58):
You learn how to use hormetic stress things like exercise, heat, code,
light and nature to turn your body into a resilience
building AIDS defying machine. You'll also master the four pillars
of psychological hardiness. You'll also get clarity on how to
reclaim your energy you're focusing your health. You'll connect with
(01:20):
like minded people who are also on this journey, and
you'll get a signed copy of my leader's book, the
Hardiness effect. Then over the six week program, you'll have
access to my Hardiness app that has workouts, breathing and
meditation sessions, educational videos, and a ritual board to help
you build healthy habits. It will keep you accountable, it
(01:42):
will give you a structure, help you connect with others
in the workshop, and help hardwire these habits into your life.
So if you're serious about showing up as your best self,
whether it's at work, at home, and for the people
who matter most, then this workshop and program is for you.
So early bird ricing is still in effect and spaces
(02:02):
are limited. So if this resonates with you, jump onto
my website www Dot Paul Taylor dot biz and booked
your place there And now only the podcast. Hey everybody,
welcome to another edition of Wisdom Wednesdays. Today I am
going to talk about some new research that offers a
little bit of tantalizing hope for Alzheimer's disease. And it
(02:27):
is all about a compound called lithium.
Speaker 1 (02:30):
Now you may have heard of it before, you may not.
Speaker 2 (02:34):
It has actually been used for decades as a psychiatric medication,
most famously for bipolar disorder. But what you probably don't
know is that lithium is also a naturally occurring trace
element that's found in our soil, our food, and even
more relevant for this, in our brains. And a recent
(02:54):
fascinating study out of Harvard Medical School has generated some
real buzz suggesting that tiny amounts of lithium, particularly in
a form called lithium or rotate, might have powerful effects
on brain aging and even help protect against Alzheimer's disease. Now,
before we start thinking we finally found the long awaited
(03:17):
silver bullet, let's really unpack the research and tell us
what is the state of play, what's exciting, what is
still speculative, and why we should be cautiously optimistic. So
let's first of all talk about the Alzheimer's challenge. You
would have heard me talk many times on this podcast
about Alzheimer's disease being one of medicine's greatest unsolved puzzles
(03:41):
because billions of dollars have been spent on drugs and
with no avaal to this point. Now, Alzheimer's is the
leading cause of dementia worldwide, and we really have only
made a very modest progress in its prevention and treatment,
and for decades it has been framed as an amyloid
(04:04):
versus tao battle, with these amyloid beta plaques and toy
tau tangles viewed as the central villains. But some researchers
have actually called that into question and said that even
though we see these things appear in the brain, they
might not be the cause. And this new study introduces
(04:24):
a third player. The trace element that we talked about
lithium measured in micrograms, and this might be very very important.
So in this harvardly had study, researchers examined post more
than brain tissue for people who had either normal cognition,
mild cognitive impairerment, which is often a precursor to Alzheimer's
(04:46):
or other forms of dementia, or full blown Alzheimer's disease.
And they measured twenty seven different metals and they find
that only lithium was consistently lower in people with cognitive decline,
and even more interestingly, lithium wasn't just missing, it was
actually misplaced. The team found that amyloid plaques actually trapped
(05:10):
lithium inside them, acting like molecular sponges, and that meant
that the brain regions most affected by Alzheimer's, particularly the
prefrontal cortex, were effectively lithium deficient, and the lower the
lithium levels in these healthy brain regions, the worst the
person's memory and cognitive test scores had been before death.
(05:35):
And this suggested that disrupted lithium distribution might not just
be a side effect, it could actually be part of
the disease process itself. So let's talk about testing the
theory what happens when the brain runs low on lithium.
So to explore that idea, the researchers turned to mouse models,
(05:57):
including what's called transgenic mice that develop Alzheimer's like pathology,
and they compare them to normal aging mice, and they
cut dietary lithium by about half, which in turn reduced
brain lithium levels by roughly fifty percent.
Speaker 1 (06:14):
And what happened was remarkable.
Speaker 2 (06:16):
Those lithium deficient mice began to show all the early
features of Alzheimer's disease, including more amyloid plaques and more
phosphorylated taul, increased brain inflammation, loss of synapses, axons, and
mile in sheath, which is the coating around the nerves
(06:37):
in the brain, and importantly clear deficits in learning and memory.
Even normal aging mice who don't usually develop amyloid pathology
showed faster cognitive decline when lithium was low. So just
lowering lithium alone was enough to trigger Alzheimer's like changes
(06:57):
in the brain. So let's talk about the molecular break
to understand how this happens. What the researchers did was
was looked at one of lithium's best known targets. It's
an enzyme and they all have silly, ridiculous earning names.
It's glycogen synthius kinikinis three beta or GSK three beta.
(07:20):
This enzyme is actually at the heart of Alzheimer's biology.
Speaker 1 (07:24):
Now this gets a little bit complicated, but what it.
Speaker 2 (07:26):
Does is it promotes tall phosphorylation, it drives amyloid production,
and it ramps up inflammation and under normal conditions, lithium
acts as a natural break on this enzyme, keeping X.
Speaker 1 (07:41):
Activity in check.
Speaker 2 (07:43):
But in the study, lithium deficiency unleashed this enzyme GSK
three beta, pushing it into a hyperactive state, and the
result was the perfect storm. When it comes to brain aging,
which included the development of tau tangles. In inflammation demilation
as in stripping off the mielin from the nerves and
(08:05):
synaptic loss, and when the researchers chemically blocked GSK three beta,
those changes largely reversed. So there's a real smoking gun here.
We understand the process and aim by damaging or stopping
the process, the damage actually reversed. And it's a really
strong hint that lithium's protective role in the brain may
(08:28):
stem from its ability to keep this enzyme under control.
So the next logical question is can we just give
lithium back If low lithium drives disease, can replacing it
fix the problem? In theory, yes, but the practical challenge
has always been formulation and safety. The lithium that has
(08:50):
typically been used clinically, lithium carbonate, is effective for mood disorders,
but comes with a very narrow therapeutic window. Doses high
enough to impact the brain can cause kidney and thyroid toxicity,
and in Alzheimer's most of that lithium ends up driven
into these amyloid plaques, where it's essentially useless. So the
(09:13):
Harvard team then screened sixteen different lithium salts to find
one that could deliver lithium into healthy Brian tissue without
binding to amyloid, and they found one that stood out,
and it's this lithium oratate. Lithium ritate is basically a
smarter delivery vehicle. It turned out to have a much
(09:37):
lower affinity for the amyloid plax, meaning it didn't drive
itself there and it stayed free in Brian tissue with
the neurons actually need it. And then the Alzheimer's prone
mice long term treatment with tiny doses of lithium oritate,
achieving blood levels similar to those seen naturally in humans,
(09:58):
actually produced dramatic effect. What they found was the amyloid
and tau accumulation were almost completely blocked, brain inflammation was
markeably reduced synaptic density and mielin integrity were preserved, and
on learning and memory tasks that traded mice performed as
well as cognitively normal controls. Even normal aging mice benefited.
(10:23):
Lithium ooritated reduced markers of brain inflammation, preserved synaptic connections,
and largely prevented age related cognitive decline, and crucially, it
did so at very low, non toxic doses. The doses
they used were several thousand times lower than those used
(10:43):
to treat bipolar disorder. So let's talk about human evidence. Now,
this obviously is still animal data and humans aren't big mice,
but there's alrarely a small body of human work hinting
that lithium could slow cognitive decline. Over the past two
several randomized trials have tested low dose lithium carbonate in
(11:05):
people with mild cognitive impairment or early Alzheimer's, and in
one two year study, lithium treatments stabilized memory and attention
while the placebo group declined, and their biomarker analysis that
they did showed reduced phosphorylated tawel and the higher levels
of alpha beta forty two in this cerebral spinal fluid,
(11:28):
which suggested slower amyloid accumulation. I know that's all a
bit geeky, but basically this is a good thing. And
then a smaller trial found that even microdoses three hundred
micrograms per day helps stabilize cognition in people already diagnosed
with Alzheimer's disease. When all the data are pulled, meta
analysis suggests that lithium therapy, usually in very low doses
(11:52):
produces the modest but measurable slowing of cognitive decline. And meanwhile,
observational data are are also interesting. People prescribe lithium for
mood disorders appear to have a roughly forty percent lower
risk of developing Alzheimer's disease.
Speaker 1 (12:10):
And though you know, we've got to say that correlation.
Speaker 2 (12:13):
Doesn't prove causation, but certainly evidence is starting to stack up.
Now what makes lithium oority it so exciting is that
it could overcome two major barriers that have limited lithium's
therapeutic potential, and that being the poor brain bioavailability ie
lithium's hard to be taken up by neurons and toxicity
(12:35):
at higher doses.
Speaker 1 (12:37):
Because the lithium.
Speaker 2 (12:38):
Orty it crosses the blood brain barrier more readily and
doesn't get trapped in amyloid, it could theoretically deliver the
same neuroprotective benefits at much lower, safer concentrations. And if
these findings translate to humans, we might finally have a
low dose, low toxicity way to restore natural levels of
(13:01):
lithium in the aging brain.
Speaker 1 (13:03):
Now is still early days, but all of this.
Speaker 2 (13:06):
Data provides a strong rationale for the first clinical trials
of lithium oritate in mild cognitive impoerment and early Alzheimer's disease,
and you can bet your bottom dollar they're already starting
to design these studies. Now, before you start googling lithium
oritate supplements, let's talk about safety and lithium in any
(13:28):
form is not something to just pop like vitamin C right.
Even tristosis can accumulate over time, and the margin between
therapeutic and toxic levels is pretty narrow. Lithium toxicity can
damage the kidneys, the thyroid, and in severe cases, the heart,
and we simply don't have enough long term safety data
(13:50):
on lithium ooritate in humans, particularly in older adults who
may already have reduced kidney function. So for ANWYE, this
is not a do it yourself experiment. Lithium should only
be used under medical supervision, with regular monitoring of seri
lithium levels, kidney function, and thyroid function. And it's also
(14:14):
worth noting that lithium is not recommended during pregnancy, as
it can cross the placenta and slightly increase the risk
of birth defects or pre term breaths. Now, despite all
of those caveats, and this study really does change how
we think about lithium. It reframes it as a nutrient
for brain resilience, something that the brain uses naturally to
(14:37):
keep key enzymes in signaling pathways and balance. And much
like ourn deficiency leads to anemia, a lithium deficiency might
accelerate neurodegeneration.
Speaker 1 (14:50):
And restoring lithium to its physiological.
Speaker 2 (14:53):
Range safely and in the right form could be one
piece of the Alzheimer's prevention puzzle, although we're not there yet,
so I'm not recommending that you go out and take
lithium or go out and buy it.
Speaker 1 (15:08):
Do I take it? Yes, I do.
Speaker 2 (15:11):
Because of this, I take lithium or TAD five milligrams
a couple of times a week. But I am not
suggesting that you do this, and I am certainly suggesting
that you talk to your doctor if you're even thinking
about taking any form of lithium at all. But this
certainly is a very, very exciting development, and I'm sure
(15:34):
that there are clinical trials right now being designed and
registered both to determine the safe and affected dose of it,
just like any drug has to go through that process
and then as interventions for people with Alzheimer's disease and
mild cognitive impowerment. But it is certainly a space that
(15:55):
is worth watching and that I think we will get
to those answers pretty dumb quickly.
Speaker 1 (16:02):
So that's it for this weeaks folks. Catch you next time.
Hey folks.
Speaker 2 (00:09):
Before the podcast, a quick announcement for me. I'm running
a special event called The Hardiness Effect. It's a full
day workshop plus six week app based program designed to
literally rewy your body and brand to thrive under pressure,
whilst helping you optimize your health and live longer.
Speaker 1 (00:28):
Now, this isn't.
Speaker 2 (00:29):
Fluffy self help bullship. This is based on my published research.
The same intervention we tested in a recent randomized control trial.
The results on average people saw a twenty seven percent
improvement in mood, a twenty six percent reduction in perceived stress,
and a twenty six percent jump in gratitude. On top
(00:50):
of that, we also measured enhanced cognitive function.
Speaker 1 (00:54):
So this isn't theory. It works. Here's what you'll get
on the day.
Speaker 2 (00:58):
You learn how to use hormetic stress things like exercise, heat, code,
light and nature to turn your body into a resilience
building AIDS defying machine. You'll also master the four pillars
of psychological hardiness. You'll also get clarity on how to
reclaim your energy you're focusing your health. You'll connect with
(01:20):
like minded people who are also on this journey, and
you'll get a signed copy of my leader's book, the
Hardiness effect. Then over the six week program, you'll have
access to my Hardiness app that has workouts, breathing and
meditation sessions, educational videos, and a ritual board to help
you build healthy habits. It will keep you accountable, it
(01:42):
will give you a structure, help you connect with others
in the workshop, and help hardwire these habits into your life.
So if you're serious about showing up as your best self,
whether it's at work, at home, and for the people
who matter most, then this workshop and program is for you.
So early bird ricing is still in effect and spaces
(02:02):
are limited. So if this resonates with you, jump onto
my website www Dot Paul Taylor dot biz and booked
your place there And now only the podcast. Hey everybody,
welcome to another edition of Wisdom Wednesdays. Today I am
going to talk about some new research that offers a
little bit of tantalizing hope for Alzheimer's disease. And it
(02:27):
is all about a compound called lithium.
Speaker 1 (02:30):
Now you may have heard of it before, you may not.
Speaker 2 (02:34):
It has actually been used for decades as a psychiatric medication,
most famously for bipolar disorder. But what you probably don't
know is that lithium is also a naturally occurring trace
element that's found in our soil, our food, and even
more relevant for this, in our brains. And a recent
(02:54):
fascinating study out of Harvard Medical School has generated some
real buzz suggesting that tiny amounts of lithium, particularly in
a form called lithium or rotate, might have powerful effects
on brain aging and even help protect against Alzheimer's disease. Now,
before we start thinking we finally found the long awaited
(03:17):
silver bullet, let's really unpack the research and tell us
what is the state of play, what's exciting, what is
still speculative, and why we should be cautiously optimistic. So
let's first of all talk about the Alzheimer's challenge. You
would have heard me talk many times on this podcast
about Alzheimer's disease being one of medicine's greatest unsolved puzzles
(03:41):
because billions of dollars have been spent on drugs and
with no avaal to this point. Now, Alzheimer's is the
leading cause of dementia worldwide, and we really have only
made a very modest progress in its prevention and treatment,
and for decades it has been framed as an amyloid
(04:04):
versus tao battle, with these amyloid beta plaques and toy
tau tangles viewed as the central villains. But some researchers
have actually called that into question and said that even
though we see these things appear in the brain, they
might not be the cause. And this new study introduces
(04:24):
a third player. The trace element that we talked about
lithium measured in micrograms, and this might be very very important.
So in this harvardly had study, researchers examined post more
than brain tissue for people who had either normal cognition,
mild cognitive impairerment, which is often a precursor to Alzheimer's
(04:46):
or other forms of dementia, or full blown Alzheimer's disease.
And they measured twenty seven different metals and they find
that only lithium was consistently lower in people with cognitive decline,
and even more interestingly, lithium wasn't just missing, it was
actually misplaced. The team found that amyloid plaques actually trapped
(05:10):
lithium inside them, acting like molecular sponges, and that meant
that the brain regions most affected by Alzheimer's, particularly the
prefrontal cortex, were effectively lithium deficient, and the lower the
lithium levels in these healthy brain regions, the worst the
person's memory and cognitive test scores had been before death.
(05:35):
And this suggested that disrupted lithium distribution might not just
be a side effect, it could actually be part of
the disease process itself. So let's talk about testing the
theory what happens when the brain runs low on lithium.
So to explore that idea, the researchers turned to mouse models,
(05:57):
including what's called transgenic mice that develop Alzheimer's like pathology,
and they compare them to normal aging mice, and they
cut dietary lithium by about half, which in turn reduced
brain lithium levels by roughly fifty percent.
Speaker 1 (06:14):
And what happened was remarkable.
Speaker 2 (06:16):
Those lithium deficient mice began to show all the early
features of Alzheimer's disease, including more amyloid plaques and more
phosphorylated taul, increased brain inflammation, loss of synapses, axons, and
mile in sheath, which is the coating around the nerves
(06:37):
in the brain, and importantly clear deficits in learning and memory.
Even normal aging mice who don't usually develop amyloid pathology
showed faster cognitive decline when lithium was low. So just
lowering lithium alone was enough to trigger Alzheimer's like changes
(06:57):
in the brain. So let's talk about the molecular break
to understand how this happens. What the researchers did was
was looked at one of lithium's best known targets. It's
an enzyme and they all have silly, ridiculous earning names.
It's glycogen synthius kinikinis three beta or GSK three beta.
(07:20):
This enzyme is actually at the heart of Alzheimer's biology.
Speaker 1 (07:24):
Now this gets a little bit complicated, but what it.
Speaker 2 (07:26):
Does is it promotes tall phosphorylation, it drives amyloid production,
and it ramps up inflammation and under normal conditions, lithium
acts as a natural break on this enzyme, keeping X.
Speaker 1 (07:41):
Activity in check.
Speaker 2 (07:43):
But in the study, lithium deficiency unleashed this enzyme GSK
three beta, pushing it into a hyperactive state, and the
result was the perfect storm. When it comes to brain aging,
which included the development of tau tangles. In inflammation demilation
as in stripping off the mielin from the nerves and
(08:05):
synaptic loss, and when the researchers chemically blocked GSK three beta,
those changes largely reversed. So there's a real smoking gun here.
We understand the process and aim by damaging or stopping
the process, the damage actually reversed. And it's a really
strong hint that lithium's protective role in the brain may
(08:28):
stem from its ability to keep this enzyme under control.
So the next logical question is can we just give
lithium back If low lithium drives disease, can replacing it
fix the problem? In theory, yes, but the practical challenge
has always been formulation and safety. The lithium that has
(08:50):
typically been used clinically, lithium carbonate, is effective for mood disorders,
but comes with a very narrow therapeutic window. Doses high
enough to impact the brain can cause kidney and thyroid toxicity,
and in Alzheimer's most of that lithium ends up driven
into these amyloid plaques, where it's essentially useless. So the
(09:13):
Harvard team then screened sixteen different lithium salts to find
one that could deliver lithium into healthy Brian tissue without
binding to amyloid, and they found one that stood out,
and it's this lithium oratate. Lithium ritate is basically a
smarter delivery vehicle. It turned out to have a much
(09:37):
lower affinity for the amyloid plax, meaning it didn't drive
itself there and it stayed free in Brian tissue with
the neurons actually need it. And then the Alzheimer's prone
mice long term treatment with tiny doses of lithium oritate,
achieving blood levels similar to those seen naturally in humans,
(09:58):
actually produced dramatic effect. What they found was the amyloid
and tau accumulation were almost completely blocked, brain inflammation was
markeably reduced synaptic density and mielin integrity were preserved, and
on learning and memory tasks that traded mice performed as
well as cognitively normal controls. Even normal aging mice benefited.
(10:23):
Lithium ooritated reduced markers of brain inflammation, preserved synaptic connections,
and largely prevented age related cognitive decline, and crucially, it
did so at very low, non toxic doses. The doses
they used were several thousand times lower than those used
(10:43):
to treat bipolar disorder. So let's talk about human evidence. Now,
this obviously is still animal data and humans aren't big mice,
but there's alrarely a small body of human work hinting
that lithium could slow cognitive decline. Over the past two
several randomized trials have tested low dose lithium carbonate in
(11:05):
people with mild cognitive impairment or early Alzheimer's, and in
one two year study, lithium treatments stabilized memory and attention
while the placebo group declined, and their biomarker analysis that
they did showed reduced phosphorylated tawel and the higher levels
of alpha beta forty two in this cerebral spinal fluid,
(11:28):
which suggested slower amyloid accumulation. I know that's all a
bit geeky, but basically this is a good thing. And
then a smaller trial found that even microdoses three hundred
micrograms per day helps stabilize cognition in people already diagnosed
with Alzheimer's disease. When all the data are pulled, meta
analysis suggests that lithium therapy, usually in very low doses
(11:52):
produces the modest but measurable slowing of cognitive decline. And meanwhile,
observational data are are also interesting. People prescribe lithium for
mood disorders appear to have a roughly forty percent lower
risk of developing Alzheimer's disease.
Speaker 1 (12:10):
And though you know, we've got to say that correlation.
Speaker 2 (12:13):
Doesn't prove causation, but certainly evidence is starting to stack up.
Now what makes lithium oority it so exciting is that
it could overcome two major barriers that have limited lithium's
therapeutic potential, and that being the poor brain bioavailability ie
lithium's hard to be taken up by neurons and toxicity
(12:35):
at higher doses.
Speaker 1 (12:37):
Because the lithium.
Speaker 2 (12:38):
Orty it crosses the blood brain barrier more readily and
doesn't get trapped in amyloid, it could theoretically deliver the
same neuroprotective benefits at much lower, safer concentrations. And if
these findings translate to humans, we might finally have a
low dose, low toxicity way to restore natural levels of
(13:01):
lithium in the aging brain.
Speaker 1 (13:03):
Now is still early days, but all of this.
Speaker 2 (13:06):
Data provides a strong rationale for the first clinical trials
of lithium oritate in mild cognitive impoerment and early Alzheimer's disease,
and you can bet your bottom dollar they're already starting
to design these studies. Now, before you start googling lithium
oritate supplements, let's talk about safety and lithium in any
(13:28):
form is not something to just pop like vitamin C right.
Even tristosis can accumulate over time, and the margin between
therapeutic and toxic levels is pretty narrow. Lithium toxicity can
damage the kidneys, the thyroid, and in severe cases, the heart,
and we simply don't have enough long term safety data
(13:50):
on lithium ooritate in humans, particularly in older adults who
may already have reduced kidney function. So for ANWYE, this
is not a do it yourself experiment. Lithium should only
be used under medical supervision, with regular monitoring of seri
lithium levels, kidney function, and thyroid function. And it's also
(14:14):
worth noting that lithium is not recommended during pregnancy, as
it can cross the placenta and slightly increase the risk
of birth defects or pre term breaths. Now, despite all
of those caveats, and this study really does change how
we think about lithium. It reframes it as a nutrient
for brain resilience, something that the brain uses naturally to
(14:37):
keep key enzymes in signaling pathways and balance. And much
like ourn deficiency leads to anemia, a lithium deficiency might
accelerate neurodegeneration.
Speaker 1 (14:50):
And restoring lithium to its physiological.
Speaker 2 (14:53):
Range safely and in the right form could be one
piece of the Alzheimer's prevention puzzle, although we're not there yet,
so I'm not recommending that you go out and take
lithium or go out and buy it.
Speaker 1 (15:08):
Do I take it? Yes, I do.
Speaker 2 (15:11):
Because of this, I take lithium or TAD five milligrams
a couple of times a week. But I am not
suggesting that you do this, and I am certainly suggesting
that you talk to your doctor if you're even thinking
about taking any form of lithium at all. But this
certainly is a very, very exciting development, and I'm sure
(15:34):
that there are clinical trials right now being designed and
registered both to determine the safe and affected dose of it,
just like any drug has to go through that process
and then as interventions for people with Alzheimer's disease and
mild cognitive impowerment. But it is certainly a space that
(15:55):
is worth watching and that I think we will get
to those answers pretty dumb quickly.
Speaker 1 (16:02):
So that's it for this weeaks folks. Catch you next time.
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