Welcome to the VP Life Podcast, the show
where we bring you actionable health
advice from leading minds.
I'm your host, Rob.
My guest today is Joel Green, author of
The Immunity Code and the Way, and a
pioneer of immune-centric nutrition whose
work has completely reframed how many of
us think about metabolism,
aging, and the gut immune access.
Expect to learn why excess iron and the
Fenton reaction may be the hidden driver
of oxidative stress,
ferroptosis, and accelerated aging.
How lactoferrin, food-first strategies,
and the smart use of tools like IP6 and
phlebotomy can help control iron while
supporting gut and immune health.
And Joel's latest thinking on metabolism,
muscle gain, sugar diets, and how his
deep range fits into the bigger picture
of long-term health and performance.
Now, on to the
conversation with Joel Green.
Good morning, John.
Thank you for being here
and joining us on the podcast.
I know it's early there, so yeah, thank
you for being flexible.
Like I mentioned, or fair, this is a
conversation I've been pretty sacked out
for a while now, so yeah, like I said,
bit fanboyish, but what can I say?
So I suppose I first heard
about you, learned about you,
when a lot of people did back when you
first appeared on Ben Green's Perfels
podcast, or was that kind of circuit
2020, 2021, somewhere around there.
In any case, yeah, like I said, you
pretty much framed, reframed everything I
sort of understood about sort of biology,
and especially as it
pertains to nutrition.
And again, sort of, I spent five years in
textbooks, and then sort of took a long,
deep sort of soul searching, looked at
everything and thought, why?
Anyway, that's me, of course.
And I know that while there are many on
our audience who are likely familiar with
you and your story, there
are probably those who aren't.
So yeah, just your backstory, we have
plenty of time for the details.
Over to you.
Yeah, well, first of all,
thank you for having me.
It's a pleasure, and
looking forward to the condo.
Just kind of briefly, my backstory,
I just, my mother was, my mother was just
a failed competitive athlete, I think, in
the sense that she never really competed,
but she was hyper competitive.
And so she always encouraged us or me.
And so just from the time I was five, you
know, fitness was part of my life.
Growing up watching Jacqueline, and then
I was kind of my family's personal
trainer, like, you know, trying to get
him to do calisthenics at age seven, and
then get them to run around the block.
And I got into weightlifting about fourth
grade, where I just took apart a hammock.
And I just started kind of because my
brother used to beat me up all the time.
So I thought maybe if I could do this,
you know, I could, so I started just
doing curls, whatever I
could figure out with these bars.
And I actually started gaining a little
bit of muscle oddly, you
know, like in the fourth grade.
So and then I wanted to
be fast in the fifth grade.
And so I started going to the blacktop
during the summers and sprinting, because
I really wasn't very fast.
And the running craze kind of blew.
So this is way back.
This is like way back during the 70s.
So the running craze kind of bloomed, and
I got into running, and I could see that
my quads were coming out as a kid.
I didn't really
understand like what that was.
I just thought it was cool.
So I was always into it.
I was always tracking bodybuilding really
kind of just, I would just say you're
prototypical consumer, like if you could
just stamp like, you know, like sycophant
consumer, that was me.
And so I was lucky enough to go to high
school in San Jose, California, where at
that time during the, I guess it was the
mid 70s, late 70s, early 80s.
But a treasure trove of Olympic athletes
trained at this local junior college, you
had the gold medalist in the discus, Mack
Wilkins, you had Bruce Jenner, you had
you know, all these
Olympic athletes training there.
And there was a spillover to my high
school because my high school coach was
himself an Olympic level pole halter, who
was pretty renowned in the
area as the best vault coach.
And so all the Olympic athletes would
come over to train there.
So we had quite the quite the advanced
weight training program.
I mean, it was it wasn't bodybuilding.
It was it was Soviet style power, Soviet
style training, like like cleaning jerks,
and you know, stuff like that.
So and my big thing was, yeah,
yeah, exactly.
Yeah.
My big thing was I had a growth spurt
right about one of us right about age 12.
And I shot up to six
to by the time I was 12.
And I was 160 pounds.
So I was so skinny.
I was I was I was I was embarrassed to go
to school, like because I was so skinny.
So I always wear long sleeve shirts,
because I didn't want
anybody see how skinny I was.
And so I just started going to the gym
every night and just doing
what the power lifters were doing.
So I was just doing cleaning jerks, you
know, like, like nonstop.
And it just became part of my life.
So I became your
prototypical bodybuilding.
Sick of fan.
Yeah.
And I was just I would devour everything
and anything in the magazines.
And, you know, starting in the early 80s,
when Tom Platts exploded, and, you know,
just I just tracked everything.
And back then, the interesting thing was,
the way that information was
disseminated, you didn't have
influencers, which you
had was the magazines.
And then the magazines kind of promoted
who they wanted to be stars.
And so you had this
controlled information source.
And so you had this this thing of like,
you know, well, how do
I get to look like you?
What do I have to do?
I'll do whatever you do.
And of course, it was
all a giant deception.
It was, you know, the huge scam, because
all these guys were on steroids.
And they just lied their butts off about
it, like literally everybody.
And so the thing was like, you could
never actually look like that.
Okay, you might get close, you might look
pretty good if you're genetically gifted,
but you're never gonna be like that,
because they're there, they've got a
secret you don't have.
So I went down that track as a consumer.
And because I was so voracious as a
reader, whatever came
out, I would jump on.
So like, I remember, I think it was 86,
there was a supplement that
came out called hot stuff.
And the marketing was
very different back then.
Like back then, the marketing was they'd
write an entire page, and
you would read the whole page.
You would go long from copy.
Yeah.
And just get sucked into it, you know,
and so out came this supplement with
boron and, you know, wild game and you
know, all of these things that a lot of
them actually worked like yo and vine.
And stuff.
And I just started whatever came out, I
would just use so that led into that led
into MCTs kind of in the late 80s, when I
was in college at UCI.
And then in the early 90s, the big big
thing for me was the
meal replacement craze.
So metrics came out.
And I didn't,
I wasn't that was the the original sort
of meal replacement in the same space,
wasn't it just about
well, it was it was the first
that really thought about it.
So that so prior to that, what it did was
it changed the category.
So prior to metrics, they were called
metabolic optimizers.
And the leader was champion nutrition,
and other guys that were
sticking MCTs in theirs.
And then Dr.
Scott Conley came out.
And he really thought his thing through
and he really knew
what he was talking about.
So his big thing was he stuck in
glutamine and lactoferrin in metrics.
And that was light years and I had a few
conversations with him actually, because
he owned a gym right where I lived.
And so and he would work the front desk,
like an MD working
the front desk at a gym.
So I just I would go in and after
training, just kind of ask
him like, Hey, does this work?
And he would just he would go down the
bio babble role, and I would just kind of
sit there kind of glazed over like maybe
picking up every hundredth
word he was talking about.
But so that led me down this road of a
lifetime of doing that stuff.
Which is ironic, because today where I
sit is I you know, I go to the gym once
or twice a week, I do that
stuff once or twice a week.
But it's not the main thing I do.
And it's certainly not the thing that I
think keeps you young.
I think it does the reverse, I think it
destroys the body over time.
But the irony of that was that now that's
where all the doctors are.
So they've all adopted meat headology.
They've all adopted the the
the pattern of of, you know,
they call they don't call it 70s
bodybuilding, they
call it strength training.
Oh, no, you got to do strength training.
Yeah, it's a Gabriel lines of the world
that sort of approach.
Yeah, when you break down what they're
talking about what to do, well, what is
it I should be doing?
Well, strength
training, what's that look like?
Oh, well, see, here's a lat row.
Oh, the thing we were doing in the 70s.
Yeah.
Okay, here's a behind the neck press.
Yeah, yeah, that one too.
What else?
What else you got a T bar row?
Yeah, yeah, that was in the 70s too.
So bodybuilding.
So the answer is bodybuilding.
No, no, it's not because I
tell you, I've been there.
It's not.
So about 2006, I kind of culminated for
me, I was, I was running a company, we
had our revenue had just shot up to like
25 million in just
two years from nothing.
And it's not bad.
Yeah.
And, and like a lot of entrepreneurs, I
was working crazy hours of crazy stress.
And for me, the kind of hands on
discovery was that that stuff only works
when you're in the fitness bubble.
Yeah, if you get out of that bubble, and
it doesn't work that great.
And I just I got really well, the
interesting thing is, um, I was training.
So I was huge.
I mean, I was, I was just big, I was
about 260 pounds, I was fat.
So I was both hugely
muscular and fat at the same time.
Super strong muscles, like but fat.
And so I kind of came out of that,
rethinking things and that led to where
I'm at today, basically.
Thank you for that.
That was, that was an amazing story and
one I've heard before.
And yeah, just speaks volumes to what
you've been able to sort of develop over
the years consequently, because I know
you've fundamentally just worked all of
this out, sort of on the back end of
different life
experiences that you've had.
And I know you've obviously talked about
this a lot on various podcasts, including
Mark Bell's one, I believe, when you
originally, I think was a Daisy Carter
protocol that you originally did, and
then you sort of got down to what was it,
single digital body fat, and he was
completely sort of just in disbelief of
this fact at the time.
Is that more or less correct?
Yeah.
So basically it was, it was 2007.
I had been, I had been at it for about a
year, just whittling down all the fat I'd
gained during that period, working.
And I was about 229 and pretty, pretty
muscular, you know, but,
but still kind of not peeled.
And then I did the, I
did the Daisy Carter.
And that was probably for me, the single
most shocking body fat thing in my entire
life ever still to this day, because I
went from 229 to 212 in seven days.
And then I went into a local place that
measures your body fat in water.
And it was, it was either between six and
seven, it was pretty low.
And that was, that was after, that was
after pigging out, like for several days
coming off the day because the Daisy
Carter will make you insane.
So coming off that I was just eating
pizza or whatever I get.
So I'm sure I was probably lower.
And then there was just a, I was in a
tech stream with Mark Bell and quest
owner Ron Pena and Carl Carlin or and
Mark, I was telling about that and Mark's
like, I don't believe you prove it.
So I just, I just sent him the, the PDF,
I called the place up and said, Hey, I,
you know, can you give me the PDF?
And they sent it to me
and I just sent it to Mark.
And so fair.
Anyway, perfect.
Okay.
So what I really want to do
today is to dig into iron.
I know that people are always
interested in the sugar diet.
And to be honest, that excites me about
as much as watching paint dry.
We'll keep the, we'll, we'll
aim to keep the people happy.
And maybe we can chat
about that a little later on.
To start with, I think it would be, maybe
it would be best if we just step back a
little to discuss the
immune system as a whole.
I know that's fundamentally the lens
through which you sort of view metabolism
and health in general, and just to
provide some context, maybe
the rest of the conversation.
Now, obviously, I started off with with
the immunity code, your first book, which
for anyone who's not read
it is, is absolute gold.
So yeah, get a copy.
Now, of course, I know from here, we
could go into 30 different directions,
all of which are fundamentally going to
be come back to the fact that by
regulating the immune system of the gut,
you can make a dent in a lot of health
conditions and challenges.
So yeah, I'll ask the lazy question,
which is, what problems were you trying
to solve with the immunity code, and
subsequently, your follow up the way?
The primary problem is really the problem
everybody runs into, which is, there's a
force pushing against you over time.
Loosely, we could describe that as aging.
But the big picture of that is that it
has multiple pathways for dysregulation.
So, you know, one is that body fat is
going up, senescent cells are going up,
inflammation is going up,
mitochondrial density is going down,
muscle is going down, body fat
characteristics are shifting into a
pro-inflammatory pattern, all kinds of
all kinds of things are
happening all at once.
And everybody faces these problems
collectively, they haven't really been
well defined as a group to say, okay,
well, let's make a list and let's start
with number one and go down the list.
Let's do that.
And even if they were made into a list,
the problem you're still going
to have is the issue of time.
The average person, so the big secret in
the fitness bubble is
just two hours a day.
I mean, no one's ever
going to tell you that.
But that is the C, if you were to follow
anybody around, you're going to see
they're putting into it.
That's like two hours a day.
That's like, who has that?
Who has two hours a day?
Yeah.
So that's the problem.
The problem is you've got
this problem of decline.
And then the only solution that you've
been given to solve it is, oh, that's no
problem, just increase time.
Just increase time, that'll solve it.
That doesn't work for most people.
So for me, the issue really was just
coming down to economy and looking at,
well, if we only had a couple of minutes
a day, what would be the most important
things that we could hit
in a couple of minutes?
What would be the 80-20?
It wouldn't be doing barbell curls.
That wouldn't really be the thing.
What would it be?
And when you begin to go down that road,
where you're going to wind up at is the
intersection between the immune system
and several different organ sets and
systems in the body.
One way or another,
you're going to run into that.
So fundamentally,
let's start with oxygen.
Just getting oxygen into the body.
What's happening with most people with
age is that the
airway begins to collapse.
The tissue at the back of the throat
begins to push into
the back of the throat.
So you're getting apnea
events during sleeping.
You're getting desats during sleeping.
You're getting stabilized
hypoxia as a result of that.
And that alone will sink the whole ship.
That alone will kill you.
Just that.
Hypronorpha levels, right?
Yeah.
That alone will sink the entire ship.
We don't even need to look any farther
than that if you were going to just start
with, well, what's number one?
That's number one,
really, if you think about it.
And that converges on a key mechanism
that essentially is a switch, helping the
body flip its metabolic state between
oxidative respiration
and then glycolysis.
When you look at that, and
that master switch is HIF-1,
hypoxia-inducible factor one, it
regulates not just the general switching
between metabolic states, but
tissue-specific and cell-specific.
And when you get cell-specific, it gets
very, very interesting and compelling.
So when you begin to look at the effect
of that on immune cells, it can be
massively beneficial or
catastrophically disastrous.
It just depends on the tissue and what.
But in terms of our coming back out of
the deep dive into what's our simple fix,
it's let's fix that first.
Why don't we fix that?
And that converges on the immune system.
And so that whole line of thinking, that
way of thinking led me down this road.
Okay.
Fair enough.
And then just specifically, what about it
is, I suppose, just to maybe elaborate
that a bit more for the audience, how
does the immune system then regulate and
govern the subsequent inflammatory
responses in the body that then drive so
much of this dysfunction at a level?
So it's a big question.
One of the key functions of the immune
system is to sort of allocate when to use
what we would call weapons.
Okay.
One of the weapons the immune system has
is to induce an inflammatory state.
Now that can be massively beneficial in
the case of an infection, because you
want to kill the infection.
So the immune system can ramp up and it
can produce free radicals and shoot
superoxide through immune cells and
pathogens and invaders.
And that's a good thing.
That's not such a good thing when you
have billions of cells that have
stabilized into a senescent state and are
essentially trafficking out signals to
recruit the immune system.
That's not such a good thing at all.
Because then what happens is the immune
system sort of acts like an echo chamber.
And it propagates these signals across
the entire body and recruits more and
more and more resources into dealing with
this problem that it thinks is an injury,
but it really it's just getting old.
So what it is, would that be a case where
maybe somewhere like excess fasting could
actually be an issue,
an actual detriment?
Yes.
Yes, because this gets to the
body needs to balance itself.
It needs a balance between growth
pathways and degradation pathways or
however you want to put it, you know, the
body's autophagic pathways.
There needs to be a
balance between the two.
And when you see an excess of either one,
you're going to see some kind of
pathology either way.
So if you see too much growth, you're
probably going to see cancer.
If you see too much, too
much autophagy, too much
action with respect to protein
degradation, then
you're going to see issues.
So
that's just homeostasis.
So that's an interesting thing.
I don't want to spend
too much time on this.
But homeostasis is such a simple concept.
It's so simple to get this.
It's just simply
balance.
Like the thing needs to be balanced.
You can't be too much on either side.
Okay.
That's so simple.
And you wouldn't know it, listening to
the world of influencers nowadays,
because it's all polarized thinking.
It's all, "Oh yeah, fasting's only good.
Meat is only good.
Saturated fats is only good.
Carbs are only bad."
You know, there's this polarity of
thought that to me reflects a bigger
problem, a problem of thought.
But the fact that such a simple concept
is missing from the picture and it's
essential just blows my mind.
Yeah, I know it is interesting that you
mentioned that actually.
I mean, there are sort of, and I'll just
use it in the literal sense, sort of very
left and far and right leaning
individuals just sort of on
the vegan and the carnival side.
And it's interesting just watching your
poor saladinas and such over the world
with these sort of extreme views.
And what I've just found over the years
is that a lot of these people with these
extreme views on nutrition generally tend
to fall back to the middle, whether it's
reintroducing honey or carbohydrates, or
what have you, or reintroducing meat.
So many, yeah, just to sort of maybe sort
of build on your point.
Balance is key and it's just interesting
to note that people with sort of extreme
views ultimately do come back to sort of
this fairly centered state.
And Joel, I'd like to sort of maybe take
a little bit more into that, into the gut
side of it quickly before we carry on.
Now, I know obviously sort of the gut
being sort of the hub of the immune
system to an extent anyway.
A lot of your work sort of that you've
put out there revolves heavily around
sort of rebuilding the gut and that you
aren't generally speaking a fan of
prebiotics and that you would,
probiotics, excuse me, that you generally
sort of prefer prebiotics as a whole.
Obviously, again, within the industry and
there's always been a
push for probiotics.
And I'm in two months about that.
I deeply admire the work of Dr.
Mark Ruschow, who you might know of, and
he is a very sort of probiotic
forward-facing and he's very adamant that
they are effective at helping
to modulate the immune system.
I know at least having listened to other
podcasts you've done that you share,
maybe someone to have a
different take on that.
Could you sort of just guard us through
your thoughts on probiotics versus
prebiotics in general as it pertains to
the gut and maybe the
immune system more broadly?
Well, the merger point
in the road is bacteria.
That's all we're talking about is taxa
and representation of species.
That's what we're talking about.
The question is, how do we get there?
That's the only thing
we're talking about.
So to say that probiotics work is to say
that certain taxa can
exert beneficial effects.
Duh.
I mean, we all know that.
Everybody knows that, right?
So it's just how do we get there?
What's the optimal way to get there?
Keeping in mind not the
short term, but the long term.
And that's a problem.
That's a big problem though, because
we're in an industry
that equates results to...
We're in an industry that has no regard
for the impact of the most important
variable, which is time.
It doesn't exist.
Time does not exist.
You listen to the most high level
influencers and they'll talk as if the
outcome we get now is going to be the
outcome we're always going
to get because we got it now.
And again, that's going back to this
paucity or poverty of
thinking that is just...
It's similar to homeostasis.
When you begin to inventory, why aren't
you taking this into account?
There's no good reason.
Only stupidity.
So the issue becomes,
okay, so there seems to be sort of a
youthful profile that more or less seems
to be consistent among young people.
And you see a lot of Bifidobacteria,
healthy representations
kind of in this respect.
And it's quantifiable to some degree.
So the question is, how
can we proximate that?
How can we get there?
I'm not against probiotics at all.
I think that they can
be incredibly helpful.
I'm just against their indiscriminate
use, particularly among consumers,
because as soon as you tell consumers,
hey, our clinical results showed an
improvement of blah, blah, blah, blah,
blah, taking our probiotic.
First, they're probiotic.
Yeah.
Well, then they become chiclets.
They become like M&Ms
or just gummies.
They become like just candy.
And the net result of that, once we
insert the variable of time, is that
you're probably going to do more harm
than good long-term.
A lot of SIBO problems now are the result
of a lot of probiotic usage going back.
And so the question becomes, what's the
optimal way to get what we want?
And the really
surprising thing is how powerful food is,
to completely, completely retune the gut
in very short periods.
And this is empirical in its nature.
Going back to 2009, there are studies
that show that you can rapidly recolonize
the gut in just a few days with food.
So with that in mind,
as a generality, if food is so powerful,
where do we need probiotics?
And that becomes a
medical issue then, I think.
And I do believe the rightful home of
probiotic strain usage is probably with
practitioners who can look at something,
look at a GI map and say, "It seems like
maybe if we added this
strain for a few weeks."
Now that, to me, is really intelligent.
That's really smart.
And I think that's kind
of the right way to do it.
It's just really a question of what's
going to do more harm than good.
And it's probably the
indiscriminate use of probiotics.
Fair enough.
Just speaking of those tests quickly,
there are a bunch of them
out there, various labs.
Well, as you
mentioned, there's the GI map.
There are a bunch of them.
What do you think about their validity
and their specificity?
Again, now that we're just on this track,
I'd just love to get
your thoughts on this.
You often hear practitioners on podcasts
talk about the fact that they sent off
two samples of the same piece of stool to
the same company, and they would have got
back completely different results on
their GI map or their whatever.
I mean, the gut is your
game, let's be honest.
Do you have any thoughts
on GI testing in general?
Do you think it's there yet?
Or is it still a bit of a north star
we're trying to get to?
I think it could be useful.
I think the mistake is to see it as
the gospel.
I think it's a mistake to
calcify it into like, "Oh, ha!
Well, this is me.
That's it.
Nothing more to know."
What I never hear are seldom, very
seldom, what you'll hear is a breakdown
of mechanistically,
"How'd you get that answer?"
When you begin to ask,
you'll get crickets because
I've found a lot of
practitioners don't know.
They actually don't know
how they wrote that answer.
When you begin to break that down, what
you find is that many of
those tests rely on a single gene.
They're looking for one gene, the 16RS
ribosomal RNA, and they have a database
that they're matching
that gene up against.
The outcome you're getting is only as
good as your database.
Then there are several
problems within that.
We could list what those problems are,
but just suffice to say that a good
example is acromancia.
I think in the last couple years, there
have been several new
strains discovered of acromancia.
One of the most common things that I hear
is, "Oh, I did a GI map
test and I have no acromancia."
My response to that
usually is, "Yeah, you do.
They just can't test for it."
"No, how do you know that?"
"Because you'd be dead,
probably, if you didn't."
Yeah, it's more than just
meanest failure in existence.
The truth is there's probably dozens of
strains we haven't yet found.
To get a GI map test back, and it says,
"Oh my gosh, I have no acromancia.
I better go start taking
pendulum or some tool like that."
Well, again, it's like,
"Mm, yeah, you probably do."
It's just the tests
don't have that in there.
They don't have these undiscovered
strains in the database.
That's the answer.
Fair enough.
I often think that this is a sort of
wildlife-ure approach.
It reduces it to the bare basics and then
just sort of builds upon that instead of
trying to sort of isolate variables that
we don't have access to.
I really like the way you frame and
conceptualize things.
To be honest, I'm not very bright.
I doubt that.
I seriously doubt that.
I tend to just look towards using
frameworks to try and understand complex
topics and data sets.
Then, yeah, maybe it's just a result of
looking at information from that point of
view, but I always end up trying to find
flaws in a given model, a
stress test the best I can.
Well, to me, I can then form an opinion.
I can then try and find
limitations based on that
opinion relative to that model.
I can then sort of make cross-reference
things and try and come to some sort of
logical conclusion,
whether it's correct or not.
I know that's a fairly convoluted, but
it's kind of served me well.
Of course, it doesn't mean I'm right.
It's just the way I think through things.
I'd love to sort of explore the way you
think through things and whether you
think there are any sort of limitations
to the model that you've put forward when
it comes to helping people work through
various health challenges.
I'm sorry, that was probably 10 questions
in one and very convoluted, but I'm sure
you follow the logic.
Yeah, no, I like it.
I like it.
I kind of approach things
from a macro perspective in that
there's a bit of a dichotomy with respect
to how do we get the answer?
People always want to
know, what's the answer?
What's the answer?
We're led to think that the
individualized factors just are the
answer, that they're so overpowering that
the only way that I can know me is I got
to go do all these tests that tell me me.
Just in my experience, what I have found
is it's the generalities
where all the horsepower is.
If you take five massive generalities,
like let's take vitamin D levels, let's
take hypoxia, let's take the microbiome,
and you see where I'm going with this.
You can just kind of go down this road of
things that are just generalities.
Then you take someone who their metabolic
state is and optimal
isn't what they want it to be.
We just apply the
generalities to them consistently.
What you will see are these massive
game-changing improvements
that are life-changing.
That's not getting to the level of like,
"Well, I see you're
missing a genetic snip for it."
It's not getting to that level.
It's just taking the generalities.
So I generally tend to approach things
like, "Let's fix the low-hanging fruit.
Let's go after that and
then see where we're at."
Then usually with what's
left, that's called medicine.
Usually with what's left, now we're
talking about things that don't fit the
generalities, things that require very
types of specific tests.
That's really for doctors to do.
I think that's great.
I think that's where it should be.
But all that to say, it's that what we're
missing here is that in the simple
things, the big things, the generalities,
there's so much horsepower, so much power
for change that you should really,
collectively, it makes sense to take a
look at those things first
and then see where we're at.
That's just how I approach things.
The other piece of the
equation for me is math.
I've just found historically that
everything boils down to math.
Everything boils down to
the law of large numbers.
Everything boils down to
percentages and probabilities.
That lends me to think in a couple
different directions.
One is that it's very difficult to know
anything with certainty.
It's just very difficult to know it, but
the mind loves certainty.
The mind loves,
"Ah, yes, this is it."
You really see that in the social media
sphere where you have influencers that
speak with salesman-like certainty on
topics they don't actually understand.
Then a few years down the road,
completely revise their stance.
That's called a learning curve.
What would serve them and everybody else
better is to just begin to introduce some
maybes in there and some mightbees and
possibilities rather than
speaking with abject certainty.
We're always up against degrees of
probabilities, probabilistic space.
We can begin to say things like, "Well,
we're creating very strong probabilities
that we might get the
outcome that we want."
I'm just really just cloaking math talk
by talking like that, but
that's how I approach things.
Okay, perfect.
Thank you very much.
I just had to ask.
I love the way you build on
the data that you've always gotten.
It's just so elegant the way you are able
to frame and construct relationships.
A bit of a selfish question, but anyway.
I recently had the chance to chat to Dr.
Thomas Seafreet.
I'm sure you're familiar with, and for
those in the audience who aren't or maybe
haven't listened to that podcast, he's
currently championing the idea that
cancer is fundamentally a metabolic and
mitochondrial disease.
That's by regulating glucose metabolism
in some way, shape, or form, you can
essentially starve cancer cells
selectively and reduce the need to some
extent for additional or
adunctive cancer therapies.
Obviously, his work is based in the
backbone of what Otto Warburg did, I
think probably around a century ago now.
In any case, he's obviously a big
proponent of
carbohydrate reduction in general.
Unfortunately, we ran out of time.
I wasn't really able to ask him about his
thoughts on how different types of fatty
acids, polyunsaturated fatty acids,
saturated fats, et
cetera, might affect his model.
I'm not a cancer biologist.
I'm strictly the imagination, but when
you look at his glucose ketone index,
which I know he's now making more
publicly available for people to
understand their own metabolic health,
it's very much
focused on the macro level.
It doesn't seem to really
focus on the fatty acids.
I know this goes into the order of
operations side of it as well.
But what do you generally think about
when you start talking about fatty acids
in particular and the
immune system in the gut?
What do you think about
this approach in general about
removing one macronutrient, be it
carbohydrates, to
improve the health of a system?
And then, yeah, if you've got any
thoughts on maybe how we overly rely on,
I suppose that's the C to all debate.
Let's leave that if you, yeah, the first
part would be great.
Again,
the variable that's missing
in my opinion would be time.
So you could inject that question in
under the eugis of the variable of time
and say, "Hey, what about for a little
bit of time if we
restrict this macronutrient?"
We might see some very significant
improvements depending on
what we're talking about.
However, when you begin to look at the
long term, which is what
we always have to look at,
there are a couple of magnetars that are
always pulling at us.
Okay, one of them is insulin.
And it's very difficult to obtain real
and lasting health without insulin
functioning optimally.
Really, you're not going to.
That's just the answer,
unless insulin's functioning.
Because it's so pleiotropic in its
nature, it affects so many things.
So the problem you get into with that is
that in order to properly stimulate
insulin, there's an inventory or a suite
of hormones that need regular stimulation
through foods, through macronutrients.
And they oppose each other.
So I've spoken quite a bit about the
example of glucagon
because it's kind of in our face.
But it's a fun one to pick on because
glucagon has been the
hero of a low carb movement.
And if you go down that road far enough,
what you'll see is that actually by
overstimulating that, and by not
stimulating other hormones, particularly
insulin now to connect in through key
types of carbohydrates, you
actually get insulin resistance.
And then the result of
that is hyperinsulinemia.
So sort of briefly in the muscles, one
might argue though, that the macular
glucose bearing effect,
what would you say to that, that long
term ketosis drives this peripheral
insulin resistance, but it's typically
just within the muscle.
Yeah, I would say that probably doesn't
hold up to scrutiny for
some very good reasons.
One is that
in order...
So I did a debate with
Sean Baker that never aired.
And I really...
I was going to ask about that.
Yeah.
I really crushed this particular aspect
of it, which was to look at like, is
long-term ketosis really even something
we'd want to consider?
And I don't know how deep you want to go
down this road because it's quite
complex, but I would offer no for lots of
reasons that nobody's talking about, but
just to kind of sum it up.
So long-term ketosis, we're going to need
a fuel source for that,
which is oxaloacetate.
So you're going to need
that for a subtle CoA.
Normally your source for oxaloacetate is
glycolysis, but what's going to happen is
that when you're doing oxaloacetate for
extended periods, you got to switch to
the liver to produce it for you.
Okay.
Well, the issue that you get into there
then is you get a mismatch between the
TCA cycle and fatty acid oxidation.
So you begin to get kind of an incomplete
oxidation that happens.
And then that incomplete oxidation will
lead to a spillover of very specific
types of acyl carnitines into the serum.
And some of these moieties or very
distinctive types of acyl carnitines are
going to drive
systemic insulin resistance.
And it's all a result of basically you're
creating this backlog within the
mitochondrial membrane of transporter
mechanisms that aren't, and then that
spills over into the serum.
Yeah.
And so, and it really gets to
is the liver equipped to supply a
glycolysis to the entire body on an
extended basis, you know,
to every cell in the body.
And I think we can make a pretty good
case that it's not that, that, you know,
you begin to see over time, these
disparities between fuel sources and
things that are
required to sustain this state.
And then you begin to
see a buildup of things.
So again, the missing variables time, if
we will just insert time as the master
framework and then begin to accept the
notion that this is a dynamic
system, not a static system.
And that is the massive logic error in a
lot of these arguments is that the
assumption is we're
dealing with a static system.
It isn't.
What it is, is it's a system that seeks a
dynamic equilibrium.
That's what we're talking about here.
And so in a system that
seeks a dynamic equilibrium,
you can get in my book, the way I talk
about this, I call it the forces of time.
It's accumulation.
You can get an accumulation of something.
You can get a degradation of something.
You can get a compensation of something.
You can get attenuation of something.
So all of these forces
of time begin to play out.
And in the case of oxaloacetate,
acylcarnitines, and, you know, all of
these sort of intermediates required to
sustain ketosis over time, you begin to
see a buildup of certain things that you
can make a very good case will drive
systemic insulin resistance.
And in some cases,
perhaps it's not recoverable.
Okay, I'm going to relisten to that,
especially that last part.
Thank you for that.
That's definitely a sort of solidified a
few thoughts in my head.
Joe, I'd love to talk
about metabolism all day.
I really would.
And maybe I can convince you to join me
for another episode at some point.
A bit deeper into that.
But I think just of the sake of brevity
and time, I'd love to
sort of jump into iron.
Young Gut Ultra, I know that's a new
product you've launched.
It's exciting.
And it looks to solve the problem of sort
of excess iron brought up in the body.
Now I know there's a
lot to dig into here.
And maybe we can start with why excess
iron is an issue, maybe from the
perspective of the Fenton reaction, maybe
it's a sort of a decent
sort of lens to view it from.
But yeah, why did you sort of choose to
focus on iron as an issue with developing
that product, I suppose?
Yeah, it wasn't really so much out of a
need to deal with iron.
It's more out of a need to deal with very
specific problems that are intractable
for everyone over time.
One of those problems has to do with the
impairment and degradation of the
peroxisome membrane within the
intracellular space.
So if you're in the audience and you're
not familiar, peroxisomes are an energy
organelle within the cell.
And they're kind of
co-partners with the mitochondria.
There's this notion that the mitochondria
kind of exist at the top of the hill, you
know, by themselves.
And it doesn't really
hold up to scrutiny.
It's more like a co-emperor sort of
situation at the top of the hill where
the peroxisomes of the mitochondria form
a single system and they very much peddle
the bicycle together.
So the issue you get into with age is
that there are these transporter proteins
in the mitochondrial
membrane called PEX proteins.
And they begin to malfunction.
And so part of the function of the of the
peroxisomes apart from energy production
is to basically dismutate hydrogen
peroxide down into water.
The hydrogen peroxide by itself can be an
extremely important signal molecule as a
free radical within the cell.
It's very much
involved in insulin signaling.
The problem is that if you get too much
of it, it really kind of becomes maybe
just by again by virtue of math, by
virtue of sheer weight and sheer numbers,
possibly the most detrimental free
radical in the body.
Now on an individual basis, it's not
nearly as damaging as something like the
hydroxyl radical or superoxide when
superoxide goes wonky.
But because there's so much
of it, it's really a problem.
And so what happens with age is that you
get a buildup of hydrogen peroxide in the
cell and at the same time we tend to
build up iron with age.
That's bad.
That's very bad because hydrogen peroxide
can mediate through iron a reaction
called the Fenton reaction that produces
a very damaging free radical
called the hydroxyl radical.
And you get a lot of you get a lot of
cell damage from this.
You could make the whole argument that
that's where your
gray hair is coming from.
Is that it tends to torch the
polyunsaturated fats
in the cell membrane?
Is that right?
Yes.
In addition to, well, in particular,
the mitochondrial membrane
takes a lot of damage from that.
So that's a huge problem that needs,
we're all going to face.
And like, let me just make it simple.
Everybody wants to
fix for their gray hair.
What's the fix?
We got to fix this problem because it
isn't just your gray
hair that it's affecting.
Your gray hair is just a marker for how
fast the damage is progressing.
So that's a big problem.
And that was the motivation behind it.
The other thing was that when I first
really laid into this focus of how can we
modulate a few switches in the immune
system to get massive results?
One of the key variables in that is
lactoferrin because lactoferrin, I guess
the best way to describe it is that it's
kind of like the glue
of the immune system.
It sort of holds the whole thing together
and it acts as an intelligent
intermediary with the immune system.
So it sort of acts as the
glue that drives homeostasis.
And in my first iteration of this back in
the 20 teens, there
wasn't really a way to do it.
We didn't really have
human lactoferrin back then.
And so it's going to be my next question.
Yeah.
So the focus was, go ahead.
No, I was just going to say the
difference there being the difference
between human lactoferrin and then
obviously bovine and
other forms of lactoferrin.
Why is lactoferrin coming from bovine
sources or other sources?
Maybe such an immunological issue.
Why is it sort of less preferential than
finding the, I think it's Iphira, is that
the brand of human lactoferrin?
But yeah.
Yeah.
So bovine and human
lactoferrin are very similar.
It depends on who you're reading.
They're somewhere
between 68 to 77% identical.
So that's not bad.
That's pretty good.
The difference is binding sites.
So bovine and
lactoferrin has five binding sites.
Human has three.
But the issue you get into really becomes
one that it's a foreign protein.
So lactoferrin is a glycoprotein.
And you run a bit of a risk for an immune
reaction like the body would
have to any foreign protein.
So where lactoferrin, generally speaking,
human lactoferrin is meant to be the
master regulator of the immune system,
bovine lactoferrin can
actually trigger the immune system.
Now, I want to be fair, that's not true.
Probably in a majority of cases.
Yeah.
Like bovine lactoferrin
can be highly beneficial.
So I don't want to sit here and just go,
"Eh, mine's the only stuff that works."
But no, bovine lactoferrin can
be highly, highly beneficial.
In fact, it's one of the reasons why
dairy is really so beneficial in the long
term for so many reasons.
That just triggered off
a firestorm right there.
But we'll let that go.
I can hear all the anti-dairy
crowd just going, "Ah, click."
But all that to say that
there's a thing called glycosylation.
So I'm trying to tailor
this to the audience here.
I don't want to...
Yeah, we've been pretty deep here.
So let's just go there.
So much of the information and
communication in the body happens based
on what are called PTMs or
post-translational modifications, which
are things that happen after
transcription, after making proteins.
They're modifications to the proteins.
One of those modifications is adding
sugars to those
proteins to form glycoproteins.
And then those sugars, depending on their
structure, essentially act as a second
messenger system or a
communication system.
So the specific structure of those sugars
carries information.
And so lactoferrin...
Go ahead.
Sorry, would that include ATEs as well?
Just out of interest?
Yeah, all glycosylation related
activities are information carriers.
So in my first book, this was actually
going to be a chapter and I gave up
because there was no way to do it.
It was a book talking about PTMs.
It's just way too much.
Suffice to say that apart from DNA,
there's a whole information-bearing
system in the body based on the structure
of sugar proteins, glycoproteins.
So anyways, all that to say that
bovine lactoferrin and human lactoferrin
share a lot with respect to
glycosylation, but
there's also some differences.
And those differences translate into very
practical things like
how absorbable is this.
And the human lactoferrin just is always
going to be more absorbable
than the bovine lactoferrin.
You're going to need more of the bovine
to get the same results.
In fact, so in milk,
the best estimate so far is that there is
1.5 to 2 milligrams per gram of bovine
lactoferrin in milk.
So at a kilogram level, roughly 150 to
200 milligrams of bovine lactoferrin, but
then the absorption is not the same.
So in other words, like in my young gut
ultra product, there's 200
milligrams of human lactoferrin.
To get that same dose in bovine
lactoferrin, you'd need
a kilogram and a half.
That's a lot.
Yeah.
So that's a lot.
Yeah.
And then I'm sorry, I jumped some
completely sidetracked here, but then how
is lactoferrin, I suppose, sort of
solving broadly
speaking, the ion problem?
So lactoferrin, the interesting thing
about lactoferrin is that
it drives iron homeostasis.
So if you have too little iron or too
much iron, it tends to push the pendulum
back towards the middle.
So lactoferrin, it's a member of the
transferrin family, which
are iron binding proteins.
The thing about lactoferrin is its iron
binding capacity is so astoundingly high.
It's hundreds of times
higher than your ferritin.
And so lactoferrin,
it's like a sponge.
It has this amazing
ability to soak up iron.
Kind of a simple way to put it.
Fair enough.
That's perfect.
And then, yeah, I suppose there are other
few competing molecules out there on the
market, things like IP6 phosphate, or I
suppose the main mechanism is probably
phyto-gasol to some extent
binding up iron in the gut.
And then obviously, you can go down the
copper route to which I know Morley
Robbins has done a pretty deep dive on.
I mean, I think he's based the latter
part of his career around that.
And the idea that by regulating coppin,
ceruloplasma, you can sort of convert
excess ferrous iron, let me get this
right, I think, to ferric iron.
And then that can then be transported,
combined to transferrin and then get
yanked out of the bloodstream.
What do you think about that as an often
not a competing product or competing
theory, but as an odd competing mechanism
to sort of regulate iron, the idea of
just sort of increasing copper intake?
Well,
first of all, I don't want to do a
disservice to his work.
Just anecdotally, what I've heard is that
he's had some very good outcomes.
And I'm not 100% expert in his work, so I
don't want to misspeak.
As I understand it, which I will say up
front has room for error.
So please correct me if I'm wrong.
So a significant portion of the actual
protocol involves dietary modifications.
And when I look at those dietary
modifications, what the net, which I
haven't heard anybody talk about, that
they're going to do is you're going to
produce a shift in the gut taxa that
favors bacteria with
iron binding cytoform.
So what you're going to get is this
variable that doesn't get
talked about a lot, which is that,
and this gets to the phytic acid thing.
As you increase certain taxa in the gut,
like the phyto bacteria,
they bind iron in the gut.
And then in terms of your IP6 problem,
that actually prevents that
from binding iron in the gut.
So shifting the gut taxa can have this
tremendous impact with respect to a
number of variables that we could kind of
anecdotally attribute to
quote unquote the protocol.
But it's really possibly to some extent
has to do with just
simply shifting the gut taxa.
That's kind of the theory I'd offer on
that with respect to copper.
The thing is,
lactoferrin can also bind copper.
And I would just offer that the master
regulator of iron naturally
in the body is lactoferrin.
So if I were to approach the problem, I
would kind of start with what exists
naturally, which is not to say that maybe
he's not having fantastic results too.
So I don't claim to have the market
cornered on solving the lactoferrin iron
problem or the iron problem.
So that's what I would say.
Yeah, that's perfect.
And of course, no disrespect to Molly,
though, I'm actually getting more on the
podcast in a few weeks.
So I'm just always interested in speaking
to individuals obviously with opposing
but similar sort of understandings of the
problem, just looking from a different
lens and just trying to
get a broader picture of it.
I mean, ultimately, all rosary trim.
And I suppose one could also just stick a
needle in the ROM and just do some sort
of venus section as well.
I'm sure that is
effective as well as anything.
But yeah,
Joel, you'd be amazing.
And I just want to be
respectful of your time.
But I've got a few rapid-ish fire
questions that I'd love to
go through if that's okay.
Perfect.
Okay.
To keep the sugar diet crowd happy.
I know you've covered this
on your Instagram recently.
And seemingly, it has more to do with I
suppose, one of my other protein
restriction, although as we chatted about
earlier, if you sort of remove a
macronutrient entirely, you're going to
get a massive sort of swing in
metabolism generally speaking.
And I know that there's obviously an
issue there with high fat diets sort of
triggering an increase in FGF21
hepatically, which is why maybe that's
not the best way to
sort of protein respect.
But just overall, I suppose, what's your
take on the sugar diet?
And do you think it's efficacious?
I know time will be available, but yeah.
So first question,
can quote unquote the sugar diet work to
help you lose body fat?
Answers, yes, absolutely.
Yeah.
Is there anything new there?
No, nothing.
That's been known for decades that just
take any macronutrient to
zero and you can see fat loss.
Mechanistically,
personally, I don't think any of the
reasons apart from protein restriction
are what's going on.
The two big reasons
nobody's really talked about.
Number one is glycolysis.
So again, this gets to kind of my
worldview, which is math
always drives the equation.
In a carbohydrate restricted state, you
have less substrate
available for glycolysis.
And so you're going to have less
glycolysis in general.
When you reintroduce substrate into the
equation, remember, we're talking about
trillions of cells here.
Every one of them can run glycolysis.
So when you have more substrate
available, you're going
to increase glycolysis.
Glycolysis will shred you up.
That's why sprinting works.
That's why high altitude training or high
altitude kind of
hypoxia works to lean you up.
It's been proven.
So cancer patients know
this glycolysis leans you up.
So when you increase glycolysis through
increasing substrate,
you're going to get lean.
The other variable that no one's talking
about is just simply that you're
recolonizing the gut.
And I think it's something that a lot of
low carb influencers have stumbled onto
and they don't even know it.
And it's just simply
that I've experienced this.
When you recolonize the gut rapidly,
there are very specific proteins that are
related to fasting and fat loss.
One of them is ANGLP4, PT4, or FAFE,
fasting induced adipose factor.
That is a protein that is secreted during
fasting that actually
drives fatty acid liberation.
And what you will find is that that same
protein can be
stimulated by the microbiome.
So when you increase taxa during a fed
state that produce this protein,
you drive fat loss.
It actually helps prevent fatty acid
storage and drive fatty acid release.
So you can actually drive fat loss
through the microbiome through mimicking
fasting through that.
So you have glycolysis and you have the
recolonization of the microbiome along
with protein restriction.
So those are three variables that all
work together all at once.
And so that explains things, I think
pretty well, would be my answer.
Okay, that's perfect.
And do you think maybe a bit more that I
spoke not really, it's not like we
haven't talked about anything technical
to stay listy honest.
And when somebody is going through some
sort of disease statement, maybe when
there's some impaired match or conjugal
function, there's an elevated sort of
cell dangerous responses at work.
There's obviously in those states is
going to be impaired oxfoss down
regulated use of fatty acids.
Do you envisage that being maybe a
potentially effective strategy for people
who do have some sort of matcha conjugal
impairment to sort of bypass that block
in energy production, it'd be in the
short term while you're dealing with
maybe the underlying issues.
Yeah, I certainly think so.
I think it could be.
I would just say it's
certainly something to try.
Fair enough.
Perfect.
Okay.
Last one, and then I'll let you go.
Any new molecules you're particularly
excited about, just generally speaking,
not giving away any
trade secrets or IPF course.
Yeah, there's...
So we're in the burgeoning era of
precision fermentation.
Basically, we can get bacteria to make
very specific immunoglobulins or proteins
or different things we want it to make.
And where this gets really interesting is
in the replication of milk proteins.
So lactoferrin is kind of the most
conspicuous example, but there are other
ones that are blowing up.
They're not blowing up.
You're going to see...
What you're going to see is the
introduction of additional co-factors of
unique things that are present in
mother's milk that are additive with
respect to the equation of
optimizing the metabolism.
And it gets back to
mother's milk is growth serum and it
triggers all the right things in all the
right way when you're young.
And it makes sense that there could be
some significant benefits to
replicating aspects of that.
And through precision fermentation now,
we're seeing kind of a release of that.
Okay.
Perfect answer.
Thank you.
Cheryl, like I said, you've been a star.
This is a conversation I've been wanting
to have for a while.
So thank you.
I appreciate your time and hopefully
we'll be able to do this again soon.
Just to finish off,
where can people find you?
Should they wish to connect, learn more
about what it is you do, your work, your
company, Veep, et cetera?
Yeah, probably the best
place is my Instagram.
So that's real Joel Green.
And then my link tree has
all those goodies in it.
And then I'm trying to
grow my ex, my Twitter.
I just don't post often enough, but if
you want to follow me,
same thing, real Joel Green.
And then our URL is a veepnutrition.com.
Perfect.
Joel, thank you so much for your time.
Thank you, Rob.
I really enjoyed the convo.
Really great.