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.

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 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.

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.