When we're looking at smoking versus

vaping, vaping is probably worse in

terms of the damage to the airway and

the insulin resistance that comes from

it. But this gets worse because we know

that insulin resistance is the core for

most chronic diseases that are killing

us. And there's a handful of other

lifestyle habits that's contributing to

it.

That's horrifying. So tell me

everything.

Dr. Benjamin Bikman is a leading

metabolic scientist. His research

focuses on the hidden epidemic of

insulin resistance and its devastating

consequences.

And by regaining control of your insulin

levels, he says you can regain control

of your life.

Insulin is a hormone that affects

literally every single cell of the body.

But if those cells become insulin

resistant, you start to spread the

disease. For example, they call

Alzheimer's insulin resistance of the

brain. And even the most common forms of

infertility, erectile dysfunction, and

PCOS, insulin resistance is a heavy

contributor. Now, 88% of adults in the

US have some degree of insulin

resistance. And people hear this and

think America is just fat and

metabolically sick. But we're not

actually the worst country when it comes

to this. And part of it is because of

how different ethnicities store fat. And

I'll come back to that. But there's two

roads to insulin resistance. So there's

the fast lane, and I could make you

insulin resistant in 6 hours with either

of these common three things. But if I

removed them, your resistance would go

away just as quickly. Now, the slow

lane, that's a problem. And there's

certain lifestyle habits and problems

with our diet that are massively

contributing to slow insulin resistance.

Now, thankfully, this can be resolved

through four pillars, which are very

simple.

We'll get into that. But why don't we

just cycle this off and just take his

Ozempic?

Well, because people may not know about

the negative side effects. For example,

40% of the weight that people are losing

on these drugs is coming from

Highly

I have been forced into a bet with my

team. We're about to hit 10 million

subscribers on YouTube, which is our

biggest milestone ever, thanks to all of

you. And we want to have a massive party

for the people that have worked on this

show for years behind the scenes. So,

they said to me, "Steve, for every new

subscriber we get in the next 30 days,

can $1 be given to our celebration fund

for the entire team?" And I've agreed to

the bet. So, if you want to say thank

you to the team behind the scenes at

Diabetes Canada, all you've got to do is

hit the subscribe button. So, actually,

this is the first time I'm going to tell

you not to subscribe because it might

end up costing me AN AWFUL

BENJAMIN,

WHAT IS THE MISSION THAT YOU'RE ON?

My mission is to help people appreciate

that much of chronic disease

we look at them as these siloed

individual distinct disorders with

totally distinct origins, and yet much

of them

uh share a common core. It's as if

they're branches growing from the same

tree. And the conventional clinical care

will look at these branches and give

someone a prescription for a medication,

which is only going to prune the branch

back a little bit, never actually

solving the problem.

It can just grow right back. And so, we

can look at most of these chronic

diseases that are killing us globally

and and then say, "Okay, there are in

fact some simple lifestyle changes that

can be implemented that will help reduce

the risk of not only one or two, but all

of the top killers from things like

Alzheimer's disease to

uh heart disease to type 2 diabetes to

uh liver failure or fatty liver disease.

All of them share a common metabolic

core. That's my mission.

And what is that common metabolic core?

Yeah, it's a little-known problem called

insulin resistance.

In fact, when I first started

this topic, I stumbled on one paper

that documented how when fat tissue is

growing, it increases the risk of type 2

diabetes. That wasn't a concept in the

early 2000s that was is getting a lot of

attention.

Diabesity, this kind of dual epidemic of

wherever we see obesity, we see more

type 2 diabetes. And this manuscript

outlined

something that was to me a revelation at

the time. It was so fascinating where

when fat tissue is growing, it starts

releasing pro-inflammatory proteins.

That inflammation caused a problem

called insulin resistance.

And then that got me into this realm of

understanding that other tissues of the

body as they become insulin resistant,

then you start to spread the chronic

disease.

And and essentially

coming to the conclusion that something

like hypertension, high blood pressure,

which is the most common cardiovascular

problem and the main contributor to

heart disease.

Well, insulin resistance is the main

cause of hypertension. Um they call

Alzheimer's disease type 3 diabetes or

more accurately um insulin resistance of

the brain. Even the most common forms of

infertility in men, it's erectile

dysfunction. Well, that's because of

insulin resistance of the blood vessels.

In women, the most common form of

infertility is polycystic ovary syndrome

or PCOS. That's because of the insulin

resistance affecting her ovaries and the

ability to produce the proper sex

hormones.

I guess the really important question

here is what is insulin resistance? And

can you explain this to me like I'm a

10-year-old because

for sure. Insulin resistance is it's

kind of a it's a disorder that has two

parts. It's like a coin with two sides

that as much as we think of we we think

of one side just because we hear the

word insulin resistance, but there's

another part to it that I need to that

is very important. So,

insulin first of all is a hormone that

we make from the pancreas, a long kind

of gland tucked underneath the stomach.

And the pancreas is a very busy organ.

It makes a lot of different hormones. It

makes hormones that come into the blood.

It also makes enzymes that go into the

the into the intestines to help digest

food. But among the hormones that are

being released into the blood is

insulin. Now, in the person with type 1

diabetes, their immune system has

destroyed their beta cells. So, they

don't make insulin anymore. That's why

for a person with type 1 diabetes,

insulin is a life-saving therapy. You're

giving them what they're not making

anymore. But for everybody else,

we have beta cells and they're releasing

insulin when they need to.

Now, usually the main stimulus

the main reason the beta cell is

releasing the insulin is because blood

glucose levels go up.

So, I eat sugar.

You eat sugar or not even something as

obvious as sugar, but bread or or

crackers.

White rice.

Chips. Oh, yes. Yes. So, basically

anything that falls into the family of a

carbohydrate. So, if the earth grows it,

that's a carbohydrate. Um if it's a

plant, it's a carbohydrate. Maybe that's

a better way of describing it. And so,

it's going to have starches and sugars,

which all this kind of falls into this

family of carbohydrate. Depending on how

much starch or sugars that it has, then

that will result in a bigger or a

smaller blood glucose or blood sugar

response.

But then, if blood sugar is too high for

too long, that becomes very harmful to

the body. So, insulin comes in

um and helps lower the blood glucose.

And then, having done its job, insulin

comes back down.

So, insulin comes out like a taxi and

transports all the glucose in my blood

to various places around the body to

store them.

Perfect. Perfect. Yeah,

Yeah, that's right. It's that's you can

say look at it's a shuttle. It's a taxi

saying, "Hey, glucose, come on in. I'm

dropping you off at the muscle." So,

mostly, just as an interesting tangent

of insulin before I finish answering

insulin resistance,

insulin will open the doors for blood

sugar to come in and drive the taxi in,

mostly at the muscle and the fat.

Muscle and fat tissue need insulin to

come and bring the sugar in via taxi.

However, other tissues and and the brain

a little bit as well. Other tissues will

still respond to insulin, but they don't

need insulin to tell it what to do with

the sugar. It just takes it in. But even

on those like the liver for example,

if the liver sees sugar driving by in a

taxi, it just opens the doors and lets

it in. It doesn't need insulin to come

and tell it to let the sugar in.

However, even at the liver and other

every other cell has a similar degree of

this.

The liver doesn't know what to do with

it.

So, this is back to something I'd

mentioned earlier where insulin's

thematic effect of the entire body is to

tell the body what to do with energy in

all of its forms as as these kind of

caloric rich molecules. What to do with

lactate, what to do with ketones, what

to do with fats or glucose, what to do

with pro- amino acids. So, insulin will

tell the body what to do with all of

those things. But again, it's most

famous effect is to control blood sugar.

And that's not wrong because it's most

powerful activator is blood sugar. So,

with all of that in mind,

insulin resistance is two problems

wrapped into one. The one problem is the

most obvious one, which is that insulin

isn't working as well as it used to. So,

back to the analogy of the taxis

dropping off sugar,

if the muscle tissue has become insulin

resistant, insulin is coming and trying

to pull the sugar-loaded taxi into the

muscle, but the muscle's not listening.

So, say that again. So, the

Yeah.

Insulin's coming past with the glucose

inside it.

Well, not not technically. Yeah, but

just to sort of go with your metaphor.

But maybe to use another one, insulin

comes and knocks on the doors. It's like

the bouncer

Yeah.

at the door. It's coming and knocking on

the door of the muscle saying, "Hey

muscle, I've got some sugar that wants

to come in.

Mhm.

And normally the muscle will say, oh

yeah, sure, okay, open up the doors and

let the sugar come in.

When the muscle is insulin resistant,

the bouncer is knocking. Maybe there's

even I'm almost getting ahead of myself,

but

one bouncer maybe two or three bouncers

pounding on the doors of the muscle

cell, but the muscle cell's not

listening. It's become deaf.

That's the insulin resistance of what we

call insulin resistance, where some of

insulin's effects, like helping lower

blood sugar, it's not working very well

anymore. And the muscle is just an

obvious example because there's so much

of it. You know, it is the biggest

tissue on the average individual.

Someone who's very obese perhaps now has

more fat tissue, but even people who are

overweight, most of us is muscle. So,

that's a good it's a good tissue to look

at. So, part of insulin resistance is

that of all the things insulin's trying

to do,

including lower blood sugar, it doesn't

do it quite as well as it used to. Some

of the cells or tissues of the body have

become deaf to insulin's demands.

Now, however, at the same time that's

happening,

insulin levels are higher. And that is

really important. Um and I'll I'll

mention an example in just a moment that

highlights the difference between the

two, but we have to consider anytime we

talk about insulin resistance, we think

of two things happening

um in concert. One, insulin isn't

working quite as well as it used to in

various places of the body.

At the same time, insulin levels are

higher. And that kind of takes us back

to the um the muscle cell, where I'd

mentioned getting a little ahead of

myself, that a bouncer is knocking on

the door,

and once upon a time the muscle cell

would hear that one polite knock from

that one bouncer or one molecule of

insulin, if you will, and it would open

the door and let the glucose or the

blood sugar come in. But now the muscle

cell

um the the the bouncer insulin's

knocking on the door, but the muscle

doesn't listen. It's resistant.

And so, the body has adapted, and it

learns, "Okay, well, if one bouncer

wasn't enough, let's send an angry mob

of bouncers." And then the glucose the

muscle will start to open the door. And

and and indeed it can. So, those two

problems go together. On one hand,

insulin isn't working as well as it used

to. That's what gives it the name

insulin resistance.

But there's another part that is equally

present, which is that blood insulin

levels are higher. Now, there's

um earlier at the outset of the

conversation, I mentioned that even

infertility has an origin has has some

degree of um

development because of insulin

resistance.

And it's a perfect example of both of

these parts of insulin resistance, where

in some instances insulin isn't working

very well, always with insulin

resistance blood insulin levels are

higher. So, for example,

erectile dysfunction is the most common

form of male infertility. In fact,

its connection to insulin resistance is

so strong that just a few years ago I I

was so struck by a title of a paper that

had just been published, which stated

something like, "Is erectile dysfunction

the earliest manifestation of insulin

resistance in otherwise young healthy

men?" Now, what is the connection? It's

because in a normal erectile function,

in order for the man to have normal

erectile function, he has to experience

a pretty dramatic increase in the size

of the blood vessels in his body. The

blood vessels expand, that increases

blood flow, and then he has normal

function.

Part of that signal that tells the blood

vessels that it's time to expand is

actually insulin. And so, this is what I

said earlier, where insulin does so many

things in the body, and we only think of

it as being relevant to glucose, and

that's not fair. Insulin does a a of

stuff. Again, including telling blood

vessels to expand. Now, unfortunately,

in the case of this

this unfortunate man,

his blood vessels become insulin

resistant. So, now it's insulin coming

and knocking on the doors of the blood

vessels saying, "Hey, it's time to

expand and increase blood flow."

But, the blood vessels don't respond.

They don't listen. So, they stay

constricted, blood flow stays

insufficient, and thus he has erectile

dysfunction.

Now, I don't want to be insulin

resistant.

No. No one does. No one does.

So, so tell me how it happens.

Yeah, right. Yeah, so the origins are so

important because it helps us understand

why we've gotten into the situation we

are, where it's the most common problem

worldwide. There are two pathways to

insulin resistance. So,

two two roads to get to the same

destination. Again, the destination

being insulin resistance. There's the

fast lane, which I call fast insulin

resistance, and it actually has three

lanes, which I'll describe in a moment.

Then, there's the slow insulin

resistance, which is a more it takes a

little longer to get there, but at the

same time it takes a little longer to

get away from it. So, I'll start with

fast insulin resistance because the slow

one ends up getting a little excitingly

complicated, but in a cool way.

So, with fast insulin resistance, there

are three things that I could take you

to a clinical lab, and I could make you

insulin resistant in 6 hours with either

of these three things. But, as quickly

as it settles in, if I remove those

things, your insulin resistance would go

away. So, these are fast causes, and

they're fast resolution.

They are stress

is a is a primary cause of fast insulin

resistance.

So, too is inflammation.

And then lastly, and this is going to

sound somewhat paradoxical, too much

insulin is also a cause, and I'll end

with that one because I think it's the

most important. Then transition to slow

insulin resistance. So, anytime the body

is experiencing too much stress, it will

very quickly become insulin resistant.

Now, as a professor who teaches

endocrinology, no surprise, I define

stress in the context of hormones. And

there are two primary stress hormones,

cortisol and what we call in the US

epinephrine or in the UK adrenaline.

Those are the two stress hormones. Now,

those hormones are very distinct. They

have almost nothing in common. But like

when you are feeling a little stressed,

it's both of those, especially

adrenaline {slash} epinephrine, that are

making you feel a little jittery. It's

making your heart beat a little faster.

You're a little more alert. Um that all

starts to play into a stress response.

But what those two hormones have in

common

is that they both want blood glucose

levels to climb.

It's kind of their way of saying, "Hey,

we don't really know what's going on

right now, but we want to be ready to

run away." Or that's the fight or flight

kind of aspect to stress. And so they

want to push blood glucose levels up,

and they do very well.

That, of course, puts them at odds with

the hormone insulin.

Cuz these two, epinephrine or adrenaline

and cortisol, the two stress hormones,

they're pushing glucose up, insulin

wants to push it down. So, the more of

the body is has those stress hormones

elevated because of, say, sleep

deprivation, that's a very effective way

to increase cortisol, or they are taking

too much drinking too much caffeine,

that is a way to increase epinephrine

quite strongly. If both of those signals

are too incessant, or the you know, they

they continue to be present and climb,

then insulin has to work harder and

harder. And then we have insulin

resistance. So, stress is a cause of

insulin resistance. But then next is

inflammation.

You you know, you you and I were

commenting about earlier about how,

"Boy, there's a cold going around.

People it's flu season. Even then, if a

person were wearing a continuous glucose

monitor on the back of their arm,

measuring their glucose levels, they

would see their glucose levels are much

much higher like significantly higher

during the time that they're struggling

with this infection. That is a

reflection of insulin resistance.

Insulin's having a harder time keeping

the blood glucose levels in check.

Anytime inflammation is up, insulin

resistance will be up as well. Even in

things like autoimmune diseases, there

are reports in humans that document the

degree to which someone has say active

rheumatoid arthritis. Their their joints

are achy and because of of an autoimmune

attacking of the joints,

they will note on some days, like every

autoimmune disease, there is an ebb and

a flow. Some days it's good, some days

it's bad. And on the bad days, if you

measure their insulin resistance, it is

absolutely locked with the degree to

which their immune system is turned on

or off or higher or lower. So,

inflammation is another cause. And then

the last one of the fast lane of insulin

resistance is too much insulin itself.

Now, the astute listener will realize

the kind of circular thing I've just

presented by invoking high insulin as a

cause of insulin resistance because they

will also think, "But wait a minute,

Ben. You just said that high insulin is

also a consequence of insulin

resistance." That, you know, back to the

bouncer knocking on the the the door of

the muscle cell, if one bouncer wasn't

enough or one molecule of insulin wasn't

enough, the body will say, "Okay, well,

let's send 10 molecules of insulin."

So, high insulin is both a consequence

of insulin resistance, but it's also a

cause. And this is reflective of a

fundamental principle in all of biology

that if there is too much of a stimulus,

a cell, if it's capable, will try to

become resistant to that stimulus. This

would be like a funny analogy of in in

in my in the Bickman home, my darling

wife is home with the children. That is

what she wants to do. She She is

full-time mom. When I'm home, and I try

to be home as much as I can, it's funny

for me to note the difference in how

quickly we each respond to our children.

I will hear my child saying, "Mom. Mom.

Mom."

And she's not responding. Mom has heard

this for so much that she's become kind

of selectively deaf to when my children

are demanding her attention. I'm not as

around my children quite as much cuz I'm

working during the day. And so when I

hear that, it's a very fresh signal to

me. I've not heard it so much that I've

become deaf to it. And so I will respond

even though I'm in the other room

because I'm so much more sensitive to

the clamoring for attention.

This is like the body in response to

insulin. If there is always insulin,

it's always going up, always going up,

the body will start to say the muscle

cell will start to say, "Boy, insulin,

you are knocking on my door all the

time. This is getting old. I'm not

responding anymore. I'm not going to

listen as much as I was before." So in

that sense,

insulin, too much insulin becomes a

cause of insulin resistance. And back to

what I said earlier, I could take you

into the lab, start infusing you with

just a little drip of insulin to

increase your insulin, and over just a

few hours, you would become demonstrably

less sensitive to it than you were

before we started. But again, as I would

take that away, give your body a few

hours, and it's back to normal. In every

one of those instances, it's a fast

onset, and it's also a fast solution if

we can take it away.

If we can take it away, but if we can't

take it away, does it become sort of

chronic?

Yes, so that especially all of these can

contribute to a more lingering insulin

resistance, but especially insulin.

Where I focus on that one the most

because of not only its relevance to the

slow lane, but also just how present it

is where 70% of all calories globally

are carbohydrates. And now, perhaps with

the best of intentions, our experts are

telling us that we should be eating six

times a day.

And so, we

eat we wake up in the morning, insulin

has finally been coming down while we've

been fasting overnight. Insulin gets to

take a little bit of a break. We're

fasting. Then we break that fast by

eating breakfast. And in the UK as it is

in the US, by and large, this is going

to be a very starchy sugary breakfast.

It's toast with some jam or a cereal or

it's bagels.

That is going to be that is almost pure

glucose. And so, what do we do? We wake

up, we eat breakfast, we spike our blood

sugar levels, and insulin has to come

up.

Insulin will take longer to come down

than the blood sugar will.

It will wait in the blood to make sure

that all the blood sugar has gone back

to normal. So, depending on how much

carbohydrate we ate for breakfast, it

could take our insulin levels three or

even four hours to come back down to

normal. Long before it's had a chance to

come back down to normal, we've had a

mid-morning snack, of course. We need to

go get a sugary coffee and another bagel

or something. And so, after just a

couple hours, we do it again. And once

again, before insulin has had a chance

to come back down, we have a starchy

carbohydrate-heavy lunch, then an

afternoon snack, and then a

carbohydrate-heavy dinner, and then of

course we have to have an evening snack

before we go to bed. So, the average

individual is spending every waking

moment in a state of elevated insulin.

And thus, the signal never really goes

away because they they never give

themselves a break. But one of the

consequences of that I mentioned, which

is that it directly causes insulin

resistance.

But, when insulin is high,

it starts to have a signal on the fat

cell. And that then brings us to the

slow insulin resistance, where you have

something happening in the fat tissue

that begins to set the stage for insulin

resistance in the entire body. And it

takes longer to settle in, but it takes

also longer to go away. That's why I

call this one slow insulin resistance.

Now, in the case of insulin,

most people So, the the the the key with

the

Yeah, I'll explain it this way first.

So, the most relevant feature with fat

tissue contributing to insulin

resistance is the size of each fat cell.

When we typically think of fat, we would

maybe say, "Okay, Steve has um I'll do

this in kilos for the UK audience. Steve

has 10 kilos of fat on your entire body.

That's probably too much for you. Ben

has 20 kilos.

And yet, it's possible that I'm

healthier metabolically than you.

Um and that's because it's not the mass

of fat that matters most. It's the size

of the fat cell that matters. This is

why women, despite universally being

fatter than her male counterparts, are

healthier with regards to insulin

resistance and every single metabolic

problem. It's because women, as a result

of her particular sex hormones, have

more fat cells, but they're smaller. So,

she has more fat, but smaller fat cells.

And small fat cells are healthy, insulin

sensitive, anti-inflammatory

fat cells.

The but the bigger the fat cell gets,

the more it initiates a cascade of

events or a series of events that

creates insulin resistance.

Am I right in thinking we have the same

amount of fat cells for our whole life,

pretty much?

That's really, really safe assumption

for most people. Yeah, for most people

the a fat cell um sometimes students

will hear that fat cells are immortal.

That is not true.

But, they're long-lived. Fat cells will

live about 10 years. And so, typically,

by the time you if you think of if you

look at a newborn, during infancy,

childhood, and puberty, the number of

fat cells is going up up up up up. Once

they finish puberty, so mid to late

teens for a young woman, late teens or

even early 20s for a young man, usually

at that point the number of fat cells

they have is going to be very static.

This is something people don't really

understand, and I actually need to

discover it from doing this podcast and

speaking to so many experts about this,

that

we pretty much, especially as an adult,

have the same amount of fat cells,

really regardless of what we eat.

Yes.

And it's actually just the fat cells we

have shrinking

Or growing.

or expanding.

Exactly. That's exactly right. Now,

there are differences across

makes liposuction a pretty bad

idea.

it in fact, it makes things worse.

Please, let's make sure we come back to

that.

Okay, I'll write that on my list.

Because it really becomes the person

ends up their vanity ends up really

ruining their their their future

metabolic outcomes.

But, there are differences across

ethnicity. Like um this is a little

oversimplified, but not much. On one

end, you'd have Caucasians, kind of

northern European Caucasians. On the

other wind end, you'd have East Asians,

like uh Chinese, Japanese, uh Korean

East Asians.

And And then, if you look at that same

spectrum of people making fat cells

through their life,

an East Asian will be making fat cells

and then stop right about here.

About sort of

So, very few fat cells, relatively

speaking, across all the ethnicities.

They have very few fat cells. A

Caucasian on the other end of the

spectrum,

they went way higher.

And so, this guy, let's say American Ben

versus Chinese Ben, overly simplified,

but but here we are. Um

so much of fat mass isn't the number of

fat cells, even though American Ben has

more, it's the size of the fat cell. So,

I could be the same percent body fat

really as Chinese Ben,

um but that would just be because my fat

cells were just that much smaller. But

this is the problem then.

If you have

let's say American Ben and Chinese Ben

both gained 10 kilos of pure fat over

the next 10 years. Very easily done.

Most people do that quite often.

Caucasian Ben just doesn't look as good

in his speedo.

Um which is a pasty Caucasian, he's not

going to look particularly good in that

speedo anyway. But I'm just indulging a

little more than I was before, but

otherwise I'm healthy. My blood pressure

is fine, my blood sugar is fine,

everything is normal.

Put that same 10 kilos of fat on Chinese

Ben,

hypertension, type 2 diabetes, fatty

liver disease, infertility.

Um and that is because Chinese Ben had

fewer fat cells to start with. And so

those fat cells, as the body was told to

store fat, those fat cells were getting

much, much bigger, much sooner.

And the fat fat cell

promotes insulin resistance very, very

readily. And so that logically moves

into this the question of what makes fat

cells grow?

And it is

two essential variables that we only

ever look at calories.

And yet, if you take a person with type

1 diabetes

and say, "I want you to eat 10,000

calories, but don't give yourself your

insulin injection." They cannot gain

weight. It is It is literally impossible

for the type 1 diabetic to get fat if

they are skipping their insulin

injections. In fact, this is so known

that if you take Let's imagine a young

woman who would maybe have more pressure

to be thin than her male counterpart,

although it's happening more in males,

too.

Imagine a young girl who gets diagnosed

with type 1 diabetes at the age of 13 or

14. Very impressionable time. She's very

worried about how how she looks and how

thin she is.

She learns that wait a minute, I can eat

whatever I want and all I have to do is

not inject my insulin and I'll be as

skinny as I want and it works. It works

so well that it's actually a formal

eating disorder called diabulimia.

So this the fact that this exists is

absolute proof

that the growing and the shrinking of

the fat cell is more complicated than

just calories being high or low.

Because like I had said earlier when I

talked about hormones, hormones are a

way for the bot for the very tissues of

the body to know what it ought to do

with energy.

And so a fat cell will have energy all

around it and if it doesn't have insulin

to tell it what to do, it won't do

anything with it. And or maybe to make

this more direct back home in my lab

my students my students are growing fat

cells in Petri dishes. These fat cells

are swimming in a little sea of

calories, lots of glucose, lots of fats

and yet they stay really small

until we add insulin. The moment we add

insulin into that little Petri dish, if

we check those cells 4 hours later,

they're immediately fatter. If we check

them 4 hours later, they're fatter

still.

Now they know what to do with the energy

they have. So with slow insulin

resistance

it develops when fat cells get really

really big. It's like a because they

have to tell insulin, insulin you

continue you you are telling me to keep

growing, I can't keep growing. I'm so

big that I'm going to pop. I mean

literally the fat cell can get so big

that it degrades its membrane. It's like

a water balloon that a naughty little

boy has overfilled and it's about to

burst.

The fat cell doesn't want to burst and

so it tells insulin, insulin you are

trying to make me grow. You're telling

me to grow. I can't listen anymore. I'm

becoming insulin resistant to stop

growing.

So insulin makes you fat?

Oh very much. Now, if you So, so I A

moment ago I said that the big fat cell

has two variables. You must have both.

You must have both a signal to tell the

fat cell to get big, which is insulin.

It is the There's no other signal that

can do it. You can in a human just

simply take away the insulin, like type

1 diabetes. It doesn't matter any other

hormone in the body, it does not matter.

They cannot get fat. They could Again,

they can eat thousand They could eat

10,000 calories of chocolate cake. They

cannot get fat. Not only can they not

get fat, they can't hold on to their

fat. Cuz if there's no insulin to tell

the fat cell to hold on to it or get

big, it has to shrink. It's breaking

down its fat. So, the body goes into

such a dramatic fat burning state in the

absence of insulin that keeping fat

becomes impossible. So, the insulin

signal's necessary to tell the fat cell

what to do.

But, the fat cell will say, "Okay,

insulin, you're high. You're telling me

to grow, but what am I going to grow

with?" That's where the calories come

in. Now, the fat cell will say, "Hey,

fats and glucose in the blood, insulin

has told me to get big, and so I need to

pull you in to help me grow. You're

going to give me the bulk."

And if you have one without the other,

it is death.

So, if I'm eating 2,000 calories and I

have a different insulin sensitivity to

you. Say we both eat 2,000 calories

and I'm insulin resistant, doesn't that

mean that I will

You'll store more as fat.

Oh, okay.

Yeah. Yeah, so so your body now it would

partly depend on There are people where

you you if your if all of your fat cells

had reached its maximum point, then

you're done. You're not going to gain

more fat. You're just going to become

more and more and more insulin

resistant.

Okay, fine.

So, you kind of start limiting yourself.

But, there are studies in humans to show

that if you give humans isocaloric diet

meals, so the exact same number of

calories,

but they in the same amount of protein,

but you differ those meals based on the

amount of carbs to the amount of fat.

So, let's say two meals, exact same

calories, 2,000 calories, or that's in

one meal, that's too high. 1,000

calories in one meal.

One version of this is the conventional

way of eating, which is lower fat,

higher carb.

The other meal, same number of calories,

but it's lower carb, higher fat.

This lower carb, higher fat version will

have a lower insulin response,

and they they will store less fat from

that meal. And their meta- And someone

would say, "Well, where do the calories

go?"

You can't this it's the laws of

thermodynamics. You can't destroy

energy. The metabolic rate will go up.

So, when insulin is low, if you have

someone going a full day eating the same

number of calories, but lower carb

calories, their metabolic rate will be

almost 300 calories higher in that day.

And metabolic rate is the

the total amount of energy that it just

costs you and I to just live.

Okay. So,

It was going through the day. But that's

But that's a significant amount. Like,

if you and I were to go exercise and

say, "Let's go burn 300 calories." We

got to be on the stair stepper for an

hour or something. So, it's 300

calories, but at the same time,

if your insulin is low,

you're burning so much fat that you

start making ketones. And I I don't

intend to get onto that topic quite yet,

but suffice it to say,

every molecule of a ketone has a has a

caloric load roughly similar to glucose.

And one of the And And what the body

when it starts making a lot of ketones,

it starts eliminating the ketones. So,

every time someone is breathing out

ketones, they're literally breathing out

calories.

Or they're urinating, and they're

urinating out ketones if they have

higher ketones in their blood. They're

urinating out calories, because ketones

have energy.

And so, this is the way that if insulin

is low, it becomes impossible for the

body to hold on to its energy. It is so

determined to spend energy that it will

both increase metabolic rate, and it

will make the energy, the calories be

wasted in the breath and in the urine,

and and in the form of ketones because

ketones have calories. Ketones are

energy. Now we're just dumping them out

into the universe.

It's worth, before we talk about how to

keep my

insulin levels low so that I can benefit

from all the health benefits we've

talked about, it's probably also worth

just spending a little bit of time

trying to understand the evolutionary

basis of insulin resistance.

There are some theories that are very

interesting that attempt to explain why

is it that we became so fantastically

different from let's say our closest

animal relatives, other primates like

chimpanzees or or apes.

What was the difference that had us

become so different than them? One of

the leading theories is a is a theory

called the expensive tissue hypothesis.

And it actually does have something to

do with ketones.

In the expensive tissue hypothesis, as

the theory goes,

our earlier ancestors deviated in this

kind of animal family line because we

started eating more meat. We started

eating food that was so nutritious, so

nutrient dense, so loaded with good

calories and all of the fats and

proteins that we need, that it allowed

two very distinct changes to occur in us

compared to other primates. One, our

intestines became significantly shorter.

So if you compare the human digestive

tract to any other

primate animal, if if we are a primate,

um then if you look at the intestines,

they're fantastically different,

particularly the large intestine or the

colon. Because

our ancestors, as the theory goes, began

eating meat, we didn't need the the as

much. Um and

the colon is a place for food to

ferment.

And so, if you're eating a lot of plant

matter, like other primates do, you need

a much, much larger colon.

So, we started eating food that was so

nutrient-dense, our colon shrunk

considerably. We didn't need to waste

energy on a big, busy colon. At the same

time, as we were eating food that was so

nutrient-dense and so loaded with good

fat,

it allowed us to have more time to be

curious and explore. And so, at the same

time our intestines were shrinking,

because we didn't need them to be so

big, our brain was growing.

And and it's because it had so much

nutrition,

including ketones. So, ketones are

an extraordinary fuel for the brain. In

fact, one of the reasons why a baby that

is born premature

will be more likely to have learning

disorders later in life, is because

premature baby didn't have time to get

very fat.

And fat baby is healthy baby. And fat

baby gets into ketosis.

Let's say you and I were to to fast

straight for 2 days.

If you took a 6-month-old baby, that

baby would be in a deeper state of

ketosis in 2 hours than you and I would

be in 2 days.

Because the baby is burning so much of

its beautiful chubby fat, and the more

the body burns fat, the more it makes

ketones. And the tissue of the body that

appears to benefit the most

in response to ketones is the brain. The

brain, the moment ketones hit the blood

stream, the brain immediately starts

taking in ketones for a fuel. Very

often, I have students who have had a

professor, perhaps with the best of

intentions, but ignorant nonetheless,

tell the student that the brain the main

fuel for the brain is glucose, that the

brain prefers glucose. And I show them

just one or two papers to prove that

wrong immediately.

And it is reflected in in in this idea

which

if if to use some convenient UK units,

if blood glucose is 5 millimolar, that's

a concentration, a way of measuring an

amount of of something.

Blood glucose may be 5 millimolar or 80

mg per deciliter for the American

audience. Um that would be a normal

glucose. And if you and I were to fast

for 24 or so hours, we may get up to

about 1 millimolar of of ketones. And

yet even then, the brain has already

switched to get the majority of its

energy from the ketone.

And so don't tell me that in this

dynamic the brain prefers this one

because this one's five times higher

than this one. And even in that

scenario, the brain is already getting

more than half of its energy from the

ketone. So all of this is my long-winded

way of saying, when we look at the

principles of evolution, one of the

leading theories is this idea that we

began eating essentially a meat-heavy

diet that again is so nutritious that it

allowed our brains to grow. Maybe one

final point on this, although it is a

bit of a barbed comment,

people may find this somewhat amusing or

disappointing or frustrating, the title

of a book just published which is that

vegetarians have smaller brains.

This is seen in humans that the less a

human eats meat,

then the smaller the brain becomes. The

brain is so dependent on the nutrient

density that comes from animal-sourced

foods that it will suffer

um when it doesn't get them.

Interesting. I mean, that's a

controversial thing to say.

It is, and you can cut it out.

But it really is it's a real thing. And

why does depression go up so much when

people stop eating animal-sourced foods?

It's because you are depriving the brain

of what it needs.

What is it exactly you're depriving the

brain of in that situation?

Yeah. Yeah. So at least among other

things, at least it would be the the

essential omega-3 fats.

So there are three omega-3s, and you

humans can only we can only get one from

plants, but it's one that the humans

don't use. We need the other two, and

they only come from animal source foods.

And you could supplement.

Absolutely.

Right. I mean, that's what I was

Yeah, you can, but but that that So, the

the solution in that regard is the vegan

must be educated enough to know what

they're deficient in, and then wealthy

enough to afford the supplements to make

up for it.

So, is that the the only evolutionary

sort of hypothesis towards why we

develop this insulin resistance?

Mm. Oh, yeah. In fact, it's funny that

you bring the question up again because

I realized I didn't quite answer it that

way. So, insulin resistance, why would

it exist at all? It would probably be a

way for the body to know when it was

needed to hold on to energy a little

better.

So, now Now, I say that now, and and

someone would think, well, but you just

why would I want to hold on to energy in

a way where it's causing hypertension

and Alzheimer's disease and increasing

the risk of heart disease?

Not all versions of insulin resistance

are negative. So, there is um there is

what all the insulin resistance that you

and I have been talking about is

pathological insulin resistance, or

harmful insulin resistance. Insulin

resistance that serves no good purpose,

and it's making us sick.

However, there is insulin resistance in

human development, which is

physiological, or helpful. It's supposed

to happen. And that is the two P's of

physiological insulin resistance,

puberty

and pregnancy. Because in both of those

instances, as we outlined earlier, when

the body's insulin resistant, insulin is

high.

That's not always bad, because insulin

wants things to grow.

It is like a fertilizer in the body.

Now, sometimes it's misplaced, and

results in problems, like increasing the

risk of cancer, for example.

But in other instances, if you have a

young child who needs some explosive

growth during puberty,

well, then that's really helpful.

Insulin's telling the body to store more

energy, to build up tissues, including

muscle and bone, but also including fat.

So, in pregnancy, insulin's playing a

role in growing the placenta.

is.

The breasts.

Yes, so in the woman, after she's

finished puberty, the only other time of

growth she'll ever have will be

pregnancy. And and so, those are the two

instances where the body has become

insulin resistant to take advantage of

the heightened scenario where it can

grow.

Because the woman's body needs to more

fat.

goodness, yes. Yes, so her body not only

needs to grow tissue mass, like the

uterus has to get much bigger. She has

to grow a placenta. She also needs to

become a little insulin resistant to

give a little more glucose to her baby,

because she is after all now living for

two people. And so, as she as her body

becomes insulin resistant, it actually

facilitates the growth of the baby a

little more rapidly. But as you noted,

it helps her store more fat, and

progesterone is another hormone that

even accelerates that process.

But basically, it's the her way of her

body's way of saying,

"Hey, I am committing to growing another

human, and it's going to be

metabolically very demanding, and so I'm

going to have as much extra fat or much

as much extra energy as I can in order

to ensure that if there's any sort of

scarcity in food that happens during the

course of the pregnancy, I'll have

enough energy to get through it all. And

then maybe I'll even have enough to

continue to feed the baby with lactation

after the baby's born."

What is gestational diabetes?

Yeah, it's a great question. Gestational

diabetes is essentially type 2 diabetes

of pregnancy. So, it's perfectly timed

question because

if you look at the average woman um who

is very healthy, very insulin sensitive

at the beginning of her pregnancy. So,

glucose is normal and insulin is normal.

Over the course of her pregnancy,

she stays normal healthy pregnant woman,

which is to say she has physiological

insulin resistance. She doesn't get

diagnosed with gestational diabetes

though, which means her glucose is

normal. But to keep her glucose normal

because she is insulin resistant, but

for a purpose to help her body grow, her

insulin levels are high. And then the

glucose is still in a normal range. And

then in some women, especially if she

has a family history of type 2 diabetes,

the insulin resistance goes too far.

Now, she has high insulin, like all

pregnant women do, but she's not able to

keep her glucose levels in check.

So, if I'm eating loads and loads of

sugar throughout pregnancy,

That will compound the problem.

Absolutely. So, then she will go from

the normal insulin resistance of

pregnancy into the insulin resistance of

diabetes. So, it really is like type 2

diabetes, but a microcosm of it, a mini

version that was really instigated or

initiated because of the pregnancy

combined with a bit of a genetic

predisposition combined with her eating

the worst possible way.

Does that then impact the future baby?

Oh, for sure it does. Yeah. So, think

about it's almost like the baby is

develop literally developing in a

hyperglycemic hyperinsulinemic

environment. So, the baby's get the baby

gets hardwired

to want to continue to exist in a state

of high insulin and high glucose after

the baby is born. And so, yes, the

offspring of mothers who have

gestational diabetes are significantly

more likely to gain weight and be

chubbier or fatter than their

counterparts and to later develop type 2

diabetes. Yeah, a resounding yes.

I read in your book that these infants

have a 40%

higher chance to be obese and have

metabolic complications in their teenage

years and beyond.

Yes, I mean a significant thing and I I

say that with all of the sympathy I can

for the mother who may be struggling

with this, but it is certainly a

motivation for mom to just be mindful of

what you're eating.

One of the things that that I saw the

other day on social media, which I

wanted to ask you about, was this. I've

got a picture of it here.

Um

it was someone online that posted this

photo, and they said, well, this graph,

and they said, we need to figure out

what's going on here. Um this is the

graph. I'll put it on screen for anybody

that's watching, but also it'll be

linked in the comments section below.

Um it essentially shows that over the

last, let's say, 20 years, there's been

a really significant rise in cancer

amongst women, but when we look at

cancer amongst men, it's pretty flat.

Mhm.

Um and this is cancer incidence by age

and gender up to 49 years old.

Mhm.

And I was wondering if you had any

thoughts on why this is happening.

Yeah. Yeah. Yeah, a few thoughts come to

mind. Um whenever I see these kinds of

reports, I always make sure I look

firstly at the What are they actually

measuring? So, just to set the stage,

this is the number of women who are

being diagnosed with cancer, so not

dying from cancer, but it's going up.

So, one one simple explanation, although

perhaps the most disappointing, could be

that more women are going in for testing

younger, and so we're just seeing kind

of an artifact of more women are just

going in sooner, and they're detecting a

problem that they wouldn't have

otherwise detected, you know, for 10 or

20 years. And which is a good thing. You

want to detect cancer as soon as

possible. So, that's the boring answer,

that it could be a reflection of just

more women going in for ultrasounds or

MRIs or mammary scans, whereas men don't

ever get tested for anything,

which is why we die more from

everything, possibly. But to give a more

exciting answer, this is very, very

likely almost entirely driven by breast

cancer. Um breast cancer is the main

cancer for women um by far. And so, if I

had to guess, I bet almost all of this

increase in cancer incidence is because

of breast cancer. Why might that be

going up? I would suggest there's

probably a couple instances. One, um

although people might not appreciate

this, is that one of the best ways for a

woman to reduce her risk of breast

cancer is actually having babies. It's

very well known,

um very well documented, that if a woman

um has a fam- it has babies and

breastfeeds, her risk of um breast

cancer goes down.

So, yeah, in fact, it's very meaningful.

I actually don't know um the reasons for

it. It could be the changes in estrogens

during lactation phase.

I've just I've just actually done a

quick search here to I put a picture of

that graph into AI and asked it the same

question, and it said pretty much what

you said. It said, "There's a rising

breast cancer incidence according to

Cancer Research UK." The other one that

it came up with is obesity trends.

Oh, yeah. I promise I was going to talk

about that. I wouldn't leave that. Yeah.

Sorry for interrupting there.

No, no, no problem.

Uh and then the other one was delayed

childbearing.

That's what I'm saying.

Which is what you were saying.

Yeah, so as child rates as childbirth

rates are going down, it does increase

the risk of breast cancer. Now, as I I'm

a cell biologist, right? I like to

understand the direct mechanism. And so,

as much as I invoke the perhaps lower

rates of childbirth among women, I don't

know the mechanism, so I'm sort of loath

to describe it. The mechanisms I'm very

familiar with are the metabolic,

um which is if you take a breast tissue

that is tumor tissue and compare it to

like if you take a breast tumor and

compare it to the normal tissue right

next to it, like that it would have

shared its origins with, the cancer from

the breast will have seven times more

insulin receptors than the normal breast

tissue. So, the idea of this tracking

quite nicely with obesity rates going up

over the past 20 years, I wouldn't say

that it's the obesity per se, but I

would say it's the entire metabolic

milieu, which is the insulin resistance,

that as much as the high insulin is

promoting fat cells getting bigger, that

high insulin is also accelerating the

growth of the tumor cells. Because

again, the main one of the main

mutations in breast cancer is a

sevenfold so a seven times increase in

the number of insulin receptors. And

insulin wants to tell things to grow. So

it's no surprise that almost every tumor

that's ever been measured for having

insulin receptors will have a lot more.

It's basically telling its neighboring

cells, "Insulin's going to come by and

it's going to tell us all to grow. I

want to grow more than you." And that's

what cancer is. Cancer is growth,

unregulated growth. Insulin tells things

to grow. So the connection between

obesity with the rising incidence of

breast cancer is very, very likely a

consequence of the rising incidence of

insulin resistance.

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You know, one of the big subjects you

touched on at the start was the was

Alzheimer's and dementia.

Yes.

And I have heard several people on this

podcast tell me that they think of

Alzheimer's as type three diabetes.

Worldwide, there is a new case of

dementia every 3.2 seconds.

Um it seems like I don't know if this is

true, but is Alzheimer's and dementia on

the rise?

Oh, yes. Yeah, it is. In fact, it went

from not being even on the radar to

being a top 10 killer.

Um now, it's interesting how people even

die from Alzheimer's disease. It's a

very kind of vague death.

But yeah, Alzheimer's disease is one of

the top 10 diseases now. Um certainly in

the West.

Um and and I would argue it's because it

has a metabolic origin. Now, one of the

interesting things about Alzheimer's

disease is we have spent

billions of dollars on Alzheimer's

research trying to identify the the

plaque. So so just to set the stage here

so that people listening can appreciate

this this paradigm shift that's occurred

in Alzheimer's research. Originally, and

even in many people still, people

thought that Alzheimer's disease is the

result of these plaques accumulating in

the brain. These kind of little

proteinaceous little

thick things that are preventing neurons

from sending the signals throughout the

brain for the brain to think and and and

have normal cognition.

And and yet, there are those of us and I

am proud to say I have long been one of

them

who has said that the plaque-based

theory doesn't make sense. We have had

drugs that have been available for human

use for years that have effectively

reduced plaques in the brain and yet did

nothing to improve cognition. So that is

an immediate challenge of the

plaque-based theory of Alzheimer's. Even

further,

even beyond older than that evidence,

when you would look

postmortem or look at tissue donor,

people who passed away, you would look

at the brains of people who died with

confirmed Alzheimer's disease at the

time of death

and look at the brain of someone who

died without any evidence of any

cognitive decline or any compromised

thinking whatsoever. And you would be

just as likely to find plaques in both

brains.

So the So whether the brain had

Alzheimer's disease not, you would still

see plaques in the brain. So the whole

idea that plaques mattered has long been

controversial. And just to put a fine

point on it before transitioning to the

metabolic origins,

about two or three years ago,

they found out that the very first

published papers that implicated plaque

as a cause of Alzheimer's disease were

based on fabricated data.

So the scientists who published those

first reports that led to the entire

theory that Alzheimer's disease is

plaque-based

were called out as fraudulent. And and

indeed, all of it was fabricated. So the

entire idea that Alzheimer And and we

have spent billions of dollars on

studies to try to

how determine how do plaques cause cause

Alzheimer's disease? Why when we reduce

plaques, it doesn't appear to help the

disease.

Because the plaques had nothing to do

with it. That's just something that some

brains have. Some brains have more of

these little specs than other brains,

and they don't contribute to Alzheimer's

disease at all.

Now, what did

can what kept rising to the top, and I

would hope now is the dominant theory,

is that people with Alzheimer's disease

almost always have some detectable

instance of insulin resistance, if not

full-on diabetic type 2 diabetes. Now, I

will say personally, I don't like the

term type 3 diabetes because it makes it

sound

like it's a whole new version of

diabetes.

To say it more succinctly and

accurately, it is simply insulin

resistance of the brain. And the brain

is a very hungry organ.

It is in what I teach as as a tri a

trinity of high metabolic rate organs.

That there are three organs in the body

whose metabolic rate is so high that it

just really sets it apart from

everything else. And the brain is one of

them. The brain has a very high

metabolic rate. So this is a very hungry

organ that that a lot of energy all the

time.

But the brain is unique in that it

primarily will only use two fuel

sources, and I've mentioned them, namely

glucose and ketones.

But glucose in that section of the brain

that gets compromised with Alzheimer's

disease, the glucose can't just come

straight in. It needs someone to open

the door for it, and that is insulin, of

course, just like we described with the

muscle cell.

Where in order for the glucose to go

into the muscle, insulin had to come and

knock on the door, if you will. And then

the muscle, being a polite, responsive

host, would open and allow the glucose

to come in. The brain is similar.

That in that section of the brain, it

has doors that need insulin. It's locked

until insulin comes and opens them. So,

even though glucose levels may be high

in the blood,

like in type 2 diabetes, you would

think, "Well, the brain can just get all

the glucose it wants." And yet it cannot

because it has insulin regulating the

entrance of the glucose. And if the

brain is insulin resistant, there's not

enough glucose coming in. And thus the

brain is forced to rely on the only

other fuel that it can rely on, namely

ketones.

But the same person who's eating all the

time to keep their blood glucose high

all the time has so much insulin in

their blood that they're never making

enough ketones to fill the gap. You

know,

mind the gap, and the brain has an

energy gap now. And where where the

brain needs, you know, an amount of

energy, I'm kind of acting it out for

those that are watching, but the brain

has a certain energy demand that it

needs. And if there's a lot of glucose

in a healthy insulin-sensitive person,

glucose will fill all of that need. But

as the brain becomes progressively

insulin-resistant, it cannot get all of

its energy from glucose. And thus

there's an energetic gap.

And in the absence of ketones, there's

nothing to fill that gap, and the brain

says, "Well, I don't have enough energy

to keep functioning as well as I did

before, so I have to reduce my function,

which manifests as a reduction in the

ability to think and process. In other

words, cognition goes down. But, what's

so interesting

is I just got finished describing a

scenario that scientists refer to as

brain glucose hypometabolism,

or a reduction in the amount of glucose

the brain is using. There are scientists

that measured this. We don't in my lab

because we don't do these kinds of

techniques, but you can actually infuse

people with a glucose that you can take

pictures of and see how much the brain

is taking it in and metabolizing it. In

Alzheimer's disease, the brain is not

getting as much glucose, so they call

that a hypo, or a reduction in

metabolism of glucose.

And as much as you and I are describing

that scenario as relevant for

Alzheimer's disease, you can essentially

open up the book of neurological

disorders and see the same thing.

Depression

has a brain glucose hypometabolism to

it. Migraines have a brain glucose

hypometabolism.

Epilepsy um and Parkinson's so all of

these disorders of the brain, of the

central nervous system, the one thing

they all have in common is the brain

isn't getting enough energy from

glucose.

And another way of saying that is the

one thing all of those seemingly

unrelated brain problems have in common

is that they all have some degree of

insulin resistance. But, then it's no

surprise that they all benefit

when ketones can swoop in to save the

day.

Um but that only can happen if the

person is giving their body a break from

the insulin long enough to actually

start making ketones.

Really, really interesting on this point

about Alzheimer's because I don't think

people have spent enough time talking

about the link between insulin

resistance and Alzheimer's. Um

and

one of the things I was I was looking at

there was how many people with

Alzheimer's have meet the criteria for

insulin resistance.

And some studies have it at 40%. There's

a study I found here that has it at 70

to 80%.

Um which I wanted to cite. Um

Exact percentages vary, but one example

is a study in the Journal of Neurology

in 2011 that found insulin resistance at

approximately 40% of individuals with

Alzheimer's.

Um but another study

uh in Alzheimer's patients sometimes

found it to be as high as 70 or 80%. For

instance, research by Dr. Suzanne de la

Monte

Mhm.

at Brown University has drawn attention

to the concept of type 3 diabetes.

Yeah, again, I don't love the term, but

I appreciate the use of it, which is it

does suggest a metabolic origin. But

even you look at those ranges, Stephen,

you'd say, "Well, one was 40, one was

80. Boy, what a difference." I suspect a

lot of that is just how did they measure

insulin resistance? If they were looking

at the glucose like so many do, you're

just going to miss a lot of people.

Yeah, it's quite hard to

I think there's different criteria,

right, for how one defines someone as

insulin resistant.

Well, there Yeah, and that's just that's

right. That's because there's not enough

training, which is at the beginning of

the conversation you asked my mission.

One of my missions is to help people

learn what to look for.

What do they need to be looking for?

Yeah, they need to be looking at

insulin. So

Is that easy to measure?

Well, it is technically easy to measure.

It's just that we have we don't have

enough systems in place to allow to

enable it. Like again,

if if someone listening in the UK were

to go to their GP and say, "Can you

measure my insulin?"

In many instances, they literally can't

get it done. The system just isn't in

place to take it to the lab and and

measure it. Now, some do. I know some

physicians in the UK who do so, and they

have developed their own way of getting

it done, and they're incredible

advocates of this whole idea. But it is

harder in the UK and Canada um where the

system is such that they have said, out

of ignorance, but perhaps well-placed or

or well-intentioned, they will say,

"Well, insulin isn't a marker that

matters."

It is. And if you're measuring insulin

resistance, just to put things back to

where we had talked about it earlier,

many people with insulin resistance have

normal blood glucose levels. It's the

insulin that's high. And so, I would say

if a person can get their insulin

measured, get it measured. In US units,

if it is anything above about 10 micro

units per mil, that's a warning. In UK

units, if it's anything above about 40

picomoles, that's a warning. Insulin is

high, you could have insulin resistance.

And you could be skinny

Oh, yes.

and have insulin resistance.

Yes, that's especially depending on the

ethnicity. Like if someone listening to

this is East Asian and they say, "Well,

I'm quite thin. I don't have insulin

resistance." You very well could. Um it

it depends. Even in in young women, a a

group out of northern Canada,

which is of course pretty far north,

they found that even in young healthy

weight women with PCOS,

they if they compared them to their

identically matched other women without

PCOS, they were more insulin resistant

in the other group. So so anyway, that's

my

way of saying even if you look at

yourself and think, "Well, I'm kind of

lean. I'm not insulin resistant." You

very well could be.

Okay, so I've got a friend who's a a

woman

Mhm.

who has PCOS.

Yeah.

And one of the things that she often

says to me is that

she gains weight easily. Is this true?

Oh, for sure. And in fact, I wouldn't be

surprised if she does because the fact

that she has PCOS is not absolute

evidence, but very likely evidence that

she has insulin resistance, which would

mean at any given moment her insulin is

at the risk of being a little higher

than her non-insulin resistant

counterparts.

So if she goes and gets the test done,

I bet her insulin would be high.

Um and so, all that would mean is which

is good. I mean, knowledge is power. And

my hope would be that as someone goes

and gets their insulin measured, and

there are a handful of other tests they

could also look at, but that's the most

succinct. Then it would be all the more

impetus or encouragement to say, "Okay,

I heard I listened to Steven and Ben. I

really do need to start making some

changes." And even in PCOS,

there are reports that document the

absolute reversal of the disease with

nothing more than just dietary changes.

I was looking also at second here cuz we

mentioned ethnicity a few times and it

says the research I was looking at says

that East Asians have East Asians have

fewer fat cells and they're more

resistant to obesity-related metabolic

issues.

Well, that's second part of that

statement is not true. They're more

resistant to obesity,

but they are like if it's an interesting

dichotomy cuz

Right. Okay, I got you.

Yeah, so they're more you you like to

find a Japanese man who's as fat as the

average American, boy, you're going to

have to look. It's hard. It's hard, but

to find a Japanese man who has is just

as much likely to get diabetes, type 2

diabetes, very easy.

Africans have

more fat cells typically?

Yeah, so so on that ethnicity, if now

there's a lot of kind of wiggle room

here, but on one end we'd have

Caucasians, blacks would be right

nearby. African ethnicities would be

quite close

um to the to the kind of northern

European ethnicity. And then we would

move through and and I don't mean to

miss anyone here, but on the other end

it would be East Asian and then

sprinkled through that would be um

uh

Latino.

Latino would be somewhere in the middle

and Hispanic. And then other Southeast

Asian and then East Asian kind of on the

worst end or the least sensitive or the

most sensitive to their fat. The most

sensitive to their fat. This actually is

a concept that has been presented called

the personal fat threshold, which is

this really interesting idea born from a

group in Australia suggesting that

across every individual body, which of

course is heavily influenced by both

ethnicity and sex, like we mentioned

earlier, a body is going to have a rate

at which it can store fat in a healthy

way. And then once that threshold is

met, any further pressure to store fat

will start creating insulin resistance.

And that threshold is essentially

how big, how many fat cells do you have,

and how much room do they have. So if

you have more fat cells, you have a

higher fat threshold. You can get fatter

before it starts to hurt you.

Does your fat distribution also matter

here? Because

does.

different races, this research is

telling me

have different fat distribution. It's

saying that Africans have better fat

distribution, lower visceral fat, and

less metabolic risk because of that.

Yeah, yeah, yeah.

Caucasians moderate fat cell quantity,

more prone to subcutaneous fat

accumulation, which

Subcutaneous.

Which is that's the fat around the

organs.

Yeah, so Caucasians and so so let's say

northern European African, both store

more of their fat subcutaneously, which

is the fat just beneath the skin, or the

fat that you can pinch and jiggle.

That has an ability to expand more

because there's nothing really to limit

it. Um however, the other place for

people to store fat is their visceral

adipose, which is the fat that is tucked

within the abdominal cavity, so tucked

around the organs. It's sort of

surrounding the kidneys and the

intestines and the liver. That is an

unhealthy place to gain fat, but an East

Asian, all things equal, is putting much

more fat there than they are

subcutaneously. The advantage of

subcutaneous fat is

Which is the fat on the outside.

Yeah, yeah, so the the fat beneath the

skin. Yeah, the yeah, the loose belly

fat, the fat that can pinch and jiggle.

That fat has a greater ability to make

new fat cells. So as much as earlier you

and I said fat cells remain static, for

the most part they do, there's a little

bit of wiggle room, where it can go up.

And that's purely subcutaneous.

And Hispanics have higher fat cell

quantity, more visceral fat,

Yes.

and increased risk of obesity related

conditions.

Yes, and so the problem with visceral

fat is this is such a finite space.

There's so little room within the core

of your body that if we allowed those

fats to multiply, it could theoretically

start physically compressing on tissues.

Right.

And so those fat cells only grow through

hypertrophy, which is the thing we

talked about earlier with slow insulin

resistance. Subcutaneous fat cells are

more abundant but smaller. Visceral fat

cells are fewer but much larger. And so

any ethnicity including Hispanic or

Asian that promotes relatively more fat

storage in the visceral space is going

to suffer from the consequences of that

fat much sooner. And again, it still

comes back to size. The bigger the fat

cell, the sicker the fat cell.

According to Alzheimer's Disease

International, the total number of

people living with dementia globally is

expected to reach 139 million by 2050,

which is up from around 55 million in