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Hormone Expert: The Fastest Way to Insulin Resistance & the Big Lie About Calories! | Dr. Rob Lustig

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Insulin is the bad guy. I can't say it

any simpler than that. Yes, glucose is

bad, too. I'm not saying it's not.

Insulin's worse. Insulin is associated

with all of the diseases of metabolic

syndrome. Type 2 diabetes, hypertension,

dysipidemia, cardiovascular disease,

cancer, dementia. And why are we insulin

resistant? Because our mitochondria is

screwed. Mitochondria are fat. So the

lower the fat that you're eating, the

less well your mitochondria would work.

actually cause the insulin resistance.

This concept of calories is useless.

It's essentially garbage. Calories come

from bomb calorimeters. Our

mitochondria, not bomb calorimeters. So

there's leptin deficiency, there's

leptin resistance. Ultimately, the brain

sees the same thing. Not enough leptin.

But leptin deficiency is a total of 14

people in the world. Leptin resistance

is about 4 billion people. 14 people, 4

billion people. Which you think you

have? You got to fix the leptin

resistance. So, what causes the leptin resistance?

resistance?

Rob, why is excess insulin a problem and

how much is too much?

Why is excess insulin a problem? So,

let's talk about what insulin is.

Insulin is a hormone. It's made in one

place, works in another. It's made by

the beta cells of the pancreas. Works on

not quite every cell, but almost every

cell on the body. Now, for years, we

thought that insulin only had one job,

and that was to deposit glucose into cells.

cells.

Okay, that is

true, but it's way more than that. And

what it really is is it deposits glucose

and fatty acids into different types of

cells and the process

causes energy storage.

So it basically takes energy away from

the mitochondria that would burn it and

puts it in places where the mitochondria

can't necessarily get to it. And the

reason is because mitochondria

are like funnels

and you can basically fill a funnel

slowly in which case the funnel will be

able to direct the flow of uh the fluid

into the bottle you're trying to funnel

it into. But if you over stuff that

funnel and basically provide the liquid

or the even the solid too fast, what

will happen is you'll get it all over

the place. And ultimately your

mitochondria can only take energy at a

certain rate. And so insulin is the way

to divert energy away from the mitochondria.

mitochondria.

So the higher your insulin goes, the

more that's telling you that the

mitochondria are overwhelmed. And when

your mitochondria overwhelmed, that

causes them to be dysfunctional.

And the extra substrate is going to go

into a another storage form of chemical

energy which is not necessarily good for

you in the form of liver fat or you know

peripheral fat. And so high insulin

means energy storage rather than energy

burning. And what you want to be doing

is energy burning. So high insulin is a

bad guy in the story.

Insulin is high insulin is associated

with all of the diseases of metabolic

syndrome. Type 2 diabetes, hypertension,

dysipidemia, cardiovascular disease,

cancer, dementia, fatty liver disease,

polycystic ovarian disease. All eight of

those diseases are associated with high

insulin, i.e. insulin resistance.

That your insulin's not doing its job.

And the reason is because your

mitochondria are not doing their job and

that's why your insulin had to go up.

Okay. So the very top of this chain is

mitochondria becoming overwhelmed, too

much energy.

Let's talk about how they signal to the

body they don't want anymore and how

that leads to more insulin.

Well, I don't think we know how they do

that yet. We have some um uh you know

interesting uh clues to it though. Uh

when your mitochondria are in distress,

they send out distress signals and those

distress signals include mitochondrial

DNA. So you can find mitochondrial DNA

as a sign of mitochondrial um uh shall

we say exhaustion and also extracellular ATP.

ATP.

And that also is a sign that your cells

are on its last legs. It's kind of an

agonal event. And it basically tells the

body um I'm in trouble and it's time for

inflammation to help clean up the mess.

So this is work from Dr. Bob Navio at uh

University of California, San Diego, who

basically looks at mitochondrial uh

function and this concept of

salogenesis, which is the concept of

healing and how the mitochondria are

hooked to this concept of healing. And

it turns out that, you know, when your

mitochondria are not happy, they um they

they they tell you,

okay, so I'm just trying to piece this

together. we have too much glucose in

the system

or fructose in the system.

So either way with either one of those substrates,

substrates,

is insulin bringing that into the cell

to a point until the mitochondria say no more?

more?

Well, no. What's doing is insulin is

diverting it away from those cells so

that the mitochondria have a chance to basically

basically

burn it all the way through.

But doesn't the glucose need the insulin

to get into the cell?

Yes, that's the and that's the problem.

That is the problem. Certain cells need

insulin for glucose to get into the

cell. So, which cells need glucose to

get into the cell? Okay, the liver

and the fat tissue.

Now the muscle does not need glucose to

get into the cell because if the gluc if

if if muscle needed insulin to get

glucose into the cell then every type 1

diabetic would be paralyzed.

Now insulin does have effects on the

muscle, no question. But it's not for

glucose. It's for amino acids.

So insulin is necessary to get amino

acids into the muscle cell. And that's

for growth. In order to increase muscle

size, muscle mass, you need those u

amino acids to make the actin and the

meosin that basically make the muscle fibers.

fibers.

So insulin is very important for muscle

growth, but it is not necessary for

muscle burning.

Okay, let's take another cell besides muscle.

muscle.

So insulin's needed to get that glucose

into the cell. Mitochondria become overwhelmed.

overwhelmed.

Let's take brain as an example. There's

insulin made in the brain. There are

insulin receptors in the brain. So your

brain must need insulin, right? On the

other hand, if you have no insulin, your

brain still works fine.

Okay? As type 1 diabetics, they're not

unconscious. They're not comeosse.

Okay? In fact, glucose gets into neurons

without insulin. And the reason is

because insulin affects really only one

glucose transport, two glucose

transporters, glute 2 and glute 4. Okay.

Glute 5 is the fructose transporter.

Glute 3 is insulin independent and glute

one is insulin independent. Glute one is

the one that's in the brain. So in fact

your brain does not need insulin to get

the glucose into the brain. It goes in anyway.

anyway.

So what's insulin doing in the brain?

Why are there insulin receptors in the

brain? And are there insulin receptors

on all brain cells? No. Where are the

insulin receptors? They're in the hypothalamus.

hypothalamus.

They're in the vententral tegmental

area. They're in areas that are related

to food intake. So insulin is a driver

of food uh uh metabolism. It when your

insulin is working right in your brain,

it's one of the signals that tells you,

"Hey, I'm in the middle of metabolizing

a meal. Cut it out. Don't eat anymore."

So, it's part of the acute satiety response,

response,

but it's not forcing glucose into cells

like it is in say the liver or the

muscle or the fat. All right. Well,

let's take fat for example here. We'll

leave the brain aside too, muscle aside.

I just want to try and get most upstream

to understand the fundamentals here

where in my understanding insulin comes

in allows that glucose to get into the

cell and then it's going to go to the

mitochondria. But then I want to tie

this back to what we said before about

the mitochondria becoming overwhelmed.

Then it's going to signal, we're not

exactly sure how,

that we have enough energy here. I'll

have you take it. What the insulin did,

what the insulin did was it forced the

glucose into the cell, but it didn't

necessarily say go to the mitochondria.

It might be going to fat

for storage. It's basically taking the

uh the weight of the of what you're

bringing in and diverting it away from

the mitochondria so that the

mitochondria don't get even more

dysfunctional than they already are. So

insulin is driving energy away from

mitochondria, not toward mitochondria.

So it's going into cells, but it's not

going toward mitochondria.

Okay. So what takes it from somewhere in

the cell to the mitochondria?

The lack of insulin.

Um so the first step is glucose has to

be converted to pyrovate and that's and

that is the process called glycolysis.

So that gen generates a little bit of

ATP. There is a glucose uh uh uh uh

there's an enzyme that increases glucose

uh uptake into cells. That enzyme is

called PI3 kynise phosphotidal andositol

3 kynise. This is the enzyme that Luke

Canley at uh first at Harvard and then

at Cornell uh discovered and showed that

this is the primary way by that cancer cells

cells

snarf up glucose is that their P3 kynise

is turned on way high and they'll grab

all the glucose they can irrespective of

the insulin level. Okay. And so they're

not it's not necessarily insulin

dependent. The the PI3 kinace will grab

and snarf whatever glucose is floating

by. And the more PI3 kinace that's

activated, the more glucose will enter

the cell because cancer cells need lots

and lots of glucose because cancer cells

don't have functional mitochondria.

They ferment to make their ATP. they

don't burn it in mitochondria to make

their ATP.

So cancer cells and also fetal cells by

the way you know during pregnancy same

thing you don't you need ATP but you

don't necessarily

need um uh insulin to uh uh uh generate it.

it.

So uh insulin will come in uh sorry

glucose will come in sorry insulin

basically tells the cell don't send it

to mitochondria send it to storage.

Insulin is the energy storage hormone.

More insulin

more energy stored either as glycogen in

the liver and as fat everywhere else.

Okay let's talk about our fat cell here.

Somebody consuming too much sugar, too

many carbs,

blood sugar goes up, insulin goes up,

the fat cells getting this glucose

deposited within it,

fatty acids, right?

right?

Okay, explain that part. The fatty acid

on top of that.

So the fatty acids will be in the LDL

or in the VLDL, the triglyceride, either

or. And the glucose will be you know on

its own glucose circulating and the u

insulin will stimulate the glute for

transporter for glucose to get across

into the fat cell and then that glucose

can be turned into triglyceride in the

fat cell to increase fat stores.

In addition, the insulin will stimulate

another enzyme on the fat cell called

lipoprotein lipase. And that enzyme will

snarf and soak up and suck up

circulating lipid off LDL and VLDL

and throw it into the cell where it then

gets um uh turned into uh triglyceride

as well. So you have two things two two

different transport mechanisms in the

fat cell and both are insulin driven.

The glute 4 transporter is insulin

driven and lipoprotein lipase is insulin

driven. The glute 4 transporter is for

the glucose.

The lipoprotein lipase is for the fat.

Either way you're making more fat. So

insulin's really good at making fat.

Well, let's take the story even further.

Somebody's doing this over a long period

of time. Fat cells are continuing to get

That is the body's natural way of

storing energy. When does that become problematic?

problematic?

Right? So, how much fat is too much fat?

That's the question you're asking.

Well, first remember that there are

three fat depots in the body. Okay? The

fat depot that you're thinking about

right now and that we'll talk about this

moment is the subcutaneous or big butt

fat. But there are two other fat depots

that we have to deal with and we'll do

that after. Okay. The other one the

other two are the visceral fat or the

big belly fat and also the liver fat. So

we have big butt fat, big belly fat and

liver fat. And they're not all the same.

They have different qualities. They have

different regulatory mechanisms. They

have different stimuli. And they have

different blood supplies. And they all

do different things for your body or

against your body.

Before you get into this, let me set the

scene. We're taking in too much energy.

The body storing fat. You've talked

about these three different areas that

it can go into.

Does it go into one before the others?

Which fat depot it goes into depends on

the metabolic status of the individual

at the time the fat came in

that the energy came in. So I can't

answer that question because everybody's

different at at different times of the

day and at different points in their

life. And uh you know it's it's it's

much more complicated than one takes

precedence over the other. Now if you

are insulin sensitive

insulin sensitive

the preferential storage place will be

the subcutaneous or big butt fat. So in

an insulin sensitive person subcutaneous

fat will get the uh the energy first.

Okay. Now,

how much fat can you gain before your

subcutaneous fat becomes a problem?

There is a limit. Everyone has a limit.

And once you go above that limit, then

you start getting into problems. On

average, about 10 kilos, 22 lbs.

So you can most people when they're

insulin sensitive can gain 22 pounds and

show no signs of metabolic mayhem

but at a certain point you reach a an asmtote

asmtote

a a peak and at that peak things then

start to decompensate. So why do they decompensate?

decompensate?

your fat cells snarfing fat or glucose

into the fat cell and building fat and

the fat droplet, the fat vacule gets

bigger and bigger and bigger and so your

fat grows. Your fat cells don't grow,

okay? I mean, sorry, your fat cells

don't multiply, they grow. Okay? You

don't make more fat cells. You grow the

fat cells you have. So the fat vacule in

each fat cell gets bigger and bigger.

And at a certain point, the perilipin

border that circles that fat vacule

where the fat's been placed

can't stretch wide enough. Kind of like

a balloon. Okay? Every balloon has a

point at which it can't hold the air

anymore and it bursts. Well, kind of

like that for a fat vacule. You put so

much in, you put so much in, you put so

much in, it gets bigger, bigger, bigger,

bigger, and finally the perilipin border

can't hold it all. And when that

happens, it starts leaking. And then the

fat that should be in the fat vacule now

ends up in the cytoplasm of that cell

and that chokes off the cell and now

that cell will die.

You have killed that fat cell. Well, now

you have basically a uh you know a uh a

grease uh um uh uh problem. Okay, you

got to clear the grease. Okay.

So, what do you do? You recruit that

fat, that dead fat cell with all those,

you know, uh with all those fatty acids

that have now spilled out and have

killed that cell. Okay. That has to

ultimately be um uh you know, you have

to call in the the cleanup crew and

that's the macrofasages. And so, that

recruits the macroofasages to come and

chew up all that grease and you know,

get it out of the body. Okay. In the

process, those macrofasages secrete

cytoines which basically bring more macrofasages

macrofasages

and so now you've got an whole

inflammatory process going on. And then

those macrofasages, those cytoines end

up in the bloodstream.

And the level of the cytoines like TNF

alpha and IL6 will go up.

The question is do they go up to the

point where they start affecting other organs

organs

and the answer is depends on how much

fat you're dealing with and it also

depends on the volume of distribution of

the liquid which happens in this case to

be blood. So the volume of distribution

of the peripheral you know blood system

of your body which is you know basically

you know all the blood is 6 L.

Okay. So you're basically increasing

protein concentrations, you know, these

inflammatory proteins in the blood and

you're putting it into a 6 L volume.

Well, 6 L is a lot of blood and so the

you know that you have to generate a

huge increase in those cytoines

before it will reach a concentration

that will ultimately affect the liver or

affect the brain or affect some other

part of the body in a negative fashion.

So in general

your subcutaneous fat can expand by

about 10 kilos

before the uh amount of cytoines that

are generated by those you know dying

fat cells reach a point that it causes

metabolic mayhem.

Okay, that's where your body wants to

put the fat, put the extra energy. Now,

Now,

there are two other places. There's the

visceral fat and there's the liver fat.

So, let's talk about each one of those

separately. Now, visceral fat.

What drives visceral fat accumulation?

What drives big belly fat accumulation? Answer,

Answer,

not calories.

The answer is cortisol.

Now, how do we know that? Okay, cuz in

general, big belly fat goes up when big

butt fat goes up, too. They go up

together. Okay, it's un it's rare for

one to be separate from the other, but

it happens. And that's the key is when

does it happen that the big belly fat

goes up and the big butt fat goes down?

And the answer is depression.

Depression, major depressive disorder.

So we have there are patients who are

admitted to the hospital to keep

themselves from themselves. Okay? They

are suicidal. They are major depressive

disorder. Life has lost all meaning and

they want to die. Okay? and we have to

admit them to the hospital, you know,

emerently usually to basically prevent suicide.

suicide.

You take those people, they're not

eating, they're anhydonic, they derive

no pleasure from food, they are losing weight.

weight.

Major depressive disorder results in

weight loss. It's one of the questions

on the Beck Depression Inventory.

do you have weight loss? And the reason

is because people who are depressed

don't eat. They're losing weight.

But you stick them in a scanner

and it turns out their visceral fat's

going up. At the same time, their

subcutaneous fat is going down.

So if visceral fat were due to food,

that wouldn't be happening.

Visceral fat is due to cortisol.

Cortisol increases visceral fat

accumulation. And anything that

increases your stress is going to

increase your visceral fat. Why does

this happen? Because your visceral fat

is much easier to lift the fat out of

than the subcutaneous fat. Subcutaneous

fat is kind of stuck there. It's very

hard to lift it out. That's why women

find it so hard to lose that big butt

even when they're dieting. Okay? They'll

lose it from their belly, but they won't

lose it from their butt because

subcutaneous fat is much harder to fish

it out. Metabolically active fat is the

visceral fat. And so when you're in a

stress situation,

that's your um go-to in terms of getting energy

energy

is the visceral fat. And the reason is

because the visceral fat drains directly

into the liver, drains through the

portal vein. Remember we talked about

the volume of distribution being 6 L for

the subcutaneous fat. Well, for visceral

fat, the volume of distribution is about

250 cc's.

quarter of a liter. So 6 L a quarter of

a liter 24 times the concentration.

So when you start um accumulating

visceral fat,

those cytoines come and they're

releasing those cytoines into the portal circulation

circulation

and the concentration is 24 times

greater because the volume of

distribution of the portal system is way

smaller than the volume of the general

systemic circulation. And that means

that your liver and your brain are going

to see higher levels of cytoines

for a smaller amount of fat that's been

been accumulated.

And so visceral fat is much more potent

as a driver of metabolic disease than is

subcutaneous fat. Visceral fat is a much

bigger problem and that's why stress is

such a an issue in our society because

it's generating visceral fat.

And then finally we have number three

liver fat. Now liver fat.

What makes liver fat? Two things. Sugar

and alcohol.

Sugar and alcohol make liver fat. Does

dietary fat make liver fat? Nah.

What about other foods?

Branch chain amino acids can make liver

fat too, you know. So, lucine isolucine

veene. So, shall we say low quality protein?

protein?

Branch chain amino acids like what is in

protein powder. So, you need those to

make muscle. But when you're not making

muscle, then those end up becoming liver fat.

fat.

uh Chris Nuggard at Duke University for

you know demonstrated this very nicely

is that branch chain amino acids are

part of the problem of liver fat. So

what makes liver fat? Glue uh fructose

alcohol and branch chain amino acids.

You know what that's called? That's

called ultrarocessed food.

So ultrarocessed food drives

calories, therefore subcutaneous fat.

Okay. Does it drive visceral fat? Not

specifically, except that people who are

stressed often try to find solace in

their stress by eating ultrarocessed

food. So it becomes an indirect driver

because of the cortisol which increases

your appetite and then finally it

generates liver fat directly.

Now how many kilos or pounds of liver

fat can you store before you see

metabolic mayhem?

I would be guessing I'll say quarter pound.

pound.

Half a pound. Half a pound. Okay.

Quarter of a kilo. Half a pound. So 10

uh 22 lb of subcutaneous fat equals

about 4 lb of visceral fat equals about

a half a pound of liver fat in terms of

causing problems causing metabolic

problems. So which is the worst?

Sounds like liver.

Liver fat's the worst. And what makes

liver fat? Ultrarocessed food

and alcohol.

And alcohol. Well, that's ultrarocessed.

Okay. So, so it depends on which Fat

Depot. It depends on what the driver is

and it depends on your metabolic status

when it happens. So, not a simple

calculus. It's not something where you

say, "Oh, this then that." You know, you

have to know who the patient is, and

that will tell you where the fat's going

to go.

All right, that was brilliant. I want to

follow up in a lot of different areas here.

here.

Starting with visceral fat. So we know

cortisol is the root cause there.

But if somebody is taking in a lot of

carbs, a lot of sugar,

is there some overspill

from subcutaneous fat? Now, I shouldn't

say overfill because that's two

different systems, but if the body's overwhelmed,

overwhelmed,

can that build up with an abundance of

energy as well? secondarily.

Oh, absolutely. Cuz insulin will drive

energy into visceral fat, but cortisol

is the big driver. But remember, when

you have high cortisol, you're going to

eat a lot.

That's what happens in Cushing syndrome.

Okay? Cushing syndrome is

hypercortisolism and you end up with

this enormous big belly. You end up with

muscle wasting. You end up with thin

arms and legs, but you end up with this

huge big belly. And the reason is

because the cortisol directed all the

fat, you know, all the energy to the

visceral fat.

Okay. Earlier you mentioned the fact

that our fat cells with the subcutaneous,

subcutaneous,

they don't actually multiply. They just

grow in size. Isn't there some of

multiplication? Yeah, explain that.

They multiply till age two.

Okay. So, no multiplying once you're an adult.

adult.

Yeah. Right. Basically, you're you're

done. Now having said that, having said

that fat cells don't multiply but there

are things called patiposytes.

Now they look like fibiberblasts

but they're padatyposytes

and in response to insulin and cortisol

those piatices can turn into fat cells.

So in that way you can grow your fat but

it's not like it's not because they

divided. They're already there. They're

just kind of stringy little wispy things

until they get hit with the hormones

that basically get them to, you know,

finish their differentiation and then so

they can become fat cells. But there's

no cell division that goes on past age two.

two.

So they're kind of like atyposites in obeyance.

obeyance.

They're kind of like, you know,

emergency atyposites, but they're there.

They're just not dividing.

They're waiting to be ballooned up by

the right hormonal environment.

Kind of like having a spare tire that

doesn't have any air in it.

It's there. God forbid you should need

it, but you got to put some air in it

for it to work.

Let's zoom back and talk about our

thesis as a whole. So, we're having too

many carbohydrates, too many sugars.

We're raising insulin.

You talked about the chronic diseases

associated with that throughout the

body. But let's get into physiology

wise. What's actually happening there?

Every cell in your body has a point in

time in its life when it wants to grow.

And every cell in your body has a point

in time when it wants to burn.

growth, burn, growth, burn. Now, the

substrate for both is glucose. Glucose

causes growth. Glucose causes burning.

That's true. But there's a switch in the

cell that determines, am I going to grow

or am I going to burn?

Now, let's do a little thought experiment.

experiment.

Each of us starts out as a one cell, a

zygote. Okay? sperm and egg meet, you

get a zygote. One cell. Now that one cell

cell

becomes two.

Those two cells become four.

Four cells become eight. Okay? Eight

cells become 16. Okay? You starting to

get to an embryo, right? And then and

there's a doubling and a doubling and a

doubling and a doubling and you end up

with a baby. And then that baby has to

then become an adult.

Okay? So you start out with one cell

and that has to become an adult of 10

trillion cells.

So you go from one cell to 10 trillion cells.

cells.

How many doublings does it take to get

from one cell to 10 trillion cells?

Probably less than we think because when

we start getting up there

it's an exponent. So, it's 2 to the what

equals 10 trillion?

I don't know. I'm just assuming it's

like the penny doubling thing where it

seems like it's nothing and then

eventually it's just like flips on a

dime. I'm assuming similar kind of thing.

thing.

So, how many is it, Jesse?

35.

You're not not too bad. Way closer than

most. 41.

2 to the 41 doublings gets you to be an

adult. You go from zygote to adult. 41

dlings. Now, some of those will have

occurred in uterero and some of those

will have occurred after birth.

Now, how many of them how many of the

doublings occurred in uterero and how

many of the doublings occurred after

birth? So, I need two numbers that add

up to 41.

Okay, I'll say

39 and two.

Not quite, but you got the right idea.

Okay, it's 36 and five.

So 2 to the 36 gets you to a newborn

and then the last five gets you to an

adult. People freak out when you think

about that, but I mean I'll I'll do it

for you. Okay, standard baby 7 lb. Okay,

first doubling 14 lb. Second doubling 28

lb. Third doubling 56 lb. Fourth

doubling 112 lb. Fifth doubling 224 lb.

So adult with metabolic syndrome. Okay.

So 2 to the 41 36 in uterero and five

after birth.

Kind of cool, huh?

When you think about it. So

there has to be a method for the body to use

use

to go from

growth in uterero

to slowing down growth and ultimately

burning as an adult.

How does that happen? And the answer is

whole bunch of hormones.

Okay? But ultimately there are three

enzymes in each cell that determine

which way the glucose goes. Those three

enzymes, we mentioned one of them

before. PI3 kynise, that's the spigot

that lets the glucose in. The second

one's called AMKase.

That's the fuel gauge on the cell to

tell it whether or not it needs to burn

because ATP is running out.

And if ATP is not running out then you

won't send it and you might send it to

growth instead the glucose. And then the

last one is called mTor mamalian target

of raprapamy. And what that enzyme does

it determines whether the cell's ready

So if your cell is in burning mode, your

PI3 kinace is low, your AMP kynise is

high and your mTor is low.

Conversely, if you're in growth mode,

then it's the opposite. Your PI3 kynise

is high, your AMP kynise is low, and

your mTor is high. So you have burning,

you have growth, and those three enzymes determine

determine

which way the glucose is going to go. Is

it going to growth or is it going to

burning? Okay? And it can't do both.

It's got to do one or the other. Okay?

Think of it like a cord of wood. Okay?

You can do two things with the cord of

wood. You can burn it in a fireplace for

heat, or you can build furniture, but

you can't do both.

Okay, one or the other. And these three

enzymes determine which way it's going

to go. So if you're in growth mode, you

grow. If you're in burning mode, you

burn. And the three enzymes have to be

in synchrony with each other in order to

do that. What if those three enzymes are

not in synchrony? What if they're off?

What if they're not doing exactly what

growth or burning would dictate

everyone? So basically you've got three

enzymes two veilances high low or on off

that means you have two to the three

permutations you have eight permutations

one of them is growth one of them is

burning that means there are six more

every one of those is a chronic disease

it is the dynamy

of those three enzymes that lead to the

chronic disease and so the question is

what did that and the answer is that's

our envirment environment. That's our nutrition.

nutrition.

Turning those on or off. It turns out

those three enzymes are all kinases.

They're all phosphorolatable.

So that's what a kynise is. You get

phosphate put on it and it changes the

enzyme, changes the activity. Okay? So

kynise can turn on, can turn off based

on its phosphorilation status. Well,

what determines the phosphorilation

status? the metabolic status inside the

cell reactive oxygen species

which your mitochondria make. So when

your mitochondria make ROS's it tells

those three enzymes to go one way and

not the other way. So everything is in

concert as long as those three enzymes

are doing what they're supposed to all

at the same time. When they go when they

fall out of synchrony that's when you

end up with disease.

And those are determined by what the

mitochondria is doing. Fix the

mitochondria. Fix the whole thing.

I had asked about insulin

and its contribution to the chronic

diseases. Connect that piece with what

you just said. Well, so when your

mitochondria are not working, the

insulin is going to basically have to go

up in order to divert the glucose away

from the mitochondria, the pyrovate away

from the mitochondria to go to something

else. So the pyrovate can be used in the

Randall cycle to make uh uh proteins or

it can be used in the denovo lipogenesis

to make lipids or it can be used in the

um uh pentos phosphate shunt to make

ribos for DNA. Okay. So you can grow the

cell. Yeah. I mean you can sorry you can

you can you know grow the cell so it can divide.

divide.

Okay. Now you don't want the cell to

divide if you're supposed to be in

burning mode. That's what happens in

your coronary arteries. You get coronary

artery smooth vasc vascular muscular um

uh growth. That's what makes the uh the

coronary artery that much uh thicker and stiffer.

stiffer.

And then it's a lot easier for a plug,

you know, for a thrombus to come, you

know, plug it up and now you have a

heart attack.

Okay. In addition, that insulin is a

growth factor. And so when the insulin

goes up, it causes glands to grow. And

when glands grow, much more chance for a

tumor to develop. So there's your breast cancer.

cancer.

Okay? And insulin causes diversion of

energy in the brain away from neurons

because the insulin receptors are on

astraytes. Okay? And so they end up

storing glycogen. And when they store

glycogen that starts the phosphotau

thing and that's been associated with Alzheimer's.

Alzheimer's.

So the more insulin,

the more growth

and the more growth when it's not

supposed to grow, the more risk for disease.

disease.

In this whole thesis of too many carbs,

too much sugar, raising the insulin,

there's a double-edged sword here. We

just talked about the insulin piece and

the damage it can cause, but elevated

blood glucose can cause small vessel

damage as well. Bring that piece in. So

glucose is like grains of sand. Okay?

The higher your blood glucose goes, the

more grains of sand you got. Okay? Now,

if you only have a couple grains of

sand, like you've got liquid going, like

no big deal. Okay? But what if you have

a lot of grains of sand and you have

liquid going? it might actually damage

the inside of your um of your uh vascule.

vascule.

So high glucose causes

uh dysfunction of the internal vascule

especially small vessels. So causes

microvascular disease causes

retinopathy, nephropathy, neuropathy,

you know problems in the eye, problems

in the nerve, problems in the kidney. So

high blood glucose due to say type 1 diabetes

diabetes

will take its toll irrespective of

insulin or not. But

But

high blood insulin will cause

macrovascular disease because of that

growth that we just talked about

irrespective of the glucose.

So they do two different things to the vascule

vascule

and they're both bad, but they're

different. So the high blood glucose

causes small vessel disease. The high

blood insulin causes large vessel disease.

disease.

And usually you end up with both because

that's what diabetes is, is high blood

glucose and high blood insulin. So you

end up with both.

So there's type two diabetes for you.

What's I've always found interesting as

a pediatrician, you know, we always had

type 1 diabetes. You know, that was

always in our portfolio, but now we have

type 2 diabetes too, which we never had.

You know, when I entered medical school,

type 2 diabetes in children was unheard

of. It was reportable. Now it's

one-third of all patients.

Okay? And it happened on my watch. And

so when I learned diabetes, I learned

type one.

And what we learned was that it took

years and years and years of high blood glucose

glucose

to affectuate that microvascular disease problem.

problem.

But what was interesting was when type 2

diabetes came around.

We could see patients in clinic,

pediatric patients, adolesccents who

didn't have diabetes yet, but they had

high blood insulin. They had insulin resistance.

resistance.

They were obese, but they were not

diabetic. They had normal blood

glucosis. They had normal glucose

tolerance. So, it wasn't from hypoglycemia,

hypoglycemia,

but they already had albumin in their

urine. They had micro albuminura.

They already had the renal the kidney manifestation

manifestation

of insulin acting on the kidney.

and they were adolescents,

not 40 years later. They were already

kids. They were just kids and they

already had signs of insulin damage.

So people think diabetes is because of

high blood glucose. They think that all

the damage is due to the high blood glucose.

glucose.

That is wrong. That is a mistake. That's

because they didn't live through it like

I did.

In fact, in 2008, the group at um at uh

Joselyn, okay, Suda Biddinger was the um

uh first author, but this was in Ron

Khan's lab, developed my favorite mouse

in the whole world. I love this frigin

mouse. Best mouse ever. Okay, this mouse

basically sends everybody back to

medical school because it is so paradoxical.

paradoxical.

It is so out of line with everything we

learn in medical school. And it's true.

And you know, I mean, it's because what

we teach in medical school is wrong.

Okay? And this is the mouse that proves

they're that they're wrong. Okay? This

mouse is called the Padurkco mouse. P O

D I R KO.

What is it? It is the insulin receptor

has been lifted genetically out of the

kidney of this mouse. Okay. The rest of

the mouse is perfectly fine.

Wild type mouse everywhere except the kidney.

kidney.

No insulin receptor in the kidney.

So this animal has normal glucose

tolerance because the beta cells work fine.

fine.

This animal has normal liver because the

liver works fine. This animal has normal

brain because the brain works fine.

But this animal has the worst diabetic

nephropathy, worst diabetic kidney

disease of any animal model on the planet.

planet.

Normal blood glucose,

worst diabetic nephropathy.

If glucose is the cause of the kidney

disease, how does this animal that has

normal glucose have the worst kidney disease?

disease?

That's why everyone has to go back to

medical school to figure that out.

Okay. And the answer is because it's not

the glucose that caused the damage.

It's the insulin.

So these animals have normal insulin,

but the insulin is not working at the

kidney. And so they end up with diabetic

nephropathy. They end up with diabetic

kidney disease.

That's telling us that it's the insulin

that's the problem. And that's why these

adolescents who don't have diabetes yet

have micro albuminuria which is the

first sign of of the you know transition

to metabolic syndrome to to diabetic

kidney disease even with normal glucose.

So insulin is the bad guy. I can't say

it any simpler than that. Yes, glucose

is bad too. I'm not saying it's not.

Insulin's worse.

Hence why I opened up with that and

we've been focusing on it.

Well, insulin's a good thing to focus on.

on.

What's the youngest you've seen somebody

acquire type 2 diabetes? And the reason

I asked that is because in our world,

it's common knowledge that insulin

resistance can go on in the background

for a decade or even more.

Oh, yeah.

Before somebody becomes type 2 diabetic.

So I would assume

in kids it would still take a period of

time before they get to that point. So

what's what's the youngest you see?

Age five. Wow.

Wow.

I've seen a 5-year-old type 2 diabetic. Crazy.

Crazy.

Yeah. Now there are genetic forms of

type 2 diabetes which are you know even

earlier like for instance rebs and

mendenhole and leprechonism. Okay. They

have genetic defects in the insulin receptor.

receptor.

So they have basically, you know,

insulin receptor deficiency to start

with. They're like the pedural mouse

many times over because it's in every

organ. Okay? And you find those out like

in the normal newborn nursery because

they're they're sick as hell. And their

blood glucose ends up in the hundreds.

And when you measure their insulin, it's

also in the thousands. Okay? But the

insulin because there's no receptor to

bind to can't bring the glucose down.

Those babies, the leprechauns

especially, they die by age one. Okay?

Nobody, nothing can save them. Okay? We

haven't figured out how to fix those

babies yet. And I took care of those

babies, you know, as a pediatric

endocrine, you know, endocrinologist.

You know, they're rare, but they come,

you know, I would say probably one every

five years, you know, so I've taken care

of like three of them. Okay, they're

always always disasters.

But that's not what's happening in most

people. Most people it's insulin

resistance occurring not because of a

genetic defect but because of some

functional defect. And that functional

defect is usually mitochondrial dysfunction.

dysfunction.

Okay, so insulin's the bad guy today.

We mentioned the fact that this can go

on in the background for over a decade

causing disease silently in the background.

background.

Given that, what are some symptoms

people can look to

without going to the doctor to realize

if they're in that period of say 10, 15

years where things are a show

behind the scenes? And then objectively

when they go see their doctor, what

testing can they have done to see where

they're at on the spectrum, right?

So the question is, how do you diagnose

high insulin? And the answer is by lab

tests. But are there s signs or symptoms

that will tell you that? And the answer

is yeah, there are a few. There are a

few. Okay. So the first of course is

increasing waist circumference.

That'll tell you you're insulin

resistant. Okay. The second is insulin

doesn't just bind to the insulin

receptor. Insulin also binds to the

epidermal growth factor receptor, the

EGF receptor. This is on your skin and

it's particularly prevalent on extensor

surfaces of the skin. So like your

knuckles or the back of your neck or

behind your knees or in the cleavage

areas like under your uh bra strap,

okay? Or under the mammary gland, okay?

And what will happen is it will thicken

it up. Okay? Look like sort of like um

um alligator skin. Okay. And often uh

it'll change color. It's particularly

noticeable in African-Americans.

Okay. And so this has a name. It's

called aanthosis nigricans. Aanthosis.

When I was a med student in 1976.

Robin's pathology textbook had one

sentence on athtosis nigricans.

Okay. It was rare. I never saw it in

pediatrics all through my residency.

And now every kid in America has it if

you know where to look.

And so what that's telling you is that

the insulin level in the blood is high

because that's a manifestation of

insulin binding to this epidermal growth

factor receptor on the skin. So when you

see that, you don't even have to draw

the blood. You already know you got a problem.

problem.

And I would point this out to parents in

clinic. I would say to the mom, say,

"Mom, come over here. Look at the back

of the neck." Okay. What do you see? Oh,

rash. It's not a rash. Okay. Okay. You

um or ring around the collar. A lot of

them think it's ring around the collar.

I say, "Have you ever tried to wash it

off?" And they say, "Yeah, doesn't come

off." I said, "Right. Doesn't come off."

And so then I would go to the computer

and I would type in aanthosis nigricans

and so all the images would come up. I

say does that look like yours kid? Oh

yeah. Yeah. Okay. So I explained to them

this is extra insulin working on the

skin. This is a sign of high insulin. So

I don't even have to draw your kid's

blood and I already know what the

problem here is. Okay. And here's the

problem lady. Okay.

Your kid eats insulin's high straight to

fat. Your kids eats insulin high

straight to fat. Kid grows bigger bigger

bigger bigger until finally could get so

huge, so gargantuan, so enormous that

your pancreas, which makes the insulin

in your in your abdomen can't even make

enough for as big as your kid will have

gotten. Your kid basically your kid will

have outgrown its insulin supply. his

insulin supply. And when that day comes,

there won't be enough insulin to the

fat. Then the blood sugar stays in the

blood, starts to rise, and now you got

type two diabetes. That's where this is headed.

headed.

So she goes, "Oh my god, that's

terrible." I go, "Yes, it is. But the

good news is you're here and we could do

something about it if you choose to." Of

course, I won't choose to, right? I say,

'Well, the only thing we can do is get

the insulin down.

Get the insulin down. And the mom say,

'Well, how do you do that? I go, best

way, don't let it go up.

So, what makes it go up? Of course, she

doesn't know. I go, two things. Refined

carbohydrate and sugar.

That's what makes insulin go up, which

is true, by the way. Oh, branch chain

amino acids also make it go up, but

that's a little too much for them at

that point. But that's basically how we

handled all these patients,

you know, basically explaining to them

the clinical manifestations that we

could show them

linked to the pathophysiologic process,

linked to interventions that we know are successful.

successful.

And when they see it on their own kids'

neck and they see that it's a thing on

the computer, okay, it goes away. You

know, the belief system aspect of it

goes away and they start understanding

that they have to start taking in

factual information and that they

actually have to do something

lifestyle-wise to change their uh to to

to change their uh kids trajectory in

terms of metabolic risk.

And I would say 50, you know, based on

our clinic data, 50% of the time that

That wasn't always enough, but it was

enough a lot for an adult that's

noticing they have a lot of belly fat.

They're figuring they're

on this continuum we've been talking

about of insulin resistance.

They come to see you. What's the full

panel of objective tests you do on them

to see where they're at?

We do a bunch of tests, but um you know

the the the best tests are the most

expensive and we don't usually do those

and some of them are research you know

only. So we don't do those. So what do

we do? You know, I mean when when they

come in what what labs do we draw? Okay,

basically here's what we draw. draw a

fasting insulin.

We draw a hemoglobin A1C, but that's the

last thing to change. We draw a fasting

glucose, but that's even, you know,

later to change. Okay. Uh we draw um a

lipid panel and specifically we're

looking at apoan triglycerides

and we also draw an ALT alanine amot

transansferase because that tells us

about liver fat.

That's sort of the basics. That's the

basic package of the lab tests that we

draw. Oh, oh, I forgot. We also draw

uric acid.

And the reason for that is because sugar

makes uric acid go up and uric acid

increases risk for hypertension and gout.

gout.

So, we basically, you know, do cheap,

simple tests that are easily available

that insurance will cover.

And that gives us, I would say, 90% of

what we need to know.

Now, is there more to do? Sure.

But in general, that's enough. You know,

you know, we can get in the weeds on

what the other stuff is. But, you know,

in general, that that's that's what we

can do and that's what insurance will cover.

cover.

Let's come back to fructose. We

mentioned it was one of the three

culprits when it comes to liver fat

along with branch chain amino acids and alcohol.

Let's talk about physiology of fructose

entering the body, the liver and beyond.

You consume fructose.

Okay, first thing is something sweet

hits the tongue. Message goes tongue to

brain. Sugar's coming. Message goes

brain to pancreas. Sugar's coming.

Release the insulin.

Now, if the something sweet turned out

not to be fructose, but to be say an

artificial diet sweetener,

you still get the message release the insulin.

insulin.

Okay? So, keep that in mind. Okay? Sweet

alone generates the insulin, you know,

part of the insulin response. Now, the

rise in the blood glucose will be the

rest of the insulin response. But you

know the sweet alone will have primed

the beta cell to release insulin. So you

get that even before the uh food gets to your stomach.

your stomach. And we can prove that because there's a

And we can prove that because there's a phenomenon called the syphalic phase of

phenomenon called the syphalic phase of insulin secretion.

insulin secretion. You take a patient, you admit them to

You take a patient, you admit them to the hospital overnight.

the hospital overnight. They wake up in the morning, they're

They wake up in the morning, they're fasting, their blood glucose is 70,

fasting, their blood glucose is 70, everything's fine, right? You bring a

everything's fine, right? You bring a tray of food into

tray of food into the room and you let them look at it.

the room and you let them look at it. You let them smell it, but you don't let

You let them smell it, but you don't let them eat it.

them eat it. Got it? And then you take the tray out

Got it? And then you take the tray out of the room.

of the room. What happens to the blood glucose?

What happens to the blood glucose? Nothing. because they didn't eat

Nothing. because they didn't eat anything. What happens to the blood

anything. What happens to the blood insulin? It went up.

insulin? It went up. The more obese, the higher it went up.

The more obese, the higher it went up. But the insulin went up not because the

But the insulin went up not because the glucose changed, not because they ate

glucose changed, not because they ate anything, not because there were

anything, not because there were calories to work on. The insulin went up

calories to work on. The insulin went up because the brain

because the brain thought the food was coming.

syphalic phase of insulin secretion well known dates back you know to the 1970s a

known dates back you know to the 1970s a guy at University of Indiana by the name

guy at University of Indiana by the name of Terry Pley did this work you know way

of Terry Pley did this work you know way back when okay I actually worked on a

back when okay I actually worked on a disorder of that brain to pancreas

disorder of that brain to pancreas connection called hypothalamic obesity

connection called hypothalamic obesity that's how I got into the obesity

that's how I got into the obesity business in the first place with brain

business in the first place with brain tumors that basically

tumors that basically um uh destroyed that area of the brain

um uh destroyed that area of the brain that controls energy, metabolism, energy

that controls energy, metabolism, energy balance, and food intake. And so these

balance, and food intake. And so these kids would become massively obese after

kids would become massively obese after their brain tumor. And I was at St. Jude

their brain tumor. And I was at St. Jude Children's Research Hospital, and I was

Children's Research Hospital, and I was I was charged with figuring out how to

I was charged with figuring out how to help them. Okay, 350 400 lb. Okay, these

help them. Okay, 350 400 lb. Okay, these were kids who were normal weight and

were kids who were normal weight and height until their brain tumor

height until their brain tumor and then all hell broke loose and I had

and then all hell broke loose and I had to figure out what to do for them. And

to figure out what to do for them. And what we did was we gave them a drug that

what we did was we gave them a drug that suppressed insulin release

suppressed insulin release because we postulated that their problem

because we postulated that their problem was that the brain thought they were

was that the brain thought they were starving because that area of the brain

starving because that area of the brain was dead. And so their vag nerve, which

was dead. And so their vag nerve, which was telling the pancreas what to do, was

was telling the pancreas what to do, was telling it generate more insulin because

telling it generate more insulin because we can't see the leptin level. We can't

we can't see the leptin level. We can't see that you know that that energy

see that you know that that energy balance is normal. We think this b that

balance is normal. We think this b that the patient is starving. Therefore

the patient is starving. Therefore release more insulin and so the insulin

release more insulin and so the insulin levels would go skyhigh and that would

levels would go skyhigh and that would drive everything into fat. But we

drive everything into fat. But we couldn't fix that because the brain was

couldn't fix that because the brain was you know that area of the brain was

you know that area of the brain was dead. So what we did was we basically

dead. So what we did was we basically stopped the pancreas from making extra

stopped the pancreas from making extra insulin and lo and behold they started

insulin and lo and behold they started losing weight. But even more

losing weight. But even more importantly, they started exercising

importantly, they started exercising spontaneously. These were kids who sat

spontaneously. These were kids who sat on the couch, ate Doritos, and slept.

on the couch, ate Doritos, and slept. And now, because we got their insulin

And now, because we got their insulin down,

down, they had energy to burn instead of to

they had energy to burn instead of to store.

store. And so, they started being much more

And so, they started being much more active. And the parents would say, "Oh

active. And the parents would say, "Oh my god, I got my kid back." And the kids

my god, I got my kid back." And the kids would say, "This is the first time my

would say, "This is the first time my head hasn't been in the clouds since the

head hasn't been in the clouds since the tumor.

tumor. We reversed their metabolic mayhem by

We reversed their metabolic mayhem by getting their insulin down.

And that's just at the level of the tongue.

tongue. Okay. So now

Okay. So now the fructose goes further down gets into

the fructose goes further down gets into the stomach. Okay. It doesn't do

the stomach. Okay. It doesn't do anything in the stomach but then goes

anything in the stomach but then goes into the dadum.

into the dadum. And then the question is what happens to

And then the question is what happens to it there?

it there? And several things happen to it there.

And several things happen to it there. The first is that

The first is that your intestinal cells

your intestinal cells can actually turn fructose into fat.

can actually turn fructose into fat. Intestinal denovo lipogenesis. And so

Intestinal denovo lipogenesis. And so about 10% of the fructose load will get

about 10% of the fructose load will get turned into fat in the intestine

turned into fat in the intestine right away and get absorbed through the

right away and get absorbed through the lactals and into the lymphatic system

lactals and into the lymphatic system and come out and it's ky they're

and come out and it's ky they're kyomicrons and they get circulated and

kyomicrons and they get circulated and they go to the liver and they get

they go to the liver and they get cleared

cleared just 10% of the fructose load

just 10% of the fructose load but that leaves 90% of the fructose load

but that leaves 90% of the fructose load still there. And what happens then?

still there. And what happens then? So there's an enzyme in the intestine

So there's an enzyme in the intestine and it's called TXNP. TXNIP, thod

and it's called TXNP. TXNIP, thod thyroid inhibitory protein. Thyroidxin

thyroid inhibitory protein. Thyroidxin inhibitory protein. And this enzyme

inhibitory protein. And this enzyme basically

basically ratchets up the ability to absorb

ratchets up the ability to absorb fructose.

fructose. So, if you've never seen fructose and

So, if you've never seen fructose and you get a big bolus,

you get a big bolus, you don't absorb it. And the reason is

you don't absorb it. And the reason is because you haven't activated this

because you haven't activated this enzyme yet. And so, you end up with bad

enzyme yet. And so, you end up with bad diarrhea.

diarrhea. And pretty much anybody who goes crazy

And pretty much anybody who goes crazy on Halloween knows about bad diarrhea.

on Halloween knows about bad diarrhea. It's because they hadn't activated

It's because they hadn't activated enough of their TX nip. Okay? But if you

enough of their TX nip. Okay? But if you had Halloween every day,

had Halloween every day, then you wouldn't get diarrhea. you'd

then you wouldn't get diarrhea. you'd get fat instead. And it's because you

get fat instead. And it's because you ratcheted up your TXNIP. This is work

ratcheted up your TXNIP. This is work from Richard Lee at Harvard of this

from Richard Lee at Harvard of this whole TXN thing. Okay? that increases

whole TXN thing. Okay? that increases fructose absorption at the level of the

fructose absorption at the level of the intestine. And then that fructose goes

intestine. And then that fructose goes to the liver

to the liver and the glute 5 transporter in the liver

and the glute 5 transporter in the liver will suck that fructose out of the

will suck that fructose out of the portal system

portal system to a point. There's a limit to how well

to a point. There's a limit to how well that glute 5 transporter will work. If

that glute 5 transporter will work. If you over

you over uh uh stimulate, if you basically, you

uh uh stimulate, if you basically, you know, drink a 20 ounce Coke, which has

know, drink a 20 ounce Coke, which has way too much fructose for the u for that

way too much fructose for the u for that glutive transporter, then the liver will

glutive transporter, then the liver will grab what it can, but it can't grab

grab what it can, but it can't grab enough. And so you will end up with a

enough. And so you will end up with a serum fructose level that will be pres

serum fructose level that will be pres present in the peripheral circulation.

present in the peripheral circulation. So normally your fructose level in your

So normally your fructose level in your blood is zero because it doesn't make it

blood is zero because it doesn't make it past your liver. It goes intestine to

past your liver. It goes intestine to liver and goes, you know, and that's it.

liver and goes, you know, and that's it. But if you overwhelm your liver's

But if you overwhelm your liver's capacity,

capacity, then you will end up with a fructose

then you will end up with a fructose level. So what happens if you do that

level. So what happens if you do that and you drink that 20 oz Coke? Turns out

and you drink that 20 oz Coke? Turns out there are fructose receptors on beta

there are fructose receptors on beta cells and that makes them secrete more

cells and that makes them secrete more insulin because they have to clear it.

insulin because they have to clear it. And that's like a real disaster because

And that's like a real disaster because now you've got everything going wrong.

now you've got everything going wrong. But what happens in the liver to the 85%

But what happens in the liver to the 85% or so that gets cleared by that glute 5

or so that gets cleared by that glute 5 transporter goes into the cell. Fructose

transporter goes into the cell. Fructose gets converted to fructose 1 phosphate

gets converted to fructose 1 phosphate by the enzyme fructokinace.

by the enzyme fructokinace. And fructose 1 phosphate then gets

And fructose 1 phosphate then gets chopped up into two two three carbon

chopped up into two two three carbon fragments. and then they get turned into

fragments. and then they get turned into pyrovate at the level of the

pyrovate at the level of the mitochondria. They do not uh get turned

mitochondria. They do not uh get turned into glycogen.

into glycogen. So fructose does not go to glycogen.

So fructose does not go to glycogen. Glucose does go to glycogen. Fructose

Glucose does go to glycogen. Fructose does not go to glycogen. Fructose goes

does not go to glycogen. Fructose goes to the mitochondria. And that's one of

to the mitochondria. And that's one of the reasons why the mitochondria get

the reasons why the mitochondria get overwhelmed

overwhelmed because there's too much pyrovate at the

because there's too much pyrovate at the level of the mitochondria for the

level of the mitochondria for the mitochondria to handle because there was

mitochondria to handle because there was too much fructose coming into the cell

too much fructose coming into the cell in the first place.

in the first place. And so that's when the mitochondria go

And so that's when the mitochondria go don't do that and send that pyrovate off

don't do that and send that pyrovate off to become citrate then ail coa and then

to become citrate then ail coa and then that ail coa becomes malanil coa and the

that ail coa becomes malanil coa and the malanil coa then gets turned added two

malanil coa then gets turned added two carbon fragments at a time and you end

carbon fragments at a time and you end up with um fatty acids. That's how you

up with um fatty acids. That's how you end up with triglyceride. That's how the

end up with triglyceride. That's how the fructose becomes triglyceride. It goes

fructose becomes triglyceride. It goes to pyrovate first, then tries to enter

to pyrovate first, then tries to enter the mitochondria, can't. Gets thrown off

the mitochondria, can't. Gets thrown off as citrate. The citrate becomes acoa,

as citrate. The citrate becomes acoa, then malanil coa, and then fatty acids.

then malanil coa, and then fatty acids. Then those fatty acids get packaged with

Then those fatty acids get packaged with like the microsal transfer protein. And

like the microsal transfer protein. And now you have a VLDL. Now you have a

now you have a VLDL. Now you have a triglyceride molecule. And that

triglyceride molecule. And that triglyceride molecule can leave the

triglyceride molecule can leave the liver and increase your serum

liver and increase your serum triglycerides and serve as a substrate

triglycerides and serve as a substrate for either obesity or cardiovascular

for either obesity or cardiovascular disease. Or that triglyceride molecule

disease. Or that triglyceride molecule won't make it out of the liver at all

won't make it out of the liver at all and will precipitate as a lipid droplet

and will precipitate as a lipid droplet and now you have fatty liver disease.

and now you have fatty liver disease. And when you have fatty liver disease

And when you have fatty liver disease that generates the insulin resistance

that generates the insulin resistance and now your pancreas is going to make

and now your pancreas is going to make more insulin to make the liver do its

more insulin to make the liver do its job.

job. So, you've got the high insulin,

So, you've got the high insulin, you've got the fatty liver,

you've got the fatty liver, and you have the metabolic mayhem.

and you have the metabolic mayhem. Let's come back to the leptin piece.

Let's come back to the leptin piece. Make sure we all understand that.

Make sure we all understand that. Let's first talk about in a normal

Let's first talk about in a normal healthy body how that works and then how

healthy body how that works and then how insulin

insulin blocks

blocks leptin and how that works in the brain

leptin and how that works in the brain for somebody that's insulin resistant.

for somebody that's insulin resistant. So this is actually work I did um I'm

So this is actually work I did um I'm published in this u quite a while ago.

published in this u quite a while ago. Um so there's this hormone leptin. We

Um so there's this hormone leptin. We discovered leptin in 1994.

discovered leptin in 1994. Okay. And what leptin does is it's a

Okay. And what leptin does is it's a signal from the fat cell to the brain.

signal from the fat cell to the brain. Hey, I have enough energy on board. I

Hey, I have enough energy on board. I don't need to eat so much. I can also

don't need to eat so much. I can also engage in expensive metabolic processes

engage in expensive metabolic processes like puberty, pregnancy.

like puberty, pregnancy. Okay. No leptin, no puberty. No leptin,

Okay. No leptin, no puberty. No leptin, no pregnancy.

no pregnancy. Leptin is a permissive factor for

Leptin is a permissive factor for using energy for expensive stuff that

using energy for expensive stuff that costs energy because the leptin's

costs energy because the leptin's telling the brain, "I got it. Don't

telling the brain, "I got it. Don't worry. I got your back."

worry. I got your back." All right. Now, leptin deficiency,

All right. Now, leptin deficiency, therefore, is read by the brain as

therefore, is read by the brain as starvation.

But these people aren't starving. They're

these people aren't starving. They're fat.

fat. Why do they keep gaining weight? If

Why do they keep gaining weight? If leptin tells your brain you have enough,

leptin tells your brain you have enough, why doesn't it stop you? It should, but

why doesn't it stop you? It should, but it's not. Something's broken with the

it's not. Something's broken with the negative feedback. The servo mechanism

negative feedback. The servo mechanism is not not working because the leptin is

is not not working because the leptin is not telling the brain what's going on.

not telling the brain what's going on. That's called leptin resistance.

That's called leptin resistance. So there's leptin deficiency, there's

So there's leptin deficiency, there's leptin resistance. Ultimately, the brain

leptin resistance. Ultimately, the brain sees the same thing. Not enough leptin.

sees the same thing. Not enough leptin. But leptin deficiency is all a total of

But leptin deficiency is all a total of 14 people in the world. Leptin

14 people in the world. Leptin resistance is about 4 billion people.

resistance is about 4 billion people. 14 people. Four billion people. Which do

14 people. Four billion people. Which do you think you have?

you think you have? All right.

All right. 14 people, you know, we can give them

14 people, you know, we can give them shots of leptin

shots of leptin and we're replacing the leptin that's

and we're replacing the leptin that's missing and that make basically fixes

missing and that make basically fixes the problem. But if you have leptin

the problem. But if you have leptin resistance, giving extra leptin is not

resistance, giving extra leptin is not going to do anything because you already

going to do anything because you already got enough. It's just not working. You

got enough. It's just not working. You think it's going to work better from a

think it's going to work better from a bottle than it will be from your

bottle than it will be from your bloodstream. Forget about it.

bloodstream. Forget about it. You got to fix the leptin resistance. So

You got to fix the leptin resistance. So what causes the leptin resistance? And

what causes the leptin resistance? And this is the research that I've done. We

this is the research that I've done. We showed that insulin blocks leptin

showed that insulin blocks leptin signaling

signaling in the brain. Insulin blocks leptin

in the brain. Insulin blocks leptin signaling.

signaling. So the higher your insulin goes, the

So the higher your insulin goes, the less well your brain sees leptin.

less well your brain sees leptin. Now,

Now, that is the cut in the servo mechanism.

that is the cut in the servo mechanism. That's what basically turns a negative

That's what basically turns a negative feedback into a positive feedback. That

feedback into a positive feedback. That insulin blocks leptin.

insulin blocks leptin. Now, here's the question of the ages.

Now, here's the question of the ages. Why would God do that to us?

Why would God do that to us? What's in it for him for this to have

What's in it for him for this to have occurred as a you know a standard

occurred as a you know a standard phenomenon that only seems to create

phenomenon that only seems to create disease

disease that insulin should block leptin.

that insulin should block leptin. And the answer is we think

And the answer is we think evolutionarily you know thinking like

evolutionarily you know thinking like God now okay there are actually two

God now okay there are actually two times in your life when you actually

times in your life when you actually have to gain weight

have to gain weight and they are puberty and pregnancy.

and they are puberty and pregnancy. [Music]

[Music] If you don't gain weight during puberty

If you don't gain weight during puberty during puberty species dies out.

during puberty species dies out. If you don't gain weight during

If you don't gain weight during pregnancy

pregnancy species dies out.

species dies out. So if your leptin worked right all the

So if your leptin worked right all the time,

time, you could never gain the weight

and the species would die out. So, doesn't it make sense that the same

So, doesn't it make sense that the same hormone that's driving the weight gain

hormone that's driving the weight gain peripherally should be the same hormone

peripherally should be the same hormone that's blocking the leptin signaling to

that's blocking the leptin signaling to keep you eating

keep you eating centrally

centrally that they would be yolked together

that they would be yolked together so that insulin

so that insulin can tell the body and the brain store

can tell the body and the brain store and keep eating.

and keep eating. Because if insulin didn't block that,

Because if insulin didn't block that, then you would store and you'd stop

then you would store and you'd stop because the leptin would go up and that

because the leptin would go up and that would reduce your food intake and so you

would reduce your food intake and so you would never gain the weight. You would

would never gain the weight. You would be the 97 lb weakling on the beach,

be the 97 lb weakling on the beach, never being able to bulk up and

never being able to bulk up and therefore never being able to actually

therefore never being able to actually reproduce either.

So insulin blocking leptin actually makes perfect evolutionary sense. And

makes perfect evolutionary sense. And the reason is because we're only

the reason is because we're only supposed to be insulin resistant during

supposed to be insulin resistant during puberty, which by the way is a normal

puberty, which by the way is a normal part of puberty. Insulin resistance and

part of puberty. Insulin resistance and also during pregnancy. And insulin

also during pregnancy. And insulin resistance is a normal part of

resistance is a normal part of pregnancy.

pregnancy. The problem is we're insulin resistant

The problem is we're insulin resistant 24/7, 365,

24/7, 365, not just during puberty and pregnancy.

not just during puberty and pregnancy. And why are we insulin resistant?

And why are we insulin resistant? Because our mitochondria is screwed. And

Because our mitochondria is screwed. And why are mitochondria screwed?

why are mitochondria screwed? For all the reasons we've already

For all the reasons we've already discussed, the fructose, the alcohol,

discussed, the fructose, the alcohol, the branch chain amino acids, all the

the branch chain amino acids, all the extra calories. The good news in all

extra calories. The good news in all this,

this, all roads lead back to insulin.

all roads lead back to insulin. And it's a very straightforward process

And it's a very straightforward process to bring that back down. You've already

to bring that back down. You've already mentioned it.

mentioned it. That's not fair. That's not It is not

That's not fair. That's not It is not straightforward. If it was

straightforward. If it was straightforward, it would be easy. It is

straightforward, it would be easy. It is not easy.

not easy. Okay, I'm not saying it's easy, but it I

Okay, I'm not saying it's easy, but it I do believe it's straightforward when

do believe it's straightforward when people have the right information. We

people have the right information. We got to lower the sugars, get rid of

got to lower the sugars, get rid of them, and get rid of processed foods.

them, and get rid of processed foods. Ultrarocessed foods, the bad guy. I also

Ultrarocessed foods, the bad guy. I also want to talk about some of these foods

want to talk about some of these foods that are in a gray area,

that are in a gray area, especially for people that are

especially for people that are metabolically unhealthy like fruit.

metabolically unhealthy like fruit. But the obvious first step is the two we

But the obvious first step is the two we started with there. get rid of those.

started with there. get rid of those. Bring the blood glucose down, bring the

Bring the blood glucose down, bring the insulin down, regain your leptin

insulin down, regain your leptin signaling

signaling and prevent chronic disease and the

and prevent chronic disease and the conditions associated with the elevated

conditions associated with the elevated blood sugar like small vessel disease.

blood sugar like small vessel disease. So, it all leads back to this.

So, it all leads back to this. I'm going to call it a simple strategy,

I'm going to call it a simple strategy, but people don't have the right

but people don't have the right information unless they're tuning into

information unless they're tuning into something like this.

something like this. Well, indeed. You know, the bottom line

Well, indeed. You know, the bottom line is if you think a calorie is a calorie,

is if you think a calorie is a calorie, you're screwed.

you're screwed. It's that simple. Because then you're

It's that simple. Because then you're just going to monitor calories. You're

just going to monitor calories. You're not going to be monitoring your

not going to be monitoring your carbohydrate. You're not going to be

carbohydrate. You're not going to be monitoring your fructose. You're going

monitoring your fructose. You're going to say, "Well, carbohydrate and

to say, "Well, carbohydrate and fructose, they're four calories per

fructose, they're four calories per gram. Fat is 9 calories per gram.

gram. Fat is 9 calories per gram. Therefore, if I'm trying to eat less

Therefore, if I'm trying to eat less calories, I should eat more

calories, I should eat more carbohydrates than fructose and less

carbohydrates than fructose and less fat." Wrong.

fat." Wrong. But that's what we did for, you know,

But that's what we did for, you know, basically 60 years.

basically 60 years. is exactly that. And things only got

is exactly that. And things only got worse.

worse. And that's why they got worse

And that's why they got worse because we basically induced

because we basically induced mitochondrial dysfunction. By the way, m

mitochondrial dysfunction. By the way, m you know what mitochondria are made of?

you know what mitochondria are made of? Bacteria. Ancient bacteria.

Bacteria. Ancient bacteria. Ancient bacteria. But what are they made

Ancient bacteria. But what are they made of?

of? Fat.

Fat. Fat. That's right. They are fat. Okay.

Fat. That's right. They are fat. Okay. Mitochondria are fat. Okay. when you

Mitochondria are fat. Okay. when you take mitochondria and you you know do a

take mitochondria and you you know do a chemical analysis on you know what the

chemical analysis on you know what the structural components of mitochondria

structural components of mitochondria it's fatty acids

it's fatty acids okay so the lower the fat that you're

okay so the lower the fat that you're eating the less well your mitochondria

eating the less well your mitochondria would work

would work actually cause the insulin resistance

actually cause the insulin resistance so you know we got this all backwards in

so you know we got this all backwards in the you know 1940s50s60s7s8s

the you know 1940s50s60s7s8s 90s all the way up. And the reason is

90s all the way up. And the reason is because we thought fat was the bad guy.

because we thought fat was the bad guy. Turns out fat is not the bad guy. Trans

Turns out fat is not the bad guy. Trans fats are the bad guy. No argument there.

fats are the bad guy. No argument there. And trans fats were everywhere. And they

And trans fats were everywhere. And they were they just called those fat. Trans

were they just called those fat. Trans fats are basically poison.

fats are basically poison. Okay. Trans fats are not even

Okay. Trans fats are not even metabolizable because you can't break

metabolizable because you can't break the trans double bond. So you can't even

the trans double bond. So you can't even turn them into energy.

turn them into energy. So you know this concept of calories is

So you know this concept of calories is useless. It's essentially garbage

useless. It's essentially garbage because calories come from bomb

because calories come from bomb calorimeters. You know that's the

calorimeters. You know that's the measurements. We are not bomb

measurements. We are not bomb calorimeters. Our mitochondria are not

calorimeters. Our mitochondria are not bomb calorimeters.

bomb calorimeters. they, you know, depends on,

they, you know, depends on, you know, what they're made of, depends

you know, what they're made of, depends on what comes in, depends on whether AMP

on what comes in, depends on whether AMP kynise is activated or not, depends on,

kynise is activated or not, depends on, you know, a whole bunch of things that

you know, a whole bunch of things that have nothing to do with calories but

have nothing to do with calories but have to do with the, you know, uh,

have to do with the, you know, uh, orbiters of metabolic health.

orbiters of metabolic health. And you know all those previous

And you know all those previous investigators you know in the past

investigators you know in the past basically ignored all of that and

basically ignored all of that and basically led us down a primrose path to

basically led us down a primrose path to destruction.

destruction. So

So insulin is the monitor. It's the arbiter

insulin is the monitor. It's the arbiter of whether you've got a problem or not.

of whether you've got a problem or not. Because when your insulin is low, that

Because when your insulin is low, that means your mitochondria are working.

means your mitochondria are working. Because you don't need to divert energy

Because you don't need to divert energy away from the mitochondria because they

away from the mitochondria because they can take what's coming in. The funnel is

can take what's coming in. The funnel is flowing.

flowing. But when your insulin goes up, that

But when your insulin goes up, that means your mitochondria can't take it.

means your mitochondria can't take it. So what do you need to do? You need to

So what do you need to do? You need to take the load off.

take the load off. Well, what's the load?

Well, what's the load? refined carbohydrate and sugar.

refined carbohydrate and sugar. Insulin's the new calorie.

Insulin's the new calorie. Instead of bringing our calories down,

Instead of bringing our calories down, let's bring insulin down.

let's bring insulin down. I That's what I've been saying for the

I That's what I've been saying for the last um

last um uh 18 years.

uh 18 years. No, I guess I can't trademark that then.

No, I guess I can't trademark that then. No, afraid not. I can't trademark it.

No, afraid not. I can't trademark it. Um, but that's that's been my stickick,

Um, but that's that's been my stickick, you know, for a long time now is get the

you know, for a long time now is get the insulin down any way you can

insulin down any way you can and it works, you know, if you if you

and it works, you know, if you if you can do it, but you have to understand

can do it, but you have to understand what causes it in order to be able to do

what causes it in order to be able to do it. You brought up trans fats there. I

it. You brought up trans fats there. I want to go back and do a 101.

want to go back and do a 101. When we have that double bond, it goes

When we have that double bond, it goes from cyst to trans.

from cyst to trans. luckily now banned in the food supply,

luckily now banned in the food supply, but they can still sneak them in if

but they can still sneak them in if they're under a certain limit.

they're under a certain limit. Where I want to focus though is on

Where I want to focus though is on making them in the kitchen.

making them in the kitchen. That's where I want to go. So talk about

That's where I want to go. So talk about what oils people are using or fats and

what oils people are using or fats and how they can go about making them in the

how they can go about making them in the kitchen so they can avoid that.

kitchen so they can avoid that. Basically, any fat that you use for

Basically, any fat that you use for cooking

cooking can be a trans fat.

can be a trans fat. except lord.

except lord. Except animal fat. Animal fat is

Except animal fat. Animal fat is triglyceride. Animal fat is saturated

triglyceride. Animal fat is saturated fat. Well, if it's saturated fat, then

fat. Well, if it's saturated fat, then there's no double bond. If there's no

there's no double bond. If there's no double bond, there's no way to turn a

double bond, there's no way to turn a cis fat into a trans fat. So, basically,

cis fat into a trans fat. So, basically, there are two kinds of fats. There's

there are two kinds of fats. There's saturated and there's unsaturated.

saturated and there's unsaturated. And there's polyunsaturated. But, you

And there's polyunsaturated. But, you know, ultimately, they're all in the

know, ultimately, they're all in the same category. They have a double bond

same category. They have a double bond in them. somewhere. Now, the double

in them. somewhere. Now, the double bonds are helpful in some cases because

bonds are helpful in some cases because there are hormones and cytoines and

there are hormones and cytoines and factors in our body that need those

factors in our body that need those unsaturated fatty acids to build

unsaturated fatty acids to build specific inflammatory and or metabolic

specific inflammatory and or metabolic machinery.

machinery. Okay. In addition, uh uh omega-3s which

Okay. In addition, uh uh omega-3s which are highly unsaturated. Okay. help

are highly unsaturated. Okay. help membrane fluidity and help neuronal

membrane fluidity and help neuronal transmission. Really important and

transmission. Really important and necessary for your brain, you know, to

necessary for your brain, you know, to to work, right? Okay. So, God knows we

to work, right? Okay. So, God knows we need unsaturated fatty acids.

need unsaturated fatty acids. Saturated fatty acids though won't

Saturated fatty acids though won't uh have no double bonds.

uh have no double bonds. So, you can heat a saturated fatty acid

So, you can heat a saturated fatty acid to any level you want and that will not

to any level you want and that will not turn into a trans fat because there's no

turn into a trans fat because there's no double bond to flip. When you put enough

double bond to flip. When you put enough heat across a double bond, it'll flip.

heat across a double bond, it'll flip. It'll go from a cis to a trans just like

It'll go from a cis to a trans just like that. Okay?

that. Okay? And virtually all of the fats that we

And virtually all of the fats that we cook in, because they're oils,

cook in, because they're oils, pretty much anything that's an oil and

pretty much anything that's an oil and not solid

not solid has double bonds.

has double bonds. So then the question is, are there

So then the question is, are there certain oils that are more likely to

certain oils that are more likely to flip than others? And the answer is yes.

flip than others? And the answer is yes. The more double bonds that are in the

The more double bonds that are in the fat, the more likely one of them will

fat, the more likely one of them will flip. And if they flip, they they're

flip. And if they flip, they they're flipping to become a trans fat. So the

flipping to become a trans fat. So the amount of heat you put across that

amount of heat you put across that double bond will dictate whether or not

double bond will dictate whether or not you're creating trans fats in your own

you're creating trans fats in your own cooker at home, in your own skillet. And

cooker at home, in your own skillet. And that's a problem. And that's one of the

that's a problem. And that's one of the reasons why smoke point became an issue.

reasons why smoke point became an issue. So, what is the um uh uh what is the fat

So, what is the um uh uh what is the fat we cook in the most but has the lowest

we cook in the most but has the lowest smoke point?

smoke point? Olive oil.

Olive oil. Olive oil is terrific. Olive oil is

Olive oil is terrific. Olive oil is wonderful. Olive oil solves a lot of

wonderful. Olive oil solves a lot of problems except for one.

problems except for one. It can heat it high.

It can heat it high. Olive oil was not meant for frying.

Olive oil was not meant for frying. Olive oil was not meant for sautéing.

Olive oil was not meant for sautéing. Olive oil was meant to be used room

Olive oil was meant to be used room temperature on a salad.

temperature on a salad. Okay? And the minute you put um heat

Okay? And the minute you put um heat across that double bond in olive oil,

across that double bond in olive oil, it's going to flip. So you can turn

it's going to flip. So you can turn olive oil into a poison with enough

olive oil into a poison with enough heat. Okay. There are other fatty, you

heat. Okay. There are other fatty, you know, the fatty acids that we use.

know, the fatty acids that we use. There's, you know, um, uh, uh,

There's, you know, um, uh, uh, polyunsaturated fatty acids like canola

polyunsaturated fatty acids like canola oil. They'll turn into trans fats, too.

oil. They'll turn into trans fats, too. And they often have two double bonds

And they often have two double bonds instead of one. Okay? Omega-3s have

instead of one. Okay? Omega-3s have three double bonds. You definitely don't

three double bonds. You definitely don't want to heat omega-3s. In fact, you

want to heat omega-3s. In fact, you don't want to use omega-3s for energy at

don't want to use omega-3s for energy at all. You want to use omega-3s for their

all. You want to use omega-3s for their neuronal um, stabilization properties.

neuronal um, stabilization properties. Okay? So, you take those, you know, as

Okay? So, you take those, you know, as omega-3 pills or you eat fish. Okay? But

omega-3 pills or you eat fish. Okay? But you don't necessarily want to, you know,

you don't necessarily want to, you know, heat the hell out of them. Okay. Then

heat the hell out of them. Okay. Then there are mediumchain triglycerides like

there are mediumchain triglycerides like coconut oil. Okay. And those are

coconut oil. Okay. And those are triglycerides. Those are saturated fat,

triglycerides. Those are saturated fat, but they're shorter.

but they're shorter. So they can be heated high. So a lot of

So they can be heated high. So a lot of that's why a lot of the paleo people use

that's why a lot of the paleo people use coconut oil because you're not going to

coconut oil because you're not going to turn those into trans fats. Okay. The

turn those into trans fats. Okay. The problem with medium chain triglycerides

problem with medium chain triglycerides is they're absorbed a different way.

is they're absorbed a different way. They're absorbed through the portal

They're absorbed through the portal vein, not through the lactals and the

vein, not through the lactals and the lymphatics like we talked about. They

lymphatics like we talked about. They don't get turned into the kyomicrons.

don't get turned into the kyomicrons. They go straight to the liver. And so if

They go straight to the liver. And so if your liver is having a problem,

your liver is having a problem, um mediumchain triglycerides will hit

um mediumchain triglycerides will hit them hardest fastest and that can be a

them hardest fastest and that can be a problem. So it's not like an automatic

problem. So it's not like an automatic that mediumchain triglycerides are good.

that mediumchain triglycerides are good. Depends. Yes. No. Um then you have omega

Depends. Yes. No. Um then you have omega sixs. Omega sixs are you know what's in

sixs. Omega sixs are you know what's in seed oils.

seed oils. And the problem with omega sixs is they

And the problem with omega sixs is they are the precursors to arachidonic acid.

are the precursors to arachidonic acid. And arachidonic acid is the precursor to

And arachidonic acid is the precursor to thromboxines, lucatryins and icosenoids.

thromboxines, lucatryins and icosenoids. Okay. And those are all the things that

Okay. And those are all the things that are necessary for inflammation.

are necessary for inflammation. So, when you add a lot of omega sixs,

So, when you add a lot of omega sixs, you have an increased risk for

you have an increased risk for inflammation.

inflammation. So, we talk about omega 6 to omega-3

So, we talk about omega 6 to omega-3 ratios. Bottom line is if you're

ratios. Bottom line is if you're consuming too many omega sixs, you're

consuming too many omega sixs, you're setting yourself up for inflammatory

setting yourself up for inflammatory response. In addition, in addition,

response. In addition, in addition, omega sixs are usually what are used in

omega sixs are usually what are used in frying

frying and so you get a lot of trans fats. So

and so you get a lot of trans fats. So you can because those omega sixes, you

you can because those omega sixes, you can flip those double bonds. They have a

can flip those double bonds. They have a higher smoking point and they're cheaper

higher smoking point and they're cheaper like soybean oil. Okay? And so you will

like soybean oil. Okay? And so you will use those in friars

use those in friars and that will increase the risk

and that will increase the risk and so uh of metabolic disease because

and so uh of metabolic disease because you've basically turned those omega sixs

you've basically turned those omega sixs into trans fats. So, number one, they're

into trans fats. So, number one, they're precursors to inflammatory uh cytoines,

precursors to inflammatory uh cytoines, and number two, they can be easily

and number two, they can be easily flipped trans fat-wise, and they're

flipped trans fat-wise, and they're cheap, so we use them in friars. So,

cheap, so we use them in friars. So, omega sixes tend to be problematic.

omega sixes tend to be problematic. And then, of course, trans fats

And then, of course, trans fats themselves are, you know, the absolute

themselves are, you know, the absolute worst because they're already bad.

worst because they're already bad. So different fats, different effects,

So different fats, different effects, different risks, everything's different,

different risks, everything's different, you know. So the food industry will tell

you know. So the food industry will tell you a carbohydrate is a carbohydrate, a

you a carbohydrate is a carbohydrate, a sugar is a sugar, a calorie is a

sugar is a sugar, a calorie is a calorie, a fat is a fat, a protein is a

calorie, a fat is a fat, a protein is a protein.

protein. Garbage. Absolute trash. They tell you

Garbage. Absolute trash. They tell you that to assuage their own culpability

that to assuage their own culpability for what they're putting into the food

for what they're putting into the food supply.

supply. But you have to practically be a

But you have to practically be a nutritional biochemist to figure this

nutritional biochemist to figure this all out,

all out, which of course is why things are so

which of course is why things are so screwed up.

screwed up. Whether it be olive oil or one of the

Whether it be olive oil or one of the seed oils like canola,

seed oils like canola, are they ever heated in processing?

are they ever heated in processing? And if so, wouldn't they have to

And if so, wouldn't they have to mark trans fats on the label? I would

mark trans fats on the label? I would assume those would be formed in

assume those would be formed in processing and then they'd have to label

processing and then they'd have to label it. Explain that part.

it. Explain that part. They don't have to label it because they

They don't have to label it because they didn't start with trans fats, but they

didn't start with trans fats, but they can make them. So, there is a uh machine

can make them. So, there is a uh machine at your local ultrarocessed food

at your local ultrarocessed food manufacturer and it is called an

manufacturer and it is called an extruder.

extruder. Okay? It's what makes Cheetos. Do you

Okay? It's what makes Cheetos. Do you ever wonder how you got from corn to

ever wonder how you got from corn to Cheetos? That's how in an extruder. And

Cheetos? That's how in an extruder. And in order to force the stuff through to

in order to force the stuff through to give it that puffy, you know, cheesy

give it that puffy, you know, cheesy flavor thing, you know, and make these,

flavor thing, you know, and make these, you know, long, you know, things that

you know, long, you know, things that look like, you know, little orange

look like, you know, little orange poops. Um, you have to force them

poops. Um, you have to force them through at high temperature through an

through at high temperature through an extruder.

extruder. And that extruder has such high

And that extruder has such high temperatures that they can take the fat

temperatures that they can take the fat in the you know in the in the recipe and

in the you know in the in the recipe and because of the high heat they can end up

because of the high heat they can end up on the other end as trans fats because

on the other end as trans fats because you didn't add them to start with they

you didn't add them to start with they don't have to report them at the end.

don't have to report them at the end. So if you look at the bag it won't say

So if you look at the bag it won't say whatever trans fats were acquired during

whatever trans fats were acquired during processing.

processing. Nope.

Nope. Wow. I didn't know that. What about

Wow. I didn't know that. What about oils? like canola oil because I've heard

oils? like canola oil because I've heard they do some pretty crazy stuff

they do some pretty crazy stuff processing those oils including

processing those oils including deodorizers and go through a whole

deodorizers and go through a whole process.

process. So we don't know enough about what what

So we don't know enough about what what happens to those and what ultimately you

happens to those and what ultimately you know whether it changes their their

know whether it changes their their character and whether it changes their

character and whether it changes their functionality and whether it changes

functionality and whether it changes their metabolic risk. But yeah I mean

their metabolic risk. But yeah I mean you have to do a whole lot of things to

you have to do a whole lot of things to all these oils to make them even

all these oils to make them even palatable. Um uh I am not unfortunately

palatable. Um uh I am not unfortunately an expert in that. So I don't know all

an expert in that. So I don't know all the things that are done. What I do know

the things that are done. What I do know is that what happens to food in your

is that what happens to food in your kitchen is possibly more dangerous than

kitchen is possibly more dangerous than what happens to food at the food

what happens to food at the food processor.

processor. Question regarding the seed oils.

Question regarding the seed oils. if they're unheated.

if they're unheated. You're no expert on what they're doing

You're no expert on what they're doing in processing, but would you use them in

in processing, but would you use them in your own kitchen without heating them?

your own kitchen without heating them? Things like canola oil. Yeah, I do. I

Things like canola oil. Yeah, I do. I mean, you know, I'm I'm careful with

mean, you know, I'm I'm careful with them. I tend to use more olive oil and

them. I tend to use more olive oil and avocado oil and sesame oil and peanut

avocado oil and sesame oil and peanut oil. I would say those are my four go-to

oil. I would say those are my four go-to oils in general for um preparing food

oils in general for um preparing food and cooking.

and cooking. There's people talking about a

There's people talking about a connection between the seed oils and

connection between the seed oils and insulin resistance. Have you ever seen

insulin resistance. Have you ever seen that in the research?

that in the research? Well, so the question is what happened

Well, so the question is what happened to the seed oils? Were they heated or

to the seed oils? Were they heated or what? There is a terrible movie going

what? There is a terrible movie going around on on Vimeo or on the internet.

around on on Vimeo or on the internet. It might be on YouTube too. and it's

It might be on YouTube too. and it's called the big lie

called the big lie and it's all about seed oils and it's

and it's all about seed oils and it's basically four talking heads talking

basically four talking heads talking about seed oils that seed oils are the

about seed oils that seed oils are the the devil incarnate.

the devil incarnate. Okay, I think that

Okay, I think that spent seed oils that is seed oils heated

spent seed oils that is seed oils heated up to ridiculously high levels either

up to ridiculously high levels either because of sautéing or frying or

because of sautéing or frying or extrusion.

extrusion. Okay, those are the, you know, those are

Okay, those are the, you know, those are terrible.

terrible. But I'm not sure that an omega6 fat

But I'm not sure that an omega6 fat at baseline

at baseline is

is truly the bad guy.

truly the bad guy. Okay. Um, I think that, you know, this

Okay. Um, I think that, you know, this requires a fair amount of nuance and you

requires a fair amount of nuance and you sort of have to know what happened to

sort of have to know what happened to the seed oil before it got to your mouth

the seed oil before it got to your mouth in order to be able to say anything. And

in order to be able to say anything. And that's not what this movie says. And so

that's not what this movie says. And so I'm a little worried that, you know,

I'm a little worried that, you know, this is misinformation. And I don't

this is misinformation. And I don't think it's disinformation. I think

think it's disinformation. I think they're, you know, the people who are in

they're, you know, the people who are in this movie are telling you what they

this movie are telling you what they know. But I don't think it's necessarily

know. But I don't think it's necessarily correct.

correct. All right, let's come back to the

All right, let's come back to the practical here and get into a little bit

practical here and get into a little bit more nuance before we wrap up. We've

more nuance before we wrap up. We've already been clear about sugars, refined

already been clear about sugars, refined carbs, ultrarocessed carbohydrates.

carbs, ultrarocessed carbohydrates. I mentioned things like fruit.

I mentioned things like fruit. for somebody,

for somebody, okay, we'll get into the details here,

okay, we'll get into the details here, but for somebody right now who is

but for somebody right now who is metabolically unhealthy,

metabolically unhealthy, I know there's fiber and I want to get

I know there's fiber and I want to get your opinion there on how that protects

your opinion there on how that protects the body. We've talked about it before,

the body. We've talked about it before, but let's talk about it again.

but let's talk about it again. And then for somebody that's healthy

And then for somebody that's healthy versus metabolically unhealthy,

versus metabolically unhealthy, we've made it clear the processed carbs

we've made it clear the processed carbs are out. For me, even the whole food

are out. For me, even the whole food carbs would be out in that case if

carbs would be out in that case if somebody's metabolically unhealthy. But

somebody's metabolically unhealthy. But I'll have you share your thoughts.

I'll have you share your thoughts. Fiber

Fiber is what we haven't talked about. I think

is what we haven't talked about. I think fiber is the bee's knees when it comes

fiber is the bee's knees when it comes to metabolic health. I think fiber is

to metabolic health. I think fiber is the answer to

the answer to much of what's ailing us. And the

much of what's ailing us. And the problem is we're not consuming

problem is we're not consuming nearly enough. Why is fiber important?

nearly enough. Why is fiber important? Because fiber is the food for the

Because fiber is the food for the bacteria, food for the microbiome.

bacteria, food for the microbiome. Everyone's talking about microbiome

Everyone's talking about microbiome dysfunction. That's right. I agree.

dysfunction. That's right. I agree. Okay. The easiest way to get your

Okay. The easiest way to get your microbiome to, you know, behave is to

microbiome to, you know, behave is to feed it because if you don't feed your

feed it because if you don't feed your microbiome, your microbiome will feed on

microbiome, your microbiome will feed on you.

you. So, does fruit have fructose? Sure, very

So, does fruit have fructose? Sure, very little. But it has some. But the fiber

little. But it has some. But the fiber in the fruit made that fructose

in the fruit made that fructose unabsorbable

unabsorbable and so the bacteria in your intestine

and so the bacteria in your intestine got it whereas you didn't.

got it whereas you didn't. So the fiber is actually the antidote to

So the fiber is actually the antidote to the fructose. So that's why fruit is

the fructose. So that's why fruit is good, but juice is bad because once you

good, but juice is bad because once you strain out the fiber,

strain out the fiber, then the intestine absorbs it just as

then the intestine absorbs it just as fast as it would if it was a soda. So

fast as it would if it was a soda. So when you eat it whole, when you eat it

when you eat it whole, when you eat it with its fiber,

with its fiber, that fructose basically is not for you.

that fructose basically is not for you. And that's why fruit is actually

And that's why fruit is actually associated with reduction in type 2

associated with reduction in type 2 diabetes. Whereas fruit juice is

diabetes. Whereas fruit juice is associated with an increase in type 2

associated with an increase in type 2 diabetes. The only difference between

diabetes. The only difference between the fruit and the juice is the presence

the fruit and the juice is the presence of fiber.

of fiber. Because the fiber is what's actually

Because the fiber is what's actually mitigating the type 2 diabetes.

mitigating the type 2 diabetes. So if you ate your fiber and we have

So if you ate your fiber and we have data on this, cardiovascular disease

data on this, cardiovascular disease goes down, cancer goes down, diabetes

goes down, cancer goes down, diabetes goes down. So we need to eat more fiber.

goes down. So we need to eat more fiber. We need to eat more both soluble and

We need to eat more both soluble and insoluble fiber.

insoluble fiber. Fruit luckily has both.

Fruit luckily has both. Yes, it has a little bit of fructose. So

Yes, it has a little bit of fructose. So what? Eat all the fruit you want. Just

what? Eat all the fruit you want. Just eat it whole. Don't put it in a smoothie

eat it whole. Don't put it in a smoothie machine.

machine. Don't juice it. And for God's sake,

Don't juice it. And for God's sake, don't drink the fructose in a soda. I

don't drink the fructose in a soda. I know you got to go here, but we'll end

know you got to go here, but we'll end on this. We've really hammered home the

on this. We've really hammered home the two categories of food we need to avoid.

two categories of food we need to avoid. The other lever I think is important to

The other lever I think is important to mention is fasting.

mention is fasting. Basically, I think that intermittent

Basically, I think that intermittent fasting is good

fasting is good for certain people.

for certain people. Okay, who are those people? And the

Okay, who are those people? And the answer is the people with liver fat. And

answer is the people with liver fat. And the reason is because intermittent

the reason is because intermittent fasting gives your ch your liver a

fasting gives your ch your liver a chance to get rid of the fat it

chance to get rid of the fat it accumulated.

So if your liver has fat in it, intermittent fasting is a good way to

intermittent fasting is a good way to get rid of it.

get rid of it. If you don't have liver or fat, then

If you don't have liver or fat, then intermittent fasting is basically

intermittent fasting is basically neither here nor there.

neither here nor there. Neither good nor bad.

Neither good nor bad. So know what your liver is doing and if

So know what your liver is doing and if your liver has fat in it and you can

your liver has fat in it and you can find out from your physician because you

find out from your physician because you can look at your ALT, you can ultimately

can look at your ALT, you can ultimately have a liver ultrasound or you know MRI

have a liver ultrasound or you know MRI or worse or you know pancreatic sorry um

or worse or you know pancreatic sorry um uh what's it called? fiber scan. Um, you

uh what's it called? fiber scan. Um, you know, there are ways to find out, but if

know, there are ways to find out, but if your liver has fat in it, then you might

your liver has fat in it, then you might consider inter intermittent fasting or a

consider inter intermittent fasting or a ketogenic diet in order to basically

ketogenic diet in order to basically give the liver a chance to lose the fat

give the liver a chance to lose the fat it accumulated.

it accumulated. All right, Rob, we're going to end it

All right, Rob, we're going to end it there for today. I'm going to link up

there for today. I'm going to link up your website, your social media, your

your website, your social media, your books, everything in the show notes.

books, everything in the show notes. Really enjoyed this. Thank you.

Really enjoyed this. Thank you. Oh, you're very welcome, Jesse. You

Oh, you're very welcome, Jesse. You know, we we we we went deep today. Yeah,

know, we we we we went deep today. Yeah, covered a lot of new stuff that I

covered a lot of new stuff that I haven't heard you talk on. Thanks again.

haven't heard you talk on. Thanks again. My pleasure.

My pleasure. Now that you're done, you're going to

Now that you're done, you're going to want to stick around here and catch this

want to stick around here and catch this other incredible episode. You don't want

other incredible episode. You don't want to miss it. I'll see you over there.

to miss it. I'll see you over there. Ultimately, it's not what's in the food,

Ultimately, it's not what's in the food, it's what's been done to the food that

it's what's been done to the food that matters. Everything fructose does to the

matters. Everything fructose does to the mitochondria is designed

mitochondria is designed to inhibit its functioning. Its

to inhibit its functioning. Its metabolic health

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YouTube Transcript:Hormone Expert: The Fastest Way to Insulin Resistance & the Big Lie About Calories! | Dr. Rob Lustig

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Hormone Expert: The Fastest Way to Insulin Resistance & the Big Lie About Calories! | Dr. Rob Lustig