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2:04

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2:06

and as farmers who enough a place for

2:09

conversations that matter and today's conversation going amount

2:11

of all of you because it's about the

2:13

number one thing he should all be paying

2:15

attention about which is your metabolism and how

2:18

it's messed up by shiver fructose, How our

2:20

way to control heart rate is regulated We

2:22

are in a very sticky situation to the

2:24

an American around the world because of the

2:26

increasing rates, obesity and were going to be

2:29

speaking say where the world expert in this

2:31

is Hop a sift through all the science

2:33

and the confusion. Doctor Robert Lustig

2:35

is a neuroendocrinologists with expertise in metabolism,

2:38

obesity, and nutrition. He's an emeritus professor

2:40

of pediatrics in the division of Endocrinology

2:42

and a member of the Institute for

2:45

Health Policy Studies, Edu, Csf. He's also

2:47

into leaders of the current eighty Sugar

2:49

movement. It is changing the food industry.

2:52

He dedicated his retirement from clinical practice.

2:54

Dell picks the food supply in any

2:56

way you can to reduce human suffering

2:59

and to salvage the environment by interacting

3:01

with all the stakeholders to bring them

3:03

together on. A common vision for

3:05

metabolic health. Protect. Deliver.

3:08

Fi. The got and support the brain

3:10

reading and all that. Today I doctor

3:12

List dig graduated from Mit and Nineteen

3:15

Seventy Six. He received his M from

3:17

Cornell University Medical College and Nineteen Eighty.

3:19

He also received his masters of studies

3:21

in law which is amazing at the

3:24

University of California Hastings College of Law

3:26

and Twenty Thirteen. He is also the

3:28

author popular books called Fat Chance, The

3:30

Hacking of the American Mind, and Met

3:33

A Follicles which is like diabolical but

3:35

Your metabolism. He's the chief science officer

3:37

at the nonprofit. He real he's on

3:39

the advisory boards of the U C. Davis

3:41

Innovation is to for Food and Health the

3:44

center for him he technology many other companies

3:46

is also the chief medical officer at By

3:48

A Looming Technologies Perfect and Kill and Health

3:50

a hobby into a conversation with actually estate

3:53

coming up on the Duchess Pharmacy. Welcome back

3:55

to the Duchess Pharmacy Robert It's so good

3:57

to have you back of this. You know

4:00

you an Ira like a someone Louise Hay

4:02

as far as are we going to drive

4:04

of the class as a convert of all

4:06

over again allows us not a second. I

4:09

would sometimes you have to sacrifice yourself to

4:11

get to the true but you know I

4:13

I think. We met first

4:15

as part of this film called the. That.

4:18

Up right where since a set up

4:20

with. The. Food Industry

4:23

making all of our children sick and

4:25

fat and killing them and meaning liver

4:27

transplants as teenagers and and.barrier to Surgery

4:29

as teenagers. and this movie did quite

4:31

well. And and oh yeah, musical release?

4:33

Yeah, I mean, you know you and

4:35

I were the two Talking heads. You

4:37

know, it's sort of, you know. But

4:40

we didn't get to meet until the

4:42

In L A premier. That's right, we

4:44

read and premier and and it was

4:46

a other. Was it really impactful movie

4:48

for me because I realize you know

4:50

a in that scene. Is that I

4:52

was working in In In that the

4:54

movie where I was working with his

4:56

family of five and live in a

4:58

trailer, food stamps and disabilities and had

5:00

your father was forty two and had

5:03

dialysis from diabetes and the mother was

5:05

one hundred plus pounds overweight Them six

5:07

year old kid was almost diabetic with

5:09

a body composition with indexes: Kansas Fifty

5:11

percent Fat a sexy brusatte. It sucks

5:13

you add the last two hundred thousand.

5:15

The First Fear The. Father.

5:17

Los forty five million a kidney the some

5:19

last and of me a hundred and thirty

5:21

two pounds and went to medical school and

5:24

easing look good food old and will I

5:26

just taught me that he know and people

5:28

don't know the impact of all the else

5:30

or process who they're eating the they were

5:33

trying to do the right things and in

5:35

oh so to set me up to understand

5:37

that it's really not that hard if people

5:39

understand the biology of how their body works

5:42

was sacked the matter is they've been said

5:44

a of a mess and the missus that

5:46

ultra. Processed food. Is. Food

5:48

yeah well they you know this think

5:51

they had they had all this stuff

5:53

in their kitchen that they thought was

5:55

low fat diet this healthy that and

5:57

it was all processed junk that had

6:00

high sugar even a cool web which

6:02

they thought was a healthy writers are

6:04

topping said zero trans fat on the

6:06

label. And in the. The

6:09

contain have you read the ingredients list forget

6:11

the the front of packs labeling which is

6:13

so misleading. Always safe and has a health

6:16

came on the labels use the out this

6:18

it is dangerous. I gluten free potato chips

6:20

enough and it's a zero trans fat but

6:22

was only because most the air and the

6:24

fc a through a loophole the the food

6:26

industry force them to do because evasive capture

6:29

these cases. he said if it's less than

6:31

half a gram per serving offense fat You

6:33

don't have to say transfats is oh you're

6:35

eating greens It was high fructose corn syrup

6:37

and partially hydrogenated soybean off Now. Is it

6:39

a house like wow so you're It

6:42

was so powerful and any kind of

6:44

kind of made me realize that in

6:46

a were really really have a problem

6:48

of awareness, education and our bodies work

6:51

and so years and so important to

6:53

the it unpacks the biology. Of

6:55

how food interacts with our hormones are

6:58

gut microbiome are mean system or metabolism

7:00

in ways that it's really information to

7:02

food instructions and and there's a huge

7:05

debate out there which tries me Chris

7:07

which is is to be that I

7:09

want to go into today around the

7:12

idea of is a calorie a calorie

7:14

because this is what we've been taught

7:16

in Miami's is set us up in

7:19

on what your role scientists had the

7:21

southern let's you rather than even rover

7:23

hours. After that the whole debate. And

7:25

is is a calorie calorie. And his

7:28

weight loss just about eating less and

7:30

exercising more. which has an implicit bias

7:32

toward blaming the person for not exercising

7:35

more and eating. That said, blame the

7:37

victim in my pencil. It doesn't understand

7:39

the real root causes. It's great for

7:42

the food industry. Can psycho? Doesn't matter

7:44

what cows read, it could be a

7:46

Coca Cola calorie. er, och, a twinkie

7:49

calorie. And it's the same as broccoli.

7:51

Calories on junk over your calorie counts.

7:53

And then is the other extreme. the

7:56

mar which is the carbohydrates insulin

7:58

hypothesis which essentially states It's

8:00

not what you eat, it's not how much

8:03

you eat, it's what you eat and that

8:05

the quality of the calories matter and the

8:07

different macronutrients has different effects on your body,

8:09

on your hormones and your metabolism and your

8:11

gut microbiome and your immune system, all of

8:13

which impact your weight. And there's

8:16

other schools of thought around obesogens, which

8:18

are environmental toxins that screw up your

8:20

biochemistry and make you gain weight and

8:22

there's oxidative stress theories. There's

8:24

a lot of theories out there and that,

8:26

you know, on nutrition, it's one of those

8:29

really, you know, poor black sheep of

8:31

the family in medicine where it doesn't get funding

8:33

for real research and we need to be studying

8:35

these things. But we do know

8:37

enough, I think, and you and my friend

8:39

David Ludwig have really helped understand a lot

8:42

about the role of sugar and fructose

8:45

and carbohydrates, refined carbohydrates

8:47

affect our metabolism. So

8:50

can you help us kind of navigate this whole

8:52

story and tell us, you

8:54

know, layout, you know, the

8:57

insulin hypothesis versus the energy

8:59

balance hypothesis versus the obesogen

9:02

hypothesis and how they all

9:04

interconnect and are they all sort of

9:06

right? They are all sort of right.

9:09

And they're all sort of wrong. And they're all

9:11

sort of wrong. So help us understand, you know,

9:13

whether we should be just decalincounting

9:15

or we should just be focusing on quality or

9:18

we should be detoxing our bodies or we should

9:20

be like, I don't know what. So

9:22

tell us because we're all lost. The short answer

9:24

is they're all right and they're all wrong altogether.

9:28

Last month, a group of four authors

9:31

of which I was one, the first

9:33

author is Heindel, Jerry Heindel, who was

9:35

the head of the Environmental

9:39

Endocrine Disruptors group

9:41

at the National Institute of Environmental Health

9:44

Sciences and myself and Sarah

9:46

Howard who runs HEEDS, which

9:48

is Healthy Environment Endocrine Disruptors

9:51

and also Barbara Corky, who

9:53

is the named

9:55

professor at Boston U, won the

9:58

Banting Award for the American Diabetes Association. So

10:00

not exactly light weights. Yeah, we came

10:02

out with a paper in International Journal

10:05

of obesity. We're very proud of yeah

10:07

And it's called obesity genes a unifying

10:09

hypothesis for the pathogenesis of obesity now.

10:11

How does this work? There are four

10:14

prevailing models right now on

10:18

Weight gain and how it works You've

10:20

mentioned all four, but let's put some meat on

10:23

those bones energy

10:25

balance calories Ye

10:28

too much you exercise too little and

10:30

there is absolutely no question that people

10:34

who are obese have been

10:36

shown to eat more and Exercise

10:39

us. Yeah, and I

10:41

don't argue that the question is is

10:43

why cause or effect right, right? Okay,

10:45

is it a causative phenomenon? Is it

10:48

a result of phenomenon or is it

10:50

an epiphenomenon? Okay,

10:52

and they can't Tell

10:55

us which So keep

10:57

that in mind. There's nobody in

10:59

the energy balance model camp who

11:01

can actually say that that's the

11:03

reason For weight

11:05

gain. All right. Could

11:08

it be the cause could it be the

11:10

result? So keep that in mind now There

11:12

is no question. We are eating more as

11:14

a society Okay 175

11:17

calories per day more for adult men 335

11:20

calories per day more for adult women. Yeah 275 calories per

11:22

day more For

11:27

teen boys. Okay, everyone's eating more and I want

11:29

to make a point on this before you dive

11:31

into that Yes,

11:34

we're eating more calories. Yes person But if

11:36

you look at the data from 2000 and this

11:38

is from the NHANES data a natural health

11:41

nutrition examination survey Which is a national survey of

11:43

you know, tens and tens hundred thousand people right

11:45

and what they found was from 2000 until now

11:49

Calorie Counts have gone down exact as

11:51

obesity rates have gone up, which is

11:53

kind of a paradox. It's hard to

11:56

explain with the energy balance hypothesis. Right?

11:58

Well, in fact, the. Food industry

12:00

actually argues that sugar consumption gone down

12:02

as obesity rates have gone and that

12:04

cel yes or twenty year period. So

12:07

they say well i can't be the

12:09

calories in a can't beat the sugar.

12:11

Well as you wait a sec I'd

12:13

been highly refined sugar. ah there a

12:15

lot there a lot of armed you

12:17

know cane sugar. yeah maybe by that

12:20

if the reason there a lot of

12:22

whys and wherefores to that mobile and

12:24

will get their rooms not or that

12:26

is true. In addition,

12:28

Gates people say, well, we're exercising

12:30

less and we are exercising less

12:33

Except nonetheless, twenty years insects exercise

12:35

rates of actually. Stabilized.

12:38

At the Ice Cream Legacy. Like the gyms

12:40

on every corner. Orange Theory solid core host.

12:42

well as the airport and that doesn't really

12:44

work. Is it? because you don't know what

12:47

they're doing in the semi? they're playing their

12:49

money in for initiation and then you don't

12:51

have their actually been used to have gym

12:53

memberships does not airfare and well I know

12:55

and I don't. The same as a kid

12:58

into energy up after kits. And remember there

13:00

are three kinds of energy expended. Noom. There's

13:02

arresting energy expenditure. You.

13:04

Know that Just Living which is

13:06

sixty five percent of energy burning,

13:09

there is, ah, the ceramic effect

13:11

of food, which is ten percent

13:13

of energy burning. That is just

13:15

the metabolism of food itself that

13:17

generates heat that takes work to

13:19

digest north of the just vote

13:21

for energy and in that gives

13:23

you by the heat. And then

13:26

finally, there's voluntary energy expenditure, which

13:28

you know runs between twenty five

13:30

and thirty five percent of total

13:32

energy expenditure. So if energy expenditure.

13:35

Is. Going down which it's

13:37

not, but if it was going

13:39

down, which of those three buckets

13:41

actually explain it well, in fact

13:44

none of them. So

13:46

there are a whole bunch

13:48

of issues with regards the

13:50

energy balance model to start

13:52

with kids. In addition, It

13:54

doesn't explain why when people lose

13:57

weight. They. Plateau because if

13:59

they. Here last and

14:01

they lose weight. You'd

14:04

expect him to continue to lose weight but

14:06

they don't date plateau and of course that

14:08

gets everybody's crazy and then they say i'm

14:10

a failure and then yeah they go eat

14:12

the Ben and Jerry's you know and it's

14:15

and it's all over and then you know

14:17

real your back up to where they belong

14:19

in the first place right? So. If.

14:22

Is energy balance were the only

14:24

issue. Case. If

14:26

that would that phenomenon would not

14:28

occur to their a whole bunch

14:30

of things wrong with energy balance.

14:32

In addition, energy balance does not

14:34

explains why we have newborn obesity.

14:37

And. Yeah, Why they can come out why

14:39

baby or is come out obese Now

14:42

Four separate studies, one in Israel, one

14:44

in South Africa, one in Russia, one

14:46

and in the United States over the

14:48

last twenty five years. Newborns,

14:50

Way to hundred grams more.

14:54

Than. They did twenty five years ago and when

14:56

you stick, I'm in Texas. Scanners to figure out

14:58

what the two hundred grams is is all fat.

15:00

Almost half a pound of the years half a

15:02

pound of extra fat. Before

15:04

they even. Had a

15:07

chance to eat right? Mother's.

15:09

Milk nevermind. Ben and Jerry's

15:11

ruckus. Okay, so whatever. Of

15:14

cinnamon and whatever of a model you want

15:16

to proffer to me about what the cause

15:18

of obesity is. You have to explain that

15:21

here and you can't let me see energy

15:23

balance, my is right and this, but you

15:25

know I think this to kind of double

15:27

down on this. You know it's calories do

15:30

matter like obviously but as if it's really

15:32

about. the of the

15:34

v the crotty calories and people and what

15:36

they do to your body you of us

15:39

have the saying it's a calorie burn as

15:41

a calorie burn rate calorie even if a

15:43

calories presents a that one hundred times and

15:45

was i mean is when you eat food

15:47

it interacts with your microbiome it interacts with

15:50

your immune system it interacts with your hormones

15:52

and so it's not the same and in

15:54

people say it's all by calories that i

15:56

saw how do you explain the fact that

15:59

a type one day diabetic, can

16:01

eat 10,000 calories a day

16:03

and lose weight at the same time

16:05

because they have no insulin. Because they

16:07

have no insulin. Yeah. And

16:10

so that's where the second model comes in, the

16:12

carbohydrate insulin model. Now I will tell you, until

16:14

about two years ago, three years ago, I

16:17

was a proponent of the carbohydrate

16:19

insulin model because I had done research in it

16:21

myself. So this is a model

16:24

that has been particularly proffered by

16:26

David Ludwig and, you know, appropriately

16:29

so, and I was a professor. Basically

16:33

he does what I do except at Boston Children's

16:35

Hospital. And he's one of the few people who

16:37

do randomized clinical trials. Yeah, absolutely. And he does

16:39

the most rigorous kind of research, not just population

16:42

data. He does it on humans and it's a

16:44

lot of money, but he does it. Perspective clinical

16:46

trials done with appropriate controls. David's

16:48

a top notch scientist. I

16:51

have zero, zero concerns

16:54

about his accuracy, the quality

16:56

or the veracity of his

16:59

data. Or of

17:01

his thinking. Yeah. He's solid.

17:03

Yeah, absolutely. Okay. Cross

17:05

the board and he's a friend. You know, full disclosure. Me too.

17:08

Yeah, he's a good friend. Yeah. All

17:10

right. Now I was a proponent of that model too. And the

17:12

reason that I was a proponent of that

17:15

model was because I did a similar

17:17

experiment when I worked at St.

17:19

Jude Children's Research Hospital in Memphis,

17:21

Tennessee. So you're

17:24

probably familiar with this phenomenon

17:26

called hypothalamic obesity. So

17:28

these are kids, for the most

17:30

part, adults too, but mostly kids

17:32

who get tumors of

17:34

the posterior fossa, the hypothalamus

17:37

mostly, and they require

17:40

surgery, they require radiation,

17:44

they end up with hypothalamic damage

17:47

and now they can't see their

17:49

leptin. So Leptin is a

17:51

hormone that your fat cells make that feeds back

17:54

on the brain and tells your brain, hey, I've

17:56

eaten enough. I don't need to eat anymore and

17:58

I can burn energy at a normal. Rate

18:00

because I have enough

18:03

energy stored. In.

18:06

Came so it's a survival mechanism just

18:08

like the thermostat on your house case.

18:10

So leptons basically telling yeah, but he's

18:12

high enough gay, we don't need any

18:14

more heat so you don't have to

18:17

eat anymore. Who who can? Well, these

18:19

kids. Lost their ability to

18:21

see their leptin? Yeah, because those

18:23

neurons were debt. And.

18:25

Soaks Number one, they ate

18:27

like crazy and number two,

18:29

their energy expenditure. Was.

18:32

In the sewer and the cat

18:34

cola mean levels in their urine.

18:37

Or zero. Because. For their

18:39

sympathetic nervous system, it was basically

18:41

shut down because they're trying to

18:43

conserve and because the sympathetic nervous

18:45

systems when interviewed some muscles to

18:48

work as nervous systems was innovates,

18:50

assassins to give up their fat.

18:52

Yeah, okay, so they can't give

18:54

up their fat and they can't

18:56

burn. Know they're eating like crazy

18:58

and they're burning like zero rec

19:00

cakes And so they're gaining weight

19:02

out of sight. Thirty pounds, Forty

19:05

pounds a year ad infinitum. And

19:07

there's nothing that anyone. Could do

19:09

about it. The I got the Governor

19:11

is off Like the thing the tell

19:13

you i'm fog is off as a

19:15

survey data broker, right? So I inherited

19:17

a cadre of about forty of these

19:20

kids smile at St. Jude. The outtakes

19:22

would survive the brain tumors but became

19:24

massively obese because of the therapy and

19:26

the parents would scream at me to

19:28

this is double jeopardy I have my

19:30

kids survives the tumor only to succumb

19:33

to the therapy. Yeah, and I was.

19:35

you know for not fair to say

19:37

to say the least. The Us and was

19:39

up the mess do something about. Now,

19:41

as a neuroendocrinologists, I didn't know.

19:44

That. There was this literature. Case

19:47

about something called the V M H

19:49

Lesions wrapped. The. Ventromedial hypothalamus

19:52

lesions right. Electrode

19:55

in the hypothalamus. ego. And.

19:58

Those animals become massively or. beast

20:00

also. But what was

20:02

interesting was you could cut the vagus nerve, the

20:05

nerve that connected the brain to the pancreas, and

20:08

then they wouldn't. We

20:12

assumed at that point in time, this was 1995 now, so

20:14

30 years ago, the

20:18

days of the Giants, remember them? I was

20:22

there, I graduated medical school in 87, so yeah,

20:24

I was there. So

20:26

we assumed that these kids couldn't see

20:28

their leptin, so their brains thought they

20:30

were starving. So their sympathetic nervous system

20:32

was in the sewer, and

20:34

their vagus nerve was telling their

20:36

pancreas to release more insulin in

20:39

order to drive whatever they did

20:41

eat into fat to

20:43

raise the leptin, but they still couldn't see

20:45

it because the body thought it was starving.

20:47

Because the body thought it was starving. And

20:50

even though there was plenty of food without

20:52

leptin saying stop, the body's like, I'm hungry,

20:54

so all the time, let's store fat, let's

20:56

get everything stored because I don't know when

20:58

I'm gonna get my next meal, and insulin

21:00

is that fast storage hormone. Right, exactly. So

21:02

insulin was the business end of

21:05

the equation. So

21:08

I'm not a neurosurgeon, I can't cut a vagus

21:10

nerve. But could I

21:12

do something similar? So we

21:15

gave them a drug that

21:17

suppressed beta cell insulin release.

21:20

So that drug is called octreotide,

21:22

it happens to be used usually

21:24

for acromegaly, for growth hormones, secret

21:26

tumors, but we repurposed it because

21:28

it also suppresses pancreatic insulin release,

21:31

because there are somatostatin receptors on

21:33

the pancreas, on the beta cell. And

21:36

we gave these patients

21:38

octreotide and lo and behold, they

21:40

lost weight, they lost weight, but

21:43

something even more remarkable occurred. They

21:46

started exercising spontaneously.

21:49

One kid became a competitive swimmer, two kids started

21:52

lifting weights at home, one kid became the manager

21:54

of a high school basketball team, these little kids

21:56

who sat on the couch, ate Doritos, and slept.

21:58

Okay, they had lost. All.

22:01

Ah, touch with you know, the

22:03

world around them. Yeah, because they

22:05

sell to. Micro. Awful. They

22:08

felt like crap all the time

22:10

and all the sudden they woke

22:12

up. And the parents would

22:14

room where you don't like. Within a week

22:16

they would set before there's any weight loss

22:18

is A. I got my kin back to

22:20

him and the kids were active and lives

22:22

here that my head is the first time

22:24

I had Hasn't been in the clouds since

22:26

the tumor. So what it? What is a

22:28

teacher so? well? So we did a double

22:30

blind placebo controlled trial. Proved. It

22:32

again then what we did was we

22:35

did a study in we pay don't

22:37

take this trod taking the drug and

22:39

in blocking the effect blocking these activities

22:42

or right So then we'd ask the

22:44

questions are they're adults without brain tumors

22:46

who might manifest the same problems that

22:48

is leptin resistance, not being able to

22:51

see their left and hi insulin release,

22:53

driving their weight gain and driving their

22:55

sloss and bios and by we we

22:58

would let them resistance against races as

23:00

he high levels of leptin. In

23:02

the blood see I measure. Oh

23:04

yeah, super higher interest because they're

23:06

fat was so large that they're

23:08

leptons were you know, in the

23:10

Stratosphere the I'm a company I

23:12

cofounded function House or people can

23:14

ask their laps. Their basic lab

23:16

panel includes leptin, insulin and adiponectin.

23:18

Three things need to know that

23:20

a really important for understanding insulin

23:23

and carbohydrate metabolism of whoop. without

23:25

question the appeal of explain that

23:27

to the American day basis as

23:29

kind of stuff. We. Said

23:31

our they are adults. Who.

23:33

Might have the same pacifism allergy

23:35

that is leptin resistance insulin release

23:38

driving their weight gain. and if

23:40

we gave them a true tight

23:42

with they lose weight and sure

23:44

enough they did. Not.

23:47

Every patient only twenty percent of the

23:49

total eight out of forty four. But

23:51

what was interesting about the eight was

23:53

that they are insulin response to glucose

23:55

was markedly different from the patients who

23:57

did not. was asked number one meeting

23:59

me. The higher levels of Islam

24:01

and higher spiking levels of writing

24:03

sugar right? Yeah, and what we

24:05

did in that study was we

24:07

measured arresting energy expenditure with a

24:09

metabolic cart yeah before and six

24:11

going on your basic metabolic rate

24:13

Europe based on the market and

24:15

what we saw was that the

24:18

patients who lost the weight of

24:20

responders who had the high insulin

24:22

response their. Energy.

24:24

Expenditure. Did. Not go

24:26

down. Even though they lost weight you

24:28

expected to the down payment. Once you

24:30

lose weight you know you conserve. Yes,

24:32

their energy expenditure went up. really because

24:34

we got the insulin down near. There

24:37

is a subset of patients

24:40

with obesity that are just

24:42

like these kids. Yeah, and

24:44

so insulin. Is

24:47

a linchpin. In.

24:49

Driving weight gain in every one.

24:51

but not everybody has this insulin

24:54

release problem that the kids did.

24:56

Most everybody has this insulin resistance

24:58

problem. the upsets, you know is

25:00

called metabolic syndrome some degree or

25:03

another. Some degree. Or and in

25:05

what about insolence. The bad guys,

25:07

no matter how you look at,

25:09

there is no weight gain without

25:11

insulin. You gotta get the insulin

25:14

doubts. And so once I learned

25:16

this, I changed my clinic practice

25:18

completely. Are. And instead of being

25:20

a weight loss program it was an

25:22

insulin reduction probably as get the answer

25:25

down hardly where you can and I

25:27

have been trying to promulgate this as

25:29

a modality as A as A in

25:31

A models the or other O B

25:33

C programs and only my. Former

25:36

fellows do with that way. It's and

25:38

or even more enough for one A

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wonderful. It's Wonderfield. And now let's get back

28:03

to this week's episode of The Doctor's Pharmacy.

28:06

I just want to sort of highlight this point because just

28:09

to go back to this diabetes type one diabetes, if you

28:11

have no insulin like a type one diabetic, you can eat

28:14

10,000 calories and you'll lose weight.

28:16

Absolutely. But if you eat very little and you have

28:18

high insulin, you're going to store all that fat. Exactly.

28:21

And I had a patient once that just was one of

28:23

those teaching patients. You know how you think you learn medical

28:26

school and you learn shit? No, it's actually the patients that

28:28

teach you. Of course. And she looked

28:30

like an apple. She had a big round belly. I

28:33

was convinced she was going to have a high blood sugar, high

28:35

A1C. She was going to be

28:37

having diabetes. I checked her blood sugar.

28:39

It was perfect. So let's do

28:41

a glucose tolerance test but measure insulin

28:43

also. Right. Fasting and after

28:45

one hour and two hours. Her

28:48

blood sugar never changed. Like it was at 90 and then

28:50

it went to like 110 and then 105 at two hours.

28:54

It was like perfect blood sugar. You never would have

28:56

thought she had any issues. And that's what

28:58

doctors do but they don't measure insulin. Her

29:00

insulin fasting was like I think 50

29:03

and it went up to 200 or 300. 200

29:05

or 300? 200 or 300. My kids

29:07

went up to 1200. Oh yeah, I never

29:09

saw that. But you're a pediatric

29:12

endocrinologist. You're a pediatric endocrinologist. You're just either worse

29:14

or the worst. But I was like, oh wow.

29:16

Okay, insulin is the problem here for her. She's

29:18

spiking so much insulin she can't lose weight and

29:20

she's storing it all around her belly. Bottom

29:23

line is anything that gets the insulin down ultimately

29:26

leads to weight loss. And there are different

29:28

ways to be able to do that. Obviously

29:30

caloric restriction will get insulin down. Carbohydrate

29:33

restriction will get insulin down. The ketogenic

29:36

diet which is the extreme of carbohydrate

29:38

restriction will get insulin down. Metformin

29:40

will get insulin down. And all of those are

29:44

clear. Having

29:46

lots of fiber. Yeah, high

29:48

fiber diet will get insulin down.

29:50

Thank you. Exactly right. All

29:53

of these are modalities that

29:55

basically impact insulin response.

29:57

The insulin kinetics. There

30:00

is absolutely no doubt that insulin

30:03

is the lynch pin

30:05

in weight gain. So the carbohydrate

30:07

insulin model that David held promulgated

30:09

and which I subscribed to because

30:11

of the work I had done,

30:13

I was

30:16

in that camp until

30:18

about two to three years ago.

30:20

Okay, interesting. When I learned a

30:22

little more. Yeah. Okay,

30:24

that's why you do it to me. The

30:26

thing about everything is that we polarize

30:29

everything and there's truth in everything. It's

30:31

not one thing and in functional medicine,

30:33

we understand the network effect in biology.

30:36

It's basically an ecosystem, a

30:38

set of biological networks that all interplay with each

30:40

other and there are many variables that can create

30:42

the same outcome. Agreed. So,

30:44

the bottom line is if you think it's

30:46

a nutritional issue, you'll stick with nutrition. If

30:49

you think it's an endocrinologic issue, you'll

30:51

stick with the endocrinology. If you think it's

30:53

a GI issue, you'll stick with the GI.

30:55

We have siloed medicines so severely. The fact

30:58

is, this is a systems biology issue. Yeah,

31:00

exactly. I mean, you can do

31:02

a fecal transplant and make something less insulin resistant

31:04

by changing the microbiome. Exactly. So if you just

31:06

do a poop transplant, you can lose weight and

31:08

improve your diabetes. Well, how does that make sense,

31:10

even not changing your diet? Exactly. Because

31:13

there's so many variables, right? Well, and because

31:15

there are so many different nodes

31:18

because energy

31:20

is so integral to survival of

31:22

the species that there's redundancy built into

31:25

the system. Right. That's

31:28

what cyanide does. Yeah, about four. Right. Exactly.

31:31

Exactly. All right. And

31:34

why? Because it affects the mitochondria. That's

31:37

your little energy factory, right? Because that's our

31:39

systems biology, you know, 101 for today is

31:41

the mitochondria. You're going to hear this a

31:44

lot. All right.

31:46

So about three years ago, Jerry

31:49

Heindel put together a meeting on

31:53

environmental obesogens. I've

31:55

done some of this work as well because I

31:57

worked along with Mike.

32:00

colleagues at UC Berkeley on a study called

32:02

the Chamaco study which is oh yeah children

32:04

and mothers of the Valley farm farm workers

32:06

I know about them I wrote about it

32:08

in my book and these kids

32:10

you know these were the offspring of

32:13

mothers who were exposed to high doses

32:15

of pesticides through their pregnancy and so

32:17

they measured the you know pesticides in

32:19

the pregnant mother's urine and then watched

32:21

the outcome yeah the babies yeah after

32:23

they as they grew up so you

32:26

know and then we looked at several

32:28

different phenomena we looked at growth we

32:30

looked at reproductive capacity we looked

32:32

at neurologic IQ 41

32:34

million IQ points lost in

32:38

that cohort that was striking to me and of

32:40

course we looked at puberty we looked at obesity

32:43

okay and so we know that

32:46

mothers pregnant

32:48

mothers DDE levels

32:50

which is a metabolite of DDT which hasn't

32:52

been around since 1972 but it's

32:56

still everywhere it's still everywhere

32:58

it's a forever chemical predicted

33:00

obesity in their five-year-olds so

33:03

this clearly means that there's something

33:05

going on even before birth

33:08

like for instance those newborn obese

33:10

kids we just talked about so

33:13

trying to understand how obesity

33:16

genes that is

33:18

environmental factors that can lead to

33:20

weight gain what might be

33:22

the reason for that well yeah we wrote

33:24

set three papers back in 2022 about this

33:27

44 authors

33:30

yeah I was lead author on one of

33:32

the three papers and there

33:34

are a lot of different ways that you can

33:36

make a fat cell yeah okay estrogen will make

33:38

a thin cell androgen will make a fat cell

33:40

PPR gamma will make a fat cell the

33:44

aryl hydrocarbon receptor will make me make a

33:46

fat cell bigger or make a make a

33:48

new fat cell both you

33:51

know different ones at different times and

33:53

there are windows of critical periods yeah

33:56

so the question is does it does the

33:58

energy balance model explain this No,

34:00

does the carbohydrate in the model explain this?

34:02

No. No. Okay, so

34:04

clearly, we needed some more. And

34:06

so the question is what ties

34:08

all of this together? In

34:11

walks Barbara Corky who's done a lot

34:14

of this work. And she

34:17

had done work on reactive oxygen species,

34:19

both in the dish and in the

34:21

animal. And it turns out reactive oxygen

34:23

species, which are things

34:25

you can't get away from. If you're alive,

34:28

you've got ROSs, okay? Because mitochondria

34:30

make ROSs. It's a part of normal

34:32

biology. It's hard not to control like

34:34

anything, like your blood pressure, your blood

34:36

sugar, whatever. It's like normal, but you

34:38

don't want it too much. ROSs change

34:40

the phosphorylation status of the enzymes

34:42

in the cell. In English, please. Ha

34:45

ha ha ha ha ha. Every cell

34:48

in its lifetime has

34:50

to grow or burn. Make

34:54

energy. Utilize

34:57

energy. Yeah. But not

34:59

both. They do one or the

35:01

other. And there's an

35:03

energy metabolism pathway in

35:06

every cell to teach that

35:08

cell whether it's gonna burn

35:11

or grow. And there are three enzymes.

35:14

One is PI3 kinase,

35:16

phosphatidylinositol 3 kinase. This is

35:18

the enzyme

35:20

that Lou Cantley, first

35:23

at Harvard and then Cornell, found

35:25

is basically predictive of cancer.

35:29

Because what it does is it opens the spigot

35:31

for glucose to enter the cell in

35:34

high concentration. The second

35:36

one is AMP kinase. That is

35:38

the fuel gauge on the liver

35:40

cell, pretty much every

35:42

cell. And that's regulated by metformin, which

35:45

is drug-free diabetes. Exactly, and so what

35:47

it does is it tells the cell

35:49

to make more mitochondria because- Energy

35:52

is low. When energy is low, that

35:54

goes up. I call that one of the longevity switches.

35:56

It's part of our hallmarks of aging. Correct. And

35:58

then finally, the third- enzyme is mTOR,

36:01

mammalian target of rapamycin. That's a kinase also. All

36:03

three of these are kinase. Again, I call that

36:05

one of the longevity switches, which makes protein and

36:07

is good, but it can also be overdone. Well,

36:09

it tells the cell to divide. Okay,

36:12

it's the division signal. So if you're

36:14

dividing, you're growing, okay? But

36:17

if you're burning, you're not growing. Okay, you're

36:19

doing one or the other. No cell does

36:21

both at the same time, okay? So there

36:23

is two pathways, and

36:27

the switches are these three enzymes.

36:30

Well, these three enzymes are kinases, which

36:32

means their phosphorylation status dictates whether they're

36:34

on or off. That's just a chemical

36:36

reaction that kind of regulates whether they're

36:38

working or not working, right? That's right.

36:40

And guess what makes that phosphorylation occur?

36:43

Reactive oxygen species. So

36:45

we started looking with Barbara at

36:48

the question of whether or not all

36:51

of the things that we know cause weight gain,

36:54

whether it be inflammatory

36:57

things, like for instance, air

37:00

pollution, has it been associated with weight gain?

37:03

Or environmental

37:05

obesogens like phthalates or BPA

37:09

and parabens, whether

37:13

they- All the petrochemical things are everywhere,

37:15

from pesticides to plastics and everything in

37:17

between. And whether they cause reactive oxygen

37:19

species to drive the weight gain. And

37:22

Bruce Blumberg at UC Irvine has

37:24

shown that tributyltin is a great model

37:26

for this because not only does it

37:29

cause reactive oxygen species, but it changes

37:31

the genome, the epigenome I

37:33

should say. So that

37:35

it carries forward for

37:37

at least four generations because

37:40

of reactive oxygen species. And

37:43

then we looked at the diet. And

37:45

sure enough, everything in

37:47

our Western diet generates more

37:50

reactive oxygen species. Just

37:52

the inflammatory processed food in general.

37:55

Not necessarily containing toxins, but just

37:57

polarized science food projects.

38:00

As soon as you generate

38:02

more ROS's that you can quench

38:06

You know an antioxidants of the quencher. Yes,

38:08

our way to get reactive oxygen. It's basically

38:10

like rusting So we said about is like

38:12

when you get wrinkles in your face or

38:14

car rust or that around Cataract that's going

38:16

on in your body inside not just outside

38:18

and that's normal But if you have too

38:20

much of it, it causes damage to yourself

38:22

faster you die faster. Yeah, basically it is

38:24

the aging Reaction sped

38:27

up. Yeah, okay, and it turns

38:29

out ultra processed food does all

38:32

of that and

38:34

so the question is Can

38:36

we use this? Paradigm

38:40

of reactive oxygen species generation

38:42

and lack of quenching as

38:45

the model for being able to actually

38:47

do something About yeah, we

38:49

are now in the process of

38:52

designing the study, you

38:54

know to do that Yeah, so this is you know

38:56

Robert in 2007 I

38:59

wrote an article it was titled systems

39:01

biology toxins Obesity and functional medicine and

39:03

I literally wrote and that was like

39:05

almost 20 years ago Writing

39:08

about my observations that there were certain patients

39:10

that were struggling with weight They weren't because

39:12

of what they were eating or not exercising.

39:14

There was something else. I had one woman.

39:17

She was a fitness trainer She ate perfectly and

39:19

she couldn't lose the 40 pounds or hanging on

39:21

her body I'm like, you know, I don't know

39:23

but I think there's some data that shows that environmental toxins

39:25

Maybe they show on we check what we can check

39:27

we checked heavy metal when she had high mercury And

39:30

we got the mercury out of her system. We

39:32

need to talk spider She lost 40 pounds like

39:35

that and our blood pressure probably came yeah And

39:37

I and I started looking at the data and

39:39

there was data on how environmental toxins are interfering

39:41

with Every cellular

39:43

process including metabolism and

39:45

drive in some resistance and also affect

39:48

thyroid You know one of the interesting things as people

39:50

lose weight you mentioned the plateau Well when you lose

39:52

weight where the toxins stored they're stored in your fat

39:54

tissue So they get released and then

39:56

they start to interrupt your metabolism. So they interrupt

39:58

the conversion of teeth T4 to

40:00

T3 which is the active thyroid hormone

40:03

which is your metabolic rate. So

40:06

the science then was in its infancy

40:09

but I saw it and I actually had a chapter

40:11

in my book in 2005 called Love Your Liver and

40:14

Ultra-Metallism to kind of help people understand that

40:17

detoxification and getting rid of these

40:19

chemicals from their environment and lifestyle

40:21

and also from their bodies by

40:23

a scientific detoxification approach really works.

40:26

There are a whole bunch of different things

40:28

that we are exposed to that

40:30

affect different aspects of

40:32

our energy

40:34

burning pathway. The

40:37

one that we are now most interested

40:39

in and most concerned about is

40:41

the mitochondria because after all

40:43

that's where ATP generation occurs. That's who

40:45

your metabolism is essentially isn't your mitochondria

40:47

right? Right so we can talk about

40:51

environmental obesogens, we can talk about

40:53

food or we can

40:55

talk about stress. It

40:57

turns out stress does it too. Yeah for

41:00

sure. So pretty

41:02

much everything that drives

41:05

weight gain, drives these

41:07

chronic metabolic diseases can

41:10

be basically bundled into one of

41:12

these four, one

41:15

of these three bins. The

41:17

food, the environmental

41:20

exposures or the stress. None

41:23

of this has anything to do with genetics.

41:25

Right and I would say that the calorie

41:27

quality and the amount matter so it's not

41:29

like it's an either or. You need to

41:31

pay attention to it. Well yeah of course

41:33

because calorie amount means more ROSs. Yeah and

41:35

I actually noticed this one thing I just

41:37

interrupt because I'm just thinking about all these

41:39

things but I had this meal in Martha's

41:41

Vineyard once in the summer with a friend

41:43

and we ordered from this like organic regenerative

41:45

thing. We ordered like so much food and

41:47

it was so delicious and both of us are

41:50

you know like basically fit healthy guys

41:52

who have no metabolic issues and we

41:54

ate enormous amount of food, of healthy

41:56

food and we had our containers glucose

41:58

monitors on. Right. So we call each other

42:00

at 10 o'clock and I'm like, hey Michael, what is going on? Your

42:02

blood sugar high, my blood sugar's high. So it was like my blood

42:05

sugar went to like 150 because

42:07

it was the amount of food also had this effect.

42:09

Well of course, I mean, there's no

42:11

question you can overwhelm your

42:14

body's ability to handle

42:16

or to clear glucose. And

42:18

so that brings us

42:20

to the question of should we be monitoring

42:23

this phenomenon, glucose and insulin. So

42:26

I believe that insulin

42:29

is the bad guy. I

42:32

wish that we had

42:34

a method for monitoring continuous insulin monitoring.

42:36

When are we getting that? I've been

42:39

asking that for 20 years. Five years.

42:41

Five years? Five years. Serious? Like a

42:43

patch? Five years. That's gonna be

42:45

a game changer. Because glucose is sort of fine, but

42:47

it's the last thing to go up. It's coming. Yeah.

42:50

Okay. Everybody's interested and everybody knows that's where

42:53

the action's gonna be. But

42:55

we don't have insulin right now. But we

42:57

do have glucose. But you can measure your blood test for insulin.

43:00

Yeah, fasting. You can also do postprandial

43:02

insulin if you know how and if

43:04

your doctor actually understands what they're doing.

43:07

And if you can find a lab

43:09

that will actually stick you for

43:12

glucose and insulin and send

43:14

all of them. So the

43:16

most part the insurance company won't pay for that. But it's not that

43:18

expensive. And I've been doing it for 25 years. So

43:21

you can get it done easily. I did

43:23

oral glucose tolerance test and simultaneously insulin levels

43:25

on all of my obese patients. That's how

43:27

I get into the realization insulin was the bad

43:29

guy. Yeah, me too. Me too. Exactly

43:32

right. So when is the

43:34

rest of medicine gonna wake up? When

43:36

we have the continuous insulin monitor. Yeah.

43:39

But it's coming. It's just not here yet. Point

43:42

is we can use glucose as a

43:44

proxy for insulin. Now

43:46

glucose is bad by itself. Because

43:49

high glucose leads to endothelial dysfunction. It

43:51

changes the cells inside your arteries. It's

43:53

one of the reasons for high blood

43:56

pressure. It's one of the reasons, you

43:58

know, and also generates uric acid. acid

44:00

which also increases blood pressure. And

44:03

you know, there's neuropathy,

44:05

nephropathy, retinopathy, all you know,

44:07

small vessel disease related to

44:09

you know, severe fluctuations in

44:11

glucose. So glucose is a

44:14

bad guy in the story. But

44:17

there are two worse guys in the

44:19

story. One of them

44:22

is insulin. And the

44:24

other one is fructose which is not

44:26

measured in the serum glucose. No, you

44:28

don't measure. It's

44:30

a different phenomenon. If you can measure like key gluline, you want to

44:32

see what you can measure for fructose amine. Well

44:34

you can't, yeah but fructose amine is a measure of

44:36

glucose. It's not a measure of fructose. I

44:39

wish it were true. I would be measuring it

44:41

on everybody but it's not true. Okay. I

44:44

wish it were so. Yeah. Anyway, bottom

44:46

line is there are other things to know other

44:48

than glucose. Glucose is

44:50

in my estimation about 10% of

44:53

the equation on metabolic health. Okay.

44:56

Interesting. So what we

44:58

have now and we can glean

45:00

the information on both

45:02

insulin release which is its own problem

45:06

phenomenon and insulin resistance which is

45:08

its own problem phenomenon and be

45:11

able to figure out which is

45:13

which and then be able to

45:15

address our therapies to the appropriate

45:18

pathology by understanding what's going on

45:20

with glucose. So I

45:23

am for continuous glucose

45:25

monitoring even in non-diabetics

45:28

and of course that's one reason why

45:30

both you and I, full disclosure, are

45:32

advisors to company called Levels Health and

45:35

that's exactly what they do and

45:37

I have to say that we

45:39

have data that shows that exercise

45:42

affects that glucose response, that we

45:44

have data that shows sleep

45:47

affects that glucose response in non-diabetics.

45:49

Yeah, yeah. You know normal weight

45:51

people. Oh, yeah. And we

45:53

also have data that shows that if you know

45:55

your glucose you

45:57

lose weight. Yeah. Yeah.

46:00

back mechanism. It is. It's like I'm

46:02

in shock. I'm like oh my blade's

46:04

so high when I eat that whatever

46:06

cookie. I can eat that again. So

46:08

there's data to be had that we

46:10

can access today. Is

46:12

it perfect? No of course

46:14

not. Do we need more

46:16

information? Absolutely. But you know

46:18

to ignore

46:21

this possibility I think is you

46:23

know not serving our patients properly.

46:25

I will tell you I

46:29

recently just within

46:31

the last week had dinner with

46:33

two of my former trainees and

46:36

they didn't know a thing about this. I

46:38

mean they're pediatric endocrinologists. And they

46:40

didn't know a thing about this. Tell me about my daughter's third

46:43

year medical student. My reach was learning about insulin resistance. Not really.

46:46

So there is this big hole.

46:48

About nutrition? No none medical school.

46:50

This is a big hole in medical education. And

46:53

the reason I think is because

46:56

you know what we learn in medical school and

46:58

we've talked about this you know there's a pill

47:00

for that. Yeah. Well there is no pill for

47:03

this. That's what we've learned. There is no pill

47:05

for chronic metabolic disease. Well was that big? No.

47:08

Okay let me just unpack what you said because

47:10

it's so important. I want to make sure people

47:12

got all the things we talked about. So there's

47:15

basically three to four hypotheses that

47:17

are needed to explain all the

47:19

facts. You know science is designed

47:21

to try to explain the facts

47:23

that are observed. However a lot

47:26

of times in science we misinterpret the facts

47:28

and we create meaning in ways that actually

47:30

aren't true. For example I'm reading this book

47:32

called Rethinking Diabetes by our friend Gary Tauss.

47:34

Yep. It's a fascinating history of diabetes. He

47:36

talks about how in the early days with

47:38

type 1 diabetics you had to give them

47:41

a high fat keto diet or they

47:43

would die. So Elliot Joslin

47:46

knew this. Gucas is of no use

47:48

to the body. That's a direct quote

47:50

from Elliot Joslin before he knew what

47:52

insulin was. 1893. Right.

47:55

He said this. And Fred Allen who took

47:57

over for Joslin in 1919 published

48:00

a treatise basically

48:03

saying the way to treat type 1 diabetics

48:05

was a 70% fat, 8%

48:09

carbohydrate diet. So they said that but

48:11

then what happened was years later when

48:13

they started getting insulin they

48:16

saw that all these people were dying

48:18

of premature heart disease and atherosclerosis. So

48:21

they made the observation that the fat in

48:23

the arteries was happening in these patients and

48:25

they hypothesized based on that set of facts

48:27

that it was the high fat diet that

48:29

they ate when they were younger that caused

48:31

clogged arteries. They just misinterpreted those

48:33

facts. So why I brought that up

48:35

is because we have to agree that we

48:38

have a whole set of facts that don't

48:40

meet all the theories. So we need

48:42

multiple theories to actually understand it. So is

48:44

the energy hypothesis wrong? Not

48:46

completely. Is the carbohydrate insulin model

48:49

wrong? No, it's actually mostly right

48:51

but this doesn't explain everything. Is

48:53

the obesity model the entire story?

48:56

No, not exactly because stress plays

48:58

a role. For example stress, I

49:01

found out when I was researching one of my books that

49:04

your vagus nerve and your sympathetic nervous system innervates

49:06

every one of your fat cells. So when you're

49:08

stressed it literally sends a nervous signal, a nerve

49:11

signal to your fat cells to say stop burning

49:13

calories. So these are the four things we talked

49:15

about that all play a role and have to

49:17

be encountered and you have to personalize the approach

49:20

to each person. So like oh this is going

49:22

to work for this person and that doesn't work

49:24

for that person. There is no one size fits

49:26

all. So to that point and I'm glad you

49:29

brought that up. People

49:31

think that the sympathetic nervous system

49:33

results in lipolysis because

49:35

you exercise burning fat. Burn fat,

49:37

right? And that is true in

49:40

the acute situation. In

49:42

the acute situation you release norepinephrine

49:44

from your sympathetic nervous system. Then

49:48

via the intermedial lateral cell column and the peripheral

49:52

sympathetic nerves go to each fat cell,

49:54

bind to the beta 3 adrenergic receptor,

49:57

Activate hormone sensitive lipase, That

50:00

leads to dissolution of the tray

50:02

so glycerol into free fatty acids

50:04

and glycerol which then circulate back

50:06

in the bloodstream to the liver

50:08

which than turns them into key

50:10

tones for the rest of body

50:12

is. That. Why policies

50:15

and that? What a cute sympathetic

50:17

nervous system activation shit Exercise does

50:19

a cute and by way of

50:21

aggravation. Know that insulin block fi

50:23

policy? So it may faith insulin

50:25

prevents the sad breakdowns Live in

50:27

slums? Hi, it's hard to lose

50:30

weight. That's exactly right. Insulin blocks

50:32

your ability to be able to

50:34

lose weight and that's why is

50:36

getting in some down his job

50:38

One? Yeah, for just that reason

50:40

exactly right now here's the problem

50:43

with that. Yeah, Chronic. Activation

50:45

of the sympathetic nervous system. Does.

50:48

The opposite Now. So.

50:51

Every. Sympathetic neuron in

50:53

your body. Whether. To

50:55

new perfume your spinal cord or in your

50:57

brain the matter. Releases

51:00

norepinephrine, But. Also releases

51:02

a neural peptide. Called.

51:05

Neural Peptide: Why know you and

51:07

p Why they are currently east

51:09

and turns that Mp: Why binds

51:11

to it's receptor? This

51:14

So the y two receptor and

51:16

what it does is it shuts

51:18

off. That. Were nonsense and

51:20

of lipase. So the you know

51:22

that lack of insulin and this

51:24

sympathetic nervous systems. Now instead of

51:27

just generating lie palaces you're actually

51:29

generating lipid genesis. You me Belfast

51:31

that a burn Fat Yes exactly.

51:33

And so chronic stress become Saigon

51:36

from the and that really like

51:38

Obama had his anger translator on

51:40

the rubber less excel hydra. Ah

51:42

outside point. The point is chronic

51:45

stress does the opposite and we

51:47

all know the chronic stress. As

51:49

the bad guy, us industry acute stress is

51:51

for the most part adaptive. Yeah, but chronic

51:53

stress is clearly maladaptive and it less what's

51:55

in his. i just say we a stress

51:58

free that pint of Ben and Jerry. It's

52:00

another mechanism, right? It's another mechanism. If

52:03

you eat that pint of Ben and Jerry's on top of it, it makes it even

52:05

worse. Well the pint of

52:07

Ben and Jerry's is because of what's happening at the

52:09

amygdala and at the fear center of

52:11

the brain because dopamine is

52:14

one of the ways to

52:16

basically placate that amygdala at

52:18

least short term. And

52:21

so that's what stress eating is about. And

52:24

I'm a card

52:26

carrying member of the stress eating club.

52:31

Until I did the research and understood

52:33

it better and now I'm a whole

52:35

lot more appropriate.

52:37

I know last night I was really tired.

52:39

I had a very stressful weekend and

52:42

I flew from New York to LA and

52:45

I was really... You looked pretty good. I was

52:47

really tired and I went shopping and I was

52:50

really hungry. I went shopping at Erewhon and literally

52:52

this voice in my head was buy the

52:54

ice cream, buy the ice cream, buy the ice

52:56

cream. And I literally had to like override that

52:58

because I knew if I brought it home, I

53:01

would eat the whole thing. Of course. But

53:03

I was able to manage. My higher self

53:06

kind of kicked in until I got to shut

53:08

the F up and I was able to sort

53:10

of manage the store. It was very

53:13

tough but I got out of the store safe and

53:15

didn't bring it home. But I would have eaten it

53:17

even though I know everything I know. I've written 19

53:19

books about this. It's not something

53:21

you can willfully control. Right. So the bottom

53:23

line is we have to,

53:26

number one, get the insulin

53:28

down and number two, we

53:30

have to get the amygdala

53:32

working properly. Those are

53:34

our two most important

53:36

things. Now how do you get the

53:38

insulin down? Well number one,

53:41

don't let it go up. Well can I just interrupt

53:43

for a second? Because you're basically laying out these different

53:45

hypotheses but I hear you're going back to insulin. Always

53:48

leaning more towards the carbohydrate insulin hypothesis?

53:50

Well I'm leaning more to the ROS

53:52

hypothesis. So the question is what is

53:55

ROS is do your beta cell? Turns

53:57

out it makes more insulin release. Or

54:00

Wess in the beta cell actually

54:02

generate and a bigger insulin response

54:04

to miss oxidative stress from anything.

54:07

Will I know? Toxins? sugar alter

54:09

process food or micro bombing must

54:11

up com us chronic stress. All

54:13

these variables have to be looked

54:15

at so it's exactly I just

54:17

sat there was that I'm in

54:19

obesity Nanos impact efficiency is it

54:21

different from the and will talk

54:23

about that in a minute. That's

54:26

what's the point is points everybody

54:28

who's.metabolic disease which is ninety three

54:30

percent of America. Has

54:32

a problem with one or more of

54:34

the five things you just mentioned That

54:36

staggering Robert: Ninety three percent of Americans

54:38

have some degree of this problem. Yet

54:40

even though seventy five percent overweight see,

54:42

don't have to be overweight status problems

54:44

Nice recall: skinny fat and since I

54:47

met about obese, Norm Away or. He.

54:49

Auto feasting on the outside. found the inside

54:51

and what we know is that those patients

54:54

have liver said yes to just because you

54:56

don't have. Subcutaneous fat.

54:59

Doesn't. Mean you don't have liver Sat in

55:01

the Us. have never. Just because you're healthy

55:04

doesn't mean your wealth. and just because you're

55:06

fast doesn't you said yes? And case the

55:08

the overlap is huge so is this is

55:10

a problem for everybody? Answer the question is

55:13

what do you do about it? How do

55:15

you figure it out of are you at

55:17

risk? Does your doctor know it? Will They

55:19

help you via earnest? Not how you gonna

55:22

figure it out for yourself? Well you know

55:24

that's what's you. and I are doing a

55:26

friggin' podcast or have ya sister try to

55:28

help people. Understand that? Yeah,

55:31

exactly right. And Six point

55:33

as. Insulin. Is one

55:35

of the drivers promote metabolism, get

55:37

insulin down. The other one is

55:40

to suppress inflammation because inflammation drives

55:42

insulin resistance from anything. and infection

55:44

by a virus has been linked

55:46

to obesity. right, outlet reset, and

55:49

a virus Thirty six, right? For

55:51

as for one and and others

55:53

to but mostly eighty Thirty six,

55:55

I'm point is inflammation. Drives.

55:58

Are O s because. inflammation

56:00

drives NADPH oxidase at the

56:02

level of the liver, driving

56:04

those ROSs. That's what NADPH

56:07

oxidase makes, those ROSs. Okay,

56:10

now, the ROSs... That's part of your mitochondrial processing

56:12

of the food you eat and oxygen you breathe

56:14

in it. It sort of has these little pathways

56:16

and when it goes kind of awry, it's like

56:18

going on the wrong pinball thing and it doesn't

56:20

go where you want it to go. Exactly. And

56:23

ends up causing more damage. Exactly right. ROSs have

56:25

to be quenched. Now, the quenching occurs

56:27

in the peroxisome and that's where the antioxidants

56:30

live. So in the liver,

56:32

it's glutathione or maybe vitamin E. In

56:34

other cells, it might be other... SOD,

56:37

catalase, glutathione, peroxis. These

56:40

are all antioxidants that your body makes

56:42

and they're so powerful and often they're

56:44

overwhelmed and often we don't support their

56:46

function with the right nutrients. Right, exactly.

56:48

So for instance, glutathione needs methionine. Well,

56:51

methionine is the second rarest amino acid

56:53

after tryptophane. That's the rarest and you

56:55

need tryptophane in order to be able

56:57

to turn that amygdala off. But

57:00

methionine is necessary to be able to

57:02

make S-adenosyl methionine, which then contributes to

57:04

methyl group for glutathione. Well, if you're

57:07

methionine deficient, you've got a problem.

57:09

Yeah. And glutathione is like the King

57:12

Kong of antioxidants. Exactly. Your

57:14

body makes it. My colleague,

57:16

Jackie Marr at San Francisco

57:18

General, studies the methionine choline

57:20

deficient rat, the MCD rat.

57:23

Poor rat. Okay. Not the McDonald's rat,

57:25

but it might as well be. Okay.

57:27

This is the fastest way to fatty

57:29

liver disease there is. And

57:31

the reason is because without

57:34

methionine, you can't generate glutathione. So you're going

57:36

to get naffled,

57:39

non-alcoholic fatty liver disease. And also

57:42

choline. Choline makes phosphatidylcholine, which is

57:44

part of ApoB, which helps export

57:46

the fat out of the liver

57:48

so it can go to the

57:50

adipocyte instead. Yeah. So without choline,

57:53

you can't get the fat out

57:55

of the liver. Yeah. So you

57:58

make too much and you can't clear it. And so... These

58:00

animals have fatty liver like crazy like

58:02

about almost a hundred million Americans Point

58:05

is the point is the finding and

58:07

co-ing are things that you don't find

58:09

much in processed food No, where are

58:11

they found? Well, they're found in

58:13

real food I mean the fining is found

58:15

in you know, basically good protein when I

58:18

say good protein fish poultry

58:20

eggs Okay The

58:23

ocean red meat. Absolutely. Absolutely You

58:25

know and also you need iron for

58:27

this too, you know Colleen is where

58:29

and Colleen is in red meat as

58:32

well eggs eggs and eggs our Dean's

58:34

sardines Which I have a can of

58:36

sardines here with me now for lunch

58:40

The problem with Colleen is that Colleen

58:42

can be acted on by the intestinal

58:44

microbiome Yeah to form trimethylamine TMIO and

58:46

then that gets oxidized in a Stanley

58:49

Hayes and Cleveland Clinic where you by

58:51

the way are You

58:53

know working working as well, you

58:55

know with Michael Roy's and in

58:57

their wellness program. So, you know

59:00

So, you know even though sometimes

59:03

things are good Sometimes too much of a

59:05

good thing is bad so good And so

59:07

we have this problem in nutrition also is

59:09

that we have inverted u-shaped curves for certain.

59:11

Yeah, like Colleen Yeah, yeah, Colleen used to

59:13

be called vitamin b4 You

59:16

know, so it's it's essential essential,

59:18

right? It's essential So it's

59:20

these are the things that are wrong

59:23

that we have to fix I'm saying if

59:25

for me we're going about our Right you're

59:27

going inflammation is driving this so where inflammation

59:30

is coming from if it's coming from stress

59:32

if it's coming from toxins Come sugar over

59:34

your microbiome. It's coming from our diet. That's

59:36

where it's coming from So if

59:38

you have an autoimmune disease, it's coming from your

59:40

immune system But if you don't have an

59:43

autoimmune disease, which is 90% of us 10% do but yeah 90%

59:45

of us don't It's

59:48

coming from your gut now Your

59:51

gut is a sewer What's

59:53

the definition of a sewer a pipe with

59:55

you know, what in it? Yes. Okay. That's

59:57

what the gut is. It's a sewer Well,

1:00:01

all that junk in there is

1:00:04

bad for you. You don't want it in

1:00:06

your bloodstream. It stays in your gut. So

1:00:09

there are three barriers in your

1:00:11

intestine to keep the junk out of your

1:00:13

blood. The first is the

1:00:15

physical barrier, the mucin layer. The

1:00:17

mucus. Right. And

1:00:19

it lines the intestinal epithelium all the

1:00:21

way through. The second is

1:00:24

the biochemical barrier, which is the

1:00:26

zonulins, the tight junctions that hold

1:00:28

the intestinal epithelium cells together. Lego

1:00:32

blocks stuck together. Yes, kind of sort of

1:00:34

like Lego blocks. And when they become dysfunctional,

1:00:36

then they get permeable and that

1:00:38

leads to what we call leaky

1:00:40

gut. Yeah. And the

1:00:42

third is the immunologic barrier. And those are called

1:00:44

TH17 cells. And they make

1:00:47

a cytokine called IL-17. So

1:00:49

those are white blood cells and they're

1:00:51

making inflammatory compounds. Exactly. To

1:00:53

get rid of foreign invaders. Yeah.

1:00:57

Okay. It's like the front line of

1:00:59

the military on the front lines, right? Yeah. Well,

1:01:01

you've got the guys at the front, the pawns, then

1:01:03

you've got the knights, then you've got the bishops. All

1:01:05

right? Before you get to the king.

1:01:07

Right? I mean, you have all

1:01:09

of these things in defense of

1:01:12

your bloodstream. The

1:01:14

point is all three of those are

1:01:17

failing today because of

1:01:19

ultra-processed food. The

1:01:21

mucin layer, because of the lack of

1:01:24

fiber, the microbiome will actually

1:01:26

chew up the mucin layer

1:01:28

for its own purposes because it

1:01:31

otherwise is starving. Fiber is the

1:01:33

food for your microbiome. Fiber is the

1:01:35

food for your bacteria. Fiber is the nutrient

1:01:38

you don't absorb because it's not for you,

1:01:40

it's for your bacteria. But

1:01:42

our food is fiberless

1:01:44

on purpose because you can't

1:01:47

freeze fiber. Exactly. So

1:01:49

the food industry took it out. Yeah. Well, we

1:01:51

got to put it back in. And that's what this is. Yeah.

1:01:54

What is that? You got

1:01:56

to pack it. Full disclosure, I am the

1:01:58

chief medical officer and co-founder. of

1:02:00

a fiber company and it's called

1:02:02

BioLumen and the product is called

1:02:04

MoshMosh and we just released it

1:02:06

end of November. It's doing very

1:02:08

well. And what's in it? What

1:02:10

is in it? These are microcellulose

1:02:13

sponges, seven microns in

1:02:15

diameter. So the size of

1:02:17

a red blood cell. So it flows like a powder. It's

1:02:20

colorless, odorless, tasteless, textureless because

1:02:23

your tongue can't tell six microns. Yeah, it's

1:02:25

gotta be 12 microns or greater for your

1:02:27

tongue to be able to discern that it's

1:02:30

there. So we can go into bean

1:02:35

dip, it can go into chocolate, it can

1:02:37

go into ice cream and smoothies, yogurt,

1:02:39

anything that's non-aqueous. Well,

1:02:44

you can put it in water and then drink it right away. If

1:02:47

you leave it, it'll swell. It turns to a gel

1:02:49

and you can put a spoon and it stands straight up,

1:02:51

right? Right, we don't wanna do that because then no one

1:02:54

will drink it. You

1:02:56

swallow it in the food or

1:02:58

otherwise. In the

1:03:00

stomach, it'll start expanding. It expands 70-fold

1:03:02

over its original size. Incredible. So that'll

1:03:04

give you a feeling of fullness, which

1:03:07

helps. And when

1:03:09

it expands, it exhibits the nooks and the

1:03:11

crannies in the sponge, right? Like the kitchen

1:03:14

sponge, you know, there's the holes in it.

1:03:17

Impregnated in all of those

1:03:19

are a set of proprietary

1:03:21

hydrogels, soluble fiber, which sequester,

1:03:23

absorb, soak up glucose, fructose,

1:03:25

sucrose, simple starches. Even fat

1:03:27

too? No, not fat. Not

1:03:29

fat? Not fat. It doesn't limit like

1:03:32

cholesterol because a lot of the fibers will

1:03:34

like metamute. Some of them will reduce cholesterol

1:03:36

absorption. Yeah, but this one won't. Interesting. So

1:03:38

that's one of the geniuses

1:03:40

of this is it only works

1:03:42

on carbohydrate. Interesting. Because you don't

1:03:45

wanna absorb fat because if

1:03:47

you absorb fat, number one, you get bad

1:03:49

GI side effects. That's what happens. Genocal

1:03:52

or carb. You don't wanna prevent the absorption of

1:03:54

fat. Right, exactly. And yeast fat.

1:03:56

With oral fat and that fat block or

1:03:58

anybody who's having disaster. pants with, right? This

1:04:02

is basically what's in

1:04:04

regular food and everything that's in this

1:04:07

packet is food. Yeah. All the components

1:04:09

are food. They're food grade. We get

1:04:11

them on Amazon. We just assemble them

1:04:13

in a specific proprietary way. You take

1:04:15

it before you eat essentially. You take

1:04:17

it with you. I

1:04:19

just came back from Tanzania and I met with the honey

1:04:21

hunters. I mean the Hadza,

1:04:23

which are this incredible

1:04:26

tribe. Right. The last hunter-gatherer tribe.

1:04:28

Right. And they hunt and they

1:04:30

gather and 20% of their diet

1:04:32

is honey, right? Honey. And

1:04:34

the other part of their diet is an enormous amount

1:04:36

of fiber. They eat a hundred and fifty grams of

1:04:38

fiber a day. We literally dug a root out of

1:04:41

the bottom of a tree. It was kind of a

1:04:43

wild yam. And they eat that. And

1:04:45

so, you know, we all ate about a hundred

1:04:47

to a hundred and fifty grams of fiber per

1:04:49

person a day. Now we eat about eight or

1:04:52

less. Right. And it's destroying our microbiome. It's making

1:04:54

us metabolically healthy and it's hard to

1:04:56

get that much unless you're eating. Unless

1:04:58

you're a Hadza. Yeah, unless you're a

1:05:00

Hadza. Eating tons of fiber all the

1:05:02

time. And it's hard. And I

1:05:04

think the data is really clear on other

1:05:07

studies too, like from Metamucil and Wade, even

1:05:09

things like polyglycoflex from gluca-manin

1:05:11

helps in this. Some of that in there.

1:05:13

Right. So the concept is

1:05:15

right. I mean, so this is

1:05:17

both insoluble fiber cellulose and

1:05:20

soluble fiber these hydrogels. Okay. And so it's

1:05:22

unusual because it's a combination of both. So it's

1:05:24

going to do a couple things. Tell us

1:05:26

the things that it does. So number one. Because

1:05:28

it has multiple actions in terms of its

1:05:30

effects. Six separate effects. So the

1:05:33

first thing is it gives you

1:05:35

feeling of fullness. Second, it absorbs

1:05:38

carbohydrate and, you know, especially

1:05:40

simple sugars in the duodenum

1:05:42

preventing their ability to cross into the

1:05:44

bloodstream. Thus you reduce the glucose response.

1:05:47

You reduce the insulin response. We just

1:05:49

said that's the most important thing. So

1:05:51

you slow absorption of sugar into your

1:05:53

blood and it prevents this glucose spike

1:05:55

and the insulin spike that makes you

1:05:57

gain weight. Correct. In addition...

1:06:00

It moves the food through the

1:06:02

intestine faster because fiber is a

1:06:04

lot faster. Transit time we call

1:06:06

it. Transit time decreases. That

1:06:08

means that you get your satiety signal sooner

1:06:10

because it's at the end of the intestine,

1:06:12

the peptide YY signal in the

1:06:15

ileum, the end of the intestine. In

1:06:17

addition. So what you just said

1:06:19

there was you feel full the satiety signal, which

1:06:22

is a PYY and others that get released in

1:06:24

the lower part of the intestine and activated on

1:06:26

the fiber. So that makes you actually shut your

1:06:28

brain down from wanting food. Correct. Which

1:06:31

is by the way is what GLP-1 does. Yeah. Okay.

1:06:34

And we'll get to that. Number four, it feeds

1:06:36

the microbiome so it increases microbial diversity, which is

1:06:38

a way to prevent inflammation.

1:06:41

Yeah. There's like bugs that are

1:06:43

good bugs in your gut and bad bugs. And when

1:06:45

you eat processed food, you grow bad bugs. When you

1:06:47

eat fiber, you grow good bugs. Exactly. Okay. So

1:06:51

those are what you eat. If you have inflammatory

1:06:53

bugs, you get something called

1:06:56

metabolic endotoxemia, which means your inflammation

1:06:58

from your bugs causes insulin resistance

1:07:00

independent of your diet. And do you know what does that?

1:07:03

Sugar. Because sugar nitrates those tight

1:07:05

junctions and makes them non-functional. And

1:07:08

so transiently increases leaky gut. And

1:07:10

gluten. And gluten. Of

1:07:12

course gluten. And all the food additives,

1:07:14

the emulsifiers, which destroy the lining of the

1:07:16

gut. That's destroying that mucus

1:07:18

layer. That's right. Number

1:07:21

five, the soluble fiber

1:07:24

acts as food for the colonic bacteria

1:07:26

generating short chain fatty acids, which have

1:07:28

been shown to be anti-inflammatory, anti-alzheimer's. Anti-cancer.

1:07:30

Anti-cancer. Yeah. And

1:07:33

finally, the insoluble fiber helps

1:07:36

clear cancer cells from,

1:07:38

you know, sloughing from the colon. So

1:07:41

basically- I think there's one more. What's the one

1:07:43

more? Well, you secrete extra toxins from your liver

1:07:45

into your bile. It goes in your gut. And

1:07:47

so you have environmental toxins. Yeah. And

1:07:50

you have a lot of push down as well, Fatt. Sure. So

1:07:52

you have seven there. Yeah. Seven.

1:07:54

That was a lucky number. We haven't studied that one

1:07:57

yet, but that's actually very true. The point is, what

1:07:59

this does is it recoup- capitulates the effect of

1:08:01

the fiber that was in the food to start

1:08:03

with Before the food

1:08:06

industry got to it, but it doesn't mean you can take

1:08:08

that and eat ultra processed food You want to still eat

1:08:10

well food right well? Ultimately the question

1:08:12

is can you have your take and eat it too

1:08:14

and that by the way that was just an article

1:08:16

in the Guardian three days ago

1:08:19

with that title I'm

1:08:22

not proposing we Abandon

1:08:24

trying to fix ultra process. I just have one of

1:08:26

those before my pint of Ben and Jerry's or what

1:08:29

we need We need all the tools

1:08:31

right? I bet that's what people are thinking well. We

1:08:33

need all the tools we can get yeah Okay, there

1:08:35

are sugar addicts out there who you know no matter

1:08:38

what information we give them You

1:08:40

know they're going to continue. You

1:08:42

know hitting the hitting the sodas

1:08:44

hitting the the Ben and Jerry's

1:08:46

and we have to provide

1:08:48

them with Methods for dealing

1:08:51

with their problem as well think of it this

1:08:53

way Okay, you got a

1:08:55

heroin addict Okay Why

1:08:58

is heroin bad? Because

1:09:01

it's addictive because it's addictive

1:09:03

well caffeine is addictive, but there's a

1:09:06

Starbucks on every street corner True,

1:09:10

so why is heroin such a

1:09:12

problem because during the withdrawal phase

1:09:14

you go steal a car That's why

1:09:16

all right, so what did

1:09:18

society do? we came

1:09:20

up with this thing called methadone and Methadone

1:09:24

basically is an

1:09:26

oral opioid which basically takes

1:09:28

the edge off the peaks

1:09:30

in the valleys Think

1:09:33

of this as methadone For

1:09:36

your sugar that's incredibly addiction. How

1:09:39

do you like that? I like that. I mean, okay It

1:09:42

doesn't fix the problem, but it helps mitigate the

1:09:44

dolphin on it Don't

1:09:46

is addictive so not quite methadone But

1:09:48

I I think you know I don't bring this up

1:09:51

because I a lot of criticisms about this whole food addiction

1:09:53

Theory yeah, and and there are a lot of

1:09:56

people who are pushing back and saying it's not

1:09:58

a problem that it's really just people Gluttony

1:10:00

and then it's not really a biological phenomenon and

1:10:02

doesn't meet the criteria. Actually it does meet the

1:10:04

criteria. But if you look at, I mean listen,

1:10:07

Kelly Bernal has created a whole

1:10:09

Yale food addiction score. It's a

1:10:11

valid entry. Ashley Gerhard has done

1:10:13

enormous work. Yeah. Nicola

1:10:15

Vina has demonstrated sugar addiction in animals and

1:10:18

now in humans. And I just met with

1:10:20

her. We just did the Commonwealth Club last

1:10:22

week. Yeah. We're going to

1:10:24

meet in New York next week as well. Yeah.

1:10:27

There's a food addiction symposium in London. Yeah.

1:10:30

In May. There's different degrees of it. There's

1:10:32

different degrees. But there was a really interesting

1:10:34

meta-analysis of a systematic review of 281 studies

1:10:36

from 36 countries and

1:10:38

they found that overall the prevalence of food

1:10:41

addiction, according to the Yale food addiction score, which

1:10:43

is a validated metric, was 14% in adults and

1:10:46

12% in

1:10:49

kids. And 14% of

1:10:51

the population is alcohol addicted. So it's like

1:10:53

the same as alcoholism and tobacco is about

1:10:55

18%. So let's use

1:10:57

alcohol as the template for this. Okay.

1:11:04

Let's take the American population. 40%

1:11:07

of Americans are teetotalers. Never touch the

1:11:09

stuff. 40%

1:11:11

are social drinkers. Pick up

1:11:13

a beer and put it down. 10%

1:11:17

are binge drinkers and 10%

1:11:19

are chronic alcoholics. Yeah.

1:11:23

Okay. So even though alcohol is available

1:11:26

everywhere, 80% of

1:11:29

the population does not seem to have a

1:11:31

problem. Yeah. But 20%

1:11:33

do. Right. And

1:11:35

the question is, what are you going to do for that 20%?

1:11:38

And why do they have it? And why do they have it?

1:11:40

Well, it turns out they're probably the same people. Yeah. So

1:11:42

the idea that there's no sugar addiction doesn't

1:11:45

make sense just because not everyone

1:11:47

is addicted. Right. It

1:11:50

doesn't mean it doesn't exist. Right. So

1:11:52

sugar and alcohol are metabolized

1:11:54

virtually identically. The fructose

1:11:57

molecule and the ethanol molecule basically

1:11:59

do the exact same thing at

1:12:01

the level of the mitochondria. So

1:12:04

it shouldn't be surprising that children

1:12:06

who don't drink alcohol have the

1:12:08

same diseases as alcoholics, type 2

1:12:10

diabetes and fatty liver disease, even

1:12:12

without alcohol because they have a

1:12:15

substitute. They have sugar. Yeah.

1:12:18

It's really interesting. I mean, I think that

1:12:20

the food addiction thing is fascinating because even, you

1:12:22

know, there's people say, where are the randomized controlled

1:12:24

trials? Well, David Ludwig did one

1:12:27

where he basically took, it was fascinating study called

1:12:29

the milkshake study. Yeah. I

1:12:31

know. You know about this study. Basically,

1:12:33

he's a group of overweight guys and he gave them

1:12:35

on different times different milkshakes,

1:12:37

but they were identical. So they were

1:12:39

calories, carb, fiber, protein, fat. And

1:12:43

the speed of the absorption of the sugar was

1:12:45

the only difference. So one had a rapidly spiking

1:12:47

sugar and the other one didn't. And

1:12:50

they measured their brain MRIs and

1:12:52

they measured their blood chemistries. And

1:12:55

even though they were identical in calories, the

1:12:57

group that had, and they tasted the same,

1:12:59

the group didn't know which one they were

1:13:01

eating, the ones that had

1:13:04

the high spiking sugar carbohydrate had

1:13:06

higher levels of insulin, higher levels of

1:13:08

glucose, higher triglycerides, more inflammation

1:13:10

and higher cortisol, higher adrenaline and their

1:13:12

brains in the area of addiction, the

1:13:15

nuclei succumbens lit up like a Christmas

1:13:17

tree. Exactly. And that's the same area that

1:13:19

lights up with heroin and cocaine. And I think the- Anything

1:13:22

that makes that nuclei succumbens activate

1:13:25

in the extreme is addictive. And

1:13:27

now we know there's genetics that play a

1:13:29

role. So I don't know if you do

1:13:31

this, but I- We haven't found the genetic

1:13:33

locus yet for alcohol or for nicotine or

1:13:35

for sugar. Well, we may not know exactly,

1:13:37

but we do know that there's difference in

1:13:39

dopamine receptors. So we can measure genes for

1:13:41

dopamine receptors and dopamine is the receptor that

1:13:44

feels pleasure. So in these people with dopamine

1:13:46

receptor problems, they end

1:13:48

up needing more stimulation to feel

1:13:50

the same goodness. Because the dopamine

1:13:52

receptor has been downregulated. It's the

1:13:54

law diminishing returns basically- Well, it's

1:13:56

both by- Log ends downregulated. Well,

1:13:58

there's a situation- But there's genetics

1:14:00

also, right? Well, yeah. So

1:14:03

the TAKA1 allele of the dopamine receptor,

1:14:05

so it's in about 20% of people,

1:14:07

okay? Turns

1:14:10

out they make 30% fewer dopamine receptors on

1:14:12

their neurons. They gain more weight. And those

1:14:15

are the people more likely to be addicted

1:14:17

or gain weight or have sugar addiction. So

1:14:19

you're right. It's not like, it's not people,

1:14:21

oh, sugar addiction. Not everybody's alcohol addicted. Not

1:14:24

everybody's sugar addicted. But it's a thing, and

1:14:26

it's as big a thing as alcoholism. And

1:14:28

it's causing societal devolution,

1:14:30

okay, in the same way alcohol did.

1:14:32

And so then the question is, all

1:14:35

right, if you know that something is

1:14:37

both toxic and addictive like

1:14:40

cocaine, heroin, nicotine, alcohol,

1:14:42

you have societal

1:14:46

interventions that deal with it. We call

1:14:48

it public health. What

1:14:51

do we have for sugar? Nada.

1:14:53

Not here. I mean, I just came back

1:14:55

from Chile and Argentina. Yeah, that's right. And they have

1:14:58

incredible laws that have really radically changed their food

1:15:00

consumption patterns and to reduce the amount

1:15:02

of refined sugars and

1:15:04

carbohydrates and junk food because they put black box

1:15:07

warnings on the front of the package. They have

1:15:09

eliminated advertising. I read a Tony the Tiger. They

1:15:12

have no junk food in school. So

1:15:14

there's a lot of ways that we actually can fix this. We

1:15:16

could. You're working on policy. I'm working

1:15:18

on policy stuff. So we have to get this done. Right.

1:15:22

And from that point, we've got standards

1:15:25

for sugar in California

1:15:27

down to 5 percent

1:15:30

of calories in schools. It's

1:15:32

called SB 348. And

1:15:35

my nonprofit Eat Real, which you're

1:15:37

very familiar with, and my CEO,

1:15:39

Nora Latore, is a force of

1:15:42

nature. She's amazing. Yeah. Okay. You

1:15:44

know, worked with Nancy Skinner of the California legislature to

1:15:47

push this through. We're trying to make this national. And

1:15:49

just today, the White House

1:15:51

announced that Eat Real is now

1:15:54

one of its model programs

1:15:56

for dealing with childhood obesity

1:15:58

going into 2020. We

1:16:01

are going to be taking one

1:16:03

billion meals in

1:16:07

schools and making them low

1:16:09

sugar and zero processing. That's

1:16:12

God's work. Because our kids are our

1:16:14

future and we poison our kids. We

1:16:17

have 40% plus overweight, 25% are

1:16:19

obese, we have decreased

1:16:22

performance in school, decreased

1:16:25

performance, earning capacity,

1:16:28

shorter life expectancy, 13 years of your obese

1:16:30

as a kid. It's

1:16:32

really a big deal. It is. So

1:16:35

let the audience understand

1:16:37

how this occurred because ultimately

1:16:40

when you drive into a ditch you have to know how you

1:16:42

drove in in order to be able to back out. You

1:16:45

can't just hit the accelerator and expect to

1:16:47

be able to come out the other side

1:16:50

of the ditch. You

1:16:53

have to know how you drove in. Why

1:16:55

did this happen? So when you and

1:16:57

I were kids and we are about the same age, we

1:17:00

had school and we had

1:17:02

cafeterias and we had lunch

1:17:05

ladies. My mom always made

1:17:07

my lunch. My

1:17:10

mom made me a sandwich every day and I

1:17:12

could kill her to this day. I didn't have

1:17:14

school food when I was in the audience. I

1:17:17

don't remember that. Well they had the blue hairs

1:17:19

with the hair nets. In

1:17:22

1971 the Department

1:17:24

of Education passed an

1:17:28

ordinance, an administrative law

1:17:30

called Resolution 242 which

1:17:32

basically said that all cafeterias in the

1:17:34

United States and public schools had to

1:17:36

make book. That is

1:17:38

they could not lose money for the school.

1:17:40

They had to basically fend for themselves with

1:17:42

their own budget. That

1:17:45

sent every food services director in

1:17:47

every school in America running

1:17:50

for cover. What are we going to do? How

1:17:52

are we going to solve this? Because the biggest

1:17:54

issue was personnel and the infrastructure. I'm

1:17:56

keeping it running to be able to make

1:17:58

school food. In walked

1:18:00

Aramark and Cisco and Guggenheim

1:18:02

and McDonald's and Pizza Hut.

1:18:04

He says, hey, we'll do

1:18:06

it for you. We'll

1:18:09

provide every kid with an, air

1:18:11

quote, nutritious, un-air quote, meal every

1:18:13

single day and you won't have

1:18:15

to do anything. We'll take care

1:18:17

of it and most importantly, because

1:18:20

we'll take care of it, you can take your

1:18:22

infrastructure, you can take your food preparation facilities and

1:18:24

get rid of the kitchen

1:18:26

and turn it into classrooms. And that was

1:18:28

the goal. That was the plan. No, you did a

1:18:30

deep fryer and a microwave and you're fine. Right. And

1:18:33

the point is that once you take the

1:18:36

equipment out, now you're

1:18:38

hostage to the food industry for the

1:18:40

rest of your life. That's right. And

1:18:42

1971, you can track when grades

1:18:45

in elementary school started.

1:18:47

And the reverse is true. I don't know

1:18:49

if you know about my friend, Jill

1:18:52

Shaw, who created a program called

1:18:55

MyWay Cafe in Boston where she basically

1:18:57

paid for, so Flanders paid

1:18:59

for the reinstitution of a kitchen in a

1:19:02

school. Showed how powerful it was. It got

1:19:04

the entire Boston City Schools to it and

1:19:06

now the entire inter-city Boston schools all have

1:19:08

kitchens. The menus have all been designed by

1:19:10

top chefs. The food's delicious. The kid eat

1:19:12

it. They don't throw it out. It meets

1:19:15

the school budget guidelines, the federal guidelines for

1:19:17

school lunches. And everybody's winning and they're not

1:19:19

getting food shipped in across state lines and

1:19:21

in packages of plastic with who knows what kind

1:19:24

of toxins that infiltrate the food in addition to

1:19:26

the junk that's in the food that's heated up

1:19:28

in microwaves and deep fryers. The point is there

1:19:30

are a lot of business models that work. So

1:19:32

EatReal is dedicated to finding the business

1:19:35

model that would work within any district.

1:19:37

So for instance, we started out in

1:19:39

Contra Costa County right across from San

1:19:42

Francisco. And enterprising food

1:19:44

services director, wonderful guy, Dominic

1:19:46

Mackey, he purchased a dilapidated

1:19:48

factory, repurposed it into a

1:19:50

food preparation facility for the entire district.

1:19:52

27 schools, 27,000 kids, they made 27,000 lunches per day. And

1:19:58

because they were... buying at

1:20:00

scale, they could buy cheaper and they

1:20:02

could control what was in the food.

1:20:05

And so they could get rid of, get

1:20:07

this, 10 pounds of sugar

1:20:09

per kid per year. They got rid of

1:20:12

100,000 pounds of sugar in the first year.

1:20:17

We have now gotten rid of 5 million pounds

1:20:19

of sugar from kids down. Yeah, it

1:20:21

was some great visual that Jamie Oliver did in

1:20:23

a TED Talk. We took a bathtub full of

1:20:25

sugar and that's what... School bus full of sugar.

1:20:27

What an average kid eats in a year, right?

1:20:29

Yeah, right. The point is, Dominic

1:20:32

was able to actually save money because they

1:20:34

could buy at scale. And so they made

1:20:36

it in the one central facility and then

1:20:39

shipped it out to the 27 schools each

1:20:41

day. And so every kid

1:20:43

got a real nutritious meal, a

1:20:45

hot food meal where we could

1:20:47

control what was actually in it.

1:20:50

And you saw performance get better. Everything

1:20:52

got better. Attendance got better. Behavior

1:20:54

issues got better. Exactly. Weight got

1:20:56

better. And this is

1:20:58

not our example. This was in Israel. Yeah.

1:21:02

15 years ago, the

1:21:05

Ramallah School District in

1:21:08

the West Bank had a 27% graduation rate.

1:21:12

Twenty-five percent. Not good. And

1:21:14

if you don't graduate, what happens to you?

1:21:16

You know, it's the likelihood... You can marginalize.

1:21:18

You can marginalize in terrorists, whatever. Not good.

1:21:22

And the Israeli government did not know what to do with this. A

1:21:25

entrepreneur who's done very well in the

1:21:27

tech industry, Yossi Vardy, went

1:21:30

to Netanyahu and said, give me

1:21:32

the Ramallah School District. I

1:21:35

will take care of it. They were

1:21:37

only too happy to divest themselves of it. And

1:21:41

Vardy did one thing. Change the

1:21:43

food. He fed them. He

1:21:45

didn't even change the food. He fed them. That's so

1:21:48

right. And they went from a 27% graduation rate to a

1:21:50

95% graduation rate in two years. Yeah.

1:21:54

Now I see this. I just came back from Kenya

1:21:56

and I went to this school called Little Lions where it's

1:21:58

in the war slum, Khybera slum. in Kenya. It's

1:22:00

the worst time in Africa. I went and

1:22:03

visited there, walked around. It was incredible. People

1:22:05

live on three dollars a day. There's garbage

1:22:07

everywhere. I mean, it's awful. And

1:22:09

this friend of mine started this whole school and

1:22:11

his main thing was feed these kids three meals

1:22:13

a day, real food. And these

1:22:15

kids are thriving. They're performing academically. They're going

1:22:17

to be doctors now and getting out of

1:22:19

their poverty. Why are we surprised? Your

1:22:22

brain needs nutrients. Well, let's back

1:22:24

up a little. Not just glucose.

1:22:27

It needs fatty acids.

1:22:29

It needs protein. It needs,

1:22:31

you know, anthocyanins. It needs

1:22:33

selenium. It

1:22:36

needs zinc. It needs, you know, omega-3s.

1:22:39

Where are you going to

1:22:41

get them except for food? So I

1:22:43

want to back up because this clearly

1:22:45

we need to fix our school system. We need to

1:22:47

fix schools. Eat Real is an amazing nonprofit. I'm pretty

1:22:49

sure I check it out. I'm

1:22:52

a huge fan of it. I'm a friend

1:22:54

and supporter of the whole program and Jordan

1:22:56

Schlane and Nora and you. So it's great.

1:22:59

But I want to back up because we spent a

1:23:01

lot of conversation talking about these

1:23:03

four different, not opposing, but different

1:23:05

models of thinking about the causation

1:23:07

of obesity. And if we're going

1:23:10

to address this obesity epidemic, I

1:23:12

mean, yeah, we can all take Ozempic and spend five

1:23:15

trillion dollars a year and bankrupt the country and cause

1:23:17

all these side effects and bowel destruction and so forth.

1:23:19

Or we can really address the

1:23:21

cause. And so you talked about the energy

1:23:23

balance hypothesis, which is essentially calories and calories

1:23:25

out. The carbohydrate insulin hypothesis, which is too

1:23:28

much sugar and carbs causes too much insulin,

1:23:30

which makes you gain weight and prevent

1:23:32

fat loss and dysregulate your brain. You

1:23:34

talked about environmental toxins or obesity, obesogens

1:23:36

that disrupt things in many ways by

1:23:38

destroying our mitochondria, by destroying our microbiome,

1:23:41

by causing inflammation, by causing oxidative stress,

1:23:43

by trimming our thyroid function. So many

1:23:45

different mechanisms, which I actually

1:23:47

outlined in that paper. I should send it to you. You'll love

1:23:49

it. It's like 20 years old, but I saw it coming. And

1:23:52

then lastly, this whole redox hypothesis,

1:23:54

which is all these things also

1:23:56

cause too much oxidative stress. The

1:24:00

average person listening, they're like, well, that's cool, interesting

1:24:02

science, but like, what the heck do I do?

1:24:04

So let's take the rest of the time to

1:24:06

break down what are the action steps to

1:24:08

address these things and how do we create an

1:24:11

integrated model and what is the average person going

1:24:13

to do who is struggling with weight gain, who

1:24:15

is struggling with trying to lose weight, who is

1:24:17

trying to understand all this conflicting biology, who is

1:24:19

hearing one Instagram influencer saying, you know, this is

1:24:22

garbage, another one saying this is garbage. No, this

1:24:24

is true. No, that's true. Eat this. Be

1:24:26

a carnivore. Be a vegan. No, don't

1:24:28

eat fat. It's a mess.

1:24:31

It is. It's a total mess.

1:24:33

So help us from a scientific perspective. How

1:24:35

do we break down the action steps for

1:24:37

the average person listening who wants to understand

1:24:39

how do we take these scientific advances, which

1:24:41

are really remarkable in our understanding of obesity

1:24:43

and metabolism, and turn those into action steps

1:24:45

that people can do to help their lives

1:24:47

get better and lose weight? So

1:24:52

I'm on record. You

1:24:54

can't fix health care until you

1:24:56

fix health. You

1:24:58

can't fix health until you

1:25:00

fix diet. And you can't

1:25:02

fix diet until you know what the hell is

1:25:04

wrong. And for the last 50

1:25:06

years, we've been barking up the completely

1:25:08

wrong tree. We've been working

1:25:10

on, you know, the idea that fat was the bad

1:25:13

guy. Yeah, fat ain't the bad guy. Yeah.

1:25:17

Okay. Now, what is the bad guy? Well,

1:25:19

it's a bunch of things. Basically, anything that

1:25:21

makes ROSs. All right. Well, what makes

1:25:23

the most ROSs? Okay. So

1:25:25

as it turns out, trans fats make

1:25:28

the most ROSs. Yeah. Shortening.

1:25:31

But we now know that,

1:25:33

and it's basically been banned from the American diet final.

1:25:35

You know why they call it shortening, right? No.

1:25:38

Shortening is your life. Okay.

1:25:41

Fair enough. But no, this is like Crisco,

1:25:44

right, back in the day. But it's

1:25:46

been regulated as non-grass, which

1:25:48

means generally not recognized

1:25:50

as safe. Correct. However,

1:25:52

it's still in the food. Yes, it is. It's

1:25:54

a store. It should not be there.

1:25:56

It was almost 10 years ago, and you can still find that

1:25:58

crap everywhere. You are exactly right. And for

1:26:00

the exact reason you said because they

1:26:02

round down. Yeah, so read

1:26:05

the label in other words, Scott Grundy Years

1:26:07

ago showed that two grams of trans

1:26:10

fat per day is enough to lead

1:26:12

to diabetes and cardiovascular

1:26:14

disease two grams per day.

1:26:16

Okay, if a serving

1:26:19

of Ultra-processed

1:26:21

food in America has

1:26:23

point four nine Grandmas

1:26:26

point five less than point five. Okay,

1:26:28

they can say it's zero zero right

1:26:30

because of rounding down Yeah, so if

1:26:32

you consume four Servings

1:26:34

of whatever that is, which

1:26:36

is not hard which is not hard Okay,

1:26:39

you have achieved your two grams that is

1:26:41

all still a problem. So you are absolutely

1:26:43

right We have actually not completely solve the

1:26:45

problem. Okay trans fats are bad next is

1:26:47

okay So the question is what to do

1:26:49

about all of these issues or anything that

1:26:51

causes reactive oxygen species is it is a

1:26:54

bad guy? So there's a lot of things.

1:26:56

Well, what's the next thing? fructose

1:26:59

fructose causes the Myard reaction

1:27:01

the glycation reaction the browning

1:27:04

reaction seven times crispy chicken

1:27:06

skin those creme brulee Bananas,

1:27:10

yeah, you know anything that burns. Yeah,

1:27:12

okay You know

1:27:14

barbecued q sauce on the grill. Okay, and

1:27:16

that's an oxidative stress reaction and Generates

1:27:19

100 times the reactive oxygen

1:27:22

species Ages, right? We

1:27:24

call it advanced vacation in products. Otherwise, right?

1:27:26

And so they do it can have it

1:27:28

can happen in yourself or you can eat

1:27:30

it. So dietary ages

1:27:32

Yeah, okay. So basically if

1:27:34

you take a Can

1:27:38

of sweetened condensed milk and you put it

1:27:41

in a pressure cooker for an hour you

1:27:43

get pudding okay went from white Okay,

1:27:46

that's the Myard reaction. Okay, it

1:27:49

occurs in the food Yeah, the

1:27:51

point is the sugar is what

1:27:53

drives those advanced glycolysis right any

1:27:55

kind of sugar Well

1:27:57

glucose will do it but fructose does it times

1:28:00

faster and generates 100 times the

1:28:02

ROS because of the stereochemistry of

1:28:04

the molecule. So fructose

1:28:06

is particularly egregious. Yes glucose does

1:28:08

it too but fructose does

1:28:10

it way more. Lactose,

1:28:13

galactose much less. So

1:28:16

lactose is not a big problem. People think

1:28:18

dairy is a problem. It's not a problem.

1:28:20

Okay. Don't quit your breast milk.

1:28:23

Don't quit your breast milk. Don't quit the

1:28:25

breast milk. No. We're going

1:28:27

to talk about neonatal nutrition maybe on

1:28:29

another podcast but the bottom line is

1:28:32

the amount of sugar in our diet is a mess.

1:28:35

The third thing is the

1:28:37

inflammation because that's generating the

1:28:39

ROS and there it's the

1:28:42

emulsifiers because the

1:28:44

emulsifiers are leading to that leaky

1:28:46

gut. So name

1:28:49

some. Carboxymethylcellulose, polysorbate

1:28:51

80, carrageenan.

1:28:54

By the way which food has

1:28:56

the most carrageenan? Your almond milk.

1:28:58

Ice cream. Ice

1:29:00

cream. Ice cream. And who introduced

1:29:03

carrageenan to ice cream? Is it quiz?

1:29:06

I don't know. The Eskimos is seaweed.

1:29:08

Margaret Thatcher. Margaret Thatcher. Did she like

1:29:10

her ice cream thicker? She was on

1:29:12

ice cream canvas before she was an

1:29:14

MP. What? That's a good

1:29:16

trivia. Yeah. Okay so there's

1:29:19

other ones. Xantham gum, guar gum, all

1:29:21

these thickeners that you see in even

1:29:23

health foods. Well the thickeners don't necessarily

1:29:25

mean they're emulsifiers. Emulsifiers

1:29:27

very specifically hold fat and water together. So

1:29:30

the thickeners are yet another issue. And

1:29:32

they may link to autoimmune disease.

1:29:35

Absolutely. Because leaky gut.

1:29:37

No question. Another thing that's

1:29:39

a big problem is monoglycital

1:29:42

acids. Three

1:29:46

NCPD. It's

1:29:49

a compound called E-471.

1:29:52

But you don't see it on the label of a food. Well,

1:29:54

no you do see it. It just

1:29:56

doesn't call it. They don't call it

1:29:59

E-471. What are they calling? Monoglycital esters.

1:30:01

Okay, so those are problem as well.

1:30:03

So bottom line is, here's what we need

1:30:05

to do. And the food itself is inflammatory,

1:30:08

right? So if you're eating trans-factory sugar, ultra-processed

1:30:10

food just by nature it's inflammatory. Exactly.

1:30:13

It's a whole series of mechanisms. So

1:30:15

we have to promote metabolism the best

1:30:17

way, get rid of the sugar, and

1:30:19

we have to suppress inflammation. And you say sugar,

1:30:21

you also mean flour. You also mean anything that

1:30:23

turns into sugar. Refined carbohydrate and sugar. Refined carbohydrate.

1:30:25

And we have to suppress inflammation. And how do

1:30:27

we do that? Increase the fiber,

1:30:30

get rid of the emulsifiers, increase the

1:30:33

omega-3s. Okay, so

1:30:35

get rid of the sugar, increase the fiber, increase

1:30:37

the omega-3s, and decrease the

1:30:40

emulsifiers. Alright,

1:30:42

what food looks like that? Sardines?

1:30:46

Eat the bones? I don't know. Well

1:30:48

real food. Real food, right. Real food. I

1:30:51

mean fish in particular, yes. I mean I

1:30:53

am a big proponent of fish because they

1:30:55

got omega-3s. But remember, it's

1:30:57

not the fish that make the omega-3s. The

1:31:00

fish eat the omega-3s. The algae make

1:31:02

the omega-3s. The fish eat

1:31:04

the algae, we eat the fish. That's

1:31:06

why small fish have more omega-3s than

1:31:08

large fish. Large

1:31:10

fish eat small fish. Right,

1:31:12

exactly. So how

1:31:15

do we do that? In

1:31:18

2020, I was contacted by a

1:31:21

company. But I noticed you didn't say

1:31:23

reduced calories. No, nothing about calories. You

1:31:26

didn't say? It's not about calories. Yeah,

1:31:28

yeah. Not about calories. In 2020, I

1:31:30

was contacted by a company in the

1:31:32

Middle East called Kuwaiti Danish

1:31:34

Dairy. And they

1:31:36

recognized that they wanted to be part

1:31:39

of the solution, not part of the

1:31:41

problem. Kuwait has an 18% diabetes rate

1:31:43

and an 80% obesity rate.

1:31:47

It's about 10% here, so it's almost double. It's

1:31:49

11.4 right now. Okay, geez. You can't

1:31:51

keep track. I know, I know, every day

1:31:54

keeps going up. They wanted to

1:31:56

become a metabolically health company and they wanted to

1:31:58

lead the way. a

1:32:00

privately held company so they could take the long

1:32:02

view. They didn't have Wall Street quarterly reporting they

1:32:04

have to deal with. So their business

1:32:07

model was make better food and make it

1:32:09

at a price point that they could still

1:32:11

make a profit. That was what they wanted

1:32:13

to do. They contacted me to convene a

1:32:15

scientific advisory team to help them re-engineer

1:32:18

their entire food portfolio, 180

1:32:20

items. That's amazing. And

1:32:23

so, do you know

1:32:25

Tim Harlan, who is the head of culinary

1:32:27

medicine at George Washington University? Rachel

1:32:29

Gao who ran the omega-3 for ADD

1:32:31

trial at the NIH. Andreas

1:32:36

Kornstadt who is a computer scientist out

1:32:38

of Stanford and Wolfram Alderson who's

1:32:41

been in the food business longer than all

1:32:43

of us. We started

1:32:45

the first farmer's market in Los Angeles back in

1:32:47

1979. Okay.

1:32:49

We convened the scientific advisory

1:32:52

team to basically deconstruct the

1:32:54

entire portfolio of this company

1:32:57

to determine what were

1:32:59

they doing? What ingredients were they

1:33:01

using? Did they actually meet criteria

1:33:03

for healthfulness or not? Were the

1:33:05

vendors actually telling them the truth

1:33:07

about what was in the things

1:33:10

that they were selling them? And

1:33:15

what could we do about the production

1:33:18

and the packaging in

1:33:20

order to actually improve the healthfulness

1:33:22

of the food? We came up

1:33:25

with three precepts. And

1:33:27

these are the precepts of metabolic health. I love my

1:33:29

health. And we call it the metabolic matrix. I love

1:33:31

this. Here we go. Protect the liver, feed

1:33:34

the gut, support the brain.

1:33:37

Any food that does all three of

1:33:39

those is healthy. Irrespective

1:33:42

of its processed or ultra-processed. Any

1:33:45

food that does none of the three is

1:33:47

poison. So feed the gut, support your liver,

1:33:51

protect the liver, support the brain. Those

1:33:54

are the three precepts. And you can actually determine

1:33:56

how do you do that? How do

1:33:58

you do that? Yeah. It's

1:34:00

easy when you know what each of the

1:34:03

foods, what each of the ingredients do within

1:34:05

the body. So you have to understand metabolic

1:34:07

health to be able to do that. Nutrition

1:34:11

does not answer those questions. So

1:34:13

there's a thing called food science. There's a thing

1:34:15

called nutrition. There's this thing called metabolic health. They

1:34:17

are not the same. Food science

1:34:19

is what happens to food between the ground and the

1:34:21

mouth. In the laboratory.

1:34:25

Not not when you buy an apple in the

1:34:27

grocery store. There's no food science there. Nutrition

1:34:30

is what happens to food between the mouth and the

1:34:32

cell. Metabolic health

1:34:34

is what happens inside the cell. But

1:34:36

all of these metabolic diseases are all

1:34:38

happening inside the cell. So

1:34:40

nutrition is only valuable as it informs

1:34:42

metabolic health. Food science is only valuable

1:34:45

as it informs metabolic health. But they

1:34:47

are one or two steps divorced from

1:34:49

metabolic health. So if you use metabolic

1:34:51

health as the North Star, as the

1:34:53

watchword, as the goal, and the World

1:34:55

Economic Forum has endorsed this. They even

1:34:58

came out with a white paper called

1:35:00

the True Purpose of Nutrition. And the

1:35:02

World Business Council for Sustainable Development is

1:35:05

coming on board with that as well.

1:35:07

Okay, if you use metabolic health as

1:35:09

the North Star and gear

1:35:13

your food re-engineering efforts

1:35:16

to vast concept of protect the liver,

1:35:18

feed the gut, support the brain, you

1:35:20

can actually make healthy

1:35:22

food. Yeah. Even if it's

1:35:24

ultra processed. Yeah. And that's what we have

1:35:27

done in Kuwait. And they have turned 10%

1:35:29

of their portfolio over in the last two years.

1:35:31

That's amazing. Based on the... So if you're not

1:35:33

eating Kuwaiti Danish food, what do you eat? Well,

1:35:37

we need to impress upon the food industry here

1:35:39

in America to do the same thing. It

1:35:43

is a uphill battle to

1:35:45

say the least. I love this because

1:35:47

everybody's looking for solutions. So this is

1:35:49

really a well thought out solution. Yeah.

1:35:51

I am a scientific advisor to the

1:35:53

Innovation Institute for Food and Health at

1:35:55

UC Davis, who has lines to

1:35:57

all of the food. food

1:36:00

industry at different levels startups

1:36:02

and CPG companies and the

1:36:05

goal is to get companies

1:36:07

to understand what it is that

1:36:10

they are doing basically

1:36:12

ditching the idea of

1:36:14

nutrition and focusing on metabolic

1:36:17

health instead. Yeah. Example Unilever

1:36:20

and Denone in the last two years

1:36:23

reduced their carbon sorry their sugar

1:36:25

footprint both of companies by 14%.

1:36:27

Now you think that's good

1:36:31

or bad? I

1:36:33

don't know 14%. I think it sounds

1:36:36

good but there's a catch. Well

1:36:38

I mean it's better than not yeah

1:36:40

but 14% when you are

1:36:43

you know when you use triple your

1:36:45

limit right okay in the food yeah

1:36:47

going down by 14% doesn't quite

1:36:50

get you there. Yeah it's like when they said

1:36:52

they're gonna take six trillion calories out of the

1:36:54

food supply by making Oreo cookies 90 calories instead

1:36:56

of 100 calories. Exactly. BS. Exactly BS that's exactly

1:36:59

right and they did that in 2014 and it

1:37:01

was a piece of crap then and it's

1:37:04

a piece of crap now. I'll tell you

1:37:06

realty feel Robert. I will.

1:37:09

So the point is 14% sounds

1:37:11

good. It actually got Emmanuel Faber fired

1:37:13

at Denone. Yeah. Because of it. At

1:37:16

KDD at the Squaty Danish Dairy we

1:37:19

have reduced the sugar footprint

1:37:21

of that company by 78%. That's

1:37:24

amazing. 78%. So again what

1:37:26

if without changing taste. What if people in

1:37:28

for lunch so those seem like they're this

1:37:31

all sounds great Mark what the f do

1:37:33

I eat for lunch? Alright so the so

1:37:35

obviously the easy answer is

1:37:37

real food so what's real food food that

1:37:39

came out of the ground or animals like

1:37:41

ate what came out of the ground. Yeah

1:37:43

that's real food. Alright. I make

1:37:46

it by say eat the food that God

1:37:48

made leave the food that man made. Right. I mean if

1:37:52

you think Cheetos is food I

1:37:54

mean you know you're sunk. It's

1:37:56

just that simple. So we have

1:37:58

to redefine food. What is food?

1:38:00

What is food? Okay, so what is food?

1:38:03

What is the definition of food, Mark? It's

1:38:05

something that provides nutrition to the cells. No,

1:38:07

that's not the dictionary definition of food. It's

1:38:09

something you eat? I don't know. Substrate

1:38:12

that contributes. I read a book about that.

1:38:14

Yes, you should. Substrate that contributes to either

1:38:16

growth or burning of an organism. Growth

1:38:19

or burning. Remember,

1:38:21

we said every cell has

1:38:23

to grow at one point in its life, every cell has to burn

1:38:26

at one point in its life, but it can't do both at the

1:38:28

same time. Burning or growing.

1:38:30

Okay, so does ultra-processed food

1:38:32

contribute to burning? Well, sugar

1:38:35

inhibits three mitochondrial enzymes. We

1:38:37

named them before. Sugar

1:38:40

actually inhibits burning. Okay? And

1:38:42

73% of the items in the grocery

1:38:44

store are overdosed with sugar. Does

1:38:47

sugar contribute to growth? Does

1:38:50

ultra-processed food contribute to growth? Yeah, kind

1:38:52

of. Makes you grow. No,

1:38:54