0:00

Hi, everyone. Duper out here. Today's

0:03

mini episode, we're talking all things

0:05

cancer. Specifically, we have New York

0:07

Times best selling author doctor Jason

0:10

Fung talking to us about a revolutionary

0:12

new understanding of this medical

0:15

mystery we call cancer. and

0:17

he breaks us down in his book, the cancer code, and

0:19

we're gonna get a lot of the top gems in

0:21

today's mini episode. Specifically,

0:23

we're gonna go into like what actually is

0:26

cancer. I know that's a basic question,

0:28

but we have to ask the most basic questions

0:30

if we're gonna think differently about

0:32

this approach. What is the

0:34

seed and soil analogy of

0:37

cancer and how does it change

0:39

our current model and approach

0:41

to dealing and even

0:43

treating cancer. Jason

0:45

also goes into the interview and talks about the biggest

0:48

drivers of cancer today based

0:50

on the latest research and what feeds

0:52

cancer cells. There's something that's in our diet,

0:55

especially here in America, that

0:57

we know through the latest

0:59

science and research that's out there, that it

1:01

feeds and accelerates the growth of

1:03

cancer cells. And lastly, we're gonna

1:05

talk about what you can do today to minimize

1:08

your risk of cancer. Cancer

1:10

is one of the most scariest diseases that's

1:12

out there. You know, so many people

1:14

worry about it. So many people have it in their family

1:17

or have had past friends or family members

1:19

who have had it. If you suffer from that or if

1:21

you're curious about the topic, today's mini episode

1:23

is absolutely for you. I hope you can walk

1:25

away day with a better understanding of

1:27

cancer from doctor Jason Funn.

1:30

I wanna pull a quote from your book to start off

1:32

the conversation. which

1:35

is you say and you start off in the book,

1:37

you say the most pressing question in cancer

1:39

research is the most elusive question

1:42

What is cancer? So can

1:44

we start off there? Because it's still a question

1:46

that we're asking today, which is what

1:48

exactly is cancer.

1:51

Yeah,

1:51

and that's sort of

1:52

the most important thing is

1:54

to understand disease.

1:57

You really have to understand what it

1:59

is, like, what causes

1:59

it, what, you know, what the disease

2:02

is. And really for the common

2:05

diseases, cancer stands

2:07

virtually alone because we had no

2:09

idea what this disease actually

2:12

is. So if you look at other diseases like

2:15

COVID or infections.

2:17

So we've identified viruses. We've

2:19

identified bacteria.

2:22

We've figured out fungi and

2:24

so these are external invaders for heart

2:26

disease and stuff. These are blockages

2:30

and our blood vessels which starve the heart

2:32

or the brain of blood to get heart attacks

2:34

or strokes. So we

2:36

sort of understand what the disease is,

2:38

how it develops, and that kind of thing. But

2:41

for cancer, this is sort

2:43

of a very strange

2:45

disease. So it's

2:48

it's unlike any other disease

2:50

we've ever faced, it's not a vascular

2:52

disease, like heart disease, it's not an external

2:55

invasion, like bacterial or

2:57

viruses. It's

2:59

not stones

3:01

and stuff. There's all these other but

3:03

what is this strange disease.

3:06

And it's not

3:07

that it's one of these sort of rare

3:09

diseases. It's unfortunately

3:12

extremely common. So the lifetime

3:14

risk of cancer is

3:16

somewhere around one in ten, and it's going

3:18

to affect everybody's life.

3:21

in that if you don't get it, you will

3:23

know people who will get it, almost

3:25

everybody

3:25

does. So we don't know what this is,

3:27

and this is

3:27

the whole sort of this discussion

3:30

in the book is what is this

3:32

disease? Because it's a disease

3:34

where the you have a

3:36

normal cell which is

3:38

part of your own body because it it's

3:41

derived from your own body. And

3:43

for some

3:43

reason, this normal

3:46

cell breaks

3:47

off and becomes cancerous

3:50

to the point where it can kill you.

3:52

And it kills, of course, many, many people.

3:54

It's the second biggest killer of people.

3:57

So our concept

3:59

of what this disease actually is

4:01

has been changing. So,

4:03

you know, it's changed throughout history. But

4:05

really even in the last sort of

4:07

ten years, there's been this

4:09

massive change in the way

4:11

that we look at this disease, and this is

4:13

what I call the paradigm of cancer.

4:16

That is, I'm not arguing

4:18

about, oh, this is how to

4:20

treat cancer. Like, we've done lots of studies

4:22

on you know, use this drug

4:24

and this drug and these drugs in combination

4:26

with surgery and chemotherapy and

4:29

radiation. You put them in this sort of

4:31

regimen, and you can treat cancer. And I'm not

4:33

disputing any of that. But

4:35

in the end, it doesn't help

4:37

you answer the question of what is it. So if you want

4:39

to understand what it is, then you

4:41

have to start sort of from the beginning,

4:44

go through it and say what is this disease

4:46

and that's where we've really made a broader

4:48

progress within the last sort of

4:50

fifteen, twenty years.

4:52

And most people haven't even really

4:55

appreciated it. that. And that's

4:57

what I wanted to bring forward is that

4:59

sort of recent research and bring

5:01

it

5:01

to the people. So they at least understand

5:02

what this disease is that

5:05

that is affecting so many people.

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cover shipping. That's drew salt

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dot com. I

7:24

think this is a perfect opportunity to

7:26

jump into, you've sort of set the stage for

7:28

this kind of central point that

7:30

comes into. Okay? So now that we understand

7:32

this and part of Paradigm three,

7:34

you use this sort of seed and

7:36

soil, you know, analogy.

7:39

And and I'd love to set that up just to make sure that

7:41

we get to that while I have have you

7:43

get

7:43

Yeah. So that's exactly right. So if

7:45

we understand

7:46

now, this is an evolutionary process

7:49

which goes back towards our

7:51

origins. then you just have to

7:53

say, what drives evolution? And

7:55

it's not

7:56

just genetics. So if you think about

7:58

evolution, or opinion evolution, which

8:00

is the survival of the fittest for example.

8:02

So what he had observed was that in

8:05

the Galapagos Islands, he had these

8:07

birds. And if they had these

8:09

short beaks, which were really ideal

8:12

for eating nuts, and there are

8:14

birds that these had these long beaks that were

8:16

really good for eating fruit. And in the

8:18

areas where there's a lot of nuts, you

8:20

found a lot of these short beaked animals

8:22

in the areas you had a lot of fruit. You

8:24

had a lot of these long beaked animals. And

8:26

that what he said was that's not a

8:28

coincidence. What

8:28

happens is that the environment

8:32

selects the

8:32

genes that are most successful. So even

8:35

if you have a lot of nuts, you select for

8:37

the genes, that's a selective

8:39

pressure, which favors the survival

8:41

of those genes that

8:43

produce the short thick

8:44

meat and

8:45

the areas that have a lot of fruit

8:48

have exert a selective

8:50

pressure on the genes that give

8:52

you the long narrow beats. Right?

8:54

That makes sense. It's just sort of basic

8:56

evolution.

8:56

And cancer does

8:59

sort

8:59

of the same thing. So

9:01

if it's an evolutionary process

9:03

towards this sort of original

9:06

being, caused by chronic

9:08

damage to the

9:09

cell, then it's not the

9:11

genetics, which is the important part, but it's

9:13

the environment Right?

9:15

And that is the scene of

9:17

cancer is there, but if you don't

9:19

provide that environment that

9:22

selects for this

9:24

sort of survivalist, cancerist

9:27

sort of, you

9:29

know, story.

9:30

then you're not going to get cancer.

9:32

So what you have to do then is

9:34

to say, this is not just

9:36

a genetic disease. because for years

9:38

we've been sort of thinking about it as a genetic

9:40

disease. So we think, well, it's just sort of pre

9:42

programmed into us. But

9:44

it's not. because the rates

9:46

of

9:46

cancer depend on your

9:49

environment more than what

9:51

it does on your genes. That is if

9:53

you look at, say, breast

9:55

cancer. Breast cancer, if you go

9:57

from Japan, a Japanese

9:59

woman in Japan when

10:02

they -- when you move that person to San Francisco,

10:05

their rate of breast cancer like

10:07

doubles or triples within a couple of generations

10:09

-- Right. -- vaccines. It's

10:11

the

10:11

environment But that's fantastic because

10:13

then if you can figure out what part

10:15

of the environment is what's

10:17

selecting for the damage. So in

10:19

some cases we know, It's smoking,

10:21

it's tobacco, it's viruses. Right?

10:23

In many cases, we don't know, breast

10:25

cancer, colon cancer, what's damaged prostate

10:28

cancer? We don't know. If you

10:30

can figure out what part of the

10:32

environment is

10:33

driving

10:34

this evolutionary process,

10:37

then

10:37

that's how we're going

10:40

to reduce the

10:40

risk of cancer. And

10:43

so the question is, what

10:45

is it in our environment? So they've

10:47

studied this question for a long time. So back

10:49

in nineteen eighty one,

10:51

they did a study where they're going

10:53

to estimate The

10:55

risks

10:55

so we

10:56

do something called a population attribution

10:59

factor, which is what percentage

11:01

a certain risk factor will contribute

11:03

to cancer. So tobacco smoke is the biggest,

11:06

thirty five percent So tobacco

11:08

is responsible roughly for

11:10

thirty five percent of cancer

11:12

overall. But number

11:14

two was the diet at

11:16

around thirty percent. Right?

11:18

So really, like,

11:20

very, very close to

11:23

tobacco, dwarfing

11:26

almost

11:26

everything else. So

11:28

all the stuff like the pesticides and

11:30

the chemicals and stuff like one or two percent

11:32

radiation one or two percent The

11:34

cancer was caused in large

11:36

part due to one tobacco, which

11:38

we know about, and two, the

11:40

diet. The

11:41

question never really got that

11:44

like, people didn't get that. You know? Like, he

11:46

felt him that he didn't get that.

11:48

And and and and so

11:50

they were looking for what part of the

11:52

diet. That was what the tricky

11:54

part was. So

11:56

if it's diet, then what part

11:58

of the diet is causing

11:59

cancer? Brancy

12:00

looked at fiber. It wasn't

12:03

it wasn't the case. They looked at dietary fat.

12:05

It wasn't the case. They looked at vitamin

12:07

deficiencies. who's done so many

12:09

studies like you have vitamin

12:11

A, vitamin B, folic

12:13

acid, vitamin C, vitamin D,

12:15

vitamin E, you know,

12:17

omega three fatty acids,

12:19

selenium. We've tested all of those in

12:21

multi million dollars trials and

12:23

it wasn't deficiency of vitamins that

12:25

was causing cancer. And the

12:27

answer came somewhere around two

12:29

thousand what part of

12:31

the diet was the most important.

12:33

And we didn't know this really

12:35

until about two thousand and three.

12:37

And it turns out that it was obesity.

12:40

was the biggest, biggest

12:42

driver of cancer. And probably

12:44

more specifically is

12:46

that it was the hyperinsulinemia. That

12:48

is too much insulin, which

12:50

is very typical of obesity, is

12:53

probably what's

12:55

driving cancer in those

12:57

cases. The

12:58

reason I say we didn't know is because

13:00

so I went to medical school in the mid nineteen

13:02

nineties, and we never talked about this stuff.

13:05

But in two thousand and three, a very large

13:07

study came out, which showed

13:09

that obesity actually raises the

13:11

risk of all kinds of cancers. So now

13:13

the WHO classifies

13:16

thirteen different types of cancer as

13:18

obesity related, including

13:21

breast cancer and colorectal cancer,

13:23

which are after lung cancer, sort of

13:25

the most common cancers. So

13:27

really, really important causes. And

13:29

this is what's important is

13:31

now you know, what we're doing is we have to go

13:33

past again. So this paradigm,

13:35

which gets us to evolution, which

13:37

gets us to the seed and the soil, which

13:39

is this sort of evolutionary ecological,

13:42

ecology being the

13:44

study of how the

13:46

environment interacts with an individual.

13:49

how you can change that environment

13:51

in order to prevent cancer. And

13:53

that's sort of what's sort

13:55

of exciting about this is that now

13:57

hopefully we can start to understand and then

13:59

make some changes that

13:59

are going to minimize a risk

14:02

of developing these types of

14:04

cancers and hopefully

14:06

preventing them in the future. Howard Bauchner: Yeah,

14:08

and even question basic

14:10

premises, you know, I was on the Mayo Clinic

14:12

website in preparation of this interview,

14:15

you know, there's like a

14:17

myths and there's like a

14:19

myths and facts section on cancer

14:21

and diet. And like one of the questions inside

14:23

there was sugar, you know,

14:25

somebody saying, you know, does consuming

14:27

less sugar have any impact on

14:29

cancer? Right? And it was like, There's

14:32

no research. There's no evidence at

14:34

all that consuming less sugar

14:36

has anything to do with cancer. And

14:38

again, Mayo Clinic, well established

14:40

place they're doing the best they can based

14:42

on the research and the evidence that's out there right

14:44

now. And part of the thing that you're bringing in is

14:46

that highlighting especially with your

14:48

previous books that we're really talking

14:50

about insulin resistance

14:52

and what that relates

14:54

to diabetes, especially type two

14:56

diabetes is Well,

14:58

if we know that obesity through this

15:00

big study that you were talking about plays a

15:02

major factor, and then what is it

15:04

as part of that also contributes obesity

15:06

and how do cancer cells get their energy,

15:09

then, of course, we're gonna wanna pay

15:11

attention to the

15:13

level of sugar

15:15

as one example that we're

15:17

having inside of our diet because that's

15:19

gonna cause a whole chain

15:21

of effects that ultimately

15:24

supports the growth of cancer. Howard

15:26

Bauchner:

15:26

Yeah, exactly. And so one of

15:28

the - so Dr. Luke

15:30

Cantlie, who's a prominent researcher,

15:32

cancer researcher. You

15:35

know, he was one of the ones who

15:37

sort of uncovered the link

15:39

between sort of what sugar

15:41

does, which is, you know, it contributes

15:43

to this high insulin state

15:46

and insulin other than being

15:48

a metabolic hormone is actually a

15:50

very, very potent growth

15:52

factor. So it tells cells to

15:54

grow. And if you're going to tell cells

15:56

to grow, then you're going

15:58

to tip the scales in

15:59

towards, you know,

16:02

increasing growth of cancer cells

16:04

for example. So, you

16:06

know, here's a guy who's

16:08

sort of like one of the most prominent cancer

16:10

researchers and he's like, sugar

16:12

scares me. You know, that's what he says.

16:14

in one of his articles.

16:16

He's read this, like, okay. Wow.

16:18

That's all I need to know. Right? They're

16:20

totally and and also two on the basic

16:22

premise of, like, what is chemotherapy.

16:25

Right? Yeah. Could

16:27

you explain like that link on that? Like,

16:29

how do they get these

16:32

well intentioned poisons into

16:35

cancer cells. Can you

16:37

explain that to, like, our audience through, you

16:39

know, like exactly like what

16:41

goes into chemotherapy that takes

16:43

advantage of exactly that that we're talking about.

16:45

Yeah, exactly. So when you

16:47

look at the cancer cells, you can do

16:49

something called a pet test,

16:50

which is a positron emission test. And

16:52

it basically looks at

16:55

how avidly cells take

16:58

up glucose So

17:00

when you do these tests, things

17:02

that light up are eating a lot of glucose

17:04

and those are what are identified as

17:06

cancer. So they're taking in, you

17:08

know, like five or ten times the amount of glucose,

17:10

which is a type of sugar compared

17:12

to normal cells. So

17:15

it's like, okay, when you look

17:17

on these sophisticated sort

17:19

of scans. You can

17:20

see the cancer cells

17:21

basically devouring sugar

17:24

like there's no tomorrow.

17:27

And it's like, well, you know, if I

17:29

had cancer, I certainly wouldn't be trying to eat

17:31

too much of the stuff because you know that

17:33

the one place in the body that

17:35

that loves it Ten times more

17:37

than the next guy is the thing.

17:40

Right? And then you have certain

17:42

chemotherapies which take advantage of

17:44

this try and get in, know, buy because

17:48

they mimic the sugar and that's how

17:50

they do it on the positron emission

17:52

tomography testing, for

17:54

example, They may make the sugar so that the cancer takes it up and

17:56

then it lights it up. And then people are trying

17:58

to use that to sort of target the

18:00

cancers as well. But interesting,

18:04

you know, it's

18:06

it's an interesting story of how this sort

18:08

of this new paradigm explains

18:10

so much more about the

18:13

phenomenon of cancer and how, you

18:15

know, what implications it has for

18:17

screening and this sort of

18:19

evolution of And this is sort of the

18:21

promise of this cancer

18:23

paradigm three point zero is that if you now

18:25

understand that what is happening

18:27

now is that the cell is

18:29

evolving away from normal

18:31

cells evolving into a foreign

18:34

species. Because and and people

18:36

always say, oh, that's so weird. But

18:38

that's the way the body actually looks at

18:40

the cancer cells. So

18:42

when our immune system looks at a

18:44

cell, it has a way to tell

18:47

between and non self.

18:49

That is the

18:50

the immune system is a very

18:52

powerful weapon. You don't want to use it

18:54

on its own cells. That's like friendly fire.

18:56

Right? Oh, no. You wanna type group

18:59

behavior.

18:59

Exactly. And it's very, very bad if

19:01

that happens. So your body has

19:04

these ways to distinguish between your own

19:06

cells and everybody else. So,

19:08

bacteria viruses, it will try and

19:11

kill it. And it sees a

19:13

cancer, it will try and kill it.

19:15

That's just the way that's what happens. So it

19:17

has evolved this cell,

19:19

so so you take a lung cell. this

19:21

lung cell, which was originally your own

19:23

cell, has evolved into

19:25

basically a new species that is

19:27

foreign. That's

19:27

that's why it's inside your

19:30

own body. Exactly.

19:31

And that's

19:33

the reason that

19:33

instead of trying to the third

19:36

paradigm, which is like, okay, now we

19:38

have these these cells that were originally

19:40

part of us, but they've basically broken

19:42

away and they've become their own

19:44

sort of, you know,

19:47

invader Now you say,

19:49

well, instead of trying to just get

19:51

indiscriminate killing, which was paradigm one

19:53

or genetic targeting, which was

19:55

paradigm two, Now what we're gonna

19:57

do is enhance the immune

19:59

system to identify it. So

20:01

basically, you have these sleeper

20:03

cells like, you know, you have terrorists,

20:05

sleeper cells of terrorists in your city,

20:07

and now what you're trying to do

20:09

is uncover them so that you

20:11

can get your police and your SWAT teams

20:14

in there. to kill these sort of domestic

20:16

terrorists. That's what we're doing

20:18

with immunotherapy. So

20:20

these new drugs, these checkpoint

20:22

inhibitors, are basically

20:25

uncovering. So there are certain ways that

20:27

these cancer cells hide,

20:29

and they're basically trying

20:29

to uncover them.

20:32

Right?

20:32

And this is the new paradigm. What we're gonna

20:34

do is trying to uncover these sleeper

20:36

cells, these hidden sleeper cells so that

20:38

they can be identified targeted.

20:40

We can, you know, direct the immune

20:42

system. So something like those

20:44

new drugs are talking about

20:47

those checkpoint inhibitors, then you get

20:49

CAR T, where you're actually going

20:51

to take the cancer and

20:53

then engineer sort of a

20:55

SWAT team that is going to

20:57

identify and kill them, right? That's a new

20:59

therapy based on this immunotherapy, but

21:01

it's based more specifically

21:04

on this new paradigm of looking

21:06

at a cancer as a

21:08

new foreign species.

21:10

And

21:10

it's very, very interesting because

21:13

you know, it's it's the promise is

21:15

sort of immense.

21:17

Like, we're not there yet and I, you know, I

21:19

hope that there's a lot more to

21:21

come. but it's a totally new way

21:23

of targeting cancer

21:26

and treating it based on a whole

21:28

new paradigm. and that's what gives me hope

21:30

for the future that there's more

21:32

going to be able to be applied because you

21:34

can apply these lessons

21:36

of evolutionary biology and

21:38

say, well, you know, what can I do

21:40

to to change the environment for example?

21:42

Because that's evolution, that's biology,

21:45

so things like

21:47

losing

21:47

weight and, you know,

21:50

intermittent fasting, which is another way to

21:52

lose weight. You know, trying to

21:54

reverse your type two diabetes type two

21:56

diabetics, of course, get much higher rates of

21:58

cancer because it's also

21:59

hyperinsulinemia. So getting reversing the

22:02

type two diabetes, that's going

22:04

to likely reduce your risk. to

22:07

other things like chemo

22:09

preventative agents. So there's not a

22:11

lot. They've been studying stuff to

22:13

try and prevent cancer, but there's not a lot. So only

22:15

things that might work that farm in

22:17

gets a lot of research, which is

22:19

a diabetes drug, may be

22:21

useful, and then green tea,

22:24

probably a very small effect, but there's some

22:26

data from

22:27

Japan where they do drink a lot

22:29

of green tea, that some of the the compounds

22:31

in that are maybe

22:34

effective. So, hey, maybe that's a great,

22:36

you know, great thing to do, drinking green

22:38

tea is probably good anyway. And

22:40

really, the the the two

22:42

central themes that I got out of your book after

22:44

really going to that

22:46

history is One, the future is

22:48

hopeful in a way that is really

22:50

understanding more of that

22:52

central question coming back to how we start

22:55

off the guess, which is what the heck is

22:57

cancer. So we're better shaped

22:59

for what we're developing in terms of

23:01

treatments and drugs in the future because

23:03

we're where more we

23:05

have a we have the most robust

23:07

answer that's actually getting to the source and

23:09

the root of what is cancer. And the

23:11

second component is exactly

23:13

kind of what you were talking about, which is what are the things that

23:15

you can do today to both enhance,

23:18

you know, whether it's some

23:20

of the work of, like, Walter

23:23

Longo or other people that are out there that are showing

23:25

that fasting could

23:28

support, right? Targeted fasting,

23:30

especially before chemotherapy can

23:32

or and enhance the potency

23:35

of of these drugs if somebody actively

23:37

has cancer, cutting

23:39

off the source of the

23:41

supply of food, which

23:43

is significantly reducing

23:45

the amount of glucose so that we're

23:47

not in this place of hyperinsulinemia.

23:51

And if you don't have cancer right

23:53

now and this is something that you're

23:55

paying attention to in the

23:57

future, what would be your biggest recommendations?

23:59

You know, somebody who's healthy, who's listening

24:01

to this podcast right now, and they're like, wow.

24:03

This is all super fascinating. I've

24:05

never understood this before, but now I get it. It's almost

24:07

like you just gave us a master class

24:10

on cancer. What

24:12

are the one or two things

24:14

to do today besides

24:16

not smoking that will

24:19

help us be the most

24:22

resilient to potentially avoid this

24:24

disease in the future or greatly

24:26

minimize our risk. Yeah. And

24:28

and so you you get back to

24:30

those sort of attributable

24:32

risk, which is number one, backhoe

24:34

smoke. So of course, probably the single most important thing. And

24:37

still is, is to not

24:39

smoke. And then two is the diet.

24:41

So avoiding hyperinsulinemia which

24:44

is that sort of when I talk about more

24:46

in the obesity code and type

24:48

two diabetes code

24:50

is that insulin is this

24:53

hormone which tends to make us gain weight and

24:55

also causes insulin resistance

24:57

and too much insulin is a bad

24:59

is

24:59

a is a very cool growth factor, so

25:02

that's the so if

25:04

you're, you know, you want to

25:06

avoid things that are going to try,

25:08

that are going to raise insulin, which is eating

25:10

a very diet that

25:12

is very high in refined carbohydrates,

25:14

for example. Sugar is probably some

25:16

you should best take in small

25:20

amounts. And then this other idea is

25:22

that you really should be having

25:24

a regular period of

25:26

fasting every day that's

25:28

really sort of basic.

25:30

It's the word breakfast. It's

25:32

the meal that breaks your fast because

25:34

really you're supposed to be eating at,

25:36

say, dinner time, which is say, six o'clock and

25:38

eating at breakfast time, which is maybe eight

25:41

o'clock. So you're getting somewhere between twelve and

25:43

fourteen hours of fasting every

25:45

single day. that's what's supposed to

25:47

happen. That's what that buried in the

25:49

word breakfast, right, and break

25:51

fast. That is what's supposed to

25:53

happen every day. That's not what how happens

25:55

to most of us in

25:56

twenty twenty. Because

25:59

if you

25:59

look at sort of societal

26:02

norms and stuff instead of having three

26:04

meals and then no snacks, we sort

26:06

of braised throughout the day

26:08

believing that it's actually healthy for us I

26:10

don't think it is because every time

26:13

you are eating, you're

26:15

stimulating your insulin, which is

26:17

giving growth signals to the cells, including

26:19

the cancer cells, which love

26:22

insulin. You look at

26:24

a breast cancer cell, for example, has

26:26

like five or six times the number of

26:28

insulin receptors compared to a normal breast

26:30

cell. They love this stuff. They love insulin, they

26:32

love glucose. So therefore, you

26:34

want to know it. So eating

26:36

sort of whole pro unprocessed

26:38

foods is important. That's probably the

26:40

most important thing. not eating all the time is the

26:42

second, probably the second most important

26:45

thing. And, you know,

26:47

maintaining a normal weight as best as

26:49

you can I mean, that's not always the

26:51

easiest thing to do. But if you

26:53

are overweight and try to lose that weight,

26:55

if you are type two diabetic, try to reverse

26:57

that type two diabetes, And that's the you

27:00

know, the the tobacco and the

27:02

diet are so overwhelmingly

27:04

more important than everything else.

27:07

Like you could also, you know, look at the viruses,

27:09

for example, you can get the,

27:11

you know, try to avoid the

27:13

hepatitis B and hepatitis C,

27:16

which cause cancer and

27:18

human pap Loma virus, but those are

27:20

sort of givens. But the

27:22

diet and the tobacco are

27:23

sort of in a class

27:26

of their own. Everything else is like two percent

27:28

and they're at like thirty, thirty five

27:30

percent And and, you know, I I think I

27:32

just wanna say from somebody

27:33

from the outsider has been an observer of your work and and

27:36

consuming it and just super

27:38

appreciative. The the

27:40

cigarette is is

27:42

easy, you know, tough to break,

27:44

but actually there's really a lot of

27:46

really interesting stuff that's coming out of

27:48

Johns Hopkins and other places of using

27:51

psychedelics to help break cigarette

27:53

succession. You know, maybe those things will

27:55

incorporate and we'll figure out new ways to help people.

27:57

I think it's about fifteen percent of

27:59

adult population smokes here in the United States.

28:01

So it's gone down massively and cancer rates

28:03

have gone down for that. The diet,

28:05

sometimes people listening here, if they're not familiar

28:07

with your work, can think, okay, he's just talking about eating

28:09

healthy, but really you're talking about

28:11

getting out of this central

28:13

paradigm to use the word

28:15

where we're eating sugar

28:17

in all its other forms. So people who are listening

28:19

are like, I don't really have a lot of sugar in my

28:21

diet, you know, maybe a coffee, some birthday

28:24

cake here and there, one of my parties. But,

28:26

you know, how often are you eating

28:28

those meals of refined

28:31

starches that are

28:33

a regular part of our

28:35

daily life, the big bowls

28:37

of of rice or

28:39

ultra processed foods or

28:41

or breads or other things like that, that

28:43

fine. You know, have those things

28:45

every so often as, you know,

28:48

parts of your diet. But when they become the

28:50

norm, now you understand why

28:54

so much of America is in

28:56

that pre diabetic state

28:58

where they think they might be eating healthy

29:00

because they're just a little bit

29:02

overweight, but actually diet

29:04

is constantly spiking their blood

29:06

sugar, which leads to all these problems with

29:08

insulin that you're talking about. So you're not

29:10

just talking about eating healthy, let's be a little bit more mindful.

29:12

You're talking about really actually leaning

29:15

in and getting your blood sugar

29:17

under control. Yeah,

29:20

exactly. And and, you know, one of the

29:22

ways I mean, a lot of people talk

29:24

about diets and there's all these different

29:26

opinions on diets, but what people

29:28

hadn't focused on really

29:30

at all, I think, until

29:32

a few years ago was

29:35

this meal timing that

29:38

is, is eating all the

29:40

time really the same as

29:42

eating, you know, a few times? And think

29:44

the answer is no, because the point is that

29:46

you need to let your

29:49

body sort of digest, let your

29:51

insulin levels fall so that you don't

29:53

get all these problems with

29:55

the insulin resistance and so on

29:57

because insulin is not intrinsically bad,

29:59

but

29:59

it is a hormone

30:02

that goes up when you eat. So if you eat

30:05

constantly, is that a bad thing? And

30:07

that's not been talked about a lot, and that's

30:09

what really I've really focused on is

30:11

that I think it's actually

30:13

highly detrimental to be

30:15

eating constantly. It's just not the way that

30:17

you're supposed to be doing it, then -- Which was never

30:19

done it. -- which was a little bit of a trend of some

30:21

of the advice, especially in, like, the nineties and two

30:23

thousands, eat six meals a day. You

30:25

know, great. out the day and and

30:27

really, you know, we're backing

30:29

away from that largely through the

30:31

work that people like yourself are doing

30:33

and just educating, well,

30:35

Let's actually look. Is this actually helpful? Or could

30:37

it be harmful? And it's looking like it's

30:39

not supportive of our overall

30:42

health goals. inside the body. Yeah. I

30:44

mean, I think the whole idea was

30:46

sort of silly that you

30:48

should eat, eat,

30:50

eat, eat, to lose weight. And it's

30:52

like, well,

30:53

how's that gonna work exactly?

30:55

Right? If you're eating all the time, how

30:57

are you expecting to lose

31:00

weight? And you know, of course, that

31:02

if you eat a little bit and then

31:04

stop, that doesn't suppress your

31:06

appetite. It increases it. That's what an

31:08

appetizer is. It's a small

31:10

portion of food to

31:12

make you more hungry, not less

31:14

hungry, more hungry. Right? So if

31:16

you're gonna eat small portions of

31:18

food, gonna stimulate your

31:20

appetite, then you're gonna stop.

31:22

Right?

31:22

It's like it's like when you start

31:24

urinating, you just want to finish.

31:27

Right? When you start eating, you just wanna

31:29

finish. If you were

31:31

to to go pee and you

31:33

just stop start and stop and start. It's

31:35

like, why would you wanna do that?

31:37

Like, that's the dumbest thing ever.

31:39

Right? So it's like you're gonna make yourself

31:41

hungry by taking a little appetizing

31:43

portion of food, and then you're gonna

31:44

stop. Right? It's like,

31:46

oh, well, that's

31:48

not

31:48

really useful and then you're gonna do it again

31:50

and again and again six times a day.

31:52

Well, why would you wanna do that? That's

31:55

ridiculous because it's never been done

31:57

before. Because prior

31:59

to like nineteen

31:59

seventy seven, nobody did

32:02

that. So why would you even think that it's a good thing to do?

32:04

Like, why would you even come

32:06

up with that? And the answer is that

32:08

there was no real scientific evidence

32:10

said it actually helpful. And it was just sort of

32:12

made up. People just thought it might be

32:15

good and they just said it and that's it.

32:17

Sure. Well, you know, there's that old

32:19

saying that I

32:20

don't know who discovered water, but it probably

32:22

wasn't a fish. Sometimes we're

32:24

so in the cultural norms

32:26

of the way that things have been done.

32:29

that it actually takes a lot of courage, especially

32:31

for somebody in your position, to

32:33

step back and say, wait, does

32:35

any of this make sense? Let's

32:38

start with the basics and let's question

32:40

the premise and then go

32:42

from there. If not, we're in this

32:44

rat race where today still in

32:46

the US. Unfortunately, number one

32:49

reason for bankruptcy is medical

32:51

bills. Cancer rates are continuing

32:53

to go up. Quality of life is

32:55

not increasing. Out

32:57

of ninety percent of our

32:59

insurance dollars that we pay in,

33:01

young people, old people, everybody, out

33:04

of all the insurance

33:06

dollars that we pay in, ninety percent of it is

33:08

used in the last six to eight months of somebody's

33:10

life to try to keep them alive through

33:13

these expensive treatments. Lot of them

33:15

well intentioned. Lot of them well intentioned

33:17

that are there. Some may be coming from

33:19

business perspectives, but it's not

33:21

a winning race we have

33:23

to stay step back, and we have to question the

33:25

basic idea. And that's exactly doctor

33:27

Fung, what you do inside this book.

33:29

And I wanna thank you for really

33:32

putting together some strong material. I

33:34

hope progressive medical

33:36

schools out there start to make it required

33:39

reading because, you know, as we all know in this

33:41

podcast is that It can take seventeen,

33:43

twenty years for what's the

33:45

latest literature to end up becoming part

33:47

of the practice that's

33:50

out there. So kudos to you for writing an

33:52

incredible book.