3:34

In today's episode I'm speaking with Morley Robbins

3:37

. He is a former hospital consultant turned

3:39

self-taught expert on the role

3:41

of trace minerals in health . He

3:43

strongly advocates for identifying and

3:45

correcting mineral deficiencies

3:48

as a strategy to optimize health

3:50

. In this episode , we go pretty deep into

3:52

the biochemical mechanisms of how

3:55

the body uses copper and iron

3:57

, and particularly how they relate to mitochondrial

3:59

health . We finished with a discussion about

4:01

soil mineral depletion and

4:04

the effects that monocropping , including

4:06

the widespread use of the herbicide glyphosate

4:08

, is impacting

4:10

the chelation of copper and therefore reducing

4:12

its prevalence in the food supply . This interview

4:14

is quite dense and quite technical , but it was

4:17

very interesting to get Morley's opinion

4:19

on things , and we I

4:21

cross-referenced his point of view with a

4:23

lot of the guests that I've had on previously , including

4:25

Dr Jakuz and Leslie Boros . So

4:28

have a listen , tell me what you think and

4:30

I hope you enjoy it and

4:32

I'll see you in a minute . I'll

4:36

see you in a minute

4:38

, bye , bye , bye , bye . So , morley Robbins , thanks for

4:40

coming on . The Regenerative Health podcast .

4:43

Max , I'm thrilled to be here and look forward to our discussion

4:45

.

4:46

So give the listeners a background

4:48

on yourself and how you arrived at

4:50

exploring this amazingly

4:53

interesting world of minerals and

4:55

how they affect human health .

4:57

I grew up in a very sickly family

4:59

here in the States

5:01

. The mom was an

5:03

alcoholic and dad was manic depressive

5:05

schizophrenia and

5:08

my sister became a nurse

5:10

and I was supposed to become the doctor

5:12

and fate

5:14

got in the way . I found

5:16

out I wasn't a good student but

5:19

I went into hospital management

5:21

and then consulting , did that

5:23

for 32 years and

5:26

developed frozen shoulder

5:28

from pulling a suitcase behind

5:30

my back for 20 years through airports

5:32

, hither and Yon , and

5:35

friends at a health

5:37

food store told me to go see Dr

5:39

Liz . Well , I knew that was a chiropractor

5:42

and I said I don't do witchcraft

5:44

. Well , dr Liz is

5:46

now my wife and she's the one who introduced

5:49

me to natural healing and

5:52

she sparked this interest

5:54

in me around understanding

5:58

the innate healer . I'd

6:00

never heard that phrase . In 32

6:02

years of working in hospitals and

6:05

I'd had thousands of conversations

6:07

with doctors , I'd never heard that phrase

6:09

innate healer . But if

6:11

there's an innate healer , why do we have all these

6:13

doctors ? You know why do we need doctors . And

6:16

so I took

6:18

it upon myself to really delve

6:20

into the world of metabolism

6:23

and

6:26

, as you probably know , wrote a book called Cure

6:28

your Fatigue , because what

6:30

most people don't know is that every

6:33

symptom in the Merck

6:35

manual and there's 32,000

6:37

of them that are profiled . Every

6:39

one of them begins with cellular

6:41

energy deficiency

6:44

, and

6:46

that's a really important concept for people

6:48

to realize is that if the mitochondria

6:51

start to wobble and

6:53

can't do their work , they do more

6:55

than just make ATP . They're

6:58

incredibly active organelles

7:01

, as you know . But if

7:05

the mitochondria go well , then

7:07

there goes the I

7:09

guess , the intelligence of the cell , and

7:13

that's really been my area of focus .

7:16

Interesting and this concept

7:18

of the innate healer is I understand what you're

7:20

saying is one that is very much

7:23

sidelined or not profiled throughout

7:25

medical orthodoxy , throughout

7:27

doctors' education , throughout treatment guidelines

7:29

. It's sidelined

7:31

for prescriptions for

7:34

surgeries , for various types of interventions

7:36

, and I mean that's

7:38

another whole conversation in itself . But

7:40

there's a reason why these

7:43

structures exist and profit

7:45

is made on not promoting

7:48

the innate healer within each and every one

7:50

of us . But let's start with mitochondria , because

7:52

this is a topic that I've been very

7:55

much leaning into over the past six

7:57

months , and regular

7:59

listeners to my podcast have heard

8:01

from Dr Jack Cruz , We've

8:03

heard from Dr Lazlo Boros , a

8:06

range of other guests , and I

8:10

really think that putting the mitochondria at

8:12

the center of our disease paradigm kind

8:14

of gives us the most explainability for

8:17

these so-called complex diseases like

8:19

neurodegeneration , cancer , autoimmunity and metabolic

8:22

disease , and there's so much to be said

8:24

about it . But really , basically

8:27

, there's this bacteria that got simply

8:29

enslaved hundreds of a billion

8:32

years , billion and a half years ago , and

8:34

then subsequently make energy for us in

8:37

a symbiotic relationship . So , as you mentioned

8:39

, they do a lot more than make ATP

8:41

and , critically , they

8:43

make water , metabolic water that is

8:45

deteriorated amongst a range

8:48

of other facets and they're obviously receiving light frequencies

8:50

. So

8:52

talk to us about how you think about mitochondria

8:54

in the context

8:56

of all your research and all your work

8:59

.

8:59

Yeah , Well

9:01

, it's important to put the word purple in

9:03

front of bacteria . They're purple

9:06

bacteria . There's a color to

9:08

their existence . And

9:11

how do we get the color purple ? Oh

9:14

, it's a blending of red

9:16

and blue . So

9:18

when you get into the mechanics

9:21

of the mitochondria and you

9:23

begin to explore the electron

9:26

transport chain , so

9:28

there's four complexes there , and then , when

9:30

that's working with complex

9:32

five , you have what's called

9:35

oxidative phosphorylation . As

9:37

you know Well , complex four

9:39

is the

9:42

critical step , and

9:44

we live on a planet that

9:47

has 20% poison in the

9:49

air . It's called

9:51

oxygen and

9:54

it's not our friend . It really isn't

9:56

. It's a very toxic element

9:58

, and the reason why we're

10:00

here , the reason why you and

10:02

I are having this conversation on

10:05

these very fancy devices talking

10:07

to each other thousands of miles

10:09

away from each other , is because higher

10:11

intelligence requires

10:14

higher levels of energy

10:16

that were made possible

10:19

by the harnessing of

10:21

oxygen to burn fuel . Right

10:24

, that's . Those are the fundamentals

10:26

, but the part that people seem

10:28

to gloss over is

10:30

that there can be no life on

10:33

planet Earth without copper . It's

10:36

impossible . It is

10:38

the only element on the planet

10:40

that can regulate iron

10:43

and oxygen at the exact

10:45

same time and not create

10:47

static . And

10:49

everybody misses that , and

10:53

you

10:55

probably know about the great oxygen event

10:57

3.4 billion

11:00

years ago . Right ? Who came

11:02

to our rescue ? Cyanobacteria

11:05

, right , cyanobacteria

11:07

, blue bacteria . Cyan

11:11

was a it's very important to know the colors

11:13

. So cyanobacteria

11:15

started playing with the sunlight and

11:18

releasing oxygen because they were engaging

11:20

in photosynthesis . So

11:23

it's exciting that you've talked

11:25

to Jack Cruz . But it's important

11:27

to recognize that there's three

11:29

steps to photosynthesis

11:31

there's photosystem

11:34

1 , there's

11:36

photosystem 2 , but

11:38

there's a step

11:40

in between . Did

11:42

you know that Plastocyanin

11:45

? Plastocyanin

11:48

is the critical step

11:50

and it turns out that photosystem

11:53

1 occurs second

11:55

. It was discovered first . That's why it has the

11:57

Roman numeral 1 . But photosystem

11:59

2 is the first step , Moves

12:02

the electrons to plastocyanin and

12:05

plastocyanin moves the electrons

12:07

to photosystem 1 . Plastocyanin

12:11

does not work without copper . Therefore

12:13

photosynthesis does not work without copper

12:16

. Therefore you can't release

12:18

oxygen into the air without

12:20

copper . But the

12:22

catch is you can't turn

12:25

that oxygen into

12:27

two molecules of water without

12:30

proper copper concentration

12:33

in complex 4 . And

12:36

so it turns out that complex 4 is

12:38

a two-stroke engine . There's

12:41

a downstroke that creates

12:44

hydrogen peroxide , h2o2

12:46

. And there's an upstroke that

12:49

turns that H2O2 into two molecules

12:51

of water . So what are the mitochondria

12:54

? They're water wheels . They're

12:56

water wheels . And

13:00

I see the whole deuterium issue

13:02

a little differently , because I think

13:05

that it's a sign of defective

13:07

copper concentration . One

13:12

of the great copper researchers , paul

13:15

Kobine . He's at Auburn University

13:18

. He's originally from Canada

13:20

, saskatchewan , canada , did

13:23

his doctoral work there and then became

13:25

a professor at Auburn University . Guy's

13:28

brilliant . But in 2004

13:30

and in 2006 , he's

13:32

the guy that figured out , based

13:34

on a yeast model . Yeast

13:38

are many mammals it's a very cool

13:40

concept . Their metabolic

13:42

structure and activity is identical to mammals

13:44

. It's a

13:47

lot smaller and , based on his model

13:49

, he discovered that there's 50,000

13:51

atoms of copper in the matrix

13:54

of the mitochondria and

13:58

the complex 4 that we're talking

14:00

about , where oxygen

14:03

becomes two molecules

14:05

of water . That

14:07

complex is blue

14:10

, sky blue , and

14:13

that's really important for that complex to work

14:15

by Red light . Oh

14:18

, there we go . So

14:21

what does blue tissue do ? It attracts

14:23

red light and

14:25

the mitochondria love that red light . People

14:29

swear by their red

14:31

lights and their red lasers , not

14:34

knowing that all they're revealing

14:37

is that they're copper deficient , because

14:42

what's the frequency of red

14:44

light ? Oh , it aligns perfectly

14:47

with the frequency of copper . What's

14:49

the frequency of blue light ? Oh

14:52

, it aligns perfectly with

14:54

the frequency of iron . So

14:56

you hear these two metals opposing each other , expressing

14:59

different forms of light and

15:02

it's absolutely amazing that

15:04

I think a kindergartner

15:06

could understand this better than a

15:08

physician , because they understand colors

15:10

and they think

15:12

differently , and I think the

15:15

phrase that I use and I didn't say

15:17

that to punch

15:19

you in the nose next it's just most

15:21

physicians don't know how energy

15:23

is made . Most physicians

15:26

don't know how blood is made , and

15:28

this is the fundamentals of our metabolism

15:30

, and it's important that

15:33

the way I approach it is ignore

15:35

the enemies , the

15:38

pathogens and the toxins

15:40

and the heavy metals . Let's

15:43

ignite the energy . That's

15:45

what this is all about , and I think that aligns

15:47

with your desire is to help your clients

15:50

increase their metabolic profile

15:52

so that their machinery and

15:54

their messaging , their signaling , can

15:57

be at an optimal level .

15:59

Yeah , for sure , and I'll give

16:01

you the lessons , a bit of a background about that Great

16:04

oxygenation event . And

16:06

the point that you brought up , molly , was

16:09

that the world was an incredibly unhospitable

16:11

place back those

16:13

three billion years ago . It wasn't conducive

16:15

to life as we know it existing

16:17

, and that those cyanobacteria

16:21

essentially existed in the oceans . They

16:23

used their harness solar energy

16:26

to produce oxygen

16:28

as a biproactive photosynthesis

16:30

and they bubbled along for

16:32

so many billion years that they eventually changed

16:34

the content of the atmosphere . So the dynamics

16:37

, the nutrient dynamics , change so

16:41

that we're able to evolve . This

16:43

oxygen-aerobic metabolism

16:46

was able to evolve . So

16:48

that's a very interesting point . And

16:51

what you've talked about in terms of

16:53

the specific role of copper in

16:56

the electron transfer chain in the mitochondria

16:58

is also fascinating Because , as

17:00

you've given us an overview , we

17:03

can't do these fundamental processes , which

17:05

is photosynthesis , and

17:08

oxidative phosphorylation is a

17:10

reversal of photosynthesis . I think I'll

17:12

hammer that point on Because

17:14

photosynthesis is taking light

17:17

and it's

17:19

taking water and

17:22

it's turning that into basically

17:24

sugar , essentially carbohydrate

17:26

chains , and what we do when we

17:29

burn substrates in our mitochondria is

17:31

we're taking the chains of

17:33

hydrocarbons and we're

17:35

taking oxygen and the outcomes

17:37

is water and CO2

17:40

. So

17:42

I also want to emphasize the point that you made , which

17:44

is that that fourth complex is a red

17:46

light receiver , and the

17:49

value or the role of red light therapy

17:51

. One of them is that it's

17:53

assisting in the function

17:55

of the mitochondrial electron transport chain

17:57

, and I think there's even new

17:59

evidence that the structured water in

18:01

the mitochondria is also acting

18:04

as a chromophore , is acting as a absorber

18:06

of water . So

18:08

the question , then I think that's relevant

18:11

is we're trying to optimize

18:13

these mitochondrial functions and we're doing so

18:15

through a light environment . We do so

18:17

through food substrates into the electron

18:20

transport chain , and Dr Lazer Boris , who

18:22

I agree with , advocates strongly for

18:24

fully grass-fed butter

18:26

and beef , tallow

18:28

long chain fatty acids

18:30

as well as ketones . But

18:32

what you're proposing is that we

18:34

can also tune these mitochondrial engines

18:37

by ensuring adequate amount

18:39

of these trace minerals . So

18:42

talk to us about that idea .

18:44

Yeah , so

18:47

let's go back to that GOE

18:50

Great Oxygenation Event , and

18:53

three chemicals came and saved

18:55

us . It's really important to understand

18:57

. So , to

19:00

get a little technical , there's

19:02

something called multi-copper oxidases

19:05

. These are enzymes that turn

19:07

oxygen into water

19:09

in one fell swoop . It's

19:12

actually a four-step process , but

19:14

they're called MCOs . We have a thousand

19:16

different forms of MCOs in our gut . Think

19:19

about that , but

19:22

it happens like that . So the oxygen

19:24

becomes two molecules of water at

19:27

the courtesy of this enzyme . So

19:29

that was the first really important development

19:33

. Second , you've

19:35

probably heard of melatonin , right yeah

19:39

?

19:39

of course .

19:41

It's more than a sleep aid it's

19:44

a master anti-oxygen .

19:45

Yeah , go ahead . And it evolved

19:47

, dandy . That's the point that Dr Russell

19:50

Reider has made is that it evolved

19:52

mitochondrial antioxidant

19:54

capability well before it was a

19:56

circadian signal or well before

19:58

it was a sleep inducer

20:00

.

20:02

Yeah , and it's the master antioxidant

20:04

inside the cell . So melatonin

20:06

is the master antioxidant in the cell

20:08

, inside the mitochondria . Glutathione

20:12

is the master antioxidant in the cell and

20:14

ceruloplasma is

20:17

the master antioxidant protein in

20:19

our body . And so

20:21

there's a real critical

20:23

requirement to manage this oxygen

20:25

. And so that was the second chemical

20:27

was melatonin . And

20:30

the third is my favorite , that

20:34

you've heard of cholesterol

20:36

. Right , it

20:39

was the third chemical that

20:41

came on the scene , and

20:43

it's important to understand that in

20:46

order to make cholesterol , it requires

20:48

11 molecules of oxygen . So

20:51

the production of cholesterol

20:53

is in response to copper

20:55

deficiency . So

20:58

when you don't have enough copper to

21:00

metabolize the oxygen , the body

21:02

has this wisdom to say well , I'm

21:04

going to store it in cholesterol and we'll

21:06

begin to make things from this . And

21:10

so those three chemicals are some of the most

21:12

important . And so what's happened in the

21:15

modern world is we

21:18

don't know anything about the GOE . We

21:20

think that melatonin is a sleep aid and

21:22

we don't know that it's being made in every mitochondria

21:25

of our body , and we have 40 quadrillion

21:27

mitochondria , and it's distributed

21:29

unevenly throughout the body . The

21:32

number of mitochondria in the heart is very

21:34

different than the liver . It's very different than the neurons

21:37

of the brain . Some of the neurons have

21:39

2 million mitochondria . That's

21:41

important to know . Especially

21:44

, like the substantia nigra , where

21:46

you get Parkinson's , it's

21:48

an enormously

21:51

dependent upon functioning

21:53

neurons in the neurons

21:55

of the substantia nigra .

21:58

Yeah , and I'm glad you brought that up , because this

22:00

idea of human diseases , these

22:03

complex diseases , diseases that

22:05

are killing people , so neurodegeneration

22:07

, heart disease , they are diseases

22:09

of organs with the most mitochondrial density . And

22:12

let me add in age-related macular

22:14

degeneration , because that's , the retina

22:17

has the highest density of mitochondria and

22:20

the endocrine system is also quite dense . So

22:23

if we're thinking about what's killing people and

22:25

what I see in my GP clinic , what

22:28

we see in terms of the general

22:30

medicine inpatient ward , these

22:34

are all diseases of organs of the highest mitochondrial

22:36

density . And when

22:38

you I mean bringing up the substantia

22:41

nigra , that's an excellent point and

22:44

that's a whole kind of another topic

22:46

. We can talk about melanin and neuromelanin

22:48

. But the role

22:50

of melatonin I think

22:52

of as this kind of guardian of

22:54

the mitochondrial genome . It's

22:57

a mitochondrial DNA guardian because

22:59

it's being made on site to

23:02

quench this oxidative stress that's

23:04

occurring as a natural byproduct

23:06

of oxidative

23:08

metabolism , and

23:11

maybe we'll talk about this . Maybe it's a bit of a detour , but

23:14

the idea of quenching oxidative stress is not

23:16

necessarily a good idea when

23:19

these kind of biofotons are also being

23:21

used in a very , very finely tuned signaling

23:23

mechanism . So it's not always the best

23:25

idea to get rid of them

23:27

all . But I really love it

23:29

how Dr Robert Fozbrie

23:31

presented this idea of

23:34

melatonin in mitochondria and he described

23:36

a cooling and a lubrication system . The

23:39

cooling is the melatonin because it's

23:41

being made on site and the lubrication was

23:43

the red light because in

23:45

terms of helping those

23:48

mitochondrial complexes operate

23:50

. So let's

23:52

continue the discussion about mitochondria

23:54

. I think you're onto a good thing .

23:57

So , again , the goal

23:59

is and

24:02

I think I don't know , that I've ever

24:04

talked with anyone who understood the link between

24:06

quote disease and

24:08

density of mitochondria , so

24:10

I had soft tea for that . That's a very nice

24:12

way to describe it , because

24:14

that's in fact true . And

24:17

what

24:19

happens to the mitochondria is

24:21

they're great recyclers

24:23

of substrates . They're

24:26

recycling calcium , they're recycling

24:28

amino acids , but one of the most important

24:31

things they need to recycle is called iron

24:33

. If

24:35

you hear something you may or

24:37

may not know and

24:40

I find this fascinating Scientists

24:44

and clinicians do

24:46

not know how

24:48

oxygen gets into

24:50

the mitochondria . If

24:53

I were to ask you , you'd say what's diffusion

24:55

? No , we're talking about

24:58

the master pro-oxidant . It's

25:00

the second most reactive element on the planet After

25:03

flooring gas . Oxygen is number

25:05

two . So we're not going to have passive

25:07

diffusion of a gas into

25:10

the mitochondria . So it's an active

25:12

transport . And the

25:14

people who came the closest were Wittenberg

25:16

Wittenberg husband and wife team back in 2007

25:19

. And they threw up their hands

25:21

and said we don't know how it happens . No

25:23

one knows how oxygen

25:26

gets into the mitochondria

25:28

. The most provocative

25:31

theory about it is Dr

25:33

Solis Herrera son

25:36

man down in Mexico . Have

25:38

you had a chance to talk with him ?

25:40

I haven't , but I'm culturally

25:43

aware of his work . Go on .

25:46

Brilliant guy , and his whole theory is

25:49

that the melanin is

25:51

on the outside of the mitochondria and

25:53

so it's engaging in photosynthesis

25:55

and releasing the oxygen . Still

25:58

, I'm not sure that he knows how it's getting in there

26:00

, but there's this back and forth

26:03

between melanin and the mitochondrial

26:06

activity . It's a brilliant model

26:08

. It makes so much sense conceptually

26:11

. I think he's still challenged

26:13

to be able to prove it , but he has a wonderful book

26:15

on human photosynthesis which is

26:17

just phenomenal to read . But

26:20

I think people need to understand that there's some real

26:22

gaps in our understanding . There's

26:25

just this well , the oxygen gets into the mitochondria

26:27

. It's like well , wait , let's start right there

26:29

. How did that happen ? And it's

26:31

happening at a very fast rate , right

26:33

? And so the

26:35

other thing that people , a lot

26:38

of people , don't know is that everyone

26:40

puts the electron microscope

26:42

on complex four . Oh , it's copper dependent

26:44

. What turns out ? The complex

26:46

one , three , four and

26:48

five are all copper dependent , and

26:53

complex two is just an enigma

26:55

. I don't , we

26:57

won't go there right now . But the thing is , if

26:59

one , three , four and five are

27:02

copper dependent , well , let's talk about

27:04

that . Let's talk about the fact

27:06

that the gears of the mitochondria

27:09

start to grind to a halt . And

27:12

what ? And if the mitochondria

27:14

can't make heme , that's

27:17

really where critical breakdown

27:19

is , as you likely know . And

27:21

the thing is there's eight enzymes to

27:24

make heme . Four of them are

27:26

occurring inside the mitochondria , in

27:28

the matrix . There's a lot

27:30

of copper in that matrix , right ? So

27:32

four occurring inside the mitochondrial matrix

27:34

and four occurring outside the mitochondria

27:36

, so the ones that end

27:39

in the word oxidase . It's a pretty

27:42

good bet that copper's involved , because

27:44

copper has a unique ability to

27:47

work with oxygen , to oxygenate

27:49

and to harness that energy

27:52

. And that is lost

27:54

in the world of conventional

27:56

medicine . Again , I

27:58

don't think practitioners understand

28:00

how energy is made and

28:03

they don't understand the mechanics of what

28:05

the mitochondria are doing , nor do

28:07

they understand the signaling . Do

28:09

you know much about the PAM

28:12

enzyme ? Pam enzyme

28:14

have you ever heard of that ? So

28:17

there's an enzyme . It's

28:19

called peptidoglycine

28:22

, alpha-amidating

28:24

monooxygenase . It's

28:28

35 letters long and

28:30

max . I get a dollar every time I say it , but

28:34

it's . There

28:37

are 4,700 signaling

28:40

peptides inside our body

28:42

and what

28:44

may surprise you is

28:46

that those peptides are

28:48

made in the form of parked cars . Does

28:52

your car in the driveway allow

28:54

you to get to the store ? No

28:57

, you've got to turn it on right . You've

28:59

got to start the engine right and

29:02

the

29:05

signaling peptides need

29:07

to be turned on and

29:10

there's a glycine at the end

29:12

that needs to be cleaved off

29:14

and then an amine

29:16

group is attached and then suddenly

29:18

the hormone can signal Hormones

29:21

like insulin , insulin

29:23

growth factor , you

29:26

know , just hemopexin , spexin

29:29

these are things that people have never heard

29:31

of , and they're all involved in sugar

29:34

metabolism signaling . That's

29:36

taking place inside the

29:38

tissue , inside the cell

29:40

, inside the mitochondria

29:43

, and if it's literally

29:45

when

29:49

this is on , it works right . You

29:51

called me yesterday and my

29:53

phone lit up and I decided to ignore

29:56

the fact that I didn't know who the phone number was , thank

29:58

God . But the point is , I got

30:01

a call , the phone worked and that's

30:03

great and we were able to

30:05

come to consensus . But

30:09

if the tissue can't communicate with

30:11

itself , if

30:14

the insulin can't tell all

30:16

of the other many peptides

30:18

that it's on the scene , that's

30:21

what we're up against . And here's the most important part

30:23

. The PAM enzyme

30:25

is copper dependent . It

30:28

doesn't work without copper , why ? Because it's

30:30

working with oxygen monooxygenase

30:33

, and so I've

30:38

talked to probably

30:40

100 doctors . I've

30:42

yet to meet a doctor who even

30:44

knows what I'm talking about , and

30:47

to me we're

30:49

at the basis of how the

30:52

metabolism communicates

30:54

with itself . Think

30:57

about hey , we got some incoming

30:59

, we got something to do , we got . And

31:01

if they can't get the signal through , if it's

31:03

just static or if it's an incomplete

31:05

signal , it's like it's one bar as opposed

31:08

to five bars , and

31:10

people aren't aware of that

31:12

. And so the cornerstone of

31:15

the root cause protocol is

31:17

missing . Information equals

31:20

missing truth . If

31:22

you don't know that the mitochondria

31:25

do more than just make ATP

31:27

, if you don't know that , as

31:29

you pointed out , that disease

31:31

is highly expressed in mitochondrally

31:34

dense tissue , if

31:36

you don't know that these organelles

31:39

need to communicate with each other

31:41

, to me , the mitochondria

31:44

are the brains of the outfit . The

31:46

nucleus is just a Xerox machine . And

31:49

what I really want to know and I'm hoping

31:51

that you can give me some insight on this who's

31:55

writing the mitochondria ? There's

31:58

got to be an orchestra leader , right , there's got to be someone

32:00

saying , hey , we're going to do this

32:02

, we're going to do that . Who's doing that ? I've

32:05

yet to find the . Is

32:07

it the hypothalamus ? Is it some

32:10

nucleus within the hypothalamus

32:12

or I'm

32:14

just ? That's one of my greatest

32:16

quests to find out Where's the nerve

32:18

center that's running the mitochondria

32:21

? Within the cell , within the

32:23

tissue , within the organ , within

32:25

the organism . That's

32:27

the part that absolutely fascinates me .

32:34

You're raising so many fascinating points

32:36

, molly , and I will just

32:38

say what initially just came to my mind

32:40

in the answer of your most recent question , and

32:43

it speaks to this idea of centralization

32:46

versus decentralization . And if

32:49

we've thought about the model

32:51

of medical care and science

32:53

, up till now it's been DNA

32:55

RNA focused . It's about finding

32:57

monogenic causes of disease , it's about

33:00

targeting single gene pathways to

33:02

solve problems medically . But

33:05

what I think we're both in

33:07

agreement about is that this is the stories

33:10

in the mitochondria and this

33:12

is a story of decentralization . And

33:14

it's a story of this decentralized

33:16

system where we're

33:19

essentially more worried about our mitochondrial

33:21

DNA than our nuclear DNA . And

33:24

if we're taking this centralization and

33:26

decentralization lens , then

33:29

I think the answer to your question

33:31

is that there's not one place in the body

33:33

. These bacteria , these

33:35

antibacteria , they're environmental sensors . And

33:38

when we manipulate the

33:40

mitochondria to increase their efficiency with

33:43

light , with

33:45

red light , with UV light , with

33:47

different light wavelengths , when we

33:49

manipulate their function with cold , which essentially

33:52

reduces the space between those

33:54

respiratory proteins and increases the efficiency

33:56

of electron tunneling , when we

33:59

increase their efficiency with ketone

34:02

bodies or long chain fats and

34:04

this is a story of environmental sensing

34:06

I'm inclined to think that it's

34:09

ungrounding . We haven't even mentioned grounding the free

34:11

electrons that you can get , so

34:14

I would say that they're coordinated in a decentralized

34:17

way by sensing the environment that they're in

34:19

.

34:19

Yeah , and

34:21

to me , the piece that I've

34:23

elected to focus on just because

34:26

it makes the sense intuitively

34:28

and it's worn out in the research

34:30

is the

34:33

bioavailability

34:35

of copper . Is what ties it all

34:37

together . One

34:39

of my most amazing

34:41

conversations via one

34:44

of my students down in Australia she's a

34:46

naturopath . One of her

34:48

mentors is a . He's

34:51

a chiropractor of 40 years , a naturopath

34:53

of 40 years , but he's been an alchemist

34:55

studying copper

34:58

and iron for 30 years . It

35:00

was a fascinating conversation . His name is John

35:03

and he said you know more lately it would be important

35:05

for you to know that the copper has

35:07

a magnetic attraction for light , he

35:10

went . Well , that makes so much sense when you think about

35:12

photosynthesis , he said

35:14

. But it also has a magnetic attraction for ammonia

35:17

. So what does that represent

35:19

? Sunlight and ammonia ? Well , that's the

35:21

beginning and end of life . And

35:23

copper has a relationship . People

35:26

don't realize that there's four enzymes

35:28

to break down ammonia . The first is

35:30

a copper dependent enzyme , and

35:32

if that obligate enzyme doesn't work right , well

35:34

, you're going to have a buildup of ammonia

35:37

and you're going to have brain fog . And

35:39

where is this happening ? In the liver , and

35:41

there's probably a component of it that's happening

35:44

in the spleen as well . And the

35:46

second point is people are not aware of

35:48

the thousands of activities

35:51

, enzymatic activities

35:53

, that are being regulated

35:56

by the activity

36:01

of oxygen and iron , by

36:03

copper hiding behind a curtain . And

36:05

how do we spell curtain ? C-u-r-t-a-i-n

36:10

, so we can see the symbol for copper , and

36:13

that's . You made the point earlier . There's

36:15

no money in a cure . How

36:18

do we spell cure ? Oh yeah , c-u-r-t-a-i-n

36:20

. And so the

36:22

basis of the conventional model

36:24

is on illness , is

36:26

on lack of energy , and

36:29

the world doesn't know that . I

36:32

think it's a very small percentage of practitioners

36:35

who really understand the way

36:37

you do that . There's this energy

36:39

dynamic that's really behind

36:41

the quote disease dynamic

36:43

, and that's

36:46

the amazing work of Douglas Wallace

36:48

at UPenn , amazing

36:50

writer and thinker , and

36:52

if it were up to me I'd give him a Nobel

36:54

Prize or two for his

36:57

work so far . But it's just , it's

36:59

amazing that more people don't know about

37:01

the central role of energy

37:03

regulation to drive

37:05

the whole signaling and all the other

37:07

dynamics that we're talking about .

37:09

Yeah , you took the words out of my mouth

37:11

. I was just about to reference Dr Doug Wallace

37:13

for the listeners and his

37:16

seminal work on mitochondria

37:18

and the bio-energetic

37:21

, the mitochondrial bio-energetic etiology disease

37:23

, which is basically giving

37:25

explanatory power to all

37:28

these diseases that we're dealing with in the clinic

37:30

, that the medical paradigm

37:32

isn't able to provide

37:35

any kind of useful treatment

37:38

. And I think that gets to the

37:40

crux of what you're saying , morley , which is , if

37:42

you understand the fundamentals of what's

37:44

going on , then you can reason by

37:47

deduction to work out what

37:49

the most effective treatment is . But if you don't

37:51

understand how the system works , if

37:53

you don't understand how an engine works , then

37:55

you're going to be pouring vinegar into

37:57

the fuel tank instead of fuel . So

38:03

that's a bit of analogy for where we are . And

38:05

, before we go into , start talking

38:07

about the clinical implications and

38:09

we need to talk . I think we need to talk

38:11

about these quantum biology concepts and

38:13

we need to talk about this idea

38:16

that the

38:18

proteins and complexes

38:22

inside the body , the acting , is

38:24

semiconductors , and no

38:27

one has talked about this more than Jack

38:29

Cruz and

38:31

he's incredibly complex

38:34

and deep . But there's an idea that these physical

38:36

quantum properties are occurring within

38:38

the body . So talk to us about

38:41

how you integrate those ideas

38:43

into this copper and

38:45

kind of mineral centric

38:47

view .

38:49

Again , it's about the efficiency

38:51

of interaction , and

38:55

you talked about red light

38:57

being the oil . I've

38:59

never heard it described that way , but it makes so much sense

39:02

. It's

39:04

being able to efficiently harness

39:07

the light and the energy

39:09

that is intended

39:11

to be a part of our cellular

39:13

structure , and so I

39:16

think the challenge is a

39:19

lot of people aren't grounded

39:21

in mitochondrial enzyme

39:23

activity . They don't know about

39:25

the handoffs of electrons and

39:28

what the enzyme activity is

39:30

that enables that movement of the electrons

39:32

, and that , more

39:35

often than not , those handoffs are

39:37

made courtesy of copper , the

39:39

bioavailability of copper and

39:43

in 1985

39:45

, earl

39:49

Frieden , who was then the

39:51

preeminent iron biologist on the planet

39:53

. He theorized that ceruleoplasma

39:56

, which is the master

39:58

protein , copper protein , was

40:01

the supply line for the mitochondria

40:03

. There's

40:06

this constant sourcing of

40:09

copper to the mitochondria throughout

40:11

the body . Well , he was resoundly

40:13

criticized for that and

40:16

in 2017 , zach Baker

40:18

proved that he was right

40:20

. Without

40:23

a steady supply line

40:25

, the mitochondria don't work

40:27

right and the electrodynamics

40:32

of the mitochondria don't work right . There

40:36

was a time we've

40:39

heard of the telegraph wires and the

40:43

communication that took place with telegraph . The

40:45

original wires for the telegraph were

40:48

iron back in the 1850s

40:51

, and then someone figured out

40:53

that copper was three times faster to transmit

40:55

electrons . And so then , suddenly , everyone

40:57

adopted the copper

41:00

side . And the way I look at it

41:02

is what

41:04

makes a tall

41:06

building stand still

41:09

? It's

41:11

steel girders , right . And

41:13

what are they made of ? Iron , right . But

41:16

what is it that makes a tall building move

41:19

? Well , it's

41:21

copper , because it runs the

41:24

plumbing and it runs the electricity . And

41:26

I think it works the exact same way in our body

41:28

and inside our mitochondria . The

41:31

way I describe it , max , is that in

41:34

the world of conventional science

41:37

and conventional medicine is

41:40

they love

41:42

to liken the mitochondria

41:45

to a kitchen . And every kitchen

41:47

has a stove , right , and

41:49

we put a big spotlight on the stove

41:51

. What's the stove made out

41:53

of ? What's made out of iron , right

41:56

. And but

41:58

does the stove , does the stove

42:00

know what is

42:02

going to be cooked that day ? Does

42:05

the stove know what temperature the

42:07

burner should be ? Does the stove know what

42:10

the temperature should be in the oven ? No

42:13

, no , turns out there's

42:15

actually a chef . I call

42:17

it a cuisine artist . Well

42:20

, again , got to spell it right , right . And

42:22

so no

42:24

one talks about the cuisine artist

42:26

inside the kitchen managing

42:30

and regulating the stove . And

42:32

it turns out that when you get inside

42:35

the minority , you get inside complex

42:37

four , there's he may

42:39

and he may three . Right

42:43

, how do you make he may and he may three ? Oh

42:46

, you got to have copper . That's in the literature . It's

42:48

copper dependent . And

42:50

so what is he may and he may three ? It's

42:53

actually the stove that

42:55

holds the oxygen , so

42:57

the copper can slice and dice it and move

42:59

the electrons and hydrogen atoms in to

43:02

enable it to become water

43:04

, but everyone is fixated

43:07

on the stove and no one

43:09

can see the chef . And

43:12

then the other member of the restaurant

43:14

that's so important is the waiter

43:16

. Right , 70%

43:19

of the iron in our body is

43:21

a waiter , carrying oxygen

43:24

, carrying carbon dioxide

43:26

Right , if we include myoglobin

43:28

, it's 80% of the iron in the body is

43:31

a waiter . Well

43:33

, do we go to our restaurant for

43:36

the waiter or are we going there for an

43:39

experience with the food ? I

43:41

would contend that it's . We go there for the chef

43:44

, not the waiter . And so I

43:46

think all of the optics and thinking about

43:48

how energy is made , how

43:50

energy is regulated , how energy is expended

43:53

, is more copper centric

43:55

than anything , because

43:57

of the very nature of how the

43:59

process takes place , and

44:02

I don't think there's enough sensitivity

44:05

to that in a lot of the discussion

44:08

is that the physics of

44:11

the mitochondria is

44:13

copper dependent Because we're moving

44:15

electrons , because we're moving photons

44:17

, and it's a very copper

44:20

dependent process .

44:23

The analogy to the building

44:25

and the electricity transmission really gives

44:28

me more context and really helps me

44:31

understand . That makes intuitive sense . Anyone

44:33

who's touched a copper pipe or

44:36

a copper spoon . It conducts heat

44:38

, it conducts electricity that much quicker than

44:40

those metals . So from

44:42

a biological point of view it makes sense to

44:45

me that if we're trying to handle electrons

44:47

in the most efficient way and

44:50

that's a great point to make , to hammer home this idea

44:52

that mother nature is the

44:55

most experienced and the most

44:58

expert engineer and

45:00

she has crafted these organisms

45:02

over periods of billions of years

45:04

through the most robust

45:07

system , which is trial and error and

45:09

the simple failure of organisms

45:11

that didn't have the most thermodynamically

45:14

efficient makeup . So

45:17

it's a fascinating way to think about it , Molly

45:19

. So yeah , that's really great . Maybe

45:22

we can now talk about the kind of clinical

45:24

implications or try

45:27

or zoom out from mitochondrial level to kind

45:29

of whole body and physiology

45:31

and discuss how copper

45:34

is regulated , Because the

45:36

corollary of what you've just talked about to

45:38

me , and I'm thinking that

45:40

we need to avoid a Frank

45:42

total body copper deficiency if

45:44

we want those mitochondrial

45:47

function to be optimized

45:49

.

45:52

Great point and look forward to the discussion

45:54

. Now we have to get past

45:56

the meme that runs the planet . The

46:00

main , the central meme on planet Earth is

46:03

your anemic and

46:05

your copper toxic . And

46:08

you'd be amazed where that

46:10

is woven into the thought process

46:12

of the individual and

46:15

their practitioner . And

46:17

the

46:20

fact of the matter is . The truth of the matter is it's

46:23

just the opposite . One of

46:25

the most central paradigms

46:28

of understanding metabolism

46:30

is to know that an

46:33

animal you and I are animals

46:35

, whether we like it to think of that . But

46:37

when an animal is denied copper in

46:39

its diet , iron builds

46:41

in its liver . That's

46:44

been well established . It was back to 1928

46:47

, the University of Wisconsin , dr

46:49

Hart , steenbach , waddell and Elviem , in

46:51

March of 1928

46:54

, proved that . Then , in May of 1928

46:57

, dr McCarg James McCarg at

46:59

University of Kentucky , was able

47:01

to prove that denying copper to an animal

47:04

caused iron to build in

47:06

the red blood cell . That's

47:08

not necessarily good . And

47:11

so there's this really critical

47:13

seesaw if you deny

47:15

copper , iron builds . And

47:20

we've been talking for almost it's

47:22

been about 50 minutes . So

47:24

every second

47:26

of every day . So

47:28

50 minutes times 60

47:30

times 2.5

47:33

million red blood cells need

47:35

to be replaced every

47:37

second In the course of 24

47:40

hours , we need to replace over 200

47:42

billion red blood cells . That's

47:45

a lot of red blood cells , but

47:48

what that's predicated on is the ability

47:50

to move iron out

47:52

of the tissue because it needs to

47:54

be recycled , because it turns out

47:56

that , believe it or not , it's

47:59

about 215 billion red

48:01

blood cells . To

48:04

replace that many red blood

48:06

cells , you need 25 milligrams

48:09

of iron . Average

48:13

man has about 5,000 milligrams of iron

48:15

, average woman about 4,000 . And

48:18

that's

48:20

a lot of iron , especially in a

48:23

body that's run with just 100 milligrams

48:25

of copper . So it's a 50 to 1

48:27

ratio of copper to iron , or iron

48:29

to copper . And so here's

48:33

the most important part , though we

48:35

need 25 milligrams every

48:39

24 hours to

48:41

replace 215 billion red

48:43

blood cells , and

48:45

24 of those

48:47

25 milligrams of iron

48:50

come from a recycling system

48:52

called the verticuloendothelial

48:55

system . I don't think it's taught

48:57

in practitioner school anymore . I

48:59

think what doctors are taught is that we

49:01

need to eat 25 milligrams of iron

49:03

daily , when in fact , we have

49:06

this very sophisticated system of

49:08

recycling the iron , and

49:10

it's got to get out of

49:12

the recycling macrophages

49:14

, principally in the spleen . And

49:17

if the iron gets stored in the liver , it's

49:19

got to get out of the hepatocytes , but

49:22

it's got to be released back into

49:24

the recycling system to

49:26

get to the bone marrow to support the

49:28

production of 2.5 million red blood

49:30

cells a second . So we're taking 2.5

49:33

offline . We're replacing with 2.5 every

49:36

second . That's

49:38

really important to understand that . And

49:40

so 95%

49:43

of the iron is

49:46

copper dependent because

49:49

the recycling macrophages have

49:52

an iron doorway . It's

49:54

called ferroportin iron

49:56

doorway and the iron doorway

49:59

is run by a copper doorman . That's

50:02

the work of Giovanna

50:04

Moussi in Italy , 2014,

50:07

. Amazing article about the

50:10

copper driven ferroportin

50:12

pathway and what

50:14

practitioners are being trained is that hepsidon

50:17

regulates ferroportin . Well

50:20

, hepsidon is a negative regulator

50:22

. Ferrooxidase

50:25

is a positive regulator . What's

50:28

the difference between positive and negative ? Positive

50:30

would be like your mom making sure you get up on

50:33

time to go to school . Negative

50:35

regulator would be like a SWAT team coming and

50:37

grabbing you out of your bed and throwing you into

50:39

the school . Big difference between those two

50:41

, right ? And so the

50:45

body runs on positive

50:47

regulation , unless there's a

50:49

crisis . When does hepsidon

50:52

come on the scene ? When there's copper

50:54

deficiency . That's the work of Dr

50:57

Welch at the University of Utah in 2007

50:59

. So , again , doctors aren't taught that

51:01

. And so the very basis

51:04

of responding

51:06

to your question you've

51:09

got to ground your understanding about . Where

51:11

does copper and iron intersect

51:13

in the body in order to support

51:16

the metabolism of the body , and

51:18

so that recycling

51:20

of iron that we were talking about earlier

51:23

, that recycle or the remaking

51:25

of heme , that's

51:27

copper dependent too , because you can't

51:29

put iron into

51:32

a heme molecule . There's

51:35

an enzyme called ferrokeletase . Well

51:38

, guess who's running the Guess who the

51:40

crane operator is . It's copper

51:42

. It brings iron

51:44

and drops it in the center of . Doctors

51:48

don't know that . So if you don't know the

51:51

cornerstone of how it's done , then

51:53

downstream there's going to be a lot

51:55

of confusion about the

51:57

mechanics of it . So

51:59

people need to accept

52:02

the fact that the meme your

52:04

anemic and your copper toxic is

52:06

a lie , when in fact

52:08

we exist on a planet now where

52:11

the amount of glyphosate is

52:13

killing the soil , as

52:15

you probably know , and

52:17

glyphosate is a perfect

52:19

copper chelator . It

52:22

will chelate copper a billion

52:24

times faster than it will chelate

52:26

magnesium . It will

52:28

chelate copper a thousand times

52:31

faster than it will chelate iron , and

52:34

so we can't relate

52:36

to those numbers . So

52:38

there was a time , max , when I could run an

52:40

eight minute mile . I was very

52:42

proud of that . I was never a

52:45

great athlete , but at the time

52:47

when I could run an eight minute mile . My

52:49

younger son clocked a 402

52:52

mile when he was in college and

52:55

I called him up and said you going to go for it ? He said

52:57

no . He said

52:59

I could work for months and maybe not shave those

53:01

two seconds off . But

53:03

his old man was curious , so

53:05

I went to a gym to see what it was like to run

53:07

a four minute mile and

53:10

I got on the treadmill and cranked it down

53:12

and was holding on for dear life and

53:15

then realized wait a minute , the machine's doing all the work

53:17

. I'm just holding on and almost

53:19

killed myself trying to get off of it . The

53:22

thing is we can't relate to a

53:24

thousand times faster , a

53:26

billion times faster , because

53:28

we barely know people who are twice as fast as

53:31

we are , and so we get

53:33

lost in the , the

53:35

bio dynamics of the

53:37

minerals and these chemicals

53:39

that we're now exposed to , and

53:41

the brainwashing

53:44

that , oh , we need more iron

53:46

and oh , be careful of that copper , it's

53:49

going to cause you a problem . We need to flip

53:51

that narrative and that's why I appreciate the

53:53

chance to have this conversation so

53:55

that more people can understand that , wow

53:57

, there's more to the story and

54:00

just by way of a

54:02

parenthetically comment , I

54:05

renamed what the condition

54:07

was back in 2020 , around

54:10

April or May of that year . The

54:12

COV stands

54:14

for coppers vanished and

54:16

ID stands for irons dysregulated

54:19

. And we're back to Hart

54:22

and McCarg realizing that

54:24

copper is missing , iron's building

54:26

, and that's what the research is now

54:29

showing , what that whole event was all about . And

54:31

people don't know that . And what

54:34

does that do to our mitochondria ? It

54:37

kills the mitochondria . They can't . They

54:39

can't process , they can't engage

54:42

in their constant

54:44

activity of recycling and regenerating

54:47

ATP . And it's just

54:49

, it's amazing how these

54:52

fundamental cornerstone facts

54:54

are not being taught to

54:57

understand how the higher level functioning

55:00

of the tissue is dependent upon

55:02

that process .

55:05

Yeah , let's to explore that . Molly , I'll

55:07

make a quick point on the glyphosate

55:09

before we launch into iron dysregulation

55:12

. But this idea of glyphosate

55:14

, when it was brought out , was you know , it's a

55:16

benign compound , it doesn't harm

55:19

, you know , it doesn't harm human health , it's

55:22

all well and good . And it's subsequently been

55:24

sprayed on you know

55:26

how many , maybe millions

55:28

of billions of hectares of land and

55:31

I want to

55:33

make quick mention of the episodes where I've talked

55:35

about glyphosate . So , and the mechanisms

55:38

of toxicity . So it disrupts the chikimate

55:40

pathway , which is a enzymatic

55:43

pathway that we need to make tyrosine

55:45

, a bunch of other tryptophan

55:47

, a bunch of other critical amino

55:50

acids , by nuking our gut microbiome

55:52

. It's an endocrine , and I talked

55:54

to Stephanie Seneff about that . It wrecks

55:57

our deuterium excretion process so

55:59

we're less able to deuterium deplete our bodies

56:01

. It acts as an endocrine disruptor

56:03

after it's chelated probably

56:06

copper or some other main minerals , and

56:08

I talked to Dr Anthony J about that it

56:11

disrupts the exclusion zone

56:13

water that gets formed on

56:16

hydrophilic surfaces . So there's

56:18

so many ways that glyphosate is

56:20

harming human health and none of them are being emitted

56:22

by the

56:24

agricultural companies that make the stuff

56:27

. None of them are being emitted by government

56:29

regulators who continue to endorse and

56:32

push this idea that it's a safe

56:35

and tolerated chemical and

56:37

none of these effects are aware of

56:40

being unknown by clinicians . So

56:42

I'm glad you brought up the glyphosate

56:45

and maybe we can talk about that more towards

56:47

the end of the discussion when we talk about the

56:49

agricultural implications

56:51

. But let's dive

56:53

into iron dysregulation , because you

56:56

mentioned the

56:59

effect of iron in COVID . When

57:01

the pandemic first hit , I was working

57:03

in COVID wards and emergency department

57:06

and we were measuring esterine

57:08

ferritin and it was a hallmark

57:10

of the degree of

57:12

inflammation and it was used as a prognostica

57:15

for who we're likely going to need to be sending to ICU

57:17

and who we're going to need to be putting on

57:20

respiratory support . So

57:23

in that situation the ferritin was

57:26

, as I understand it was being used as a

57:28

kind of acute phase reactant , meaning it was

57:31

a marker of inflammation in the body . Going

57:34

back to how I see it in

57:36

my clinical practice , I always interpret

57:38

it in the context of a seroactive protein

57:40

which is again an inflammatory mediator

57:42

, because if it's ferritin

57:45

is high and CRP is high , it's not giving

57:47

us a good indicator of iron status . It's

57:49

simply just reflecting the background information in the body

57:51

. So talk to us

57:53

about this use of ferritin

57:55

as a kind of marker of iron store

57:57

, as a marker of information , and how you

57:59

conceive of these concepts ?

58:03

Great . So first we have to understand that there's

58:05

three different forms of ferritin

58:07

in the body . There's

58:09

ferritin heavy chain , there's

58:13

ferritin light chain and

58:15

then there's secreted ferritin , and

58:18

the form that the doctors are

58:20

focused on is the secreted

58:22

form . But what

58:24

they're not taught is that

58:27

, the heavy chain

58:29

. Why is it called heavy ? Because there's a

58:31

heavy metal that's running it . What's that

58:33

heavy metal ? It's called copper . So

58:36

we're back to the ferrooxidase enzyme

58:38

function running the process

58:41

of bringing iron into the core . And

58:44

what's light chain good at ? It's

58:46

good at storing , it's not good

58:48

at releasing . You've got to have the heavy chain

58:50

to let it out again . And

58:52

what happens in the liver

58:55

is where it's principally . When you see high

58:58

levels of ferritin , you

59:00

basically have a breakdown of the

59:02

liver is taking place and the

59:04

recycling of the

59:06

iron , the ferritin , is taking

59:08

place within the lysosome

59:10

of the hepatocytes

59:13

, a really important process . And

59:15

the lysosome is the stomach

59:17

of the cell and it's an energy-rich

59:21

environment dependent

59:23

upon what . Oh yeah , copper is what's

59:25

making the acidity rise

59:27

in the lysosome , and

59:30

so if it can't

59:32

complete that cycle properly , the

59:35

iron gets dumped into the

59:37

tissue , into the liver tissue

59:40

, and what gets secreted

59:42

from the hepatocyte is

59:44

an abridged form of light

59:46

chain . It's

59:48

missing about 10 amino acids and

59:51

it gets picked up in the blood test

59:53

as ferritin . But

59:56

they don't distinguish between the

59:58

ferritin missing 10 amino acids

1:00:00

and the ferritin light chain . They

1:00:03

just say ferritin's rising . Well , as

1:00:05

soon as you have rising ferritin , you

1:00:07

have iron dysregulation , principally

1:00:10

in the liver , and so when

1:00:13

you have this inflammatory response

1:00:15

, the liver is not able to

1:00:17

recycle the iron properly

1:00:19

. The flip side

1:00:21

of it is low ferritin . Everyone

1:00:24

knows it Well . Low ferritin means you need more

1:00:26

iron . No , it means

1:00:28

that the spleen is on the ropes

1:00:30

and it's a completely

1:00:32

different understanding of what

1:00:34

the role of the red pulp macrophages is

1:00:37

and their ability to store iron

1:00:39

. And

1:00:42

the missing piece of the puzzle in

1:00:44

low ferritin is hemo-siderin

1:00:46

. When was the last time you did a hemo-siderin

1:00:48

test of any of your patients ? Never

1:00:51

, because you were never taught to do that right

1:00:53

. So you're taught to do ferritin , but never

1:00:55

hemo-siderin . Why is hemo-siderin

1:00:58

important ? Because it can hold 10 times more iron

1:01:00

. It's 10 times more reactive

1:01:02

. It's violently

1:01:05

effective of the spleen

1:01:07

and the liver , both of whom can hold

1:01:09

hemo-siderin , but no one ever measures

1:01:11

it because they were never taught to measure that . So

1:01:14

the thing is that the iron

1:01:17

can get dysregulated , it

1:01:19

doesn't get recycled properly , it's

1:01:23

not able to release its

1:01:25

stores . The ferritin

1:01:27

is rising because

1:01:30

it's being released , because

1:01:32

the recycling process

1:01:34

is breaking down . Why ? Because

1:01:37

the energetics and

1:01:39

the enzyme activity doesn't

1:01:41

support it . And so the rising

1:01:43

ferritin is a sign of

1:01:45

liver metabolic

1:01:47

dysfunction . And

1:01:51

no one you knew that hypofaritinemia

1:01:55

, the cytokine storm that you

1:01:57

were treating in the wards

1:01:59

and in the hospital , could

1:02:03

have been interpreted as classic

1:02:05

raging copper deficiency

1:02:09

. But you never had that training

1:02:11

. There's a wonderful article that

1:02:13

I can send you by a world-renowned

1:02:15

MD , phd , leslie

1:02:18

Claveille , where he's talking about chronic

1:02:20

copper deficiency being at the

1:02:22

core of everyone's problem . It

1:02:25

was just published , october

1:02:27

of last year , and I believe

1:02:30

Dr Claveille will be 90 next

1:02:32

year , so he's a very active

1:02:34

researcher . He's written

1:02:36

hundreds and hundreds of articles , but

1:02:39

again , the copper side

1:02:41

of the story is not known to

1:02:43

the public , it's not known to the public's practitioners

1:02:45

, and it's really again hiding

1:02:47

behind that curtain . And so if you don't

1:02:49

know about the curtain , if you don't

1:02:51

know about the copper dynamics , you can't

1:02:54

understand the iron dysregulation

1:02:56

. And so what happens

1:02:58

, max , is that far too

1:03:00

many practitioners confuse

1:03:04

low iron in the blood

1:03:06

, in the blood work , and

1:03:09

don't think about what that really is

1:03:11

. Signaling is high iron in the tissue

1:03:13

. The reason why it's high

1:03:15

in the tissue is it can't be released

1:03:18

to

1:03:20

get back into the recycling system , and

1:03:22

so there is no blood test that

1:03:25

measures iron in the tissue . Everything's

1:03:29

in the blood . The only time you

1:03:31

can get to the tissue level is

1:03:33

to do either a Tesla 2

1:03:35

MRI , which is very expensive

1:03:37

, or you can do a needle

1:03:39

biopsy of the liver , which is very painful

1:03:42

. In both situations , you

1:03:44

first . I

1:03:46

would love to know how much iron I have in my liver , but I'm

1:03:48

not afraid to spend the money or

1:03:50

go through the pain . But the point is

1:03:53

no one knows about that

1:03:55

copper-iron dynamic from

1:03:57

the 20s . No one knows that

1:03:59

this liver is . It

1:04:02

was never designed to store iron . It's

1:04:04

designed to store copper and retinol . And

1:04:08

what are we taught now ? Oh , be

1:04:10

careful of copper and retinol , you

1:04:12

can become toxic from them , which

1:04:15

is like no , that's exact

1:04:17

opposite of the truth . And so then

1:04:19

the liver has become an iron storage

1:04:21

depot , which was never

1:04:23

designed by Mother Nature to do

1:04:25

that . I mean , it has the

1:04:27

capacity the hepatocytes have that natural

1:04:30

ability to store iron , but it was never supposed

1:04:32

to be dominant function . It

1:04:34

was supposed to be storing copper and retinol

1:04:37

to support the metabolism of

1:04:39

the mitochondria Throughout the body . And

1:04:41

the part that a lot of people don't know about is

1:04:44

the work of Dr Hammerling in 2016

1:04:46

. He'd be a great scientist for you to

1:04:49

chat with , because his area

1:04:51

of expertise is retinol and

1:04:54

how important retinol is to mitochondrial

1:04:57

function . And

1:04:59

there's something , there's a complex

1:05:01

between , or there's a component

1:05:04

, we'll call it . It's a structure

1:05:06

between complex three and complex

1:05:09

four and

1:05:11

the electrons turns out

1:05:13

. The electrons ride the tail

1:05:15

of the retinol to get from three

1:05:17

to four and what Dr Hammerling

1:05:20

has been able to prove is that it's

1:05:22

a lack of retinol that

1:05:24

causes the Warburg effect

1:05:26

. And it's like

1:05:28

wow , that's fascinating and

1:05:31

it's interesting . Dr Warburg never coined

1:05:33

that phrase . That was actually , I think it was

1:05:35

coined in the 80s . But

1:05:38

the point is , when

1:05:40

did they first know that lack of retinol caused

1:05:42

cancer ? 1925

1:05:45

. Montrose T Burroughs

1:05:47

, working at the Rockefeller Institute . He

1:05:49

gets his MD degree at Hopkins in 1909

1:05:52

. 1925 , he

1:05:54

publishes an article and four

1:05:57

articles in 1926 proving

1:06:00

that retinol deficiency causes cancer

1:06:02

. Well , what is cancer ? What's

1:06:05

a buildup of iron and the

1:06:07

lack of retinol . The

1:06:10

electrons can't flow and you

1:06:12

begin to . And the only

1:06:14

way to explain the Warburg

1:06:16

effect . So the body is designed

1:06:18

to burn oxygen in

1:06:22

the presence of copper . And

1:06:24

in the Warburg effect what's happening ? The cells

1:06:26

are choosing to use fermentation

1:06:29

to make energy Even

1:06:32

though oxygen is present . Well , there's only

1:06:34

one way to explain why they can't do the

1:06:36

oxygen there's no copper , there's

1:06:39

no bioavailable copper , and

1:06:42

the cancer cells are filling up with iron

1:06:44

, which is taking . It's

1:06:46

just , it's destroying the availability of

1:06:49

copper in that situation . So

1:06:51

it's just . It's a wholesale different

1:06:54

way of thinking about what's happening

1:06:56

inside the cells and inside the mitochondria

1:06:59

. But the iron dysregulation is

1:07:02

tremendously significant

1:07:05

. But people are confusing low iron

1:07:07

in the blood work and not aware

1:07:10

of the high iron in the tissue . And

1:07:12

once you realize that iron can

1:07:14

get stuck in the tissue and

1:07:17

famous scientists from all over the planet

1:07:19

have studied it it's

1:07:21

in the literature , there's thousands of articles

1:07:24

about it , but that wisdom

1:07:26

doesn't make it into the classroom

1:07:28

in doctor's school , it's

1:07:31

not in the clinical curriculum , and

1:07:34

that's where I think the breakdown is in the understanding

1:07:36

of the problem .

1:07:38

Yeah , A couple of clinical cases to

1:07:40

kind of analyze , given it with your

1:07:42

frame of reference . So

1:07:44

hereditary hemicromatosis is the most common

1:07:46

acknowledged kind of clinical

1:07:48

setting

1:07:50

of iron overload and

1:07:54

there's mutations in certain genes that

1:07:56

basically people of Northern

1:07:58

European descent and the thought being

1:08:00

that they evolve in situations

1:08:03

of iron , low iron in the environment . And

1:08:05

these mutations help us , you know , help

1:08:07

these people hang onto iron more efficiently . I

1:08:10

have seen heterozygotes

1:08:13

of hemicromatosis , so

1:08:15

people that carry one mutated

1:08:17

gene . They have had

1:08:19

ferritins of 500 , 600 , indicating

1:08:23

some degree of iron overload , and

1:08:25

then when they go on a very low carbohydrate

1:08:27

diet or often a carnivore

1:08:29

type diet , so they're eating a heap of steak paradoxically

1:08:33

, according to the mainstream and paradigm

1:08:35

, that iron overload

1:08:38

disappears and the ferritin actually

1:08:40

goes back under 300 , maybe it goes to 200

1:08:43

. So this is a

1:08:45

kind of a point that most

1:08:47

other doctors and GPs kind of scratch the

1:08:49

heads at , because they think that if you're eating very

1:08:53

hemoglobin , hemion-rich sources

1:08:55

of food , then that will contribute to

1:08:57

iron overload . My interpretation

1:08:59

of what was going on is that essentially

1:09:02

we were fixing a degree of metabolic

1:09:04

dysfunction that was dysregulating iron

1:09:06

but iron homeostasis

1:09:09

. So by what you're saying , it sounds

1:09:11

like we probably repleted copper

1:09:13

in that nutrient

1:09:15

dense animal food diet and that kind

1:09:18

of fixed this

1:09:20

ferritin number . So

1:09:22

obviously the patients lost a heap of weight and they're

1:09:24

feeling great . So what's your interpretation

1:09:26

of that observation

1:09:29

?

1:09:31

Yeah , the hemicromatosis

1:09:33

is basically a condition

1:09:35

of copper deficiency and

1:09:38

when we were talking about the PAM enzyme

1:09:40

earlier some very important research

1:09:43

that I'm going to come back to hemicromatosis in

1:09:45

just a second . But there

1:09:48

was a husband and wife team , betty

1:09:50

Eiber and Richard Mainz , that

1:09:53

studied this enzyme for 45 years 20

1:09:56

years at Hopkins and 25

1:09:58

years at University of Connecticut Medical

1:10:00

Center . They had funding for 45

1:10:02

years to study this one enzyme . That's

1:10:05

a head scratcher right there . But

1:10:08

in 2008 to 2012

1:10:10

, they were engaged

1:10:13

in doctoral

1:10:16

research with two of their

1:10:18

students and

1:10:20

they did a series of experiments with

1:10:22

mice and

1:10:24

they manipulated the PAM

1:10:27

gene so it lowered

1:10:29

its ability to express the PAM enzyme

1:10:31

. And in another group of

1:10:34

mice they withheld

1:10:36

copper and got the

1:10:38

same level of low PAM expression

1:10:41

. So they manipulated the gene , they

1:10:43

withheld copper and then in

1:10:45

two separate experiments

1:10:47

four years apart , they

1:10:52

fed copper to both sets

1:10:54

of mice and

1:10:57

in both experiments PAM

1:10:59

expression turned back on , both

1:11:03

with the defective genes and with

1:11:05

the copper withheld animals . And

1:11:08

the

1:11:10

student in the second

1:11:12

series of experiments his name is

1:11:14

Eric Geyer , he's an MD-PhD

1:11:17

at Harvard , he's an ophthalmologist and

1:11:20

in

1:11:23

his doctoral dissertation yeah

1:11:26

, I take the time to read those things . It's

1:11:29

like it's amazing information in there , max

1:11:31

. But he made the comment

1:11:33

that heterozygous

1:11:36

defects

1:11:39

are a sign of

1:11:41

copper deficiency . Put

1:11:44

it in black and white . And

1:11:46

so I think what we to come back to your hemochromatosis

1:11:48

topic is hemochromatosis

1:11:51

like quote gene defect or is it

1:11:53

a mineral deficiency ? And

1:11:56

to your point , people change their diet . They

1:11:59

probably would have responded better to organ

1:12:01

meats than to muscle meats

1:12:03

because there'd be even more copper there . They

1:12:06

might need copper supplementation beyond

1:12:08

that . But the point is , the

1:12:11

body's not stupid , the body

1:12:13

. Think about the wisdom

1:12:15

of the body . If

1:12:17

we can buy the fact that copper

1:12:19

is playing a central role in managing

1:12:22

light , managing energy

1:12:24

, managing the handoffs and just

1:12:27

many , many different things , if

1:12:29

it starts to sense that it

1:12:32

doesn't have enough copper , it's going to start to

1:12:34

change the expression of different genes , and

1:12:37

especially those that are handling

1:12:39

iron . And so

1:12:41

, again , one

1:12:44

way to interpret hemochromatosis is

1:12:46

well , there's no source of copper . We're

1:12:48

going to take this organism offline because

1:12:51

we know that if we start to build up the iron , it's

1:12:53

eventually going to kill the animal , and

1:12:56

that's a rather dark way of thinking about

1:12:58

it . But again , I think the body does have

1:13:00

this innate wisdom . It says we

1:13:02

don't have the requisite substrates

1:13:05

to keep energy production . So

1:13:08

we're just going to start to change the

1:13:10

dynamics and so hemochromatosis

1:13:13

will respond to phlebotomy

1:13:15

. Very important to get

1:13:17

the iron out , get the ferritin out

1:13:19

of the system . When

1:13:21

I really began to become more sensitive

1:13:24

to this whole issue , it was

1:13:26

December of 2015 . And

1:13:30

Dr Liz said you know , you've been talking to

1:13:32

a lot of people about iron . He says have you

1:13:34

studied yours yet ? I went no

1:13:37

, don't . So

1:13:39

I did a blood test and found

1:13:41

out that my hemoglobin

1:13:43

was 18.3

1:13:46

and my ferritin was 237

1:13:48

. Well , it's a

1:13:50

good thing I was wearing brown pants . When I got the

1:13:52

results back , it freaked me out , and

1:13:56

so that's what

1:13:58

I really started to take a deeper dive into understanding

1:14:00

this copper iron dynamic and

1:14:02

who's on first and what's on second . And

1:14:06

the people who understand this the best are

1:14:08

the Italian researchers , the

1:14:10

Indian researchers , the Icelandic

1:14:13

researchers . What do they all have in common

1:14:15

? Their countries begin with the letter I . I

1:14:17

don't know why , but they just have this awareness

1:14:20

about iron metabolism that most don't . But

1:14:22

the thing is , it

1:14:26

was the copper that was missing in my body

1:14:28

that was not allowing

1:14:31

the regulation of the iron . Do

1:14:34

I have heterozygous

1:14:37

genes for this ? I don't know . I don't

1:14:39

have the courage to do the gene

1:14:41

test to find out . I just know I

1:14:44

feel pretty darn good with

1:14:46

my diet and with the protocol and with

1:14:48

the supplementation that I do . I

1:14:50

guess if I was a real , true scientist I

1:14:53

would subject myself to the gene research to

1:14:55

find out . But I take

1:14:58

comfort in that if

1:15:00

the body is properly nourished the

1:15:02

body will express genes properly , because

1:15:05

I think that you have genetics

1:15:07

epigenetics

1:15:09

, because the epigenetics are

1:15:11

the environment that are influencing the gene

1:15:13

function . But what's above epigenetics

1:15:15

, energetics . When the energy

1:15:18

is being produced right , it's going to influence

1:15:20

epigenetics , which is then going to influence

1:15:22

the genes . I think we've become

1:15:24

too gene-centric . We

1:15:26

need to go back to energy to

1:15:29

drive the environment to

1:15:31

get the genes to express . Superchromatosis

1:15:35

is an enigma in that a

1:15:37

heme

1:15:40

diet will correct it , but I think you

1:15:42

nailed it . You're getting

1:15:44

other nutrients in that process . You

1:15:46

might also be getting more

1:15:49

animal-based fat . The

1:15:51

part that people need to understand is that there are

1:15:53

two critical pumps

1:15:55

that run the copper

1:15:58

enzymes . One

1:16:00

pump , called ATP7B

1:16:02

, makes soloplasmin

1:16:04

. The other pump is called ATP7A

1:16:07

. It makes all the other

1:16:09

copper enzymes . It's amazing

1:16:11

what it does , but both of those

1:16:13

pumps are activated

1:16:16

by retinol . It's actually

1:16:18

retinoic acid . It's a hormonal

1:16:20

form of retinol . That's

1:16:24

buried in the research Cousins

1:16:26

and Barber 1987 . One

1:16:30

little sentence says it all . That

1:16:33

is the cornerstone of truth . That's

1:16:35

not taught in doctor school is that

1:16:37

these pumps need retinol

1:16:40

in order to load the key

1:16:42

enzymes to regulate the iron

1:16:44

, to allow for proper regulation

1:16:47

of the system . We

1:16:51

live in a fat-free diet now

1:16:53

. Most people are afraid of fat

1:16:55

. That

1:16:57

all started in 1955 when

1:16:59

Eisenhower had his first heart attack . Ansel

1:17:02

Keys flexed his muscles and said we've

1:17:04

got to get cholesterol out of the diet . We

1:17:08

can go into all the controversy of that . What

1:17:11

they were really doing was eliminating retinol

1:17:13

. They

1:17:16

knew back in the 20s how important retinol was

1:17:18

. It took

1:17:20

a generation to be eliminated from

1:17:22

our diet . There's just been this gradual

1:17:25

erosion of the nutrient

1:17:27

density of our food , which I

1:17:29

think you understand , and

1:17:31

you advocate people going back to a

1:17:33

more ancestral diet to get

1:17:36

the nutrients that our body is designed

1:17:38

to run on . That's really what

1:17:40

it comes down to .

1:17:42

Yeah , when I'm hearing copper

1:17:44

requires retinol to function

1:17:46

, I immediately think of the

1:17:48

food foods that a code will

1:17:50

have , rich source of both copper and

1:17:52

retinol . That's

1:17:55

liver , that's a ruminant liver . The

1:17:57

other enzyme that my listeners

1:17:59

will know has a key link

1:18:02

to retinol and vitamin

1:18:04

A is the photoreceptor

1:18:07

system . All of the photoreceptors

1:18:09

are bound covalently

1:18:12

to retinol . When we're exposed

1:18:14

to a whole bunch of artificial

1:18:17

blue light , it basically destroys

1:18:19

that linkage and causes

1:18:21

all kinds of havoc inside the

1:18:23

cell . I'll

1:18:27

make a couple points about the hemochromatosis

1:18:30

. It sounds that , or

1:18:33

maybe I'll ask you how

1:18:36

can we identify copper deficiency and how

1:18:39

can we best replete

1:18:41

copper , given what you've said ?

1:18:45

Just to reinforce what you just said about the retinol the

1:18:47

retinol being

1:18:50

stored in the liver supports the

1:18:52

retinol of the eye . When

1:18:55

did they first know about that ? Early

1:18:57

1920s

1:19:02

. The

1:19:06

key is I'm just having a senior moment , Max

1:19:08

, I'm sorry . I'm sorry , I didn't make that point . No

1:19:10

, I can't remember what question you were asking me

1:19:12

. That's okay .

1:19:14

I'll also make the point that isotretinol

1:19:16

is a retinoid . It's a synthetic retinol

1:19:18

. There's evidence that

1:19:20

it can interfere with vision in certain

1:19:23

patients who take this medication for acne

1:19:25

. That's exactly right . There's a finely

1:19:27

tuned system here with

1:19:29

regard to the body's handling

1:19:31

of these enzymes and these

1:19:33

cofactors . It's

1:19:35

not surprising to me that people could become copper

1:19:38

deficient if they're not including nutrient-dense

1:19:40

sources of food . They're not

1:19:42

including liver , they're not including glass-fed

1:19:45

butter , they're not including deep-sea fish , all

1:19:48

these important sources of vitamin A . I'm

1:19:50

talking about preformed retinol , I'm talking about beta-carotene

1:19:54

, or this idea that we can get

1:19:56

our vitamin A needs met

1:19:58

through plants . It's

1:20:01

just not true . Maybe riff on that for

1:20:04

a bit more if you could .

1:20:05

Sure , in order to restore copper

1:20:08

. It's really important . I

1:20:10

came across some research just a

1:20:12

few weeks ago which was fascinating . I

1:20:17

grew up in Baltimore . My

1:20:20

nickname is Baltimorely . We

1:20:23

bought our dairy from

1:20:26

a company called Cloverland

1:20:28

. Dairy . Bear with

1:20:30

me , max , I'm not a singer , but I want to

1:20:32

share this jingle with

1:20:34

your listeners Milk and butter

1:20:37

and eggs and cheese Fresh

1:20:39

from the farm to you , if you

1:20:41

don't own a cow , call Cloverland

1:20:43

now Northfield 92222

1:20:47

. I first heard that , or I first remember hearing

1:20:49

that , when I was four years old . That

1:20:51

was 67 years ago . That

1:20:53

jingle for some reason just got stored . It's

1:20:56

critically important . With

1:20:58

the article I just found a couple weeks ago

1:21:00

Back to James McCarge

1:21:02

, 1925 , university

1:21:06

of Kentucky , he's identifying

1:21:09

the foods that

1:21:13

have copper . But

1:21:15

they also are rich in retinol Whole

1:21:19

milk , butter

1:21:21

, eggs and

1:21:24

the cheese that they're talking about is

1:21:27

curd cottage

1:21:30

cheese made from curd . How do you spell

1:21:32

curd Cu-rd

1:21:35

right ? Gotta spell it right

1:21:37

. And so our ancestors

1:21:40

depended upon that

1:21:42

basic diet . Daily

1:21:44

they were getting exposure to whole

1:21:46

milk , butter , eggs and

1:21:48

cheese , and then once a week they were

1:21:50

eating liver and they were fine

1:21:52

Back in the 30s . Back

1:21:55

in the 30s , the average intake

1:21:57

of copper was 4 to 6 milligrams

1:21:59

of copper a day . By

1:22:02

the 60s it had dropped to

1:22:04

2 to 5 , and now

1:22:07

we're supposed to believe that we can

1:22:09

get by on 9 tenths of 1 milligram

1:22:11

of copper a day . That's a complete

1:22:13

violation of the design

1:22:16

of our body and the design of our metabolism

1:22:18

. So what

1:22:20

we're bumping up against , unfortunately

1:22:22

, is we

1:22:24

buy unprocessed dairy

1:22:27

from a farmer about 15

1:22:29

miles from where we live . Milk

1:22:32

is not supposed to be white , it's supposed

1:22:34

to be yellow . This is beautiful

1:22:37

yellow milk and the

1:22:39

butter is very rich with . Obviously

1:22:42

it's got a lot

1:22:44

of beta carotene . Why is the cow important

1:22:46

? Because it turns beta carotene into retinol . Thank

1:22:49

you , cow , for that . Eggs do

1:22:51

the , or chickens do the exact same

1:22:53

thing . Eating bugs and grass

1:22:55

Turn that beta carotene into

1:22:58

retinol . Thank you , little chickens . And

1:23:00

people don't know that that chemistry is taking place

1:23:02

inside these animals' body . But I

1:23:04

think the challenge we've got now , max

1:23:06

, is to

1:23:11

your earlier points about glyphosate

1:23:13

. I'm really freaking out about

1:23:15

glyphosate , even within

1:23:17

the regenerative farming movement . I

1:23:20

have tremendous respect for the farmers

1:23:22

who are trying to bring us back to

1:23:25

what our ancestors took for granted

1:23:27

. But the thing is it's in the air , it's

1:23:30

everywhere , it's so pervasive

1:23:33

in the soil and it's like there's

1:23:35

a wow factor to it and there are ways to

1:23:37

correct it . But how

1:23:39

many farmers are taking the time

1:23:42

and the discipline to

1:23:44

make that happen ? So I think , the

1:23:46

traditional sources of copper

1:23:48

. You have to be careful . A

1:23:51

lot of people rely on nutrient

1:23:53

tables that they go to online . Do

1:23:55

you know when those nutrient tables were last updated ? It was

1:23:57

in the 1950s . They

1:24:00

have all sorts of eye candy now . They look really

1:24:02

cool online , but the raw

1:24:05

data hasn't been changed since

1:24:08

the 50s . And so

1:24:11

these historical sources nuts

1:24:13

, seeds , organ meats

1:24:15

, shellfish these were

1:24:17

all very rich sources of copper

1:24:19

. Do they still exist today ? Not

1:24:23

in the same way that they did 50 to

1:24:25

100 years ago . And so within

1:24:28

the RCP , we're very focused

1:24:30

on an ancestral diet . We're

1:24:32

very focused on getting the right nutrients . But

1:24:35

what we're also realizing ? When we first

1:24:37

started it , we relied on

1:24:40

organ meats as a source of copper

1:24:42

. What one of my students

1:24:45

did ? A very , very

1:24:47

enterprising individual . She took

1:24:49

the leading brand of

1:24:51

desiccated liver and

1:24:54

she sent it to a lab to

1:24:56

see what the mineral composition was

1:24:58

. And , according to the nutrient table

1:25:01

, there should be 9 milligrams of copper

1:25:03

and 3 milligrams of iron . She

1:25:06

got the results back from the analysis , it

1:25:09

was reversed there was more

1:25:11

iron than copper , and

1:25:13

that was sort of a shock to the to

1:25:15

the reality of what we're up against , and

1:25:18

so it was really once

1:25:20

I realized what 2020 was

1:25:23

. It was an IQ test , as we talked about

1:25:25

earlier . The

1:25:27

next year , I

1:25:29

developed a in partnership

1:25:32

with a nutrient company , formula

1:25:34

IQ . I developed something

1:25:37

called recuperate , and

1:25:39

I think what people need to come to terms

1:25:41

with is we do need to supplement copper

1:25:45

in our diet beyond the

1:25:47

foods and forgive

1:25:51

me if I sound like a supplement whore

1:25:53

I'm not . What I'm really focused

1:25:55

on is people need to get this nutrient

1:25:57

, this critical nutrient , back into

1:25:59

their metabolism , and we

1:26:02

chose to do it in a food-based form . There's

1:26:04

desiccated liver , there's spirulina

1:26:07

, there's a pinch of tumeric

1:26:09

and there's copper , copper

1:26:11

bisglycinate , and it's a

1:26:13

very bi-available form of copper

1:26:15

. I think people need

1:26:17

to realize . I've

1:26:19

got diabetic clients

1:26:21

, type 2 diabetic clients , and

1:26:26

I'm sure you have clients who are struggling

1:26:28

with their blood sugar . Did

1:26:30

you know that blood sugar is

1:26:32

a copper issue , that it's when

1:26:34

it's rising , there's a lack of copper in the body . You've

1:26:37

been trained that it's an insulin issue . Right , it's

1:26:39

actually a copper issue . That research goes

1:26:41

back into the 30s and 40s and 50s

1:26:43

. But the thing is it

1:26:47

turns out that children

1:26:50

, mankeys , children

1:26:52

mankeys' disease are

1:26:54

very copper deficient . They're

1:26:56

the most glucose intolerant

1:26:58

people on the planet . They have

1:27:00

no copper and so the

1:27:03

copper issue is really central to this blood

1:27:06

sugar dynamic . And so

1:27:08

people I've

1:27:10

got clients who type 2 diabetics taking

1:27:13

5 and

1:27:15

6 of my supplements

1:27:17

which have 2 milligrams of copper in them and

1:27:21

they have control over their blood sugar

1:27:23

for the first time in their adult life . And

1:27:26

it's like I didn't tell them to do that . I

1:27:28

say take one , maybe two , but

1:27:31

many of my clients are now realizing one , they're

1:27:33

on their own . It's kind of like this 100th

1:27:36

monkey syndrome . There's this vibe

1:27:39

out there that we need more copper and

1:27:41

they are beginning to get control of their

1:27:44

blood sugar , which is then allowing them

1:27:46

to wean off of the symptoms

1:27:48

of metabolic

1:27:51

syndrome . Yeah , go ahead

1:27:53

.

1:27:53

I would just imagine they're not eating a standard American

1:27:56

diet with that copper

1:27:58

supplementation . I'm guessing they're eating also a pre

1:28:00

ancestral type diet at the same time

1:28:02

. Absolutely .

1:28:04

Absolutely Important component

1:28:06

.

1:28:06

Yeah , the point I want to make

1:28:08

is that the I

1:28:10

think life state is and the wider

1:28:13

use of industrial herbicides is

1:28:15

this probably one of the biggest impacts

1:28:17

on both health and human health and

1:28:19

environmental health that no one's talking about . And

1:28:22

you know , I

1:28:25

think the narrative around environmentalism is

1:28:27

kind of has been hijacked to

1:28:29

myopically focus

1:28:31

on one product

1:28:33

which happens to be a waste

1:28:35

product of human respiration

1:28:39

, where we're turning a blind eye

1:28:41

to the destruction

1:28:43

of soil microbes

1:28:46

, the destruction , the chelation and deprivation

1:28:49

of these trace minerals from soil

1:28:52

and the consequent effects on

1:28:54

the food nutrient density . So

1:28:56

, and that's a massive topic

1:28:58

, and I think part of the

1:29:00

job of my , or one of my hopes with

1:29:02

this podcast is to educate farmers

1:29:04

and to get them thinking

1:29:07

about the consequences of participating

1:29:09

in an industrial food system that

1:29:11

is contributing to the poisoning of the

1:29:13

commons , that is contributing to the commoditization

1:29:16

of the food supply and the

1:29:18

subsequent , you know , metabolic

1:29:20

and nutritional , micronutritional bankruptcy

1:29:22

of populations . I

1:29:26

think that people can still

1:29:29

make the right choice in terms of

1:29:31

sourcing from local farmers and I think

1:29:33

that is still going to be

1:29:35

the best bet , and I would encourage people to

1:29:37

maybe do some testing and

1:29:39

I think the more access we could have to nutrient testing

1:29:41

and things like deuterium , things like

1:29:44

iron , things like

1:29:47

fatty acid profiles , glyphosate

1:29:49

, the better . We could make

1:29:51

informed choices and we could even

1:29:53

probably guide the agronomist

1:29:57

use of trace minerals in the

1:29:59

land to therefore increase the

1:30:01

nutrient density of the

1:30:03

food . If we can identify soil deficiency

1:30:05

, then we can then make steps to

1:30:08

improve that . My only hesitation with supplementing

1:30:10

copper in a supplement

1:30:13

form is again is

1:30:15

it in context of

1:30:17

those cofactors ? And two , does

1:30:19

it contain deuterium ? Have we deuterium

1:30:22

depleted that

1:30:24

supplement ? Because I wouldn't want to kind of be

1:30:26

giving people copper which they might need , but also

1:30:28

be giving them an extra hit of deuterium

1:30:30

that they didn't need .

1:30:33

Yeah , that's a fair comment , and

1:30:35

I can't speak to the deuterium side . I

1:30:38

take a slightly different . I

1:30:40

think you alluded to your conversations

1:30:43

with Stephanie Seneff , and one

1:30:45

of the most riveting conversations I had with her

1:30:47

was April of 2018 . We

1:30:50

were at a breakfast table

1:30:52

together and she leaned forward and she said Morley

1:30:54

, would you like to know why glyphosate

1:30:56

is so hard on copper metabolism ? I

1:30:59

thought I had died and gone to heaven , but

1:31:02

you made the point that

1:31:04

there's a relationship between the

1:31:06

clearance of deuterium and copper

1:31:08

deficiency . I think it's important

1:31:11

for people to know that these dysfunctional

1:31:14

metabolites may just be

1:31:16

an expression of a lack of this

1:31:18

critical metal inside

1:31:20

our body . I

1:31:23

can't speak to what the deuterium

1:31:25

status is of that supplement , and that's

1:31:27

not the only one . There's copper creams

1:31:30

out there that people can use . I

1:31:33

think it's important for people to stretch their

1:31:35

understanding of how important

1:31:38

this mineral is , and

1:31:40

there's been a century-long campaign

1:31:42

to lower its presence on

1:31:45

the planet . It was back to

1:31:47

the First World War . They

1:31:49

had a lot of armaments they had to get rid of . After the First

1:31:51

World War , what did the armaments have ? Npk

1:31:54

. Oh well , let's turn that into a fertilizer

1:31:56

for the farmers , not

1:31:58

knowing that that NPK was blocking

1:32:00

copper uptake in the root system . That's

1:32:03

important to know . That's

1:32:05

the genius of soil

1:32:08

grass cancer . André

1:32:11

Fawcet that book was amazing to read

1:32:13

Again , biochemist who was

1:32:15

a dairy farmer as a hobby

1:32:17

, and he was the one who figured

1:32:19

out oh , the soil

1:32:22

doesn't have the copper , it's not getting into the milk

1:32:24

, it's not getting into my customers and they're

1:32:26

getting cancer . That's a really riveting

1:32:28

series of connections for people to

1:32:30

make that they may not have known otherwise

1:32:33

, but he figured that out in the 1950s

1:32:36

. And so the thing is that was all pre-pesticides

1:32:40

that we're talking about . One

1:32:42

of my colleagues told me that glyphosate

1:32:45

is actually the ninth most toxic chemical

1:32:47

that's used in farming . I'm like what

1:32:49

? I can't imagine what the other eight are , and

1:32:52

so it's just again . We've

1:32:54

got to put it into the context . How is

1:32:57

that affecting the microzymal

1:32:59

balance , the yeast

1:33:01

and the bacteria that are supposed to be communicating

1:33:04

with each other , getting the nutrients

1:33:06

into the soil , into the root system ? Excuse

1:33:08

me , and you're

1:33:11

absolutely right . We should be doing more testing , both

1:33:14

of the soil and

1:33:17

the food and the

1:33:20

human eating the food . And

1:33:22

the testing for

1:33:25

copper and iron is at a very rudimentary

1:33:27

stage . Max , there are eight

1:33:29

tests

1:33:32

that you can do to measure the bioavailability

1:33:35

of copper . How many

1:33:37

of them are barred by the

1:33:39

Food and Drug Administration here in the States ? All

1:33:42

eight . And so we're

1:33:45

not supposed to know the bioavailability

1:33:47

of our copper , we're just supposed to know that we need

1:33:49

more iron , which is that

1:33:51

is so pedestrian and

1:33:54

ill-informed that people have got

1:33:56

to get off this iron bandwagon

1:33:58

. I think you know that . But

1:34:01

they need to start to recognize

1:34:03

the critical biochemical

1:34:06

, physiological role that

1:34:08

goes back to the beginning of time for

1:34:11

being able to harness iron

1:34:13

and oxygen at the same time . Iron

1:34:17

mass per pro-oxidant on the planet

1:34:19

, oxygen , second most reactive

1:34:21

element . And what do they like to do ? They

1:34:23

like to play together and what do they create

1:34:26

? Rust . And

1:34:28

so people need to realize that the

1:34:30

plaque and all the dysfunction inside

1:34:32

their body is an expression

1:34:34

of rust that we recognize outside

1:34:36

the body . Just , we never been told

1:34:39

that that rusting process was happening inside

1:34:41

our blood vessels and our

1:34:43

nerves and our tissue , and

1:34:46

so I think people need to

1:34:48

the test that we do within

1:34:50

the RCP community . It's

1:34:52

called the Full Monty Iron Panel

1:34:55

and there's panels available

1:34:57

in Australia and in Europe and here

1:34:59

in the States and people . There's

1:35:02

about 13 different components

1:35:05

to that test and we're looking at

1:35:07

different measures

1:35:09

of iron , we're looking at copper , we're

1:35:12

looking at ceruloplasma , we're

1:35:14

looking at urag acid Urag

1:35:16

acid building in a body is a clinical

1:35:19

sign of copper deficiency . We're

1:35:22

looking at vitamin A and vitamin D and

1:35:24

the relationship between the two and

1:35:26

a variety of other factors

1:35:28

, and people can begin to

1:35:31

get a deeper understanding

1:35:33

of their basic mechanics

1:35:37

, mineral mechanics , from

1:35:39

that blood test . And it's a very

1:35:41

easy test to do and it's just . It gives

1:35:44

the practitioner and the patient tremendous

1:35:46

insight about the ease and

1:35:48

efficiency of their energy

1:35:50

producing ability inside their body .

1:35:54

Yeah , fascinating , and we'll include that information

1:35:56

for people who are interested in diving down

1:35:58

. One last question for you , Molly Do

1:36:01

you ever do ? Have you ever looked into

1:36:03

a peripheral blood smear ? Because you

1:36:06

know Dr Cruz said once that the

1:36:08

kind of thing he's interested in is looking

1:36:10

at the oxidation state of iron Like

1:36:12

that in terms of examining

1:36:15

a blood smear . Have you ever done

1:36:17

that , and have you ever gleaned any kind of useful information

1:36:19

about copper or iron status from that test

1:36:21

?

1:36:22

No , I've never done the peripheral blood smear

1:36:24

. I would love to delve

1:36:27

into that . But what

1:36:29

I do know is that a lot

1:36:31

of people suffer from neuropathy in

1:36:35

their peripheral tissue and I

1:36:37

first connected with Dr Clavet

1:36:40

, who I alluded to earlier . It

1:36:42

was probably 10 years ago and

1:36:45

it was very gracious to take my

1:36:47

call and we've talked many times since then

1:36:49

. But he said

1:36:51

Moorley , if any of your

1:36:53

clients ever

1:36:55

present with any form of neuropathy

1:36:58

he said it's

1:37:00

a clinical sign of copper deficiency

1:37:02

. And when

1:37:05

someone of that stature makes a statement like

1:37:07

that , I take note and I've all helped

1:37:10

. A lot of people realize that that nerve

1:37:13

sensation that they were having is really

1:37:15

just a dysfunction and a deficiency

1:37:17

of the mineral . And

1:37:19

so I don't know the components

1:37:21

of a peripheral blood smear but I'll look into

1:37:23

it and see what I can glean

1:37:26

from that . But I'm pretty confident

1:37:28

that iron

1:37:31

is not being regulated properly in

1:37:33

that blood smear . The oxidation

1:37:35

state is probably not being regulated properly

1:37:37

in that blood smear and

1:37:39

it's going to go back to a series of

1:37:42

copper enzymes and their

1:37:44

dysfunction because they're not adequately energized

1:37:47

. It would be my initial

1:37:50

comment .

1:37:52

Yeah , and I would add in B12 replacement

1:37:54

. And if someone presents to me with peripheral

1:37:57

neuropathy , I'd definitely be checking their

1:37:59

serum B12 , too , which is definitely

1:38:01

a possible cause , additionally , of peripheral

1:38:03

neuropathy . I

1:38:05

think this has been a very good one

1:38:08

.

1:38:09

Do you know that you've heard of the intrinsic

1:38:11

factor ? Yeah , yeah . What

1:38:15

is the intrinsic factor called it's

1:38:18

protein ? It's a transport

1:38:20

protein called cubulin . It's

1:38:22

copper dependent it's

1:38:25

copper dependent

1:38:27

.

1:38:28

There you go there you

1:38:31

go .

1:38:31

No , I said that the symptoms of B12

1:38:33

deficiency and copper deficiency

1:38:36

are almost identical , max , and

1:38:39

so that's important for people to realize the

1:38:43

vitamin B9 folate

1:38:46

. One of my conversations with Dr Clavage

1:38:48

years ago I said I have this

1:38:51

theory that all the B vitamins require copper

1:38:53

and they regulate iron . He

1:38:55

said well , more or less , that's a very provocative theory

1:38:57

so I can't refute it or defend

1:38:59

it . He said but what I can tell you for a

1:39:01

fact is

1:39:04

that B9 is

1:39:06

copper dependent . Well

1:39:08

, when you think about what B9 does in

1:39:10

the production of

1:39:13

vitamin D , in the breakdown

1:39:15

of vitamin A , your

1:39:17

whole understanding of the mechanics of

1:39:19

those fat-soluble vitamins changes in

1:39:22

a flash because

1:39:24

you realize , oh , b9 , it's

1:39:26

reacting to the sunlight . Oh , it must

1:39:28

be the copper inside the B9 that

1:39:31

is attracting the

1:39:33

sunlight . It completely changes your

1:39:35

understanding of the dynamics of the chemistry .

1:39:37

Yeah , and that's another thing that

1:39:39

Kruse has talked about is the non-visual photoreceptor

1:39:42

function of vitamin B12 . And

1:39:44

, yeah , at the core of

1:39:46

a lot of these visual

1:39:49

properties is these minerals

1:39:52

. So , yeah , it's

1:39:55

a fascinating conversation

1:39:58

that we've had . Molly , thank you very much and

1:40:00

I'll include those If you can send me those . There's

1:40:02

that information . I'll include that in the show notes

1:40:04

. And there's a lot we haven't

1:40:06

even talked about . We haven't talked about iron dysregulation

1:40:10

as it relates to cardiovascular disease , and perhaps

1:40:13

we could talk a bit more about metabolic syndrome in another

1:40:15

time , and obviously , magnesium too

1:40:17

. So lots for people

1:40:19

to think about and yeah , so thank

1:40:21

you very much for your time and I guess , yeah

1:40:23

, we'll definitely have to talk again .

1:40:26

I look forward to it . I really appreciate the time

1:40:28

and the exchange has been fascinating .