3:40

Today I am speaking with Dr Laszlo Boros

3:43

. He is a former professor of pediatrics

3:45

at UCLA , a research scientist

3:47

and world expert on deuteronomics

3:50

. Deuteronomics refers to the study

3:52

of deuterium , the heavy isotope

3:54

of hydrogen , and how it interacts with

3:56

biological systems . This is an

3:58

almost two-hour technical interview in

4:00

which we delve deeply into the role of deuterium

4:03

in causing metabolic disease and

4:05

the deposition of visceral fat . Dr

4:08

Boros takes us down to the level of the mitochondrion

4:10

and explains exactly how foods

4:12

enriched in deuterium , such as processed

4:14

carbs and seed oils , contribute

4:17

to metabolic dysfunction by wrecking

4:19

the ATPase nanomotors in

4:21

the inner mitochondrial membrane . While

4:24

we talk a lot about mechanisms , we also

4:26

discuss some practical steps

4:28

, so you will also find out why fully

4:31

grass-fed beef fat is the optimal

4:33

human energy source . This

4:36

is a topic that I continue to learn more about

4:38

, but , based on the information that Dr Boros

4:40

and previous guests , dr Jakruz and Sarah

4:42

Pugh have presented , it makes

4:44

a very strong case that metabolic disease

4:47

is a problem of excess deuterium

4:49

. Carnivore , low carb and seasonal

4:51

ancestral diet are effective in reversing

4:54

obesity , insulin resistance , diabetes

4:56

and all these metabolic diseases , precisely

4:58

because they are low deuterium

5:01

diets . So let me know what you think about

5:03

this and hope you enjoyed the

5:05

show . Dr Lazlo Boros

5:07

. Thank you for coming on the podcast . Thank

5:10

you very much for inviting . So

5:12

I am a family medicine

5:15

doctor and I am interested

5:17

, amongst other things , in how

5:19

we can prevent metabolic diseases

5:22

like obesity , like type

5:24

2 diabetes , fatty liver , all these kind of

5:26

things . And your research

5:28

and your perspectives using deuterium

5:30

are fascinating because I think

5:32

it can offer us a lot in terms of insight

5:35

into these problems . But , maybe

5:37

because this is such a niche topic

5:39

and it is sometimes

5:41

quite technical , I think it's worth starting

5:43

from the very beginning and in terms of explaining

5:46

people what deuterium is

5:48

, before we even go down the

5:51

rabbit hole of clinical implications

5:53

.

5:54

Sure , thank you again . So

5:56

deuterium

5:59

is practically the SUV in your driveway

6:01

or in your garage where you can fit

6:03

your passenger car any longer . So

6:06

it's a hydrogen . And that's

6:08

the beginning of this whole story

6:10

. Carbon and oxygen

6:12

make up the living organisms

6:15

as the most common atoms

6:17

or elements . Hydrogen

6:19

is the smallest of all and it

6:22

helps to transfer energy

6:24

and also provide chemical bonds between

6:26

oxygen and hydrogen and nitrogen

6:29

and sulfur and so on . But the most

6:31

common ones are carbon , oxygen

6:33

and hydrogen , and hydrogen is the

6:35

ping-pong bar that oxygen and carbon

6:37

is playing a ping-pong game . In the meantime

6:39

, obviously , photosynthesis

6:41

and biological oxidation

6:44

are connected to

6:46

hydrogen itself and

6:48

practically

6:50

deuterium is the

6:52

heavy or the large

6:54

medicine bar in the

6:57

baseball game , in the

6:59

sense that so practically

7:01

it's a heavy hydrogen , hydrogen

7:04

. The nucleus of hydrogen

7:07

is a proton , is made up

7:09

by a proton and there's an electron

7:11

spinning around it , and

7:13

the deuterons or deuterium , is a

7:16

proton and a neutron

7:18

and an electron , meaning that

7:20

the nucleus of the deuteron

7:22

is twice as heavy and

7:24

twice as large as the proton

7:27

and chemically behaves different

7:29

, meaning that in chemical bonds it requires

7:31

8 to 15 times more energy to

7:34

remove that where

7:37

hydrogen would be placed

7:39

. If it's replaced by deuterium , then

7:42

the chemical behavior of the molecule

7:44

is dramatically different , involving

7:47

metabolism and so on

7:50

. More importantly , deuterium

7:53

can get into mitochondria and

7:55

ATP synthase nanomotors

7:57

, where they actually behave

7:59

like a boy in a china store

8:02

or elephant in a china store

8:04

. Practically they break these very delicate

8:06

moving proteins and nanomotors

8:09

and , for that matter , there

8:11

are going to be a lack of

8:14

T-C

8:16

cycle or Krebs-Sendier-D-Cycle

8:19

metabolism , meaning

8:21

that there's going to be a molecular

8:23

or metabolic crowding

8:25

and , because the lack

8:27

of proper mitochondrial

8:31

function to burn fuel

8:33

completely , there

8:35

is going to be a buildup of various

8:38

organic molecules

8:40

, including fatty acids , glucose and so

8:42

on , and metabolic

8:45

diseases develop and

8:47

, based on the specific tissue presentation

8:50

, human diseases develop depending

8:53

on what kind of metabolic

8:55

and how severe the

8:57

metabolic defect is or how damaged

9:00

the mitochondria are and their

9:02

nanomotors because of deuterium

9:05

effect , which is again twice

9:08

as heavy and twice as large . When we look at

9:10

its nucleus , then hydrogen

9:12

is , and hydrogen is the most

9:14

common element in our system , in

9:17

our body , and it works and

9:20

it performs most of the work as

9:22

far as energy transfers and structural

9:24

chemical bonds . And replacing

9:27

hydrogen with deuterium has major effects

9:29

on protein structure , protein movements

9:32

and so on and the activity

9:34

of metabolic enzymes and the result

9:37

of all of these , we

9:39

develop various diseases

9:41

, disease processes that you

9:43

have to handle in your family

9:45

practice .

9:47

Yeah , thanks for that explanation and

9:49

just to zoom out and really

9:51

keep a big picture before we

9:54

delve into the weeds the mitochondria

9:56

for those who are listening are these little organelles

9:58

inside almost all your cells

10:01

that are the sites of energy

10:03

production in the cell . And

10:05

what Dr Lazer was talking

10:08

about is that these mitochondria

10:10

take energy inputs in the form of food

10:13

and they also receive the cytochromes

10:15

, or can also receive a light frequencies

10:17

, and they tunnel electrons

10:20

from the food and

10:22

use it to pump these hydrogens

10:24

against a gradient . So

10:26

imagine pumping water uphill and

10:28

then at that fifth , the

10:30

fifth cytochrome of that electron transport chain

10:32

. They're supposed to flow down

10:34

this gradient like the water , supposed to flow down

10:37

a hill and run through this nanomotor

10:39

and then allow us to make ATP

10:42

from ADP . But what Dr Borosz

10:44

just explained to you is that if we

10:46

use this heavy isotope of

10:49

hydrogen instead of H+

10:51

, if we use a deuterium , then that

10:53

basically wrecks the ability

10:56

of that nanomotor to spin efficiently . And

10:59

I talked to Dr Stephanie Senef andI

11:01

like to . Someone used

11:03

the analogy of

11:05

a fat kid going down a slippery slide

11:07

at a water park and kind of getting

11:10

stuck in the middle . But it's

11:12

really more than that because , as you've talked

11:14

about it , it's not only blocking

11:16

the nanomotor from spinning and therefore preventing

11:19

us from operating efficiently

11:21

, but it's actually destroying the ATPase

11:23

. Is that correct ?

11:25

That's right . And it's not only a

11:27

destruction but it's also a

11:29

permanent chemical bond

11:31

of these proton spinning amino

11:34

acids . That means it's

11:36

irreparable as

11:39

far as the damage is delivered . And

11:41

once these nanomotors stop

11:44

functioning , we cannot transfer

11:46

protons from carbons to oxygen

11:48

. And if that occurs , then

11:51

our cellular

11:53

level energy production system is diminished

11:57

practically and those cells become

11:59

a target of apoptosis

12:02

, or information

12:04

for that matter , and those cells

12:06

, because of cytochrome C , which is part

12:09

of the electron transport chain , signal

12:11

for self destruction

12:14

. Simply , that's what the organ

12:16

disease or organ damage

12:18

and chronic disease would actually line

12:21

up . There's practically

12:23

dying cells replaced by

12:25

fibrotic tissue or inflammatory

12:28

tissues and so on . And

12:30

because of the lack of organ

12:32

function or the

12:34

lack of your cellular functions that have

12:36

these organs to perform certain functions

12:39

that could be transport of certain metabolites

12:42

, it could be storage of certain organic

12:45

materials , fatty acids , glucose

12:48

, glycogen and so on , these cells

12:50

are missing

12:52

their functions , these cells are replaced

12:54

by fibrotic or inflammatory

12:56

tissues and then organ damage

12:59

sets in and chronic diseases develop

13:01

practically .

13:03

Yes , and I really like that framing

13:05

because it gives us a framework of understanding

13:07

how things going wrong at the basically

13:10

sub molecular level can end

13:12

up manifesting as a disease in

13:15

the entire organism . And I think

13:17

it's a great place to make a quick mention of Dr Doug

13:19

Wallace and he's basically theory

13:21

of the mitochondrial

13:23

bio-energetic etiology of disease , which is exactly

13:26

what you're talking about . And Dr

13:28

Doug Wallace has made the point that

13:31

the mitochondrial dysfunction

13:33

, when that happens , when the mitochondria

13:35

start failing , the energy output of the

13:37

cell obviously fails the cell's ability

13:40

to do its job , whether that's contract

13:42

as a cardiomyocyte , whether that's

13:44

to make insulin as a pancreatic

13:46

beta cell , whether that's to transmit

13:49

a signal as a neuron in the brain

13:51

. That fails when the mitochondria

13:53

inside the cell start failing

13:55

. So it's interesting

13:57

because when that mitochondrial efficiency drops

13:59

, then things like DNA repair

14:02

, the mitochondrial DNA repair , all these processes

14:04

start impeding and then you

14:06

get this kind of feedback

14:09

or this process , this cycle that leads to

14:11

that leads to apoptosis and

14:14

basically failure of the cell . Are

14:16

you familiar with Dr Wallace's work ? Are you

14:18

up to speed with that ?

14:20

I did hear about many of these

14:22

efforts . The new

14:24

way of looking at energy production

14:27

in mitochondria is not only ATP

14:29

synthesis . The deuteronomics

14:32

or the study of deuterium in

14:34

mitochondria is

14:36

changing every day , simply

14:39

because there's so much data and information coming

14:41

in . And right now what we are

14:43

working on is extending

14:46

the energy production scenarios

14:49

in mitochondria , not only

14:51

looking at ATP , but the

14:54

actual formation of metabolic water

14:56

, which is how oxygen

14:58

and hydrogen come together after

15:00

these nanomotors are power . Now

15:03

protons are necessary

15:05

for water formation from

15:08

food and the

15:11

result of this is 280

15:13

kJ per mole energy in the

15:15

form of heat when metabolic

15:17

water is forming the mitochondria

15:19

. In the meantime , there is an additional

15:22

20 to 30 kJ per mole

15:24

energy producing the form

15:26

of ATP-ATP synthesis

15:29

. But practically the majority

15:31

of heat energy that is produced

15:34

in mitochondria is because

15:36

of the electron transport chain activating

15:38

oxygen and the proton that falls

15:40

into the mitochondrial matrix

15:43

after powering these nanomotors , and

15:45

this is what we call the explosive gas

15:47

when oxygen and hydrogen joins

15:50

together . But it's very

15:52

controlled and very precisely controlled

15:54

in the mitochondrial matrix to the electron transport

15:57

chain and those

15:59

proteins or cytochrome

16:02

enzymes . Practically

16:05

it's a very delicate , controlled

16:08

, highly energy

16:10

yielding process by producing

16:12

metabolic water and also by

16:14

producing ATP in the process

16:16

. And they all depend on these

16:19

smooth work of these

16:21

nanomotors , because those are the ones that

16:23

are able to transfer from the inter

16:25

membrane space of the mitochondria , the

16:27

protons , into the mitochondrial

16:29

matrix . The metabolic water is

16:31

formed and in the meantime that the

16:33

Crap San Diode cycle

16:35

is absorbing or recycling

16:38

this metabolic water to fumarate

16:40

hydrates and citrate synthesis

16:42

and so on . So it's practically physics

16:44

connected with biochemistry

16:47

tunneling , which means

16:49

that one of the nuclear

16:52

atomic events linked

16:54

with biochemical reactions . So

16:57

it practically covers all

16:59

that is related

17:01

to what we know quantum physics and

17:04

electromagnetic radiation

17:06

and biochemistry . And this

17:08

is why so many people work

17:11

together on these scenarios , simply

17:14

because these include

17:16

and involve all major parts of

17:18

physics and biology , as you know .

17:21

Yeah , and for the listeners who

17:24

have followed my work up till now , we explored

17:26

these concepts in the first

17:28

instance with my series with Dr Jack Cruz

17:30

and essentially

17:32

how he described what is going on

17:34

in the mitochondria are oxidative phosphorylation

17:37

is the opposite of photosynthesis

17:40

and this idea that you know it's like

17:42

a spider on a mirror doing push-ups

17:44

it's this process , that what's happening

17:47

in the mitochondria is just a reversal of

17:49

the photosynthetic process , and

17:51

the output of what we've described

17:53

is obviously ATP , but it's more than that

17:55

. It's carbon dioxide and it's this metabolic

17:58

water , and the unique idea

18:00

of the metabolic water is that it's deuterium , depleted

18:02

. I think that is the key point and

18:04

summarizing what we've talked about in the first set

18:06

.

18:06

It's important matter .

18:08

Deuterium free . Yeah , it's got no

18:10

deuterium in it .

18:12

What we desire is that the

18:14

outside is 155

18:17

ppm and the most inner part

18:19

of your cells are deuterium free and

18:21

the gradient goes in and between through

18:24

various filtering biochemical mechanisms

18:26

. And this is what practically biology

18:28

or medicine should be , as

18:31

far as understanding very basic principles

18:33

and concepts in energy

18:36

production for that matter . But

18:38

we prefer the least

18:40

amount of deuterium in mitochondria

18:42

to prevent diseases , disease

18:45

processes .

18:46

Yeah , and it's

18:49

interesting because I guess we previewed in the

18:51

first 10 minutes . The biology

18:53

has evolved very , very specifically to preclude

18:56

deuterium from the whole process of energy

18:58

generation . I think that's the point that

19:01

you've made so far . If

19:03

people can understand that concept is

19:05

that for the cell to

19:07

operate optimally , we don't want this

19:09

heavy hydrogen in

19:12

the whole process . And whether we use the analogy

19:14

of the SUV trying to fit

19:16

into a small garage , whether we use the

19:18

analogy of the eight ball I

19:21

heard you use that analogy there the Q

19:23

ball , the big eight ball that doesn't fit down the

19:25

hole , whatever analogy you

19:27

want to use , and I think the key takeaway

19:29

point for the first part of this interview is that biology

19:32

doesn't like deuterium . And even

19:34

though deuterium is present naturally in 155

19:37

parts per million in the ocean and in the

19:39

environment , there's been specific

19:42

reasons why we have evolved

19:44

to not have deuterium

19:46

inside the , in a mitochondrial

19:48

matrix .

19:50

That's right and we need to

19:52

consider deuterium as a structural

19:54

element . So some structural

19:57

proteins like collagen , proline

19:59

deuterated prolines are

20:01

very important for animals

20:03

that live in harsh conditions

20:06

, under harsh conditions in environments . So

20:08

in structural proteins and this is why

20:10

we now talk about the regulation

20:12

of deuterium Deuterium has no

20:14

place in moving proteins , energy production

20:17

or enzyme reactions and

20:19

so on , especially when tunneling

20:21

comes into the picture . Now

20:24

, in structural proteins , in very small

20:26

amounts , in certain amino

20:29

acids , deuterium is a very

20:31

important stabilizing

20:33

element and , for

20:35

that matter , it can be

20:38

high , as high as as

20:40

a 315 parts per million

20:42

in cell

20:44

collagen , simply

20:47

because those animals have to dive and

20:49

come up at very

20:51

high speed and they have

20:53

to escape from predators and so

20:55

on . So their structural element , their

20:57

skeletal elements and their

21:00

collagen have to be modified

21:03

chemically to these demands

21:05

. So now we actually use

21:08

energy production

21:10

, covering mitochondrial

21:13

and proxysomal metabolism

21:15

and how they interrelate to one

21:17

another . That's a new aspect

21:19

of deuterium research and

21:21

we may cover this in

21:24

this conversation , based on

21:26

how deep you want to dig in to

21:28

this process . And for

21:31

the structural elements of our

21:34

body , we need to regulate

21:36

deuterium according to the

21:39

need of how stable and how

21:41

structurally durable those

21:43

elements need to be . So we are looking

21:45

at in biological samples from

21:48

zero parts per million

21:50

deuterium , which is the mitochondrial matrix

21:52

, up to 315 parts

21:55

per million , which is the collagen

21:57

proline of under challenging

22:00

living conditions and

22:02

environment . So in

22:04

between there's this

22:07

human deuteronomics

22:13

project where we actually use

22:15

these various wide

22:18

range deuterium distributions to

22:20

explain phenotype and to explain

22:22

disease processes , because

22:25

what we believe is human disease

22:27

is a tissue specific presentation

22:29

of a deuterium overload or

22:31

a deuterium dysregulation process

22:34

.

22:35

Yeah , and if we think about the two major

22:37

causes of human chronic diseases , it's

22:39

neurodegeneration , like

22:41

dementia and Parkinson's disease

22:43

, and cardiovascular

22:45

disease . So heart failure , atherosclerotic

22:48

cardiovascular disease , and I

22:50

don't think it's no surprise

22:52

or it makes sense , because these

22:55

two tissues are some of the most mitochondrial

22:57

rich tissues in the

22:59

organs in the body and the

23:03

heart , having between three and five thousand

23:05

mitochondria in every cardiomyosite . It

23:09

makes sense that if we're

23:11

getting failure of mitochondria

23:13

in those organs then that in a

23:16

long enough time frame is going

23:18

to manifest as disease

23:20

. I want you to just talk a couple

23:22

more instances of the physiological role of

23:24

deuterium in the body . So we've already

23:26

established that it can't be in moving

23:29

parts in energy generation inside

23:31

the mitochondria , but it might be useful

23:33

and it is useful in structural components

23:36

like collagen . Is there an in

23:38

between here where the body is also using

23:40

deuterium physiologically ?

23:44

Well , it depends on the species

23:46

and the challenging conditions

23:48

. And this is actually a paper

23:50

from the Collinska Institute by Dr

23:52

Roman Zubarev , who measured

23:55

deuterium in seal and

23:57

pellet green falcons

23:59

and swan collagen

24:02

and he found a huge variation

24:04

based on how challenging

24:06

these animals live

24:08

their everyday lives . The swan

24:11

, which just kind of swims

24:13

around the lakes and

24:16

eats some

24:19

plants they have

24:21

155 ppm in their collagen

24:23

. Obviously their life is

24:26

not very demanding or challenging

24:28

compared to seals and

24:30

pellet green falcons . The pellet green falcons

24:32

, they come down at 300-400

24:34

km per hour and they have to slow

24:37

down using their

24:39

wings in the last 40-50 meters

24:42

of their of their diet , so

24:44

that actually puts their wings

24:47

under extreme friction

24:49

forces and so on . So they

24:51

have to develop a collagen , a

24:53

protein that actually helps their

24:55

bone structure to do to

24:58

deal with this very demanding

25:00

frictional force . To

25:02

be able to do that it takes

25:05

deuterium up to

25:07

the range of 300 parts per million

25:09

. In the meantime these

25:11

animals , because they fly so

25:14

fast and they have to

25:16

climb so fast to do before

25:18

these dives , their muscles have to be

25:20

deuterium free , for that matter , than

25:22

animal rules , meaning that their glycolysis

25:25

is controlling food-based

25:29

deuterium to get into metabolic or

25:32

cytoplasmic water through

25:34

isomerase reactions these are actually

25:36

glycolysis related enzyme

25:39

reactions where actually deuterium discrimination

25:41

effect and this discriminated deuterium

25:43

can be loaded in some other parts

25:46

of the body or biochemical

25:50

reactions , for example protein

25:52

synthesis and hydroxy protein synthesis

25:54

, which will make these collagen

25:57

proteins and it's unique

26:00

to this protein structural protein

26:02

, and cancer cells like to use

26:04

this hydro deuterium protein

26:06

as well . So this is why the cancer

26:09

, the malignant tissue's

26:11

trauma is when you touch it . You

26:13

probably in medical school

26:15

you had to rotate in surgery oncological

26:18

, surgical , surgical surgical units and

26:20

you can actually tell by touching

26:22

tumors that they are almost like bone

26:25

or cartilage type

26:27

tissues and that's

26:29

because they accumulate deuterium in their

26:31

stroma and in their structural

26:34

proteins . So it seems that

26:37

knowing deuterium or

26:39

being aware of how deuterium

26:42

is distributed among species

26:44

and also in tissues , you

26:46

can actually describe a very

26:49

critical biological behavior

26:51

type of

26:54

situations and you can argue

26:56

based on deuterium content , what

26:58

to expect from that particular

27:00

tissue , how to operate in our

27:02

body .

27:04

That's a fascinating point . I

27:06

want to just make two quick points

27:08

. One is that the

27:10

body is if you look

27:12

at the TCA cycle and

27:15

for anyone who's taken chemistry

27:17

, whether that was in school or in university

27:19

, there's a long list of enzymatic

27:22

steps that are involved

27:24

in the whole process , and it

27:27

seems to me , and what you've talked

27:29

about in your lectures , is that the reason

27:31

for those steps is because the body is

27:33

selecting for proteam

27:35

over deuterium in terms

27:38

of those enzymatic

27:40

reactions . So is

27:42

that the chief reason why there are so many enzymatic

27:44

steps ? Is it solely to select against

27:47

deuterium in the mitochondria ?

27:50

That's correct . I actually gave talks

27:52

about this at UCL back in 2017

27:55

and 2018 , talking

27:57

about glycolysis

27:59

being a deuterium scavenging mechanism

28:02

, a deuterium sorting mechanism

28:04

through water exchange reactions

28:06

and proton exchange reactions from

28:09

cytoplasmic water , which

28:11

should be diluted

28:14

by matrix water to be

28:16

low in deuterium so you can actually

28:18

exchange deuterium between

28:20

compartments of your cells

28:22

. And that's right . Glucose

28:25

, for example , has 12 hydrogens

28:27

and glycolysis have 10

28:29

reactions and one

28:32

of those reactions in a lace takes

28:34

a whole water molecule out of glucose

28:37

. So practically what glycolysis does ? It

28:39

checks every hydrogen in

28:41

a glucose molecule and

28:43

replaces it with cytoplasmic

28:46

waters protons to

28:48

make sure that there is no deuterium

28:50

can actually enter the mitochondria

28:52

as using glucose as a trojan

28:54

horse . So practically it's

28:56

a disassembly of the

28:59

trojan horse to see what's inside

29:01

and then reassembling it

29:03

to take it to the mitochondria

29:06

. And the mitochondria is hydrating

29:08

the precursors , which

29:11

is pyruvate and acetylcoenzyme

29:13

A , and it adds metabolic

29:15

water through citrate synthase , through

29:18

aconitase and

29:20

through fumarate

29:24

hydratase as the water

29:26

consuming reactions

29:29

. But in reality every

29:31

99.9%

29:33

of every enzyme reaction in our

29:36

body uses water as

29:38

the chemical solvent or

29:40

water protons to perform

29:43

that particular reaction . So every

29:46

reaction in glycolysis

29:48

and every reaction , nine

29:51

reactions of the crepseniodicycle

29:53

or the TCA cycle , use water

29:56

for that matter . So water deuterium

29:58

content and water deplete

30:01

it . Deuterium deplete

30:03

a water in chemical reactions

30:06

is a key for those reactions

30:09

to operate . So even though the

30:11

molecule itself does not

30:13

have or not necessarily deuterated

30:16

, if the water of our system

30:18

is deteriorated then those reactions also

30:20

again slow down . So deuterium

30:24

goes far farther

30:26

than we would expect . Just simply

30:29

looking at exchange

30:32

reactions , it is actually

30:34

kind of the medium

30:36

or the chemical

30:38

solvent water , and

30:41

that's why our body is made up of

30:43

so much water , because we have to provide

30:45

a solvent base for all these

30:47

chemical reactions , biochemical

30:50

reactions . And if those are not

30:52

in a deuterium or low deuterium

30:54

environment depleted

30:56

or low deuterium environment or deuterium

30:59

free environment , if we talk about the matrix

31:01

those can cause chronic

31:04

diseases and they

31:06

can actually , if it's food based , the

31:09

deuterium overload , then it can actually

31:11

cause epidemics of chronic diseases

31:14

in populations that consume

31:16

the kind of the bad food

31:18

or diet .

31:20

Yes and I use this analogy

31:22

with Dr Senef is the fascinating

31:24

way that the body has evolved this checking process

31:27

which you've just described . It's almost

31:29

like you're burning a furnace with

31:31

timber , but you've

31:33

evolved this intricate inspection

31:36

process of the logs and unless

31:38

the log is perfect , the body

31:40

is going to discard that and it's not going to

31:42

allow that log to go down and get burnt

31:44

in the furnace because it's that important

31:46

to the function of the factory which

31:48

is the mitochondria . That mitochondrion

31:51

is that those logs are

31:53

just the right thing . If it's got a branch sticking out the

31:55

wrong way which is an analogy for deuterium

31:57

then it's like no , sorry , we

32:00

don't want that . It's a great point

32:02

, sorry , go on .

32:04

And this is very important from the tunneling

32:06

point of view , because in our system everything

32:08

happens by tunnel , meaning

32:10

that those very tight enzymatic

32:13

reaction compartments , they only

32:16

can achieve chemical reaction

32:18

to occur at especially such

32:21

speed if actually those protons are pushed

32:23

around physically by other

32:25

protons and if there's a deuterium

32:27

in between , if there's a log that

32:29

stands out in different

32:32

, like as is supposed to , it can actually

32:34

stop the whole process .

32:36

Yeah , and that's a great place to talk about

32:38

fats , because glycolysis

32:40

is a process of checking these carbohydrates

32:43

for deuterons . But

32:45

what is unique about the

32:47

fatty acid molecules that make them

32:49

problematic for this process ?

32:52

Fatty acids are produced from citric acid

32:54

, which are formed in

32:57

mitochondria , so they are low in duty

32:59

. That's why fatty acids don't

33:01

have to go through glycolysis , because

33:03

our cells expect fatty

33:05

acids to be low in deuterium

33:07

, so for oxidation they are appropriate

33:10

, meaning that they can be

33:12

taken into the mitochondria , into the cell

33:15

, and into the mitochondria to this carnitane

33:17

transport proteins without checking

33:19

every proton or hydrogen

33:22

in those molecules , if those are deuterium

33:24

or not , or you don't have to

33:26

replace them with your metabolic waters

33:28

. Low deuterium protons

33:31

, so practically fatty acids

33:33

. Because nature or the creator

33:36

, I like to use both to

33:38

kind of help everybody to imagine

33:40

how this system work practically

33:44

. They it's designed

33:46

, or these reactions are designed

33:48

to kind of work

33:50

with a very efficient

33:53

, very effective deuterium

33:55

depleting mechanism when

33:57

it's necessary . Yet if

34:00

there's a perfect fuel , for

34:02

that matter it's animal based , grass-fed

34:05

, carnivore style , animal

34:08

saturated long chain fatty

34:10

acid which is very low in deuterium

34:13

, in the range of

34:15

110 ppm compared to 155

34:18

of glucose . That's

34:20

safe to use for both proxysomes

34:22

and mitochondria and for that matter

34:25

, your body has very quick access

34:27

to those because those don't have to

34:30

be checked . They are actually in

34:32

the 100 meter sprint run , they just

34:34

run . There are no blockages

34:36

or there's no gaze that they

34:38

have to hump over , and this

34:40

is why those are very

34:42

efficient fuels . Saturated

34:45

animal fat , grass-fed animal fat , is

34:47

so efficient fuel for our

34:49

cells and for our mitochondria because those

34:52

are low in deuterium and your

34:55

cells are able to

34:57

scavenge that

34:59

smaller amount of deuterium using

35:02

the ureocycle , using

35:04

various water exchange reactions in

35:07

the mitochondrial , in the TCSAC

35:09

and so on . So our biochemistry

35:11

is designed based

35:14

on deuterium intake and

35:16

deuterium scavenging and also

35:18

efficiency based

35:20

on oxygen availability and oxygen

35:22

transport . So practically it's a

35:25

stoichiometric method simply

35:27

just to deal with the right

35:29

, appropriate balance of

35:31

these systems

35:33

and mechanisms that include food , water

35:36

or nutrients that we take in oxygen

35:39

availability and

35:42

mitochondrial processes

35:44

to actually burn and make

35:46

these exchange reactions

35:49

, atomic reactions , efficient

35:52

without the participation

35:54

of deuterium itself . So

35:57

it's practically the key to health to understand

35:59

these processes and it's the key

36:01

to manage

36:03

chronic disease epidemics and

36:05

so on and to treat patients

36:07

individually using natural

36:10

patek or natural approaches

36:13

that actually limit the deuterium

36:15

intake through the appropriate food

36:17

incorporation .

36:19

Yeah , and I'm glad you brought up the grass-fed

36:21

meat and fat and we'll actually talk

36:23

about that a bit later . I'll just make a quick

36:25

flag and seed oils

36:27

which are polyunsaturated

36:30

fatty acids rich in fatty

36:33

acids , like linoleic acid . Are

36:36

they deuterium

36:38

enriched ?

36:40

At unsaturated bonds

36:42

. They are very low in deuterium based

36:44

on where they are from . If they

36:46

are actually natural or

36:49

industrial source , they

36:51

could have very different variations

36:54

or very different levels of deuterium

36:56

. If those are plant-based and

36:59

seed oil and those are not industrial

37:02

, gmo or fertilizer

37:04

or glyphosate treated plants

37:07

, naturally those

37:09

could be for certain species . Those

37:11

could be not for humans

37:13

, but for certain species those could

37:16

be useful substrates

37:18

. Their microbiome have to be

37:20

adopted to the food

37:24

that they consume . It

37:26

can be even fruit-based in certain

37:28

birds . That's when they

37:31

have a very high turnover of

37:34

microbiome , for

37:36

that matter . But

37:38

let's say this

37:41

way they poop a lot . But practically

37:43

as far as humans are concerned

37:45

, we are designed to eat

37:48

animal fat

37:50

, saturated long chain fatty

37:52

acids , preferentially

37:55

coming from bone marrow . This

37:57

is what we believe . The prehistoric men

38:00

anthropologically started

38:04

consuming brain

38:06

and bone marrow of animals

38:09

, carcasses that were left behind by predators

38:11

, because they had tools to break through the

38:14

bony skeletal structures

38:16

. Our species

38:19

or our societies

38:23

, going back to caveman's

38:25

time , prehistoric time , were all

38:28

dependent on this saturated

38:30

loaded-tium animal-based

38:34

, grass-fed fat

38:37

source . This is how mitochondria

38:40

adopted to the food

38:42

and environment . But

38:45

prehistoric men lived in and the cavemen

38:48

lived in . It's only since

38:50

the industrial

38:52

agricultural processes

38:54

set in is when chronic

38:56

diseases occurred as

38:59

we know , now

39:02

More food items are

39:04

replaced on the shelf by

39:07

processed industrial food items

39:09

, more severe chronic

39:11

disease epidemics are .

39:14

Yeah , great , we'll come back to that because I want

39:16

to delve into that a bit deeper Before we finish

39:19

. On this idea of physiological

39:21

and partitioning of deuterium

39:24

in the body , you've mentioned

39:26

that in your slides . That deuterium

39:28

is present in the serum at

39:30

around 12 millimoles , which

39:33

is higher than the other

39:35

ions in the body

39:37

. Is the body specifically

39:39

keeping deuterium there , or explain

39:42

to us the role of deuterium

39:44

specifically in the blood ?

39:48

Actually it's a lot higher because

39:50

if you look at potassium

39:53

, eukacium or

39:55

other inorganic elements , those

39:58

are actually one

40:00

tenth or one fifth of the

40:03

concentration of deuterium . Deuterium

40:05

is very common and very abundant

40:07

in circulation simply because

40:09

there are so many water

40:12

and hydrogen based

40:14

molecules circulating

40:16

and practically this is how the body gets

40:19

rid of deuterium through circulation

40:22

and kidney function urine , saliva

40:24

, sweat and poop

40:28

and

40:30

so on . So practically our

40:33

plasma is where the

40:35

first significant

40:38

deuterium exchange occurs

40:40

, in red blood cells which use

40:43

glycolysis to produce

40:45

lactic acid and in the meantime they

40:47

keep these NADP

40:49

molecules reduced because they have

40:51

to overcome the effect of oxygen

40:53

, so they have to have reducing equivalence

40:56

. So this glycolysis

40:58

that takes place in

41:00

red blood cells , very

41:03

high flux , provides lactic

41:05

acid with high deuterium . That gets

41:07

into the liver and through the core cycle

41:09

it's returned as

41:11

glucose . But in athletes

41:13

there's a vermicillin bacteria

41:16

that starts using this

41:18

high deuterium lactic acid to produce

41:20

propionic acid , which is a ketone body

41:23

. It's a low deuterium containing ketone

41:25

body which can actually replace

41:28

the core cycle to

41:30

deplete the deuterium very efficiently and

41:33

because of the high water content

41:35

of the plasma , which is 99

41:38

. Above percent , deuterium

41:42

matches practically your

41:44

body's ability

41:46

to deplete deuterium

41:49

by getting rid of through circulation

41:51

of deuterium

41:53

, mostly by dissolved urea

41:56

and uric

41:58

acid . So simply , these are

42:00

all part of a very complex

42:02

biochemical process , but very simple

42:05

biochemical process . If we just talk

42:07

about deuterium depletion and overcoming

42:09

deuterium , overloaded tissues and

42:12

it's definitely the most abundant

42:14

inorganic element in our

42:16

blood and it should be

42:19

measured just like everything else

42:21

or anything else in the plasma

42:23

. If you go to a lab

42:25

study or a

42:28

clinical or diagnostic panel

42:32

of blood work , then

42:34

those inorganic elements are

42:36

part of your history and

42:39

that's how deuterium

42:41

should be approached to

42:43

measure it in blood and in

42:45

other fluid

42:47

or liquids , for example you say at

42:50

breath , which gives

42:52

you a better idea of how much deuterium

42:55

is returned from your tissues

42:57

into the circulation . And

43:00

by those ratios

43:02

you can tell how efficient your body is

43:04

able to separate

43:06

deuterium from protons or proteome

43:09

and how to actually

43:11

keep your tissues

43:13

or tissue level operations in

43:15

the loaded tube range .

43:19

That's interesting and the usual reason in medicine

43:21

why an assay isn't performed or a test

43:23

isn't performed is because the mainstream

43:26

clinician doesn't know what to do with it , with

43:28

the result , and the

43:30

rule of one of the rules in medicine

43:32

is don't order a test that you can't interpret

43:35

. A classic example

43:37

of this is a fasting insulin level , which is

43:39

a very easy way to

43:42

give an insight into someone's metabolic health , and

43:44

a higher fasting

43:46

insulin level can give insight into the

43:49

development of insulin resistance well before the

43:51

blood glucose level starts arranging . But I

43:54

imagine that no one orders a serum

43:56

deuterium because the

43:58

implication of a high level is that we

44:00

need to be going through a lifestyle change that

44:03

you've previewed for us , which is

44:05

specifically consuming foods that

44:07

are low in deuterium . I'm

44:09

guessing I've never ordered this and I'd

44:11

be interested in the interpretation

44:14

of it but I'm guessing that if

44:16

someone has a high serum deuterium , then that

44:18

is just representing is it correlating

44:21

well to whole total body deuterium

44:23

level , and that implies that they need to be doing these lifestyle

44:26

measures . Yeah .

44:27

I'd say in between , it's what you consume

44:30

as far as food is concerned

44:32

, how hard your microbiome is

44:34

or what kind of microbiome

44:37

components or composition you

44:39

have , and also your

44:41

age , your sleeping patterns

44:44

, your ketosis

44:46

versus glucosis , your

44:48

daily activities and

44:51

also your underlying disease

44:53

processes . They all impact

44:56

on blood deuterium levels

44:58

. So for just

45:00

to dig out exactly how

45:02

those relate to diseases

45:05

, you also want to do a what

45:07

we call the organic acid test from

45:09

urine where you can actually check on

45:11

the TCA cycle intermediates

45:14

to see how your mitochondrial

45:17

branch out , the TCA

45:19

, the senioric rapps , cycle high branches

45:21

out of organic acids

45:23

. Meaning that you

45:26

can interpret your data based

45:28

on mitochondrial functions

45:30

as far as deuterium levels are concerned

45:32

. And then you would ask the patient what

45:35

kind of food , what's the source , what

45:37

they eat , where they get their food

45:39

, how much water they drink and

45:43

from these components . If

45:45

you do this with

45:48

some biochemical knowledge then

45:50

you can kind of pinpoint

45:53

to various problems

45:56

in lifestyle consumption

45:58

of certain food items , the sources

46:01

and age related

46:03

, sleep related and lifestyle related

46:06

issues . So eventually

46:08

you can and you would be able

46:11

to interpret the data

46:13

very efficiently and

46:15

with specifics of how

46:17

and what kind of diseases

46:20

to expect and how to overcome

46:22

those and usually

46:24

when I

46:26

get questions about what do

46:28

you know levels they should or

46:30

a patient should reach , I

46:33

usually start by

46:36

just simply asking

46:38

them of what their nutritional

46:41

and what their source is , because usually

46:43

that's the first obstacle

46:46

that you have to overcome of

46:48

how to deal with certain

46:50

lifestyle

46:53

and food related issues

46:55

to prevent chronic diseases

46:58

and to treat efficiently

47:00

chronic diseases and eventually

47:02

to provide a better life

47:05

expectancy and also a better

47:08

life quality for those patients

47:10

, especially obesity , diabetes and

47:12

cancer .

47:13

Yeah , great . And let's pivot

47:15

now and talk about this idea of metabolic disease

47:17

, because essentially , as

47:20

far as I'm conceiving

47:22

it , so many of the preventable conditions

47:25

that are putting people in nursing homes stem

47:28

from metabolic dysfunction , insulin resistance

47:30

, and they're

47:32

all tissue specific manifestations , whether

47:35

that's cardiovascular disease

47:38

, whether it is dementia , or whether all

47:40

these problems come down

47:42

on a hormonal level

47:44

to insulin resistance

47:47

. But on a mitochondrial level , it's

47:49

dysfunctional mitochondria

47:51

. I like to look

47:53

at things like the presence of ectopic

47:55

fat or visceral fat that

47:57

is even predating or anti-seeding

48:00

the development of a raised

48:02

fasting insulin . I

48:04

want to ask you about a critical

48:06

thing that's been on my mind , which is is

48:09

the presence of ectopic fat , which

48:11

I guess they're spilling over of energy

48:13

outside physiological

48:16

white adipose depose ? Is

48:18

that a fundamentally a problem

48:20

of excess deuterium ?

48:23

Yes , and it becomes

48:26

more clear if you think about this

48:28

process , what we call metabolite

48:31

or molecular overcrowding , because

48:33

any particular accumulation

48:36

process amyloidosis

48:41

, glucose , fat

48:44

they all indicate

48:47

a problem with complete

48:49

sub-shape oxidation , where the

48:52

products are carbon dioxide , water

48:54

and energy . This is what your Formula

48:56

One race car engine does

48:58

. It burns fuel very efficiently at

49:00

high rpm , delivering incredible

49:03

force . For that you have

49:05

to tweak it and very precisely

49:08

you have to kind of adjust

49:11

all the intake of the exhaust

49:13

parts and very efficiently

49:16

you have to bring it into a highly

49:19

precisely calculated manner

49:21

that your body can actually do

49:24

if everything works fine

49:26

, meaning that if there's ignition

49:28

and there's sufficient exhaustion

49:31

, you can actually load or

49:33

you can actually perform in

49:36

those mitochondria more efficiently

49:38

, much more efficiently if

49:40

your detune is low , if

49:42

your nanomotors are spinning at high

49:44

rotation , your metabolic water

49:46

formation efficient , your TC cycle

49:49

is able to produce carbon dioxide

49:51

, which is the optimal

49:53

gas form of any burning

49:57

or biological oxidation process

49:59

. If this set

50:01

of reactions is blocked

50:04

anywhere , that could be mitochondria

50:08

, that could be mitochondrial

50:10

nanomotors , that could be oxygen delivery

50:12

, that could be the electron transport chain . Not

50:14

enough light , not enough natural

50:18

light , not enough

50:20

exposure to

50:23

red light , for that matter . You

50:26

actually diminish these mitochondrial

50:29

functions . So there is no complete

50:31

sub shade oxidation

50:34

which results in carbon dioxide

50:36

and you can just kind of exhaust like in

50:38

a exhaust

50:41

pipe through your breath . Practically

50:43

you can exhale . If

50:46

these steps or if these reactions

50:48

are diminished , then metabolic crowding

50:50

or metabolic crowding

50:53

steps in and

50:55

you have to store those molecules

50:57

until they break down and

50:59

a certain body compartment it could be

51:01

visceral fat , it could be

51:03

compsive fat , it could be fat

51:06

tissue itself , it could

51:08

be excessive glycogen , it

51:10

could be excessive protein

51:13

of any sort based

51:15

on tissue specifics . But

51:17

it's practically a part

51:19

of a inefficient complete

51:22

biological oxidation system

51:25

where you have to store molecules

51:28

instead of burning them completely

51:31

. And once that's set in , then

51:33

you start at tissue levels , you

51:35

start building up fat . That

51:37

compromises tissue functions

51:39

, oxygen delivery , blood flow , circulation

51:42

, so on . The simple swissiosis

51:45

is practically just

51:47

stepping in in apicronic

51:50

disease where you deal with this metabolic

51:52

crowding and the truth

51:54

is we don't need glucose , we

51:57

don't need carbohydrates . Our

52:00

body is designed our liver is

52:02

designed to produce carbohydrates

52:04

from glycerol or fat , meaning

52:06

that it's a gluconeogenic

52:09

precursor . So , provided

52:11

that you eat enough fat and a little

52:13

fat , which is not the same as fatty

52:15

acids fat is composed

52:17

of a glycerol , where

52:20

all these glycerol is a three-carb

52:22

molecule and each of those

52:24

can have fatty acids

52:27

attached to them . These

52:29

are what we call triglycerides

52:31

or phospholipids , if there's one

52:33

phosphate and two fatty acids , and this is

52:35

how your liver exchanges fatty

52:38

acids with adipose tissue and heart

52:40

muscle , for example

52:43

. The most efficient way of delivering

52:45

energies in this form of this fat

52:48

, because it's very saturated with hydrogen

52:50

. A fat , a

52:52

hard hydrocarbon

52:55

is very different from a

52:57

glucose

53:02

molecule , which is a

53:04

six-carbons mixed

53:06

with six water molecules . So

53:08

hydrocarbons are carbons

53:10

in hydrogen , a carbohydrate

53:12

are carbons in water . So

53:14

practically , if you look at a hydrocarbon

53:17

, it has twice as many almost

53:19

hydrogens compared to

53:22

the same amount of carbons that they

53:24

carry and for that matter

53:26

they are much more efficient and much more

53:29

suited fuel source

53:31

for metabolic water formation , which

53:33

is oxygen and hydrogen , and

53:35

also for ATP synthesis , which needs

53:37

these protons to come into the mitochondrial

53:40

matrix . And those

53:42

are the most efficient low-duty

53:44

soft rays to deliver this hydrogen

53:46

protons and not neutrons to the mitochondria

53:49

. So hydrocarbons

53:52

and carbohydrates are very

53:54

different how they behave in

53:56

our systems . Hydrocarbons

53:59

and carbohydrates have very different

54:01

dutium contents simply because

54:03

the way they are made in

54:06

nature . Again

54:09

, photosynthesis and biological

54:15

oxidation are the reverse or

54:17

opposite processes in

54:19

a sense that , but they all will fare the same

54:21

biological role is practically to capture

54:23

the energy of sunlight and

54:26

deliver it to species

54:31

that are chemotrophic or heterotrophic

54:34

, and I

54:36

gave these talks based

54:39

on basic biochemical

54:41

or biochemistry teaching

54:44

at UCLA and Jack Rusch took

54:46

some of that in his arguments

54:48

. But practically it's a biochemical scenario

54:51

when we look at these reactions

54:53

and there are actually rows of

54:55

electromagnetic radiations

54:57

in the form of lights and

54:59

so on which actually interact

55:02

with these electron

55:04

transferred chain proteins

55:06

. And also what's very important

55:08

is that there's a

55:11

mitochondrial process , what we call these

55:13

nanoconfinement and proton , these

55:15

table stabilization processes

55:18

, which also produce energy

55:20

against the zero point

55:22

energy scales

55:25

. We actually beaming up these energy

55:27

producing scenarios

55:30

just to understand human

55:32

energy production , or you carry

55:35

out cell energy production in general

55:37

. Now we are actually linking

55:39

this with the obligatory

55:42

fatty acid oxidizing or fatty

55:44

acid modifying

55:48

cell organ and what we call peroxazones

55:50

, and the result is hydrogen peroxide

55:53

, which can be , by catalase turned into

55:55

a metabolic

55:58

water . And sleep

56:00

is very important because during sleep

56:03

you slow down oxygen delivery

56:05

and that's when molecular

56:08

oxygen , or two , steps in

56:10

and this is how you

56:12

supply your peroxazone

56:14

with oxygen and

56:17

the breathing , or the slow

56:19

breathing , during sleep serves this

56:21

process of deutym depletion

56:24

from

56:26

fat and the result is

56:28

hydrogen peroxide , which produces metabolic

56:32

water in mitochondria with

56:34

the use of catalase . But practically

56:37

, sleep is just to go into a ketosis

56:40

, a fat burning state

56:42

, without eating anything . The

56:44

problem is during daytime

56:46

, if you get hungry , you go to the freezer

56:49

, you open the door and you start eating all

56:51

kind of stuff . If you sleep , you

56:54

actually allow your

56:56

, with low oxygen tension

56:58

, simply because your breathing slows down

57:00

, these peroxazones to kick

57:02

in , even though they don't produce

57:04

much energy . They produce low

57:07

detune hydrogen peroxide

57:09

which can be taken to mitochondria

57:12

to produce low detune

57:14

metabolic water from there . And this

57:16

process is so critical and so important

57:19

that , for example

57:21

, if you want to climb to the top of

57:23

the Mount Everest , if

57:25

you want to climb

57:28

to the top

57:30

of the Himalaya without supplementary

57:32

oxygen , you have to be nutritional or

57:34

grass fat ketosis . Otherwise you're

57:37

not going to make it so practically

57:40

, as it comes to not

57:42

only chronic disease but also human

57:44

performance or extreme challenges

57:46

. In that matter , these

57:49

systems , the peroxazome or mitochondria

57:52

, or the proton destabilization

57:54

, the light effects , the heat production

57:57

, these are all interconnected in

57:59

a very simple way and that's practically

58:02

. Carbohydrates

58:04

and hydrocarbons

58:06

behave differently as far

58:08

as their energy and detune

58:10

load , so practically you want

58:12

to operate under

58:15

nutritional and metabolic

58:17

ketosis on low

58:19

detune saturated animal

58:21

fat and from then on you

58:23

can actually , metabolically

58:26

and energetically , you can challenge your

58:28

system and

58:30

you will be able to perform and

58:33

you will be able to reverse certain

58:36

disease processes , mostly

58:39

chronic metabolic diseases , simply

58:41

because now

58:44

your mitochondria is able to completely

58:47

exhaust those

58:49

stored fatty

58:51

acids , proteins , carbohydrates

58:54

, whatever those are , because of you

58:56

actually treated

58:58

metabolic crowding at the cellular

59:00

level with appropriate

59:03

low detune , high energy

59:05

substrate delivery in the form of

59:07

saturated grass fat , animal fat , and

59:10

that's key to health .

59:13

I'm blown away , lazlo . This is absolutely

59:15

amazing . I think you're really helping me put

59:18

together a whole bunch of pieces in my head around

59:21

the pathogenesis of metabolic

59:23

dysfunction . Let

59:25

me go through a couple of those things that you said in

59:28

turn , because there was so much gold

59:30

in what you've just said . Essentially

59:33

, when the state

59:35

of the art in terms of most of the metabolic

59:37

clinicians , that and kind of

59:39

thought leaders on this topic is

59:41

that metabolic dysfunction starts

59:43

in dysfunction of the adipocyte and then

59:45

the adipocyte reaches a personal fat threshold

59:48

, it can no longer store substrates

59:50

in there . So these spill out

59:52

into , you know , ectopic fat deposits

59:55

, whether that's hepatocyatosis , fat in

59:57

the liver , whether that's , you know , white adipose

59:59

, but in in in an ectopic

1:00:01

depot such as the viscera

1:00:03

in the abdomen or even within

1:00:06

the muscle , another form of ectopic fat

1:00:08

deposit . But I was never satisfied

1:00:10

by that explanation and it didn't

1:00:12

help me understand pieces

1:00:15

of evidence like circadian

1:00:17

disruption , which is this idea that and

1:00:19

there was a recent there was a study done where they had two

1:00:21

groups of mice . They fed them the exact same diet

1:00:24

but one had a circadian disrupted

1:00:26

shift work , a light environment , and

1:00:28

that group of mice developed a

1:00:31

fibrotic and inflammatory

1:00:33

adipose tissues , expansion

1:00:35

of of of their visceral and

1:00:38

subcutaneous adipose depots and they

1:00:40

developed insulin resistance . So there's

1:00:43

obviously more factors at play than what we're eating

1:00:45

in terms of developing or exceeding

1:00:47

this personal fat threshold , and then we're developing

1:00:50

ectopic fat deposits and then , on

1:00:52

the way , insulin resistance and then type 2

1:00:54

diabetes and the rest . But what you've just described

1:00:56

is that it's a backup of substrate

1:00:58

. It's incomplete oxidation

1:01:01

or incomplete combustion of these substrates

1:01:03

, that is , that is therefore being

1:01:05

altered or built up in different

1:01:07

organs , and you know any other metabolic

1:01:10

doctor that you talk to that they'll

1:01:12

make the note that certain patients can , will manifest

1:01:15

metabolic disease in different ways and

1:01:17

some get , some will get

1:01:19

, will only have the tiniest bit of

1:01:21

visceral fat , but they'll be floridly type 2 diabetic

1:01:23

. Others will have massive expansion

1:01:25

of their subcutaneous fat and

1:01:28

be metabolically fine . Others will get hypertension

1:01:30

and get kidney specific manifestations

1:01:33

. So it's all a massive spectrum

1:01:35

. But what you're helping me understand is

1:01:38

that this is a fundamental

1:01:40

mitochondrial problem and a backup of substrate

1:01:42

and and there's

1:01:44

multiple different steps that things can

1:01:46

go wrong . But you know it's

1:01:49

all kind of coming back to the mitochondrial

1:01:51

function in terms of of

1:01:53

how things are and why things

1:01:55

are going wrong yeah .

1:01:57

So you need to think

1:01:59

of , like how you come to

1:02:01

this plant . When you're a baby , when you're a

1:02:03

newborn , you have a 2.9 millimore

1:02:06

per liter glucose and and one

1:02:08

millimore per liter beta

1:02:12

hydroxy butyrate . That means

1:02:14

you you're born in ketosis , you're

1:02:17

born in a metabolic ketosis

1:02:19

, which is what

1:02:21

you reach in the morning

1:02:23

after asleep as well . So you're , you come

1:02:26

to this planet in ketosis , you

1:02:29

wake up in ketosis in your team

1:02:31

depleting ketosis , and the

1:02:33

key to this is practically regulate

1:02:35

oxygen intake and switch

1:02:37

from mitochondria to proxazone . Proxazone

1:02:40

to mitochondria , another . It's

1:02:42

more like a hybrid engine . The

1:02:44

proxazone can only

1:02:46

use and only modify

1:02:49

fatty acids and long

1:02:52

chain saturated fatty acids . Mostly

1:02:54

they produce acetylcoinsame and

1:02:56

they produce using O2

1:02:59

. So it's it's not the

1:03:02

red blood cells and hemoglobin

1:03:04

that provides that O2

1:03:07

, but it's dissolved oxygen in

1:03:09

your blood which is available . It

1:03:11

doesn't matter how slow you sleep

1:03:14

, actually sleeping

1:03:16

in deep and this is Wemhoff

1:03:19

and some other methods that

1:03:21

then you can actually improve increase

1:03:23

proxazomal beta

1:03:25

oxidation and , for that matter

1:03:27

, you can deplete duteum and produce

1:03:29

the tumor , depleted metabolic water or

1:03:32

hydrogen peroxide for

1:03:34

for mitochondria . Once

1:03:37

you wake up and you start eating , you

1:03:39

eat a mixed diet . That means

1:03:41

carbohydrates mix in if you

1:03:43

don't keep ketosis , meaning

1:03:46

that you have to

1:03:48

start dealing with

1:03:50

duteum . Some other ways and this is

1:03:52

like by glycosis is

1:03:55

inserted

1:03:57

, embedded in the system

1:03:59

. Practically during daytime you can

1:04:02

get rid of

1:04:04

certain amount of duteum

1:04:06

, but if your duteum intake

1:04:08

is overloading these systems the

1:04:10

trash holds are overloaded then you're gonna

1:04:13

start breaking mitochondria down

1:04:15

. And once you start breaking mitochondria

1:04:17

down , you're not able to completely

1:04:20

oxidize fatty

1:04:22

acids , neither fatty acids , nor carbohydrates

1:04:25

or or or amino

1:04:27

acids , and the result of that

1:04:29

is gonna be a fat storage

1:04:31

or or or a metabolic

1:04:33

, metabolic crowd , and

1:04:36

they all go down to the mitochondrial

1:04:38

mechanisms and processes

1:04:41

. It doesn't matter how and where

1:04:43

the fat shows up or how

1:04:45

extensive it is . Practically they

1:04:47

are all tissue specific

1:04:49

presentations of a duteum overload

1:04:52

and broke up , broken mitochondria . And

1:04:54

those can you . You can improve with food

1:04:57

, nutrition , light , sleeping patterns

1:04:59

and so on . There's no supplements

1:05:02

, there's no drug , there's . There's nothing

1:05:04

. You can actually fix this very

1:05:07

complex system . You as a physician

1:05:09

, use a doctor who actually talked to

1:05:11

the whole system . As

1:05:13

far as patients present their diseases

1:05:16

, you have to look at them from

1:05:18

the bottom up , meaning that you have

1:05:20

to kind of deal with the mitochondria

1:05:22

first and think over how you

1:05:24

can improve the complete biological

1:05:27

oxidation and exhaustion of

1:05:29

carbons from the whole system , because

1:05:31

that's practically the form of carbon dioxide

1:05:34

, that's the and when metabolic water

1:05:36

production . That's the whole idea

1:05:39

. Be behind a responsive

1:05:45

metabolism to challenges

1:05:47

and physical exercise and so on , meaning

1:05:50

that you are more kind

1:05:52

of ready

1:05:54

to take physical challenges

1:05:56

, you are less prone to develop

1:05:58

chronic diseases , you

1:06:01

are healthier in general , you

1:06:03

can perform some other fox functions

1:06:05

more efficiently , focusing

1:06:08

on certain things , performing

1:06:12

specific tasks . And what is

1:06:14

really very important , which we

1:06:16

observed over time , is how much

1:06:18

water you drink , because

1:06:20

water intake is also a source of

1:06:22

duteum and

1:06:25

this is the sneakiest part of the team because

1:06:27

there is no carbons involved . So they

1:06:29

actually get absorbing your tissues

1:06:32

and get diluted and

1:06:34

get mixed

1:06:36

with its cytoplasmic

1:06:38

water and first

1:06:41

through the circulation and the interstitial

1:06:43

tissue compartments and then

1:06:45

your cellular water

1:06:49

. And in the meantime your

1:06:51

brain will swell because the osmotic

1:06:54

lack of osmotic , osmotic

1:06:56

pressure and , for that matter

1:06:58

, you develop these kind

1:07:01

of low-grade . If

1:07:03

you drink too much water with

1:07:05

no salt , excessively , without

1:07:08

thirst , you can develop a diabetes

1:07:10

insipidus which is again

1:07:12

compromising your urea cycle

1:07:15

. It compromising your anti-diarrheal

1:07:17

vasopressin , anti-diarrheal

1:07:19

hormone output , because

1:07:22

the pituitary gland

1:07:24

produces sexual hormones for the

1:07:26

costimulating hormone , growth hormone

1:07:28

and thyroid stimulating

1:07:30

hormone then you can actually

1:07:33

kind of disrupt

1:07:36

all metabolic regulators and all

1:07:38

metabolism that are linked so so

1:07:40

well and so tightly together . You

1:07:44

can disrupt these , this whole process

1:07:46

and and for that matter

1:07:48

you can you will start

1:07:51

up , you will start building

1:07:53

up visceral fat

1:07:55

. Then , when visceral fat storage

1:07:58

spaces are not really sufficient

1:08:00

to store that fat , then you , you're

1:08:02

gonna build up subcontinuous fat and

1:08:05

once that starts , you , you

1:08:07

, you carrying deposit , depositing

1:08:09

fat in in various other

1:08:12

tissues , especially when

1:08:15

inflammatory cells kick in , because

1:08:17

they sense that there's cells

1:08:19

that signal to apoptosis or

1:08:21

or degenerative processes

1:08:24

set in . Inflammation

1:08:26

is always part of it , because a

1:08:29

dying cell is also

1:08:31

signaling for , for

1:08:33

phagocytides

1:08:35

or or cells that will clear

1:08:38

up the remnants of those of those

1:08:40

non-functioning mitochondria

1:08:42

bathing cells . And this whole

1:08:45

process starts with is

1:08:47

characterized with metabolic syndrome

1:08:49

, various internal

1:08:52

medical challenges like

1:08:55

high blood pressure , high glucose , high

1:08:57

circulating fat is practically

1:09:00

because you cannot exhaust all

1:09:02

those , you cannot actually get rid

1:09:04

of the carbon skeleton , the carbon

1:09:06

sources , and the only

1:09:08

way they can actually be stored

1:09:12

is in the form of their most

1:09:15

compact , let largest

1:09:17

, I would say , chain length fatty

1:09:19

acids and that's how BCD , diabetes

1:09:22

and type one type to

1:09:24

develop after

1:09:26

all , because you lose metabolic sensitivity

1:09:28

to oxygen and protons

1:09:30

and mitochondrial processes . So

1:09:33

after all , you just end up with a big

1:09:36

stuffed

1:09:38

oxidative system that

1:09:40

is not able to oxidize completely

1:09:42

the subchase that are

1:09:44

provided . I

1:09:51

can't hear you right now .

1:09:54

Sorry , On a basic level it's just

1:09:56

the use , the analogy of

1:09:58

an engine . It's like the Formula 1 engine

1:10:00

that needs the precise inputs

1:10:03

and the precise tuning . The

1:10:05

metabolic syndrome and metabolic dysfunction is

1:10:07

just a complete mismatch of the

1:10:09

fuel sources and an inefficient engine

1:10:11

that is simply not working properly

1:10:14

.

1:10:16

Imagine a Formula 1 race engine

1:10:18

that has a very tight intake

1:10:20

of air oxygen . Oxygen

1:10:23

is the only element they need burning

1:10:26

practically

1:10:29

hydrocarbons , which is a high-octane

1:10:31

fuel . Octane is the 8th carbon phalliacid

1:10:34

, phalliacidineal fuel

1:10:36

, and higher that number is more

1:10:38

efficiently those fuels burn . And

1:10:40

if you actually overload

1:10:43

your cylinders

1:10:46

with either oxygen

1:10:48

or with fuel

1:10:50

, this burning process will be insufficient

1:10:52

and immediately you drop performance

1:10:55

, Immediately you

1:10:57

drop energy production and

1:10:59

what we call is the choking of the engine

1:11:02

. We know how that works . We

1:11:04

know oxygen limited environment

1:11:07

. You have to adjust . I'm not

1:11:09

sure if you have flown airplanes

1:11:11

, but if you are flying a Cessna and

1:11:13

you reach a certain flying altitude , then

1:11:15

you have to close your oxygen intake

1:11:18

or you have to close

1:11:20

your fuel intake because your oxygen

1:11:22

is less pressurized

1:11:24

in higher altitude . So

1:11:27

you have to adopt , you

1:11:29

have to adjust your hydrocarbon

1:11:32

intake based on the oxygen availability

1:11:34

. If you keep overstuffing

1:11:36

your fuel , if

1:11:38

you keep overstuffing the system

1:11:41

with excess fuel

1:11:43

and there is not enough oxygen and

1:11:46

not enough mitochondrial processes

1:11:48

to make these two to meet the

1:11:50

hydrogen from food and oxygen from

1:11:52

air , because you overstuff this

1:11:54

, then practically you break the engine

1:11:56

and the first you see a decrease

1:11:59

in performance , and then you break the engines

1:12:01

because those engines will stop after

1:12:04

all . So these

1:12:06

have to be very tightly regulated and

1:12:08

we have all the biochemical processes

1:12:12

to regulate these very tightly , very

1:12:14

efficiently for our mitochondria . But

1:12:16

once these proportions are

1:12:19

and the due content

1:12:21

of the fuel breaks

1:12:24

the engine , or the other way

1:12:26

around , if there's too much fuel coming in

1:12:28

or there's less oxygen and these

1:12:30

are not balanced , then there's going to

1:12:32

be a major impact

1:12:34

in your fuel ruining

1:12:37

system .

1:12:38

I love that . Thank you , lazlo . And

1:12:40

I will make a quick point about how the light fits in

1:12:43

, because the near infrared

1:12:45

light is

1:12:47

helping the mitochondria produce melatonin

1:12:50

and melatonin is one of the most ancient

1:12:52

and efficient antioxidant hormones . So

1:12:55

we talked about the mitochondrial dysfunction

1:12:57

because they're building up excessive reactive oxygen

1:12:59

species . Well , if you're not getting , if

1:13:02

you're circadian rhythms disrupt , if you're not getting

1:13:04

infrared during the day to help make

1:13:06

that melatonin , then the

1:13:08

engine is again , you're not going to have enough

1:13:10

oil and then it's also going to break

1:13:12

. And if you're not getting red light

1:13:15

, which we know helps potentiate

1:13:17

the efficiency of the fourth cytochrome

1:13:19

, then again that's going to contribute

1:13:21

to mitochondrial dysfunction . And

1:13:23

then red light is also being absorbed

1:13:25

by mitochondrial water inside . So

1:13:29

it's fascinating and elegant how all

1:13:31

these parts interact and when you

1:13:33

don't get the light right or you don't get the food

1:13:35

right , you need

1:13:37

to get both right , and I talked to patients about getting their

1:13:40

light diet right and their food diet right and

1:13:42

that's plenty of grass-fed animal

1:13:44

fat and plenty of regulated

1:13:46

circadian rhythm . But you basically need to do both of

1:13:48

those . So

1:13:51

I really like that the point . I

1:13:53

just want to go back to this

1:13:55

idea of ectopic fat as a deuterium

1:13:57

depot , because I

1:13:59

got in a Twitter argument with someone

1:14:01

about this and they insisted that

1:14:03

it is . The ectopic fat is the

1:14:05

actual depot for excess deuterium and

1:14:08

a sign of deuterium accumulation

1:14:10

, and a good friend

1:14:12

and colleague , dr Sean O'Mara , is doing

1:14:15

great work in terms of recommending

1:14:17

people identify visceral fat , especially

1:14:19

through MRI , which is showing

1:14:21

them the problem . But

1:14:23

biochemically , the actual mechanism

1:14:25

is what we're talking about and this

1:14:28

idea that deuterium is

1:14:30

building up and isn't being excreted properly

1:14:32

Is that correct ?

1:14:33

Yeah , that's right . When

1:14:35

you have deuterium imbalanced

1:14:38

and you overload

1:14:41

your system with deuterium , it

1:14:43

will find a storage form for

1:14:46

itself , meaning that it's going to end

1:14:48

up in glycosis

1:14:51

and water exchange products , simply because

1:14:53

if you label glucose with

1:14:55

deuterium it's going to end up inside a plasma

1:14:57

quarter . That side of plasma quarter supplies

1:15:00

all the biochemical reactions , including

1:15:02

fatty acids in days , which is an extra

1:15:05

mitochondrial process . But the

1:15:07

substrate , not only a coenzyme

1:15:09

A , comes from citric acid . But

1:15:13

if the fatty

1:15:15

acid synthesis process , which

1:15:17

is a huge complex in

1:15:21

your cytoplasma , if

1:15:23

it has water

1:15:26

or NADPH or reducing

1:15:28

the equivalent , which is loaded with deuterium , then

1:15:30

your fat may become deuterium

1:15:32

loaded and those are again

1:15:34

stored because of the lack of biological

1:15:37

oxidation in

1:15:39

the actopic fat tissues

1:15:42

and fat accumulation . If you look

1:15:44

at MRI images , on

1:15:46

MRI images those fat pads

1:15:48

may look darker

1:15:50

because of the access to deuterium , because deuterium

1:15:53

does not allow protons to move as

1:15:56

freely and as quickly during

1:15:58

MRI . So if it's a proton

1:16:01

MRI , then you're going to see a

1:16:04

lack of signal and

1:16:06

by comparing those signals

1:16:09

you can actually determine the deuterium

1:16:11

content of your

1:16:13

fat tissue , which you can actually

1:16:16

do using these image processing

1:16:18

softwares .

1:16:19

I'm so glad you brought that up because that was

1:16:22

my exact next question , which is using

1:16:24

MRI to basically

1:16:26

identify deuterium . As

1:16:29

far as I was aware and I'm not a radiologist

1:16:31

and even the radiologists that I've talked to don't

1:16:33

seem to have any understanding of this but there

1:16:36

is deuterium specific spectroscopy

1:16:38

modes on MRI

1:16:40

that involve , and certain

1:16:42

protocols , especially in your oncology

1:16:45

, involve , ingesting deuterium rich traces

1:16:47

. But explain to us how we can

1:16:49

identify deuterium rich tissues

1:16:51

, maybe on standard MRI

1:16:53

modes ?

1:16:54

Yeah , so MRI is practically

1:16:57

a magnetic field where actually

1:16:59

you delocalize protons

1:17:01

using a radio frequency and

1:17:04

that means when they spin

1:17:07

because protons they spin they

1:17:09

use absorbed

1:17:11

electromagnetic energy

1:17:14

to change their location we

1:17:16

call it nuclear proton delocalization

1:17:19

and

1:17:21

as they return they emit

1:17:24

the energy they absorbed during

1:17:27

this changing of their positions

1:17:29

. And that's what you detect in MRI

1:17:31

Spectrically a proton moving or

1:17:33

a proton movement measuring

1:17:36

device , proton MRI

1:17:39

or magnetic resonance images . Now

1:17:42

, if there is deuterium in your

1:17:45

tissues , one single deuterium

1:17:47

, for example in ice water , can

1:17:49

actually stop a thousand

1:17:51

protons around it to resonate

1:17:54

appropriately , meaning that those

1:17:57

protons are tight in

1:17:59

their structures , meaning that they're

1:18:01

unable to delocalize and

1:18:03

they're unable to return and emit

1:18:05

this energy . So in certain

1:18:08

scan modes there's

1:18:10

two kinds of scans . One is the lattice

1:18:14

and spin relaxation

1:18:17

and the other one is the spin-spin relaxation

1:18:19

. Those are both affected by deuterium

1:18:21

, because deuterium does not allow protons

1:18:23

to move as freely

1:18:26

as just

1:18:29

simply just in proton environment

1:18:31

. So you can see a darker

1:18:33

or a diminished image . Now

1:18:35

the problem with what you refer to is

1:18:37

called deuterium . Metabolic imaging is

1:18:40

when they actually use a glucose molecule

1:18:42

that has deuterium on it and

1:18:44

as it breaks down , certain products

1:18:47

can be measured using magnetic

1:18:49

resonance imaging or spectroscopy

1:18:52

. The problem with labeling

1:18:55

glucose is that 90%

1:18:57

of the label of deuterium ends up in

1:18:59

cytoplasmic water through glycolysis

1:19:01

. So again

1:19:04

, how much is lost

1:19:06

is hard to determine based on just

1:19:08

gassing . So we

1:19:11

believe that kind

1:19:13

of getting a deutonomous type of approach

1:19:16

to MRI

1:19:18

or using MRI as a methodology

1:19:21

. Then you can actually

1:19:23

compare these images based on signal

1:19:25

strength and from there , for fat

1:19:28

tissue you can determine based on the

1:19:30

lack of proton movement or

1:19:32

the lack of signal how much deuterium

1:19:34

those tissues may

1:19:36

contain . And in the meantime you

1:19:39

can actually do water discrimination

1:19:41

, fat discrimination scans

1:19:43

and you can get closer to

1:19:45

these answers . But practically

1:19:48

anywhere

1:19:50

. When proton movements are involved

1:19:52

in any kind of biological

1:19:54

diagnostic processes indirectly

1:19:57

, those are all deuterium measuring devices

1:19:59

because deuterium compromises proton

1:20:01

movements .

1:20:03

Okay , so we should be able to get an idea

1:20:05

just using a standard MRI . We

1:20:08

don't need to use specific imaging mode or

1:20:10

most MRIs we're going to be able to use

1:20:12

. We're going to be able to visualize

1:20:15

deuterium by using this approach .

1:20:19

Indirectly , indirectly again and you have to

1:20:21

kind of again work with

1:20:23

some software aid to be

1:20:25

able to analyze those images more

1:20:28

efficiently and you have to kind

1:20:30

of consider the deuterium

1:20:32

that is embedded in connective

1:20:35

tissues , collagen , fiber

1:20:37

tissues and so on , which are also

1:20:40

part of fat tissue , and

1:20:42

you can use deutonomics

1:20:45

or deuterium metabolic imaging only if

1:20:47

you want to look at flux , but you

1:20:49

have to calculate for the loss of

1:20:51

the tracer into metabolic water

1:20:53

, which is it does not

1:20:55

make this process easier to use

1:20:57

. It's practically a different

1:21:00

angle or different window to look

1:21:02

at the same kind of problem

1:21:04

of how much deuterium there is in

1:21:06

tissues . We don't

1:21:08

recommend loading anything with

1:21:10

deuterium simply because they break down nanomotors

1:21:13

and based on their amount

1:21:15

or their level of consumption

1:21:18

, those can harm

1:21:20

especially mitochondrial

1:21:23

structures . And

1:21:25

for us it's easier

1:21:28

to work with some alternative

1:21:30

approaches , for example red light

1:21:32

, which makes interstitial

1:21:37

water in mitochondria more viscous

1:21:39

, so it improves mitochondrial functions

1:21:41

, besides improving complex five

1:21:43

, complex four and complex five , and

1:21:46

it actually makes these proton

1:21:49

bonds resonate more efficiently

1:21:52

, especially in the 670

1:21:54

nanomater range . It's

1:21:56

really interesting that my high

1:21:58

school buddy , dr Kraus , france

1:22:02

Kraus , won the Nobel Prize in Physics since

1:22:04

in 2023 . He

1:22:06

was born in May 1662

1:22:08

. I

1:22:12

was born in June 12 in 62

1:22:14

, so we are just a few weeks apart . In

1:22:16

high school we were actually competing in

1:22:18

physics very efficiently . So actually

1:22:20

my classmate in high school beat France

1:22:24

Kraus , the Nobel Prize winning physicist

1:22:26

, for the Atos second

1:22:28

laser in a high school

1:22:30

physics competition , national or international

1:22:33

physics competition , which is kind of the

1:22:35

final part of the story , but anyhow . So

1:22:37

now we are designing a project

1:22:40

where we actually use

1:22:42

this at the second

1:22:44

laser to excite biological

1:22:47

samples with

1:22:50

this very short laser impulse

1:22:52

and measure the red light output

1:22:54

of the system , just to see how

1:22:56

much proton and how much deuterium

1:22:58

is involved in the

1:23:01

chemical makeup of the sample

1:23:03

. So it seems that combining

1:23:06

resonance , which is magnetic

1:23:09

, or light , it almost

1:23:11

or electromagnetic frequency

1:23:14

it does

1:23:16

not necessarily matter , in the sense that as

1:23:18

long as you can sensitively measure

1:23:20

this or apply this

1:23:22

electromagnetic range which is in

1:23:24

the red light

1:23:26

and infrared light range

1:23:28

, you can actually mobilize

1:23:30

protons and mobilize

1:23:33

metabolic water , interfacial

1:23:35

water , more efficiently . So you can improve

1:23:37

a lot of biological

1:23:40

processes . Yet

1:23:42

in the meantime , based

1:23:45

on red light emission , if there's a

1:23:47

lack of red light emission , then

1:23:49

protons are not moving very efficiently

1:23:51

indirectly . This is a deuterium measuring

1:23:54

approach or a deuterium measuring device

1:23:56

, and this is where we are kind of tweeting

1:23:59

, just kind of establishing

1:24:01

in a metabolic research arena

1:24:03

. But there are many

1:24:06

, many new interesting things are coming

1:24:08

along .

1:24:09

Yeah , very interesting . And look the reason I was asking

1:24:11

. I wasn't proposing administering

1:24:14

deuterated tracer in terms of

1:24:16

routine investigation and management of metabolic

1:24:18

disease . It was more an academic interest

1:24:21

. But I think the point is giving

1:24:24

people an insight into their visceral fat

1:24:26

is a very powerful motivator

1:24:28

to implement the lifestyle changes that we've discussed

1:24:31

earlier . And if we could relatively

1:24:33

easily , with no additional

1:24:35

time on the MRI table , give

1:24:38

people an insight into the deuterium

1:24:40

content of that visceral fat or of their organs

1:24:42

, then that would be even more stimulus

1:24:45

, in my mind , to help them adopt

1:24:47

a low deuterium lifestyle , because

1:24:50

it's just another way of giving

1:24:54

them more impetus to make those changes

1:24:56

.

1:24:59

Yeah , I actually approach

1:25:02

this practically . I look at

1:25:04

how fast my neas are growing

1:25:07

, how long I need to sleep at night

1:25:09

to get into ketosis , measure

1:25:11

my ketone body

1:25:13

levels and measure my glucose

1:25:15

levels occasionally and eat

1:25:18

once a day at night

1:25:20

or

1:25:23

my dinomias are the main

1:25:25

courses , and those

1:25:27

are animal , grass-fed

1:25:30

animal , and I like this

1:25:32

kind of fasting , little bit

1:25:34

thirsty , kind of exhaust

1:25:36

all kind of organic

1:25:39

molecules to

1:25:41

mitochondrial complete

1:25:44

sub-shade oxidation

1:25:46

, simply because

1:25:48

you don't have to load

1:25:52

fully your system always

1:25:55

because of kind

1:25:57

of industrial-based recommendations

1:26:01

. You need to operate in

1:26:04

the optimal mode . Simply

1:26:07

, you don't fuel in all

1:26:09

kind of gasoline or diesel oil

1:26:12

when your engine is not designed for that

1:26:14

. You don't put

1:26:16

diesel fuel

1:26:19

into a formula of a race car simply

1:26:21

because it's not designed for that . It's a

1:26:23

very different idea . It's a very different

1:26:26

concept . It's a very different

1:26:28

set of principles how these engines

1:26:30

operate and simply

1:26:33

it's the easiest way to describe

1:26:35

this is that for optimal biochemical

1:26:38

operations you have to use the optimal

1:26:40

fuel source and you have to use the optimal

1:26:43

regulatory processes

1:26:45

and those are dependent

1:26:48

on how

1:26:50

you understand this

1:26:52

system . It's practically a

1:26:54

doctor , I would say , is

1:26:56

a good mechanic that can actually

1:26:58

adjust the carburetor , the injector

1:27:01

intake and the oxygen intake and

1:27:04

the exhaust pipe how clean

1:27:06

, and the catalysator and so on

1:27:08

. This we have to bring it

1:27:10

down to the mitochondrial level and

1:27:12

as long as you understand how these hybrid

1:27:15

proxysol more of mitochondrial beta

1:27:17

oxidation and substrate oxidation systems

1:27:19

work hand in hand and how they step

1:27:22

in in different stages

1:27:25

of your lifestyle or their

1:27:27

circadian rhythm , then you

1:27:29

can actually tell them or design

1:27:32

a food and the lifestyle

1:27:34

pattern that can actually help or

1:27:36

reverse chronic disease processes

1:27:39

. And it is just my

1:27:41

general kind of experience

1:27:44

that this seemed to work in every

1:27:46

case where we have an opportunity and

1:27:48

have a compliance with these .

1:27:51

Yeah , and look , I have delved

1:27:53

down very you

1:27:55

know , the evolutionary rabbit holes of

1:27:57

what is a species appropriate diet

1:27:59

, and there is debate about

1:28:01

the role of DHA in

1:28:04

terms of encephalization

1:28:06

or the development of advanced human

1:28:08

intelligence , and I think

1:28:10

that definitely played a role in terms of scavenging

1:28:13

bioavailable and very readily

1:28:15

available sources of DHA from the shores

1:28:17

. But I mean , there's no doubt that we

1:28:20

were carnivorous during

1:28:22

periods of our evolution and there is stable

1:28:25

carbon isotope data showing that

1:28:27

during periods of in the late I

1:28:29

believe it's the late middle or late

1:28:31

Pleistocene in

1:28:34

the Paleo getting my

1:28:36

, my , my periods confused

1:28:38

but there was a period where Homo erectus

1:28:40

was essentially a hyper carnivore so

1:28:42

we were hunting other

1:28:44

carnivorous animals . Just going

1:28:46

to show that we've got deeply programmed

1:28:49

genetic

1:28:51

machinery and metabolic machinery to

1:28:53

deal with with animal factors

1:28:55

.

1:28:56

Listen , if you go to the cave , art

1:28:58

you never seen , you

1:29:01

only saw hunting

1:29:03

. You know cavemen

1:29:05

. You never saw one eating carrots

1:29:08

or you know kind of gardening

1:29:10

. It's practically

1:29:12

all archaeological or historic

1:29:15

and all art data points

1:29:17

to this carnivore lobster . And

1:29:19

more fatty it is , more detuned

1:29:22

, depleted , it is more

1:29:24

beneficial for our brain

1:29:26

development . And I was actually

1:29:28

very stunned

1:29:30

and very interested

1:29:32

in exploring a 4.2

1:29:36

million years old

1:29:38

exploration

1:29:41

in North Northern Ethiopia

1:29:43

where actually they found four and a

1:29:45

half million years old carnivore

1:29:48

behavior from prehistoric

1:29:51

men . They even found those tools

1:29:53

, the stone tools that were used to break

1:29:55

in through the schools of

1:29:58

these herbivores

1:30:00

or large plant eating animals

1:30:02

, and that must

1:30:05

have been a prehistoric man who learned how

1:30:07

to use these tools

1:30:09

, the other kind

1:30:11

of species that lived in those faunas

1:30:14

or lived on those

1:30:16

biological conglomerates

1:30:20

or communities . They were

1:30:23

actually eating the

1:30:25

meat , the proteins

1:30:28

, the interiors , the visceral

1:30:30

fat and so on , but the best stuff

1:30:33

was left for this little prehistoric

1:30:35

man , which is the bone marrow

1:30:37

with the highest fat

1:30:39

content , and they didn't have to compete

1:30:42

with other predators because other predators

1:30:44

were not interested in those carcass

1:30:46

animals . So safely , with

1:30:49

plenty of food , they could evolve

1:30:51

, with less deuterium to

1:30:53

develop . They didn't have to repair nanomotors

1:30:56

, because how do you hide deuterium foods

1:30:59

? They actually could use the

1:31:01

brain and their fine finger

1:31:04

joint movements

1:31:06

to actually perform some more complicated

1:31:09

, more complex tasks memory

1:31:12

, society and

1:31:14

providing or building

1:31:16

life kind

1:31:19

of surroundings that

1:31:22

are more safe . They started cooking

1:31:24

these soups these

1:31:27

bone soups or these because they

1:31:29

moved them around and then

1:31:31

, about 400,000 years ago

1:31:33

, close to Tel Aviv , they found

1:31:35

cavemen's

1:31:38

habitats where they actually

1:31:40

used these bones and

1:31:42

they saw back the skin around

1:31:46

the bone and the bone marrow to conserve

1:31:48

these bone marrow like canned

1:31:51

food or the caveman that

1:31:53

was actually good for eight weeks to

1:31:55

consume . So it

1:31:58

was a huge part of human

1:32:00

adaptation and human

1:32:03

evolution , if you call it that way

1:32:05

. But this is how the creator

1:32:07

designed our system

1:32:09

biochemical systems , biological systems

1:32:12

to be able to use

1:32:15

these very valuable , incredible

1:32:17

, beneficial

1:32:20

low deuterium fat sources

1:32:22

or hydrocarbon sources . To

1:32:24

design to supply these

1:32:27

four mobile race car nanomotors

1:32:29

which we have as part

1:32:32

of our mitochondrial complex five

1:32:34

with the best fuel whatsoever

1:32:36

, because some of those they spin about 100,000

1:32:38

rotations per minute and those

1:32:41

are the ciliae of some

1:32:43

bacteria . They use the same nanomotors

1:32:45

. If you look at any living species

1:32:48

, as long as they use nanomotors , they

1:32:50

use the same design and

1:32:53

, for that matter , they

1:32:55

are all efficiently able to use either

1:32:57

carbohydrates or

1:33:00

fat . And , based on what

1:33:02

they use , this is what their

1:33:04

phenotype behaviors

1:33:06

and performance and

1:33:08

their abilities as species

1:33:11

or individual hunters

1:33:14

and so on , are able to

1:33:16

find the best sources food sources

1:33:18

and , for that matter , this is how and

1:33:20

why , and that's why

1:33:22

the lions are so powerful and

1:33:24

the cheetahs are so powerful , because they

1:33:27

don't mess with anything

1:33:29

else other than just saturated animal

1:33:31

fat .

1:33:35

And I want to make the comment , and I agree

1:33:37

because I think in empirical

1:33:40

, clinical practice , when you put a patient on a high

1:33:42

animal fat , grass-fed

1:33:44

beef diet , all

1:33:47

their problems go away , to

1:33:49

use a very simplistic term . And

1:33:52

I also think why the replacement

1:33:54

of saturated animal fat in

1:33:56

the human diet which was tallow , which

1:33:58

was fatty steak , which was butter

1:34:00

, the replacement of that with

1:34:02

these refined polyunsaturated

1:34:05

seed oils like canola , soy , corn

1:34:08

, vegetable sunflower

1:34:11

, has been possibly the most important

1:34:13

food issue , even

1:34:15

more so than sugar , even more so than carbohydrate

1:34:18

. I think that is a critical problem in

1:34:21

our society is because not

1:34:23

only was it the introduction

1:34:25

of these fat fats as the main

1:34:27

fatty acid source in our diet

1:34:30

collectively , but it's also the absence

1:34:32

of those saturated animal fats

1:34:34

and the fat soluble vitamins that we

1:34:36

got removed . So I talked

1:34:38

to Tucker Goodrich about this and

1:34:40

he has extensively looked into

1:34:42

the pathology of

1:34:45

why these oils

1:34:47

are so harmful , and it's his

1:34:49

opinion that it's the

1:34:51

breakdown products of linoleic acid

1:34:53

specifically that are

1:34:55

interfering with the function

1:34:57

of the mitochondria . And he's talked about the

1:34:59

incorporation of linoleic acid into mitochondrial

1:35:02

cardiolipin , which is problematic

1:35:05

. And then I talked to Jack Cruz

1:35:09

and he makes the point that it

1:35:11

is actually the presence of deuterium in

1:35:13

the seed oils that are making them

1:35:15

so toxic and

1:35:17

so harmful . So can

1:35:19

you square that this for me , or

1:35:21

help us , as the listeners , understand

1:35:24

the mechanism of harm of

1:35:26

highly refined industrial seed oils ? Is

1:35:29

it mostly the deuterium ? Is it

1:35:31

mostly this linoleic acid breakdown

1:35:33

products ? Is it both ? How do you think

1:35:35

about it ?

1:35:37

Now we wrote a paper about this in a oncology

1:35:40

called what to Eat , what Not to Eat that

1:35:42

is the question , and

1:35:44

you're right . Are

1:35:47

these plant-based oil

1:35:50

nutritional items

1:35:53

either hydrogenated or

1:35:55

treated with saturated

1:35:57

? They actually use their oily

1:36:00

, fatty nature by using

1:36:02

industrial saturation , using

1:36:05

hydrogen gas , and

1:36:07

some of those have 250

1:36:10

ppm deuterium concentrations

1:36:12

. So once you start processing

1:36:16

, using organic solvents and

1:36:19

extracting certain oil

1:36:21

types , especially unsaturated

1:36:23

fat , and you

1:36:25

want to saturate it so they actually

1:36:27

hold longer and hold better on the

1:36:29

shelf , when you put them in the

1:36:31

cellar , you know this yellow big

1:36:34

bucket of frying

1:36:36

, whatever those are , I

1:36:38

just I don't even walk through those eyes

1:36:40

, I just kind of just

1:36:43

stay out of them , simply because those

1:36:46

are probably the worst stuff

1:36:49

you can encounter

1:36:51

when as far as nutrition is concerned

1:36:53

and because

1:36:55

those are not

1:36:58

natural . Even the plant-based

1:37:01

oils are not

1:37:03

natural simply because they use organic

1:37:06

extraction processes . They use

1:37:08

various saturation

1:37:10

processes to actually make them

1:37:12

look in a certain way , make

1:37:15

them be consistent

1:37:17

in a certain way and , for that

1:37:19

matter , those are unsuited

1:37:21

for human consumption , high

1:37:23

in deuterium , because of the saturation

1:37:25

of organic extraction processes . And

1:37:28

actually we wrote a paper about this in

1:37:30

New York College . You can go and

1:37:32

check them out and when you

1:37:34

post this conversation we can

1:37:36

all link those , we can attach those

1:37:38

publications

1:37:41

, because this has been a big

1:37:43

problem for a long time

1:37:45

. There's a French team

1:37:47

, dr Robbins with

1:37:49

Dr Gabor Chomier . They did work

1:37:52

together on measuring deuterium

1:37:54

content of plant-based

1:37:57

and deuterium content of animal-based

1:38:00

oils and fat

1:38:02

products . Practically

1:38:04

those are very different because

1:38:07

plants they cannot

1:38:09

eat fat , meaning that they have

1:38:11

only access to inorganic elements

1:38:13

in the form of water , carbon

1:38:15

dioxide and sunlight . They cannot

1:38:17

deplete deuterium . They cannot . Their

1:38:20

deuterium depletion process is based

1:38:22

on light resonance , practically

1:38:24

. So they are

1:38:27

not able to control

1:38:29

deuterium in their oil

1:38:31

or in their hydrocarbon products

1:38:34

as easy as animals can

1:38:36

, because animals eat grass

1:38:38

. They use citrate mitochondrial

1:38:40

product to produce their own fat , so

1:38:42

they all have to be deuterium depleted . That's

1:38:45

why saturated animal fat is the

1:38:47

safest to eat , because they

1:38:49

have the most efficient deuterium depleting

1:38:51

process during fatty acid synthesis

1:38:53

. And that's their mitochondria , that's their citrate

1:38:56

synthase enzyme reaction which uses

1:38:58

matrix water to produce that citric

1:39:01

acid which is then through the citrate

1:39:03

shuttle , it's shuttle to the cytoplasm

1:39:05

. Non-manonar coenzyme or aceticity

1:39:08

coenzyme if it's cholesterol

1:39:11

synthesis is produced

1:39:14

. And they all come from mitochondria

1:39:16

Plants . They cannot do this plants

1:39:19

. They have their own metabolic

1:39:22

priorities

1:39:24

, simply because they depend on photosynthesis

1:39:27

. That's why they have to stay in one

1:39:29

place , soak up as much water

1:39:32

as they can , and then

1:39:34

they depend on animals to spread

1:39:36

their seeds and they wrap

1:39:38

them into these sweet

1:39:40

, addictive deuterium

1:39:43

bombs called fruits . The

1:39:45

wild boar comes , they eat

1:39:47

the apples , they walk

1:39:49

two kilometers and sorry

1:39:52

, excuse my language , but they

1:39:54

have a diary and they shit everywhere

1:39:57

. So that's how trees propagate

1:39:59

themselves , because they can produce a

1:40:02

high deuterium addictive

1:40:04

sugar , load fruits

1:40:07

and kind of embed

1:40:10

the seeds in there and the animals that eat

1:40:12

them . They go into sugar calm and they

1:40:14

start running around

1:40:19

like lunatics and they spread the seeds everywhere

1:40:22

. That's the purpose of sugar . That's

1:40:24

the purpose of carbohydrates . It

1:40:26

has no role in human nutrition

1:40:28

. The only safest food that we can consume

1:40:31

is grass-fed animal saturated

1:40:33

fat .

1:40:35

Yes , it's interesting and I want

1:40:37

to . I'll definitely include that paper in the show notes

1:40:39

. Did you

1:40:41

have specific deuterium concentrations

1:40:44

for canola oil , for sunflower oil ? Can

1:40:46

you tell me now , are

1:40:48

they 250 , are they 200 , what

1:40:51

is the deuterium level in these oils or how

1:40:53

can we test it ?

1:40:55

I can be anywhere from 150

1:40:58

to 250 , based on what kind

1:41:00

of saturation process , what kind of organic

1:41:03

expression process . They need to read

1:41:05

our paper in . What to eat . What to eat

1:41:07

? That's the question . Because that's

1:41:09

that paper was accepted in 24

1:41:11

hours by the chief editor . Because

1:41:14

he said finally finally

1:41:16

, the

1:41:19

only thing he asked me is just to reduce

1:41:21

the length of the paper from

1:41:23

like 1200

1:41:26

words to 750 words . But

1:41:28

practically it was like a light opening

1:41:30

to like a li-bob

1:41:33

kind of situation , to a

1:41:35

oncological

1:41:38

or cancer-related

1:41:40

project where they actually figured

1:41:42

that actually the ketogenic diet is not

1:41:44

working in those animal

1:41:47

models . So we looked at the

1:41:49

the supply of those

1:41:51

animal diets and sure enough it was

1:41:53

loaded with plant based oils

1:41:56

, the organic extraction

1:41:58

and organic solvent extraction . It's

1:42:01

describing that paper . So

1:42:04

my best guess is what ? 250

1:42:06

ppm or somewhere around

1:42:08

. I just you know

1:42:10

, if you look at Dr Robbins

1:42:13

papers , if you get capsaicin

1:42:16

from Paprika , which is

1:42:19

from home

1:42:22

growers , it has 110

1:42:25

ppm . Once you go and buy capsaicin

1:42:27

from any chemical company

1:42:29

, they produce capsaicin that

1:42:32

has a ppm of 160

1:42:34

. So the natural processes

1:42:36

are all very different from the

1:42:38

industrial processes and it doesn't

1:42:40

matter what the oil

1:42:43

comes from . When the industry steps

1:42:45

in you can forget about

1:42:47

the routine regulation of what nature

1:42:49

is trying to accomplish .

1:42:51

Yeah , and that really makes me

1:42:53

think that , yeah , how important the

1:42:55

deuterium is in the terms of the seed

1:42:57

oil toxicity story . And yeah , it's the omega-6

1:43:00

, yeah , it's the oxalams , but they're

1:43:03

essentially deuterium , as you , as

1:43:05

Cruz talked about the deuterium bombs , it's

1:43:08

deuterium and deuterium enriched

1:43:11

, not only because of the industrial processing

1:43:13

but also because , as you've mentioned , photosynthesis

1:43:16

is inherently the process of

1:43:18

plant metabolism , is inherently

1:43:20

unable to engage

1:43:23

in deuterium depletion .

1:43:24

So because they cannot oxidize , they cannot

1:43:26

eat fat . Practically

1:43:29

they only use inorganic

1:43:31

elements to assemble an organic molecule

1:43:33

. They don't have the luxury like

1:43:36

a cow can do practically producing

1:43:38

their own fat using mitochondria

1:43:41

.

1:43:42

And that really gets us to the next point , which is

1:43:44

why grass-fed fat

1:43:46

is so much more favorable than other

1:43:49

forms of food . And have you recorded

1:43:52

and apologies if this has already been

1:43:54

talked about in your paper have you noticed

1:43:56

a significant increase in deuterium

1:43:59

content between grain-finished