0:00

In this episode I speak with world expert

0:02

on deuterium depletion and cancer

0:04

, dr Gabor Schumli , from Hungary

0:07

. He has dedicated his professional

0:09

life to understanding and treating cancer

0:11

with methods that reduce the concentration

0:14

of the heavy hydrogen isotope

0:16

, deuterium , in the body . Now

0:18

deuterium depletion is not some fringe

0:21

or wacky alternative healing modality

0:23

. Rather , it is a thoroughly researched

0:25

scientific topic with decades

0:27

of benchside and clinical evidence

0:29

of efficacy . The benefits are understandable

0:32

when we step out of the

0:34

DNA , rna and nuclear

0:36

genomic view of cancer and into

0:38

a mitochondrial , metabolic and

0:41

bio-energetic model of cancer

0:43

, which I and others believe it

0:45

represents . Dr Schumli has

0:48

had amazing success with this approach

0:50

and has again extensively

0:52

published this in the peer-reviewed literature , as

0:54

well as making it access to people through

0:57

two published books , the most recently titled

0:59

Deuterium Depletion , which was

1:01

published in 2022 . For those

1:03

who are new to the concept of deuterium

1:05

as it relates to biology , please

1:07

check out my earlier episodes with Dr Jalal

1:09

Khan , dr Serapiu and

1:12

Dr Laszlo Boros . I

1:14

hope that you enjoyed this episode and it

1:16

offers you some further understanding

1:18

of the biochemical basis of cancer

1:20

. I particularly hope it can be

1:22

of value to other health practitioners

1:25

, particularly GPs , family

1:27

doctors and oncologists , who have

1:30

a potential role in guiding

1:32

patients through a deuterium depletion

1:34

protocol in addition to standard

1:37

oncological therapies

1:39

. Thank you and enjoy the show

1:41

. Dr

1:49

Gabor Schumli , thank you for coming onto my podcast

1:51

. You're welcome . So let's start

1:53

with this idea of deuterium

1:56

and how it relates to

1:58

cancer . You're

2:00

obviously a world expert on the use of deuterium-depleting

2:04

procedures or

2:06

regimes to assist

2:08

in cancer treatment , and I

2:11

think we could start by explaining to people

2:13

the concept of deuterium

2:15

, because that will give

2:18

us a good background for what we talk

2:20

about later in this discussion .

2:25

I was a teenager when I decided to do

2:28

something with this cancer

2:31

. The first thing I

2:33

declared that I'm not going to

2:35

find a drug , because

2:37

I don't believe that there is any drug which would

2:40

be able to effectively cure

2:42

cancer . My concept was when

2:44

I started thinking about cancer

2:46

, what should be the mechanism

2:48

and how can the cells regulate

2:50

the cell growth ? Because I

2:52

believed if we find a way how

2:55

the cells can regulate the cell growth

2:57

in that way we can find

3:00

a way to cure cancer . And

3:02

I was lucky because Albert

3:05

Sangerdi , who is one of the Hungarian Nobel laureates

3:08

, gave an interview in

3:10

the early 70s and in

3:12

his interview he said

3:14

one word . He said submolecular

3:17

. So he suggested that

3:19

it is not possible

3:22

that the huge protein molecules would be

3:24

responsible for that very precise

3:26

regulatory system

3:28

and he suggested that we should

3:30

go to submolecular level . So

3:33

I kept it in my mind that submolecular

3:35

. And he recommended that electrons

3:37

should be that small particle

3:41

and I kept it in my mind that submolecular

3:44

. One day the idea came to my mind that maybe

3:48

the hydrogen ion , which is a small

3:51

positively charged element

3:54

, should be that submolecular particle

3:56

which has a key role in that

3:59

cellular regulatory system . And

4:01

four years later I

4:04

was a student at the university and the

4:06

other idea came to my mind that

4:08

there is a heavy hydrogen

4:10

, it is called deuterium , and

4:12

that was in 1918 . So I

4:14

was sure that somehow the deuterium

4:17

hydrogen together are responsible

4:19

to regulate the cell growth . I graduated in

4:21

1982 and then I started

4:23

to find a job which on

4:25

a cancer field . But I couldn't find . So

4:29

I continued my DNA work . Later

4:33

I defeated my PhD

4:35

. Then I went to Germany and the United States

4:37

and when I came back from the United States

4:40

I started to find again a job which

4:42

is cancer related . And

4:44

at that time , in 1990

4:47

, I started to work at the Hunger

4:49

and Nations Oncology and

4:51

I started to investigate the possible

4:54

role of the deuterium in the living organism

4:56

. So the question was and

4:59

that was surprising me that everybody

5:01

knows that the deuterium is present in nature

5:03

. The ratio is 6600

5:07

to 1 between

5:09

the hydrogen deuterium . Everybody

5:12

knows that the deuterium behaves

5:14

differently in chemical reaction

5:16

because due to the 100% mass difference

5:19

and even that nobody

5:21

investigated it for 60

5:23

years . But there is any role

5:25

of the deuterium in the living

5:27

organism and I guess the reason

5:30

was that this 6600 to

5:32

1 ratio , the people believe

5:34

that we can ignore it . So

5:36

the question , what I addressed really

5:39

can be ignored at deuterium . And

5:42

it's even

5:44

more surprising that when we talk

5:46

about PPM , so if we take

5:48

1 million hydrogen , we

5:51

can find 150 , 155

5:53

deuterium out of 1 million hydrogen

5:55

. This is the reason that we talk about PPM

5:58

, of the D level , but we

6:00

explain the de-concentration in millimole

6:02

because then somebody go to the doctor

6:05

and got a blood

6:07

report . They will

6:10

find that the calcium level

6:12

is about 2.5 millimole , the

6:14

magnesium concentration or

6:16

about 1 millimole , but

6:19

the deuterium level is 12 millimole . Even

6:21

it is not on the test

6:24

. So the question was can

6:27

we ignore the deuterium if

6:30

the de-concentration is 6 times

6:32

higher than the calcium or 10

6:34

times higher than the magnesium in the blood ? So

6:37

in the very first experiment I used

6:40

deuterium-depleted water . I

6:42

prepared media for cancer

6:44

cell lines and

6:47

I checked the cell growth in

6:49

artificial media with deuterium-depleted

6:52

water and

6:55

the first data was shocking because

6:57

I found that in

6:59

deuterium-depleted media the cancer

7:01

cell growth was slowed down or

7:04

was stopped completely . The

7:07

other series of the experiment we

7:09

transplanted human breast cancer

7:11

to mice and we replaced

7:13

the drinking water with the mice deuterium-depleted

7:16

water and they found that we could

7:18

stop the cell growth and we can get complete

7:20

tumor regression in the mice drinking

7:23

deuterium-depleted water and

7:26

the very first data and results

7:28

was published in 1993

7:31

. In that paper we concluded

7:33

that the nature-occurring

7:37

deuterium is essential to keep

7:39

the normal growth rate in the living organisms

7:42

and the cells and

7:44

we combined

7:46

our data with the data

7:49

of other scientists . Other

7:51

scientists would prove that when

7:53

a growth hormone binds to the membrane and

7:56

that membrane on hydrogen out of the cells

7:58

and pick up on sodium from

8:01

the outer space of the cells

8:03

and that transportation

8:06

, increased transportation of the hydrogen

8:08

caused a pH increase in

8:10

the cell and everybody agreed that

8:12

that increase of

8:14

the pH should be responsible to

8:17

trigger the cell division . So

8:19

in our very first paper we concluded

8:22

that when the

8:24

growth hormone activates and stimulates

8:27

the membrane

8:29

and that sodium-hydrogen antiport

8:31

, that we prefer

8:33

to transport the hydrogen , which

8:36

means that activation

8:38

results a higher deuterium-hydrogen

8:41

ratio and that changing

8:43

the age ratio , a higher deage

8:45

ratio , would be responsible to trigger

8:47

the cell division . So when

8:50

we keep the cells on a deuterium-depleted

8:52

media it should lift up the age

8:54

ratio to the threshold from a lower level

8:56

and that goes to

8:59

difficulties for the cells to do that and

9:02

even we could conclude that somehow

9:05

the cancer cells are very

9:07

sensitive from the lowering

9:10

the concentration and finally

9:12

, that can cause and triggered

9:15

the octosis of the cancer

9:17

cells . So the very

9:19

first paper that the nature occurring deuterium

9:21

, essential for the normal growth

9:23

rate and for the physical processes

9:26

, With the low D level

9:28

we can trigger the

9:31

necrosis of the cancer cells

9:33

and the man is one

9:35

part of the man is how to regulate the cell

9:37

growth . It depends on the deage

9:40

ratio and that the deage

9:42

ratio increase the

9:44

threshold that can trigger the

9:46

cell division . So that was

9:48

the very first part of our study and we published

9:51

, and later we

9:53

continue our research and

9:56

we know that finally

9:59

, our D level is depends on

10:01

one , two thing the

10:03

one , what type of water

10:06

we drink and what type

10:08

of food we eat . Because

10:11

the water , what we drink , it

10:13

is about 1.5 to 2 liter per

10:16

day . That can strongly

10:18

determine the average D

10:20

level of our body . But

10:22

we every day synthesize about 0.3

10:25

, 0.4 liter water

10:28

. This is called metabolic

10:30

water , which is made in the

10:32

mitochondria . And

10:34

when the mitochondria is producing this

10:37

metabolic water , then the hydrogen

10:39

is coming from the lipids , from amino

10:42

acids or from the carbohydrate

10:45

. And so

10:48

, very first step , I went to the shop

10:50

and I bought different type

10:52

of food I mean sugar

10:55

, cottage

10:58

or land

11:00

or fat . I

11:03

brought this type

11:05

of water to the research institute

11:07

and asked them take out the

11:10

water from this food and burn

11:13

that dry food to water , because

11:15

that will be the water of what the mitochondria

11:17

will produce . We

11:20

found that the data showed that when

11:22

the mitochondria burn the carbohydrate

11:24

, that will produce metabolic

11:27

water with 150 ppm deconcentration

11:30

. When the mitochondria

11:32

burn the proteins , that

11:35

will produce about 135-38

11:39

ppm deconcentration

11:41

. But when the mitochondria

11:44

burn the fat , that will produce

11:46

118 ppm

11:48

deconcentration . So

11:52

our day-level

11:54

will depend on what

11:56

is the composition of the diet . The

11:59

more carbohydrate we

12:01

eat to cover

12:03

the calorie intake , the metabolic

12:06

water , the more fat we eat , it

12:09

means we're burning fat

12:12

and producing 118 ppm

12:14

. That means we can

12:16

lower the deconcentration

12:19

of the metabolic water . So

12:21

in our body our average

12:24

deconcentration will

12:26

be the combination of

12:28

the water we drink and the combination

12:31

of the diet we eat . And

12:33

the more fat we eat , the

12:35

lower will be the D-level . That

12:38

way we can regulate and that will determine

12:41

our deconcentration

12:43

. So what we offer

12:45

people now based upon our data , first

12:49

of all , the

12:51

biggest problem for the society

12:53

, that

12:56

the fat is said

12:58

this is a bad food and

13:01

in the last 50-60 years

13:03

it was said that we should

13:05

increase the calorie intake by

13:08

carbohydrate and

13:10

it means that the society in

13:12

the last 50-60 years leaves their

13:14

lives with a deconcentration

13:17

pretty close to the 150 ppm

13:19

, because the

13:21

ratio of the calorie intake of

13:24

the fat is pretty low . So

13:26

what we suggest ? First , change

13:28

the diet just to

13:30

reduce some but the deconcentration

13:33

of the metabolic water and

13:35

or consume due

13:38

to deprecated water . Depending

13:40

on whether you are healthy , whether

13:43

you are diabetic or

13:45

has a metabolic disease , or

13:47

depending if you are a cancer patient

13:50

, you have to consume another type

13:52

of due to deprecated

13:54

water . And if we

13:56

consider what is the

13:58

role of the deconcentration of life

14:00

and if we

14:03

and that

14:05

way we have a chance to

14:07

intervene very effectively into

14:09

that regulatory system , and

14:11

this is the reason that we believe that when

14:14

the due to depletion will be part of

14:16

the oncotherapy , we

14:18

can drastically reduce the

14:20

death caused by cancer

14:22

. And if the due to

14:24

depletion would be part of the treatment

14:26

of the metabolic disease , that will be very

14:28

, very effective and on the healthy

14:31

population , we would be able

14:33

to reduce the incidence of cancer and

14:36

to prevent the

14:38

metabolic diseases . This is how we

14:41

think today .

14:43

There's so much there . That's incredible

14:45

what you've laid out . I

14:47

really wanted to get you on because I think

14:49

that this is such a promising intervention

14:52

that people can use in

14:54

conjunction with their standard therapy and

14:56

there's no reason why it precludes

14:59

the use of existing

15:01

, maybe mainstream , oncology treatments

15:04

. And I want to go back and just recap

15:06

for the listeners , because you

15:09

said a lot there and essentially

15:11

we've got these two different types of hydrogen

15:14

. One is a heavier hydrogen deuterium

15:16

and the ratio of

15:19

deuterium to hydrogen is regulating cell

15:21

growth . So your early work showed

15:23

that when the

15:25

ratio of hydrogen to deuterium

15:27

was higher or there was less

15:29

deuterium , then the cell was

15:31

less likely to replicate

15:34

and therefore you were able to induce

15:36

programmed cell death or apoptosis in

15:38

these cancer cells . So I

15:41

think that's a key point for people to

15:43

realize or internalize

15:45

, which is that cancer

15:47

is this mitochondrial metabolic

15:49

problem and , contrary

15:53

to a lot of the messaging that we get in the mainstream

15:55

about cancer being a genetic

15:58

problem , the problem is really in

16:00

the mitochondria . So by

16:02

regulating and adjusting

16:04

the ratio of deuterium to hydrogen , we

16:07

can influence the cancerous

16:09

cell to replicate . So based

16:12

on that , you proposed this

16:14

idea of regulating our total

16:17

body deuterium using food and water

16:19

. I want

16:21

to ask you a couple of questions about

16:24

the food before

16:26

we go into the water , and you said specifically

16:28

that the fat , when you burn

16:30

it in the mitochondria , makes the most

16:33

amount of deuterium-depleted metabolic water

16:35

, and I believe , in agreeance

16:37

with you , that the anti-fat

16:39

narrative from Ansel Keys over

16:41

the past 60 years has been incredibly

16:44

harmful and obviously the demonization

16:47

of that , and for a number of reasons , but this is

16:49

just another one of it . My

16:51

question is specifically

16:53

with regard to refined

16:57

oils , or seed oils as

16:59

they're commonly known . Do you

17:01

what has been your experience and your testing

17:04

of the deuterium content of these

17:06

industrially refined oils

17:08

?

17:10

Yeah , so it's . There

17:14

is a paper published that Richard

17:17

Robbins were able

17:19

to measure the de-concentration

17:22

of the fatty

17:25

acid chain and

17:28

he could prove that the

17:30

D-level in

17:32

a linoleic acid on

17:34

the carbon 9 , the de-concentration

17:37

is 60 ppm and this is true

17:39

for the carbon 13, . Which

17:42

means that the metabolism is

17:45

so dedicated and so precise

17:47

that when the cell

17:50

is producing , synthesizing

17:52

a fatty acid

17:54

, they can specifically

17:57

modify the

18:00

D-level depending on the

18:02

number of the carbon . So it

18:04

is not just randomly distributed

18:07

in the cell , even in a given

18:09

molecules . So we

18:12

never investigated changing

18:15

or investigating different type of

18:17

oil and different type of long

18:20

chain fatty , depending

18:22

maybe on the source , depending

18:25

on the plant which is synthesizing a given

18:27

product , can modify

18:29

the distribution and the concentration

18:32

of the deuterium on a given molecules . For

18:35

example , which is very clear , with the carbohydrate

18:38

, the plant has

18:41

three systems , three chemical

18:43

way to fix the carbon dioxide

18:45

from the air . It is called

18:47

the C3 , c4

18:50

and CAM . And

18:52

even the plants , which

18:54

is a weed , for example , belongs to the

18:56

C3 way to

18:58

fix the carbon dioxide . They produce

19:01

a more depleted carbohydrate

19:03

than the other plants which , for example , the

19:06

corn , which use the

19:08

metabolic pathway according

19:10

to C4 . And the pineapple

19:13

can enrich the deuterium

19:15

in the plant . So that

19:17

shows that depending

19:20

on the plant , depending on a given

19:22

biochemical pathway , can

19:25

be even the same type of

19:27

biochemical pathway

19:29

can be different depending on

19:31

the plant , the cell and so on

19:33

. So it's an extremely complex

19:35

system and it requires lots

19:38

of science and lots of research

19:40

to figure out what's going on . When

19:43

we check the oil , the oil

19:45

deuterium level wasn't

19:47

so depleted than the

19:49

fat . So if we check

19:52

the different type of foods , the

19:54

lowest de-level is in the fat . But

19:57

for example the capsaicin which

20:00

makes the pepper very hot , it's

20:03

the concentration , only 60

20:05

ppm . Because

20:07

what we see , that in each

20:09

chemical reaction always

20:11

the hydrogen will be preferred

20:13

, because there is a tenfold difference

20:15

in the speed the

20:18

chemical reaction is running with hydrogen or deuterium . So

20:22

the more complex a molecule

20:24

we can consider , the more depleted

20:26

for deuterium . Because

20:28

during the synthesis , always

20:31

the chemical

20:33

reaction , we go faster with the hydrogen . So

20:36

that way we can differentiate

20:38

and we can consider that one molecule should

20:41

de-level , we'll be closer to 150

20:43

ppm , the other maybe

20:45

will be much lower than 150

20:49

ppm .

20:49

It makes so much sense to me , which is

20:52

that if you're eating foods

20:54

of animal origin , then

20:56

Mother Nature has kind of already created

20:59

its deuterium depleted food

21:01

source , whereas if you're eating a plant

21:04

, then you're

21:06

not benefiting from this natural process of

21:08

eating fats that

21:10

have already been deuterium depleted

21:13

. The question

21:15

, I guess , was relevant , and it's interesting that

21:18

the seed oils do have more deuterium

21:20

in them than animal fat , and I think

21:22

that is one reason why

21:24

they're such an undesirable

21:27

food for most

21:29

people , and the fact that most people have replaced

21:31

saturated fat with the seed oils

21:34

is very problematic . So

21:37

let's talk about water , and

21:39

it makes sense to me that the mitochondria

21:41

need to be burning food that is the least

21:44

deuterium content in order to produce the most

21:46

deuterium depleted water . But in

21:48

terms of drinking water

21:50

that is , having a

21:52

low deuterium concentration , can

21:55

you talk to the natural

21:57

prevalence of or concentration of deuterium

21:59

in various waters that

22:02

you might find naturally ?

22:05

So you are living

22:07

in Australia , you are

22:09

very close to the equatorial

22:12

area , so the ocean

22:15

level is 155 ppm

22:17

. And when the clouds appear

22:20

and moving to the south

22:22

and north poles easier

22:25

or easier can lose the

22:27

heavy water molecules

22:29

. It means that the rainwater

22:32

D level is decreasing . At

22:34

the farther from the equatorial

22:36

area the lower the de-concentration

22:39

of the rainwater . And

22:41

this is true when we go uphill

22:44

. The higher the altitude

22:46

on the hillside , the lower the D level

22:48

. And this is also true the farther

22:50

from the ocean , the lower the

22:53

D level . So it means in Hungary

22:55

, in central Europe

22:58

, we have about 148

23:00

ppm de-concentration

23:02

. If you go to Edmonton

23:05

in Canada , far from the ocean

23:07

and pretty north , it should be about 100 certified

23:10

ppm de-concentration

23:12

. In the middle of Africa it should be

23:14

about 155 ppm because

23:16

they've got back the same water which

23:18

is evaporated from the ocean

23:20

and that will determine

23:23

the D level of the plants

23:25

which is cultivated on a given

23:27

area and also modified

23:30

by the biochemical processes of

23:32

the plant , so that again

23:35

which can strongly modify

23:37

the D level . But it is very important to say

23:39

because you mentioned that . So we

23:41

concluded that the lower D level

23:43

can stop or can slow down

23:45

the cell growth . But when we

23:47

talk about the application of

23:49

D-tim-de-pre-tid water we

23:52

do not have to worry about that

23:55

. We'll reduce

23:57

the growth of the healthy cells Because

24:00

what we found , that the

24:03

healthy cells because

24:05

they are healthy cells and the metabolites is

24:07

perfectly working well

24:10

. They , day by day

24:12

, are able to adapt the metabolites

24:14

to the lowering D level . And

24:16

the big difference between the cancer cells

24:19

and healthy cells , that

24:21

the cancer cells has

24:23

an impaired mitochondria

24:25

. And this is the reason

24:28

that because the

24:31

mitochondria is not able to produce D-tim-de-pre-tid

24:34

metabolic water , so when

24:36

the growths form , bind to the membrane and stimulate

24:38

very easily can lift up the

24:40

D-age ratio to the threshold to trigger

24:42

the cell division . When

24:48

we modified the D level of the cancer

24:51

cells day by day , consuming the patients

24:53

due to in depleted water

24:56

, it's a challenge day by day and

24:58

that can trigger the radicals and

25:00

that radicals finally can trigger

25:02

the apoptosis

25:04

and this is how it works . So

25:07

for healthy population we

25:10

suggest to consume due to in depleted

25:12

water with 125 ppm

25:15

or 105 ppm . We

25:18

have run a phase two clinical study

25:20

with patients

25:23

having metabolic disease . They

25:26

consumed 105 ppm

25:28

, 1.5 litre per

25:30

day for 90 days and

25:33

when we checked the D level of the blood from

25:36

148 , we reduced

25:38

to 133 ppm . So

25:41

that clearly shows that consuming

25:43

DW we reduced the deconcentration

25:46

of the body and that way

25:48

in that clinical trial

25:50

we could reduce the fasting

25:53

glucose level and then

25:55

we could reduce the insulin resistance

25:57

. That way we could increase

26:00

the HDR cholesterol

26:02

, the so-called good cholesterol concentration

26:05

, and the blood count

26:07

didn't change , so we did not

26:09

cause any trouble or

26:11

drop of the blood counts or whatever

26:13

. So this is what we offer

26:15

to have CPP to

26:18

bring the D level to

26:21

the range of 125

26:23

, 450

26:25

ppm , because in that

26:27

range the mitochondria works much

26:30

properly and the insulin

26:32

signal system is also

26:34

working much properly . The

26:36

basis that I says that we

26:39

have run a three

26:41

red study . In the

26:43

red study we made the reds

26:45

diabetic and we checked whether

26:48

we can reduce the blood sugar

26:50

level of the reds . The

26:52

point was when the reds did

26:55

not receive insulin the D

26:57

level did not modify the blood sugar

26:59

level . It was pretty high in that

27:01

red . But when

27:03

the reds received 25

27:06

ppm and got insulin

27:09

, that significantly reduced

27:11

the blood sugar level of the

27:13

diabetic reds . But

27:16

in then we repeated the

27:18

experiment . If we checked not only

27:20

25 ppm but 1

27:22

, 25 and 75

27:26

, 105 . And the point was

27:28

that not the lowest D concentration

27:31

reduced the best rate of 25

27:33

ppm . And in the third

27:35

experiment we checked between 125

27:37

and 150 ppm , changing

27:39

by 5 ppm , and that

27:41

clearly showed that the

27:44

best was the 125 ppm

27:47

. And we also checked

27:49

I

27:51

don't know whether the people do

27:54

not know , I guess what the meaning of

27:56

glutathor protease is staying in

27:58

the cytosol and

28:00

when the insulin bind to the membrane and

28:03

trigger the signal system , that

28:05

will stimulate the glutathor to move to

28:07

the membrane because that glutathor will

28:09

pick up the glucose from the blood vessel . So

28:12

in that red study we checked whether

28:14

the D concentration

28:17

can modify

28:19

the glutathor concentration

28:21

in the membrane of

28:23

the red muscle and

28:25

we found that the highest glutathor

28:28

concentration was at the 125

28:30

ppm , which means that the insulin

28:32

signal system work much

28:34

properly at the 125

28:37

ppm . So this is , and after

28:39

that we checked with a human clinical study

28:41

and that was the same . We found

28:43

that when we reduce that D

28:47

level of these patients with metabolic

28:49

disease , that way we can improve

28:51

their metabolism , reduce the blood

28:53

sugar level and all these things . So

28:55

this is how it works .

28:57

Fascinating , and I'm very much

28:59

interested in metabolic disease as

29:02

well , and I really think that they're just two sides

29:04

of the same coin . When it comes to

29:06

mitochondrial dysfunction , and

29:09

whatever you have the misfortune

29:11

of manifesting with regard to mitochondrial

29:13

disease will determine whether that is

29:15

diabetes or some form

29:17

of cancer . And

29:20

125 ppm

29:23

I'll keep that in my head and I

29:25

want to talk to you about protocols . But

29:27

just before we do that , what

29:29

about the natural deuterium

29:32

depleting mechanisms of the body ? Because

29:34

if you've mentioned that the

29:37

deuterium content of our

29:39

bodies is influenced by , obviously , what

29:41

we eat and what we drink , what about our

29:43

natural ability to get

29:46

rid of deuterium ? And the reason I ask is

29:48

because there might be native

29:51

populations living at the equatorial latitude

29:53

whose water is 155

29:57

ppm of deuterium . They

29:59

eating pineapples

30:01

or bananas , mangoes

30:03

, yet they have low

30:05

incidence

30:08

of metabolic disease , mitochondrial

30:10

dysfunction and cancers , and I'm thinking

30:13

of , perhaps , maybe , populations like the Katarvins

30:15

in Melanesia . So

30:18

what mechanisms have

30:21

we evolved specifically in people who are

30:23

living equatorially or living in their natural

30:25

environment .

30:25

I understand the question and I guess this is

30:27

a very good question and important . So

30:30

I don't believe that

30:33

each population is

30:36

adapted to the de-concentration

30:38

where they live and

30:44

I have seen several podcasts

30:47

with other people . So I

30:50

don't believe that the aim

30:52

is to reduce

30:55

the de-level as much as possible

30:57

and I do not agree that the

30:59

lower the de-level the better . I

31:02

think the deuterium-hydrogen ratio

31:04

is crucial and

31:07

the question is where is

31:09

the optimal deuterium-hydrogen

31:12

ratio ? As I mentioned at

31:14

the beginning the

31:16

problem of the society that

31:18

we increased with 15 ppm

31:20

the average de-level just because

31:23

we changed the diet . But

31:25

if we can move it back to

31:28

the 125 ppm , 140

31:30

ppm , then that

31:32

would be a big step forward to

31:35

reduce the incidence of metabolic

31:37

disease and cancer In

31:40

our body . When we talk

31:42

about how can leave our body

31:44

, that belongs to , I

31:46

guess , the proteins

31:50

and the

31:52

NH2 groups

31:55

of the amino acids , Because

31:57

in a biochemical reactions

32:00

the amino groups

32:02

are collecting the deuterium

32:04

and that way we

32:06

can eliminate from the body the

32:09

de-level and the deuterium

32:11

. And I also heard

32:13

someone said that maybe the microbiome

32:17

also can be responsible

32:20

, modifying the

32:22

deuterium-hydrogen ratio and removing

32:25

it . I have read

32:27

papers that different microbes

32:30

has a very big

32:32

discrimination between deuterium-hydrogen

32:35

ratio and that way again can

32:38

modify this DH ratio . So

32:40

all these things , finally , will provide

32:43

us a given de-level altogether

32:46

. But so what

32:48

? I would like to say that the

32:51

deuterium is essential . The

32:53

deuterium-hydrogen ratio is

32:56

the way that when the cell

32:58

can modify it , because they

33:00

are deactivating the sodium-hydrogen

33:02

or because they properly

33:05

work in mitochondria and

33:07

changing the DH ratio , that way the

33:10

cells are able to send a message

33:12

to all the molecules in the cell because

33:15

in the exchangeable position always

33:17

will be an equilibrium . So

33:19

if there is an increase in the DH

33:22

ratio because the activation of sodium-hydrogen

33:24

, that will send the message to

33:26

all the molecules and that

33:29

means simultaneously

33:31

the cells can regulate the

33:33

gene expression , protein activity . Let

33:36

me tell you another experiment , what we have published

33:38

. So we know that

33:40

the small

33:42

pharma , big pharma , is targeting

33:45

a gene which was identified

33:47

to have a key

33:50

role in the cancer

33:52

development . So

33:54

we know one of the first gene was the

33:56

tisening kinase , and

33:59

so my question was whether

34:01

we can modify the gene expression , just

34:03

changing the de-concentration of the cell

34:05

. So we kept

34:08

the cells in a deuterium-depleted

34:10

media , in normal media

34:13

and deuterium-androgen media , 300

34:15

ppm , and

34:17

we were able to check

34:19

the expression of over

34:21

700 genes . Over

34:23

200 was kinase gene and over

34:26

200 was cancer-related genes

34:28

. So it is called

34:30

a nanostring technology , which

34:32

means we were able to count one

34:34

by one the copy number

34:37

of a given gene . So how many

34:39

copies was made in different

34:41

de-concentration of the cell

34:43

? And what we found ? That not

34:48

the lower de-concentration

34:50

was a key but the higher

34:52

the level was because

34:55

99% of the cells responded

34:57

to the higher de-concentration . So

35:00

when we use the deuterium-depleted

35:03

water , one

35:05

way we triggered the apoptosis because the

35:09

radicose . But

35:11

that way we simultaneously inhibit hundreds

35:13

of genes having role in the cell

35:15

division , not

35:17

just one gene , one of

35:19

the target of cancer drug

35:21

. So when we talk about

35:24

that , the cells can modify the de-age

35:26

ratio . The key message

35:28

is that no-transcript

35:30

. That way the

35:32

cell are organized and

35:35

harmonized the 2000

35:37

bicochemical processes and

35:39

the expression of thousands of genes . And

35:42

this is how it works ?

35:43

Yeah , and it makes sense to me that

35:45

the deuterium level we

35:47

adapted to a deuterium level of our environment

35:50

and I guess I would ask is

35:52

that a function of mitochondrial

35:54

haplotype and we should be eating the diet

35:56

from which our mother's lineage

35:59

has come from ? That , to me , makes the most

36:01

sense with regard to what our adapted

36:04

deuterium level is .

36:06

So when we start to consume

36:08

deuterium-depleted water , that

36:10

is challenging . We

36:12

typically say that we need about three

36:15

to four months to see the

36:17

efficacy of the deuterium depletion

36:20

, for example in cancer patients , Because

36:22

slowly there is a

36:24

decrease in the can modify

36:27

the expression of genes , the activity

36:30

of different enzymes and

36:32

the healthy cells can do that . But

36:34

challenging , challenging day by day the

36:36

cancer cells , hopefully we can trigger the

36:39

apoptosis and when

36:41

we reach the equilibrium then

36:44

all the metabolites will be adapted

36:46

to a lower de-concentration . So

36:49

when we talk about healthy people , that should

36:51

be between the 100 , 25

36:54

, 140 ppm . But

36:56

when we talk about cancer patients

36:58

, we reduce

37:01

and change the D level every

37:03

two , three months , Because then we

37:05

reach the equilibrium . Then

37:07

the cancer cells which survive

37:10

that part of the reduction

37:13

in D level , they will

37:15

be adapted to that level

37:17

and slowly they can grow again

37:19

. So when

37:21

we talk about cancer patients , we have to

37:23

gradually and

37:25

on a long period of time reducing

37:28

the level . That is the way how we can

37:30

eliminate , hopefully , all

37:32

the cancer cells from the body

37:34

.

37:35

Okay , good , because that's what I wanted to talk

37:37

about next , which is protocols and

37:39

practical implementation . Because

37:41

, like I mentioned to you

37:44

earlier , before we started recording , I

37:46

see in my clinic and

37:48

all across Australia

37:50

there are people that have cancer diagnoses and they

37:52

want to know what more they can do

37:55

to increase their chances

37:57

of a better outcome

37:59

. So the question I

38:01

have is , that is a protocol

38:04

of deuterium depletion in active

38:06

cancer . Is that something a patient can

38:09

do themselves ? Is that something

38:11

that requires close

38:13

supervision , or

38:16

how would you see the most safe

38:18

and effective way

38:21

of doing a deuterium depletion strategy

38:23

for cancer ?

38:25

This is a tough question

38:27

because our aim is and our company working

38:29

on to register deuterium depletion

38:32

water as a cancer drug . So

38:34

we have the facility to produce

38:36

deuterium depletion water in accordance to the GMP

38:39

rules and we are waiting for investors

38:41

to finance the clinical

38:44

study . So right now we cannot

38:46

say that the deuterium depletion is part of

38:48

the oncotherapy . But

38:51

my duty , I guess , and my job to

38:53

bring it to the point when all the

38:55

oncologists worldwide will

38:57

think about how to integrate deuterium

38:59

depletion to the existing therapy

39:01

. And of course I

39:03

keep working on it for over

39:06

30 years and it's

39:08

very difficult to share all

39:10

the knowledge . But this is the reason I wrote a book

39:12

. So in the deuterium depletion

39:14

this is the title

39:16

of the book I wrote

39:18

down the protocols . What

39:21

would be the best way to integrate

39:23

deuterium depletion to radiotherapy

39:25

, to surgery , to hormone therapy

39:28

, targeted therapy , immunotherapy , whatever

39:30

? Because I don't believe

39:32

that we have to replace the existing therapy

39:34

. We have to support

39:37

the therapy with deuterium depletion

39:40

and that would be the way to

39:42

win in that war which is called cancer

39:45

war . So we

39:48

have . Of course , I guess I'm

39:50

the only person who have experienced with

39:52

thousands of cancer patients . I

39:55

have been talking for over 30

39:57

years and in that book I try

39:59

to summarize the knowledge that

40:01

I collected . So there

40:04

are a couple of rules . If somebody is diagnosed

40:09

with cancer , follow the protocols

40:12

, what the oncologist says . I

40:15

never intervene and do

40:18

nothing about to replace it with deuterium

40:20

depletion water . So

40:22

the protocol should be one

40:25

example . They diagnose

40:27

the tumor and they decide to operate

40:30

. If the patients had a

40:32

couple of weeks , two , three weeks before operation

40:34

and start to consume DW

40:37

, that way we can increase the operability

40:39

of the tumor , it will be much easier

40:41

to remove . That could

40:43

be critical in a rectum tumor

40:46

, for example , whether they can

40:48

save the illness or no . And there

40:50

are other parts or other

40:52

types of cancer when

40:55

very important whether we can get

40:57

a shrinkage of the tumor and

40:59

the operation would be much better . The

41:02

other option is the

41:05

radiotherapy . What we see that and

41:07

we know that the radiotherapy

41:10

cause and trigger

41:12

radicals in the tumor and this

41:14

is the reason that the radiotherapy is so

41:17

good and so effective . So

41:19

we see very strong synergistic

41:21

effect when the radiotherapy

41:23

is combined with the deuterium

41:26

depletion . We just recently

41:29

published a paper with 55

41:32

glioblastoma patients

41:34

and within that 55

41:37

patients there were 37

41:39

. And they were lucky to

41:42

combine in DW with radiotherapy

41:44

and the medial survivor

41:46

time was three times longer than

41:48

those who just

41:50

received in the conventional therapy because it

41:52

was 47 months . So

41:55

showing that how good

41:57

combination can be the

41:59

radiotherapy with DW . And

42:02

then we can talk about hormone therapy

42:04

, for example with prostate cancer

42:07

. In

42:09

that case , somebody

42:12

diagnosed with prostate cancer , they

42:15

received the . If it's not operable

42:17

, they received the hormone therapy . After

42:19

two , three years became hormone

42:22

resistant . Then the patient received

42:24

some other and then they cannot control

42:26

it . What we suggest if the

42:28

hormone therapy is

42:31

effective , the tumor marker

42:34

values go down . Then

42:36

we recommend stop the hormone , start

42:39

to consume DW and we

42:41

keep them the tumor marker

42:43

in a low level and maybe

42:45

after half a year they

42:48

can check the PSA . It is still low

42:50

. Stop the DW and

42:52

do nothing . When they see

42:54

that there is an increase in the tumor marker

42:57

, start again with DW and

42:59

then we are not able to keep the

43:01

PS in a low level , then come back

43:04

with the hormone therapy and after

43:06

three zero six months they

43:08

can stop again the hormone therapy . We have paper

43:10

, we published paper that we

43:13

kept control for over 10

43:16

years and the patients haven't

43:19

received hormone therapy because the

43:21

DW could keep the PSA

43:23

on a low level and we

43:26

always say that combining with

43:28

the targeted therapy , the DW

43:31

again can be a very

43:33

good combination . For

43:36

example , the Herceptin . It's

43:40

a good drug to treat breast

43:42

cancer and that

43:45

would be the combination

43:47

, whether it's metabolic disease or

43:49

genetic disease the cancer because there

43:51

is connection , there

43:53

is a gene amplification

43:56

of the EGFR

43:58

, epidermal

44:01

Gross Factor receptor and

44:03

there are much more receptor on

44:05

the surface of the cell . It

44:08

means when the growth hormone binds to the membrane

44:11

and there are more receptor much

44:14

easier and faster can

44:16

stimulate the sodium hydrogen transport

44:18

system , which means much faster

44:20

can generate a higher DHS

44:22

ratio . So when we combine

44:26

the Ddela Bue with , for example

44:28

, with Herceptin , which inhibit

44:31

the binding between

44:33

the growth hormone to

44:35

the receptor and inhibit

44:39

the increase of the DHS ratio

44:41

, that again became

44:45

very , very effective to treat the

44:47

breast cancer patients with that type

44:49

of targeted drug . That is

44:52

true for tyrosine kinase inhibitors

44:54

. So that would be

44:56

the way . I hope in the foreseeable

44:59

future that the oncologist

45:01

can combine it and can integrate due

45:04

to indibition to the existing therapy .

45:06

Yeah , and I want to echo that statement

45:09

, which is that no one's suggesting that they

45:11

do discontinue , or patients discontinue

45:13

their existing therapy . This is

45:15

an adjunct , an addition

45:17

to what is also going

45:20

on from a conventional treatment point

45:22

of view , and to me it makes so much

45:24

sense that we can layer

45:26

on top of each other different protocols

45:29

that target the mitochondria and

45:31

support mitochondrial function . And

45:34

obviously in my previous podcast my listeners

45:36

will know that I've talked to Thomas

45:38

Seeger , who has advocated

45:40

for cold therapy . There's established

45:42

evidence for fasting and if we're

45:44

adding things like ketogenic diet and

45:47

deuterium depletion on top of all

45:49

these other protocols , then

45:51

that makes sense that we're

45:53

basically doing our best to support mitochondrial

45:56

function and therefore improving

46:00

the outcome . I

46:03

want to ask you again

46:05

about a bit more about the exact

46:08

approach , because

46:11

obviously people are going to be reading your book . Not everyone

46:13

can work with you . Specifically , do

46:15

people need to get

46:17

a serum deuterium level tested

46:20

before embarking on deuterium depletion , or

46:23

will some people simply just commence drinking

46:27

deuterium depleted water , as per

46:29

your protocol ?

46:32

We are just working on a paper to publish

46:34

that following . So we already

46:36

have measured the

46:38

D level of the blood and

46:40

another study

46:44

we followed how the deuterium level is changing

46:46

. So I don't believe that the

46:50

measuring of D level is a key issue

46:52

. The key issue is to consume deuterium depleted

46:54

water . But of course when

46:56

we start a clinical study we

46:59

will take the samples and measure it and

47:01

find the correlation how

47:03

fast we have to reduce the D

47:05

level , how long we have to keep

47:08

it on a low level , the D level . That

47:10

again takes time , takes

47:12

money and takes big

47:15

effort to figure out all the details

47:17

of this . What we can state

47:20

that consuming DDW

47:22

will reduce the D level and

47:25

there is a strong correlation that the lower

47:27

the de-concentration of the DDW

47:29

, the lower will be the knee

47:32

level of

47:34

the patient's de-concentration . Typically

47:38

we can say that within

47:41

two , three months there is equilibrium

47:43

with a given de-concentration . So

47:45

if we want to keep a

47:47

gradual decrease of D level we

47:50

have to change the D level intake

47:52

of the de-concentration . And it

47:54

is another question , depending

47:57

on two more types how

47:59

fast and how frequently

48:02

we change the D level of the

48:04

consuming DDW . And

48:07

it should be hundred different

48:09

times depending on staging and the conventional

48:12

therapy and all these things . But

48:14

the basic rule is that two , three months change

48:16

the D level . This is what we

48:19

say . To

48:21

measure the D-level can be important

48:24

when we talk about

48:26

whether that water is

48:29

real due to depletion , because

48:31

unfortunately it is very easy

48:33

to sell fake products

48:36

which is said due to depletion

48:38

. So sometimes

48:41

we receive samples from

48:43

patients and water samples

48:46

and that way we can measure it and

48:48

we send back what is the D-level

48:51

. We typically use precipitated

48:55

exhaled brass water which

48:57

reflects the de-concentration

49:00

of the body . So if

49:02

those who are wondering

49:05

whether the D-level is a

49:08

given , which is said about a given

49:10

water , this is a way to

49:12

either sending the water samples

49:14

or checking the

49:18

D-level of the exhaled brass

49:21

, precipitated brass

49:23

water .

49:25

Okay and say someone

49:27

embarks upon a deuterium-depleting

49:30

protocol for , say , they've

49:32

got active cancer , what are the potential

49:34

side effects or adverse effects

49:36

from

49:38

doing this ? Is there a tumour-licence that

49:40

they might have to deal with , or is

49:42

this a well-tolerated procedure on

49:45

the part ? Does it depend on the tumour type ? Let

49:48

us know about that .

49:51

So if someone starts to consume DW

49:53

, of course , depending on the size

49:56

of the tumour , the sensitivity of the tumour , they

49:59

not feel better because

50:01

when the tumour

50:03

starts to necrotize , this

50:06

is what the people can feel Tumour can

50:08

be warmer . The size

50:10

of the tumour temporary can be bigger

50:12

because we initiate

50:14

an inflammatory reaction . Even

50:19

we recommend not to go to CT or

50:21

MRI after starting

50:23

to consume DW because

50:26

in the first two , three months that

50:28

maybe you show

50:31

the bigger tumour size but that means

50:33

that there are more cancer cells . But

50:35

that is an inflammatory reaction

50:37

, that the tumour is getting bigger , that

50:39

the immune system is

50:42

going to remove the dead

50:44

cells . So lung cancer

50:46

patients starting coughing

50:49

out the tumour , the necrotize

50:51

tumour irritate the lung and

50:53

coughing out the tumour , the

50:56

colon cancer some stuff

50:59

can be removed by the faces

51:01

, can be some slight

51:04

blood in the

51:06

faces . So these are

51:08

always related to the healing process

51:11

and when we check

51:13

the blood counts of these people we

51:15

never see that we drop the blood

51:17

cell number or white blood

51:19

cell number . So we do not

51:21

reduce

51:24

the immune system activity or these

51:26

things . So this is not a so-called

51:29

chemotherapy type of

51:31

intervention . When we

51:33

are suggesting people consuming

51:35

DW , the

51:38

people feel

51:41

it more . Gain

51:43

vein , sometimes

51:45

the bone metastasis . The

51:47

pain is getting stronger

51:49

at the beginning than they can feel

51:52

the relief that

51:54

no strong pain in

51:56

the bone . So the point is

51:58

that starting to consume DW

52:01

, do not hope

52:04

that next day you feel better . No

52:06

, it takes two , three months that we can

52:09

conclude . Okay , that was the

52:11

beginning and now we are here and

52:13

to prove it with CT , mri

52:16

or other objective

52:18

numbers which prove the improvement

52:21

of the patient .

52:22

Yeah , and I want to echo

52:25

the point you made , which is that this isn't

52:27

an immunosuppressing therapy and

52:32

, contrary to what

52:34

chemotherapeutic agents are doing , or immunosuppressive

52:36

agents , this is not going

52:39

to be dampening down or

52:41

suppressing the immune system . So

52:43

I guess that is important

52:46

, because every intervention

52:48

that we prescribe in medicine well

52:51

, every medication that we prescribe in medicine has adverse

52:53

effects . But simply

52:55

deuterium , depleting

52:58

the water to

53:00

what you're

53:02

advocating for isn't

53:04

, as you mentioned , having an adverse

53:06

effect on healthy cells

53:08

. So I think that's a very

53:10

important point . So my

53:13

question is how to scale

53:15

this kind of oncological treatment

53:18

or give more patients access to

53:20

this , because it

53:23

sounds like it's quite a specialized process

53:27

that you need to follow up with someone . Or

53:29

have you found that people are managing

53:32

themselves on

53:34

just reading your book ? Or how

53:37

is the average person going with

53:39

deuterium depletion for cancer ?

53:42

I guess most of the average people

53:44

somehow got some information

53:47

about DW . They can get it

53:49

one way or other and

53:51

they start to consume . Followed over

53:53

2000 cancer patients . They

53:56

regularly came back to us , shared

53:58

the data and we

54:00

were chatting about

54:03

his or her stages . But

54:06

99% of the patients

54:08

just start to consume and

54:11

do it one

54:14

way or other . We are very

54:16

happy if someone starts

54:18

to learn something first about the

54:20

deuterium depletion , because

54:22

sometimes it's happened with our partners

54:26

that they started to consume

54:29

and after a couple of months come and

54:31

asking and maybe they did

54:33

not use the right D level , they

54:36

did not change the D level on the right time

54:38

or they did not integrate

54:40

it on the best way deuterium depletion

54:43

to the therapy . So

54:46

I guess that

54:48

should require a long time

54:50

to educate the

54:53

oncology society and to educate

54:55

the cancer

54:57

population and the healthy population and

55:01

I hope we can proceed

55:03

in that way . But the critical

55:05

step is the clinical study and

55:08

the approval from the authority

55:10

. So the rule says we

55:13

cannot claim . But this is

55:16

the way we are working on to register

55:19

DW as a drug , because

55:21

that will help us to communicate

55:23

directly and this is the only

55:25

way that we can take part

55:28

of the oncotherapy , the DW

55:30

.

55:31

Yeah , it's interesting and

55:33

important question because there's

55:36

so many potential doctors

55:38

who could assist their patients with

55:40

a deuterium depletion protocol

55:43

, given the safety and given the fact

55:45

that this isn't an immunosuppressing drug

55:47

, and to simply

55:49

guide people through this . With the

55:52

explosion in cancer diagnoses , I

55:54

think people need as many tools as possible . So

55:57

it just seems like a big challenge in my mind

55:59

is to provide enough education

56:02

to doctors and maybe

56:04

oncologist , family medicine

56:06

doctors , to be

56:08

able to have enough training to guide patients

56:10

through this protocol , so that patients

56:12

aren't simply on their own

56:14

doing a treatment

56:17

protocol by themselves without supervision

56:19

.

56:21

I guess they are waiting for the approval

56:23

from the authority . So the

56:25

step one to get the approval

56:27

from the authority , fda , ema and

56:30

then should be part

56:32

of the oncotherapy . Without that we

56:35

cannot proceed . Yeah

56:38

unfortunately .

56:40

And do you train ? Does your organization train

56:42

doctors or are there courses ?

56:43

that no , there's no , no

56:46

, no .

56:48

Yeah , okay , yeah , no , sir , because I'm

56:50

just . I'm just thinking about how we can give

56:53

wider access to people and but

56:56

, like you said , we do need more

56:58

, I guess robust studies to

57:01

satisfy the

57:03

regulatory bodies . But

57:06

from from the

57:08

30 years and the two more than 2000

57:10

patients that you've dealt with , sounds like this

57:13

is unequivocally a safe

57:15

intervention and effective .

57:18

So we were lucky to close

57:20

a phase two double my chemical trial with

57:22

prostate cancer and in

57:24

that study we could prove the efficacy of DW

57:27

. But the authority did not accept it and

57:30

then we just so

57:32

that was a so called prospective study . But

57:34

what we have done , we publish

57:36

data with a so called retrospective study

57:39

. So we collected over

57:41

200 breast cancer patients and

57:43

we published the data . Then we

57:45

published the glioblastoma

57:48

55 patients . We published

57:50

almost 200 lung cancer patients

57:52

. So in that case we

57:54

very precisely could choose and

57:58

make the subgroups depending

58:00

on the staging type of the lung

58:03

cancer , type of the therapy

58:05

. And we could prove that the

58:07

median survival time was

58:10

increased with three to seven for

58:13

the increase , which is

58:15

extremely clear evidence

58:17

that the due to depression how

58:19

effective can be . But maybe the

58:21

the best way and the fastest

58:23

way to to reduce the

58:25

death goes by cancer If

58:28

the DW would be

58:30

part of the therapy when

58:32

somebody is in a remission . So

58:35

luckily lots of cancer

58:37

patients became two more free because

58:39

surgery , radiotherapy

58:42

and all the other therapy . But

58:44

the bad news is they go back

58:46

every half a year and every

58:48

year and worrying what

58:50

the control will show and

58:53

they cannot do anything because

58:55

the therapy was completed

58:57

and waiting whether there is a

58:59

recurrence of cancer or not . So

59:01

we again published a paper

59:04

that 204

59:06

cancer patients consuming

59:08

DW was followed over a thousand

59:10

years . So that was the cumulative

59:13

follow up time and

59:15

we lost 13 people out

59:18

of 204 . Two

59:20

of them died not because of cancer and

59:23

a half of them died those

59:25

who consume DW . They

59:29

never came back and

59:31

the average time was they died 4.1

59:33

years later . Those who

59:35

regularly came back consume

59:38

DW for three , four months every

59:40

year . They never relapsed . Be patient

59:42

, the treatment

59:45

has been completed . They

59:48

are tumor-free . They

59:50

would follow that therapy Drinking

59:53

DW . We recommend tumors 105

59:55

, tumors 85 ppm . This is what I wrote

59:58

in my book and

1:00:00

they repeat it every year in the next four

1:00:02

, five , six , seven years . That

1:00:04

way we should prevent the relapse

1:00:07

. So that would be my

1:00:09

message to all the people who are tumor-free

1:00:12

now and to prevent them not

1:00:14

be cancer patients again .

1:00:17

Yeah , yeah , very interesting

1:00:20

. The question I have

1:00:22

next is regarding the metabolic

1:00:24

syndrome and metabolic diseases

1:00:26

, and you mentioned

1:00:28

earlier that 125 ppm is

1:00:30

the kind of target of the total body deuterium

1:00:33

to ppm

1:00:35

to resolve metabolic disease

1:00:38

. And is this a much less

1:00:40

hands-on process than cancer

1:00:42

for people who have , say

1:00:44

, diabetes , because we're not titrating

1:00:47

down the concentration of

1:00:49

the deuterium-depleted water ? Is that correct ? Yeah ?

1:00:52

Yeah , yeah . So that

1:00:54

would be the simplest way to again help

1:00:56

the people keep

1:00:58

the blood sugar level within the range

1:01:01

, prevent blinding and

1:01:03

the amputation of the legs and all

1:01:05

the things . And

1:01:08

even I believe that somebody

1:01:10

with a diabetes would

1:01:12

consume , for example , 105 ppm

1:01:15

for three , four months . Maybe

1:01:17

they can stop drinking DW and

1:01:20

the blood sugar level will be

1:01:22

in the normal range , maybe

1:01:24

for a couple of months . After that

1:01:26

they stop drinking DW and

1:01:29

then they can come back and start again

1:01:31

drinking DW . And

1:01:33

the longer they can keep the

1:01:36

blood sugar level within the range

1:01:38

, the better they can prevent

1:01:41

all those bad

1:01:43

consequences of the high

1:01:45

blood sugar level .

1:01:47

Yes , that makes sense . And if we again

1:01:50

go back to the beginning of the episode where we talked about the mechanism

1:01:52

, it's simply improving mitochondrial function

1:01:55

and if we think about

1:01:57

metabolic diseases as a disease of

1:01:59

inefficient or broken

1:02:01

mitochondria , then giving

1:02:03

them deuterium depleted water will

1:02:07

lead to improved efficiency

1:02:09

of mitochondria and therefore improved

1:02:11

glycemia . The

1:02:13

question about diet in terms

1:02:16

of deuterium essentially

1:02:18

it sounds like a high fat carnivore

1:02:20

diet is the most deuterium depleted

1:02:22

diet . Is that correct ?

1:02:24

Yeah , I agree , yeah , sure . So

1:02:26

we recommend people , when starting

1:02:28

to drink DW at

1:02:31

the same time , change the diet

1:02:33

, some kind of ketogenic type

1:02:35

diet . I never say be

1:02:37

restrict ketogenic

1:02:40

because they cannot keep it on a

1:02:42

long term . They should find

1:02:44

the best way when they can optimize

1:02:47

it and keep it on a long

1:02:49

period of time .

1:02:50

Yeah , and Dr Boris

1:02:53

, who I talked to earlier , was talking about

1:02:55

the benefit of high

1:02:57

fat carnivore for all the reasons

1:02:59

of promoting metabolic water

1:03:01

function and optimizing

1:03:03

mitochondrial function . So to me

1:03:05

it sounds like a

1:03:08

high fat diet , ketogenic or

1:03:11

carnivore type diet would be the most optimal to

1:03:13

do in addition to drinking the deuterium

1:03:16

depleted water . For cancer or for

1:03:19

metabolic disease , yeah , I

1:03:21

fully agree , yes , yeah

1:03:23

, and

1:03:26

again , there's no reason

1:03:28

. I think I just want to make the point for my listeners is

1:03:30

that there's no reason why we can't do this

1:03:32

therapy in addition to other

1:03:35

things like exercise , like respecting

1:03:37

our circadian rhythm and our light environment . It's

1:03:40

great that this is simply just another tool

1:03:43

in the toolbox , so that's how I kind of

1:03:45

understand it to be .

1:03:46

There are a couple of things that we do

1:03:48

recommend not to do , and this

1:03:50

is very important . So , for example

1:03:52

, I sometimes I didn't understand

1:03:54

why the people do not show any improvement

1:03:57

even consuming DW , and

1:03:59

later it's turned out those who are taking

1:04:01

antioxidants on a high

1:04:03

dose that prevent

1:04:05

the efficacy of DW , and

1:04:08

this is the reason of the radicose . So

1:04:11

when we are going to trigger radicose

1:04:13

, hopefully triggering the necrosis

1:04:16

, but if they're taking vitamin

1:04:18

C , e , a , selenium , that

1:04:21

way we have the cancer cells

1:04:24

to work again DW . This is what

1:04:26

we recommend . The other we do not

1:04:28

recommend the exercises

1:04:31

and loading tests

1:04:33

, because then the

1:04:36

electricity increasing in the blood

1:04:38

, no enough oxygen

1:04:40

and all this thing . I again

1:04:42

found that those cancer patients

1:04:44

, they were fine starting

1:04:46

to doing exercise , they

1:04:49

relapsed . And the third

1:04:51

is don't sell no

1:04:53

sauna , no hot baths , because

1:04:56

again the higher body

1:04:58

temperature modified the metabolites

1:05:01

which again somehow helped

1:05:03

the cancer cells to treat

1:05:05

the challenges

1:05:08

of the DW . So

1:05:10

the drinking DW

1:05:13

and not doing

1:05:15

that , three different

1:05:17

things to optimize the efficacy of

1:05:19

DW .

1:05:20

OK , thank you for making those points . So

1:05:22

it's very common for people to come on with a laundry

1:05:25

list of supplements N-acetyl-cystine

1:05:27

, high dose vitamin C , cursatin

1:05:31

and all kinds of plant antioxidants

1:05:33

. So that point that I'll emphasize

1:05:35

is that that is going to interfere with the mechanism

1:05:38

by which deuterium-depleted water is aiding

1:05:41

in your body's clearance of the

1:05:43

cancer cells . So that

1:05:45

makes sense . And then intense

1:05:47

exercise obviously walking is OK , but

1:05:50

you're suggesting that high intensity

1:05:52

or long distance running is a bad idea

1:05:54

.

1:05:55

Yeah , we suggest walking epoxy

1:05:58

and all this thing .

1:05:59

Yes , just

1:06:02

walking and obviously avoiding sauna

1:06:04

and high temperature . And again

1:06:06

, this is if we're using deuterium-depleted

1:06:08

water in an oncology cancer

1:06:10

type setting . And

1:06:13

this is if you're drinking deuterium-depleted

1:06:15

water for longevity or metabolic

1:06:19

disease . It's not a problem yeah don't worry

1:06:21

about it , points that you'd like to

1:06:23

make that I haven't asked you about . Specifically with

1:06:25

regard to the cancer

1:06:27

protocol , what should I ? point out relating

1:06:31

to cancer protocol , anything that

1:06:33

I haven't asked you that you think the listeners should

1:06:36

know , say if they decide to

1:06:38

start drinking deuterium-depleted

1:06:40

water with a cancer diagnosis ?

1:06:43

I guess all the key points was

1:06:45

mentioned if I'm thinking about

1:06:47

. Don't drink any other type of liquid and

1:06:49

minimize the

1:06:52

intake of other liquids . We do

1:06:54

not say that you have to use

1:06:56

for cooking the DWU , but

1:07:00

reduce those

1:07:04

foods which has a high water content , of

1:07:06

course . But the key

1:07:08

issue is , if you cover 1.52

1:07:11

liter with a body weight between

1:07:13

10 kilograms to 80 , 90 kilograms

1:07:16

, that should be

1:07:19

a good dose to trigger that

1:07:21

mechanism and keep

1:07:23

drinking .

1:07:26

And in terms of sourcing reputable

1:07:28

deuterium-depleted water . As you mentioned

1:07:31

, sourcing can be a problem and this

1:07:33

can be counterfeit product

1:07:35

on the market . What would you recommend

1:07:37

in terms of where to

1:07:39

source high quality

1:07:41

, pure deuterium-depleted water ?

1:07:45

So our product caused preventive

1:07:47

and this is , I guess , the

1:07:51

first deuterium-depleted product on the world

1:07:53

. But there

1:07:56

are other types of water selling

1:07:58

. So when I started my research the world used

1:08:00

up about 1 liter deuterium-depleted water

1:08:02

for kinetic reaction . Now

1:08:04

the world used up about 500

1:08:07

tons deuterium-depleted water

1:08:09

. So we can guarantee that the

1:08:12

D level is

1:08:15

what is on the number on the product

1:08:17

. We have 125 , 105

1:08:19

, 85 , 65 , 45

1:08:22

, and 25 PPM . So that covered

1:08:24

the range which should be enough

1:08:27

to treat any kind of cancer

1:08:29

or metabolic disease

1:08:31

. We are

1:08:33

checking it . We have a GMP facility

1:08:36

. We have a laser equipment control

1:08:38

or the production

1:08:40

of the product . So

1:08:43

this is what we can guarantee . But

1:08:45

that doesn't mean that other products

1:08:48

on the market also are

1:08:50

due to depleted . But of

1:08:52

course I cannot be

1:08:55

responsible for that

1:08:57

type of water .

1:08:58

No , not at all . And

1:09:01

finally , if a patient

1:09:03

is embarking on deuterium-depleted specifically

1:09:05

for cancer , is there is

1:09:07

a facility that they can consult with that

1:09:10

you offer or that any doctors

1:09:13

that you endorse offer in terms of guiding

1:09:15

them through the protocol ?

1:09:18

So anyone who send

1:09:20

a message , write a letter freely

1:09:24

. We discuss them and we

1:09:26

help them . So

1:09:29

, and right now , within 20

1:09:31

minutes , I will have a meeting

1:09:33

with somebody from

1:09:35

the United States who is going to asking

1:09:38

about that . So

1:09:42

this is what I have been doing for 30 years

1:09:44

sharing what I

1:09:46

have already known , and

1:09:48

to involve more and

1:09:53

more people , because the more people

1:09:55

is familiar with that , the better

1:09:57

, because I hope , easier

1:10:00

and faster we can reach the aim to

1:10:02

cure cancer .

1:10:03

Yeah , that's a very , very admirable aim

1:10:05

. So thank you very much , dr

1:10:08

Schoenlein , for talking to me , and

1:10:10

I'll point everyone to your book and

1:10:12

I'll include the information in

1:10:14

the show notes , because I think

1:10:16

that is the best resource that

1:10:19

people can embark on , given that

1:10:21

there's no real practitioners

1:10:23

, especially in Australia , who are able to facilitate

1:10:25

this . So I will include

1:10:27

that information and I guess everyone is

1:10:29

up to themselves to

1:10:31

do their own research and make their

1:10:33

own decision . And I'll emphasize again that

1:10:36

we don't recommend discontinuing your oncology

1:10:38

treatment just because you're drinking deuterium

1:10:41

depleted water . So thank you very much

1:10:43

, dr Schoenlein . Thank

1:10:45

you , thank you .

1:10:46

It was , I guess , very useful talk

1:10:48

. Thank you for your kind Thank

1:10:51

you .