3:34

In this episode I'm speaking with Steven

3:36

Hussie . Now he is bringing a quantum

3:39

biology and circadian biology

3:41

lens to the problem of

3:43

atherosclerotic cardiovascular

3:46

disease or heart attacks , and

3:49

his analysis of

3:51

this problem with regard

3:53

to the fundamentals of

3:55

biophysics and what

3:58

is occurring at a mitochondrial

4:00

level are incredibly

4:02

insightful and incredibly

4:05

refreshing for those who

4:07

are trying to understand how to

4:09

prevent the development

4:11

of heart disease or stop

4:13

them from getting another heart

4:15

attack . So if that's you , then

4:18

I would highly recommend listening to

4:20

this podcast . And

4:22

why I believe this is so important is because

4:24

, despite improvements in acute

4:26

management of heart disease

4:29

and acute myocardial infarction , we

4:32

don't seem to be getting any further in

4:34

really preventing the onset

4:36

of atherosclerosis

4:38

and we really can't

4:40

solve problems within

4:42

the same paradigm and intellectual

4:44

thought pattern that these

4:47

problems arose in . So , moving

4:49

past this biochemical biochemistry

4:52

, lipid model

4:55

of heart disease , I

4:57

think , is what is needed , and

5:00

what Steven is bringing to this

5:02

problem and his perspective and

5:04

analysis is just amazing

5:07

. So I really encourage you to listen to

5:09

the end of the podcast . And , as always , this is not

5:11

medical advice , so please

5:13

always consult your treating

5:16

clinician before making any medication

5:18

changes . Now onto the show . Steven

5:20

, I see you . Welcome to the show Thanks

5:22

for having me Happy to be here . Maybe

5:32

start with a bit about yourself , what you

5:34

do and your perspectives on

5:36

heart disease .

5:38

Yeah , so

5:40

for a living I'm a chiropractor

5:42

and a functional medicine practitioner

5:44

. I

5:47

have , obviously , dr Chiropractic and Master's degree

5:49

in human nutrition , functional medicine , and

5:51

so my day in , day out , I'm neuromuscularly

5:54

scalodally treating people , adjusting their

5:56

spines , helping them with various

5:58

problems with the musculoskeletal system

6:01

. But I also have

6:03

a passion for heart disease because of

6:05

my own health journey , and

6:08

so I spent a lot of time diving

6:10

into that topic and

6:13

the things that I found were shocking

6:15

to me along the

6:17

way , and it's been probably a close

6:20

to 15 year journey now of doing this

6:22

. But yeah , I've always

6:24

been very passionate about health in general , ever

6:26

since I learned whoever , since I had

6:28

health conditions as a child that

6:31

my parents and I kind of relied on Western medicine

6:33

to help us get through , and

6:35

it wasn't until college when I started

6:38

figuring out that the way I lived my life impacted

6:40

my ability to manage and

6:42

even reverse lots of these conditions I

6:45

had . As a child . I thought it interesting

6:47

that I never heard that from doctors

6:49

, and so that

6:51

kind of pushed me into this direction of how

6:54

can I live my life , the best way possible to

6:56

get rid of these conditions and to keep them

6:58

away and achieve health , and so I've always been passionate

7:00

about that , and specifically

7:02

heart disease , because of my own journey . So

7:06

eventually I found

7:08

myself with a bunch of information about

7:11

heart disease and I started sharing it on social

7:13

media . Eventually I wrote a book about it

7:15

, and here

7:17

we are today . People

7:20

seem to enjoy the information that I share and

7:24

it's benefiting people , so that's

7:26

what I'm doing today .

7:28

Yeah , and your history includes a diagnosis

7:30

of type one diabetes that

7:32

you had in adolescence and then you had

7:34

an acute myocardial

7:36

infarction several

7:39

years ago . So I think those

7:41

two events make

7:43

you uniquely qualified on an

7:45

experiential level to

7:48

delve into this topic , and

7:50

obviously all your own private reading

7:52

and self education around that

7:55

and has led you to this

7:57

point . And the thing that I really

7:59

admire about your work is the fact

8:01

that you're not anchored within an existing

8:03

paradigm of thought with regard

8:05

to atherosclerosclerosis cardiovascular disease and

8:08

I'm always excited to talk to people like you

8:10

who approach these traditional

8:12

problems in medicine from this

8:14

orthogonal , out of the box way

8:16

, because we get very refreshingly

8:19

unique perspectives . So

8:21

maybe start with the type one

8:23

diabetes and maybe explain

8:25

to people why glycemic problems are

8:28

an issue for atherosclerosclerosclerosclerosis

8:30

and maybe build us up to where

8:32

you are now in terms of your journey

8:35

.

8:36

Yeah , definitely . So you

8:39

know , at age nine I was diagnosed

8:41

with type one and

8:43

my only inclination that

8:46

something was wrong was that I was

8:48

peeing more often and I felt weird . I

8:50

just felt like you know , as a nine year old kid , I just felt

8:52

like claiming weird . And

8:55

I went into the doctor and they my blood sugar was like over

8:57

700 at the time . And so

9:00

, you know , learn to manage

9:02

type one diabetes by insulin

9:04

injections and things like that . And

9:06

the reason that diabetes

9:08

of any nature , where there's type one or type two , contributes

9:13

to vascular issues , cardiovascular

9:16

issues , is because blood sugars are fluctuating

9:18

. Blood sugars are higher than normal . I

9:20

might have . Well , I manage my blood sugars

9:22

, which I have very tight control . They're

9:25

still going to be higher than the average person

9:27

without type one diabetes . And

9:30

type two is different because it's

9:33

not that my , not that your body just

9:35

stopped making insulin like mine does , it

9:37

doesn't make insulin anymore . It's that you're still

9:39

making insulin but your body has gotten so sick

9:41

that it's not even responding to that insulin

9:43

. So type two is oftentimes worse

9:47

and the damage becomes or the damage

9:49

happens faster because that person's

9:51

already gotten to this poor state where they're not even

9:53

responding to insulin , whereas in my

9:55

case it doesn't happen as fast but it

9:57

still happens . And the reason that it happens is

10:00

because two

10:02

things One especially

10:04

like in the arteries . One is

10:06

that when your blood sugar is higher

10:08

, you know a certain percentage of your

10:10

, you know tissues

10:12

but especially red blood cells , and are

10:14

elements of the blood are

10:16

supposed to get quote unquote glycosylated

10:19

or filled with sugar

10:23

over a certain period of time . But

10:25

obviously if my blood sugars are higher than the average person

10:28

, then that's going to happen to more of them . And

10:30

when they're damaged by glucose

10:32

like that , they become problems . They can become

10:34

damaging to other tissues in the body . So

10:38

that's one thing . So

10:40

the elements of blood become more damaged by

10:42

glucose , or more of them do . And

10:45

the other thing is that fluctuations

10:47

in blood sugar because I'm not

10:49

a pancreas , I can't work

10:51

like one . I'm trying to predict how my blood sugars

10:54

going to react and get myself insulin . I'm

10:56

only assuming that insulin gets absorbed well

10:58

wherever I injected . It's just there's all these variables

11:00

. Because of that there's

11:02

more fluctuations in my blood sugar than

11:05

normal Same with the type two diabetic and

11:07

those fluctuations are very damaging to the

11:09

lining of the artery when we get these abrupt

11:12

increases and decreases in

11:14

blood sugar . The fluctuation seems

11:17

to be even more damaging than just having higher

11:19

blood sugar in general . So

11:21

my number one goal is to try and keep things as stable

11:24

as possible . But that's why

11:26

type ones are predisposed . And

11:28

so , you know , I spent a long time figuring

11:31

out that I could help manage that . Because

11:33

the advice I got from Western Medicine was oh

11:35

, here's this book with every fast food

11:37

listed that you could get anywhere

11:40

, listed , and the amount of carbohydrates in it , so

11:42

that when you eat these carbohydrates you give

11:44

yourself insulin for it . That's all you got to worry about . And

11:46

so that's what I did for years , you

11:49

know . And so eventually I figured

11:51

out that was not the best way and it was way easier

11:53

if I didn't eat these processed

11:56

foods . And I exercise regularly

11:58

and just on and on and on and on and on

12:00

. I've gone way down the line . It's

12:02

not just to have an exercise . And

12:05

so over the years , you know , I would

12:08

go to endocrinologists and I'd see

12:10

the . You know the postures in their

12:12

office . Like diabetics are predisposed

12:15

to eye damage and

12:17

you know diabetic neuropathy and kidney

12:19

damage and amputations and other things . And

12:22

it was all because of these vascular issues . That can happen

12:24

Because the smaller arteries get damaged quicker , faster

12:27

, and those areas

12:29

of the body you know have smaller arteries and

12:31

they can get damaged because

12:34

of that . And so , you

12:36

know , I eventually

12:39

started changing diet . It was like , you know

12:41

, it was just eating a little bit better

12:43

and then a little bit better , and then I went vegan

12:46

for a while , which was a mistake

12:48

. It is about a year and a half . I did that maybe

12:51

like 12 years ago now , and

12:54

then we'll pay Leo and then eventually went low carb

12:56

. And I went low carb

12:58

and I'm what

13:00

some in the space in the

13:02

biochemistry , lipidology space would call lean

13:04

mass hyper responder , and that when I went

13:06

low carb , you

13:09

know , and people who are lean and relatively fit then

13:11

they send , they can see these elevations in LDL

13:13

or cholesterol . Ldl cholesterol but and

13:16

I was one of them , I mean my skyrocketed . But

13:19

it varies . Sometimes it's only like total cholesterol

13:21

is only around two , 300 , other

13:23

times it's 500 . You know , it's just , it's very

13:26

. We can talk about why that is and why I think that is

13:28

. But so

13:30

, yeah , I was concerned about that at first

13:33

but then found that , you

13:35

know , there's not so much of an issue if I have metabolic health

13:37

and so then you know if my

13:39

, if my treat ratio ratio is good

13:41

and other things that signify metabolic

13:44

health were good , that's not so much to worry about . And so that's kind

13:46

of what I went into or

13:49

went in , lived my life by those

13:51

things that I should be good right , and

13:53

so I'm doing that . And I

13:56

went through a period of a very high stress , and

13:59

probably One

14:04

of the most stressful news that I got in my life happened

14:07

a day and a half before I woke up one

14:09

morning , did a very intense workout

14:11

and had a heart attack and

14:14

it was not you hear people talking about

14:16

. Oh , I was walking around with the heart

14:18

attack for a few days and I felt this weirdness

14:20

but I couldn't tell what it was and eventually went in as heart attacks

14:22

. It wasn't that at all . It was very , very

14:25

straightforward . It was yes , I

14:27

have intense chest pain right here

14:29

. I can't really function or do anything

14:32

. I should probably go to the hospital . It

14:35

was very it grabbed

14:37

my attention for sure , and it was 100%

14:39

blockage of the left

14:41

anterior descending artery , which is the biggest artery

14:43

in the heart . It's the most common place

14:46

for a heart attack to happen and

14:49

it was just a giant clot

14:51

. You know I , previous

14:53

to this , about six months earlier , I got

14:55

a CAC score , which is a measure of how much calcified

14:58

plaque there is in your arteries , and I had zero , completely

15:02

normal arteries as far as heart and

15:04

plaque , and they

15:06

say that's a good predictor whether or not you have a heart attack

15:08

. Yet here I am six months later having a heart attack

15:11

. And when they went in

15:13

to check things out and open up

15:15

the put enzymes in there to bust the clot and

15:17

go in there and see if they needed to place a

15:19

stint , they found no atherosclerosis

15:21

anywhere . So you know

15:23

, they said very , very mild , if

15:25

anything soft plaque

15:28

in an area that wasn't even where

15:30

the clot happened . And

15:33

then then there was just giant clot . You know

15:35

there was no narrowing of an artery

15:37

before there , it was just clotting material right there . And

15:40

so they busted the clot , they placed

15:42

the stint , which I could argue

15:45

they didn't need to place the stint . But that was their

15:47

clinical call and I'm grateful that I'm

15:49

here today because of what they did . So I'm

15:52

not really going to harp too much

15:54

on that . But

15:56

you know , after the fact , you know they

15:58

saved my life and here I am laying in

16:01

the hospital completely doubting everything

16:03

that for about you

16:05

know , six hours I'm just laying here like doubting

16:07

everything that I think I know and

16:10

then , after the fact , I received this care in the hospital

16:12

and for the three

16:15

days that I was there , it completely

16:17

reinforced everything

16:19

that I've learned about health

16:22

and how the body actually works . Because what they

16:24

were telling me to do was

16:27

three things . One , it didn't make sense

16:29

logically . Two , it

16:31

was clearly being pushed

16:33

by pharmaceutical and

16:36

big food and things like that . And

16:39

three , it was not reflective of the

16:41

research . You know , if the research is how you

16:43

dictate what you do , which

16:46

for some people it is , some people it isn't , and I can

16:48

make both arguments . What

16:51

they were saying , what didn't even reflect what the research says

16:53

and I was very familiar with it at that time , especially

16:55

about cholesterol and that's what they kept harping

16:57

on it's like oh , your cholesterol is high , that's why you're heart attack

16:59

. And I was like well , are you aware of the

17:01

study that shows that ? You know , they

17:03

did , like 60% of the heart attack admissions and

17:05

they measured their cholesterol within 24 hours and their cholesterol

17:08

most of them were normal or

17:11

ideal and they still had a heart attack . Like what about

17:13

that ? You know ? And they weren't aware of that

17:15

when I brought that up . So it

17:18

was clear there was a lack of knowledge

17:22

about the subject and it was I was a cookie kind

17:24

of thing , you know like someone has a heart

17:26

attack , this is what you do to them , because this is what we were

17:28

taught in school . Here it is , and

17:30

it's based on this cholesterol theory of heart disease , this lipid theory

17:32

of heart disease , and so I

17:35

was open to listening to them because

17:37

, hey , I just had a heart attack , like give

17:39

me your opinion , I want it . I don't

17:41

know if I'm going to do it , but I

17:44

want to hear it and I was taking

17:46

any information I could at that time . And

17:49

so the other thing was that clearly

17:52

there was something that I missed

17:54

too , because this still happened to me . And

17:56

, yes , I'm predisposed to type one and there's even evidence

17:58

that type ones are

18:00

less able to

18:02

handle , especially when under stress

18:05

. Let's say , we'll handle stressful things like the workout

18:07

that I did , which

18:09

I think I should not have done . Based

18:11

on my stress levels and how I was feeling at

18:14

that moment in time , I shouldn't have tried to do that workout . But

18:19

yeah , there's lots of different factors and

18:21

clearly I missed something

18:23

, and that's I

18:26

was aware of a lot of different things

18:28

when we talk about more of a

18:30

quantum or biophysics perspective . I was

18:32

very aware of them , wasn't doing

18:34

them and I have gone much

18:36

deeper into them in the last three and

18:38

a half years since this happened

18:40

and learned a ton , and it all makes sense

18:42

based on everything I knew before , everything

18:45

I know now , and to me it's

18:47

the path forward and it's what I've used to

18:50

completely heal my heart . It's 100% recovered

18:52

, which they told me would not happen if

18:54

I didn't follow the recommendations , and

18:57

I also reversed atherosclerosis in

19:00

my leg that started to develop because the

19:02

procedure they did place the stent . I

19:05

reversed that when they told me that

19:07

that would never happen either and I didn't take any

19:10

medications or follow their advice . So I'm

19:12

kind of this living example of the fact that there's

19:14

more to it than just this cholesterol theory

19:16

and placing stents and taking drugs , and

19:18

you can do it in other ways and

19:22

I hope that they figured that out soon

19:24

.

19:25

Yeah , and this is a fascinating example

19:28

of this concept of you being an N of one , which

19:30

means you're an experiment in and of

19:32

yourself , and that has amazing

19:34

power in terms of mechanistically

19:36

understanding what is actually going

19:38

on here . Couple of points and

19:40

some context for my listeners . So

19:42

what you mentioned earlier in terms of the fluctuating

19:45

blood sugars and glycemic

19:48

problems , either , as

19:50

you mentioned , in type one or type two diabetes

19:52

, are a risk factor . As

19:55

you mentioned , the fluctuations in blood sugar

19:58

, is damaging the endothelium and

20:00

I think that is just for again

20:02

, background before we delve into the minutiae

20:04

. But for everyone

20:06

that is imagining a blood vessel , if they imagine a pipe

20:08

, there's basically three layers

20:10

of the pipe and there's a really thin

20:12

layer of cells called the endothelial

20:15

layer which is lining that

20:17

inside blood vessel , and

20:19

in that endothelium is what's called a glycocalyx

20:22

, which is a bunch of glycoproteins

20:24

that stick out of the blood vessel wall , into

20:27

the lumen , into the flowing blood of the vessel

20:29

, and they have a mucin-like

20:31

, mucous-like effect which is , if you

20:33

ever touch a fish , it's very

20:35

mucous-y . That's similar to what's happening

20:37

on the inside of the blood vessel . So

20:40

what Stephen was mentioning in terms of the

20:42

glycemic dysregulation is you're going

20:44

to damage that endothelium , you're going to damage the

20:46

glycocalyx , and what

20:48

I believe is going on , and what you believe

20:51

too , and we're going to explore this , is that it's endothelial

20:53

dysfunction and endothelial injury that

20:55

is at the root of this whole atherosclerotic

20:58

cardiovascular disease problem , and insulin

21:00

resistance and hyperinsulinema is also

21:02

going to be generating endothelial

21:04

damage . The interesting point

21:06

you made was , and then coming

21:08

up to your heart attack event , your

21:11

acute myocardial infarction . You

21:13

had this CAC score the year before . It showed

21:15

symptoms 0 . And the CAC

21:17

score is a risk stratification

21:19

tool and , as you mentioned , it shows hard plaque

21:21

, it doesn't show soft plaque . So

21:23

we use it to simply really further

21:26

refine someone's risk score , but

21:29

it is not a functional test and it shows

21:31

nothing about flow or stability

21:33

or instability of the endothelium , which is a really

21:36

, really key point . So what

21:38

I think your story illustrates

21:40

is that you had a couple of issues

21:42

at the same time that precipitated

21:45

what sounds like an acute thrombotic event in

21:47

your LAD artery and

21:49

you were stressed , you were working

21:51

out intensely . Those

21:54

two are really important and

21:56

it flies in the face of

21:58

this concept of heart disease , this kind

22:01

of slow buildup and stenosis

22:03

of the vessel and then suddenly I've

22:05

had too much fat in my diet and now the artery

22:07

is blocked . What happened to you was an

22:10

acute thrombotic event , sudden onset

22:12

of symptomatic chest pain , like

22:15

it's on and off . So obviously you just threw off a massive

22:17

clot . So I think what we're going to talk

22:20

about in this interview , what I think is the crux of

22:22

the problem is that we

22:24

have to understand what causes someone to clot

22:26

and in order to help prevent this

22:28

problem . So maybe talk about

22:31

why you think you had that

22:33

acute myocardial infarction

22:36

.

22:37

Yeah , and so my

22:40

I'll call it best guess because it's

22:42

all I can do . No one's ever really going to tell exactly

22:45

what happened in that instance . All I know

22:47

is that there was no atherosclerosis

22:49

. Atherosclerosis present

22:52

first , and then all a sudden boom of a giant clot

22:54

and that's all they found . That's what they

22:56

told me was clotting material . But

22:59

if you look at atherosclerosis , it's

23:01

clotting material , like a large

23:04

percentage of it , almost 90% of it

23:06

, is fibrotic material . So the

23:08

people like clotting material , like if you cut your skin , clot

23:11

forms a scab . So think of kind of similar

23:13

to scab formation on the lining

23:15

and inside lining of your artery . And

23:18

so what

23:20

causes clotting to happen ? And then when we talk about

23:23

those things , I'll talk about the specific things that I think

23:25

happened , that caused my clotting to happen , and

23:27

so anything that can damage the lining of the artery

23:29

. So , and there's lots of layers , there's

23:32

even another layer than the ones

23:34

that you talked about . You know , there's the endothelial , like

23:36

calyx , but then there's a layer of structured water which I'm

23:38

sure we'll get into . But all those things

23:40

can get damaged , and they can get damaged

23:43

by things that want to steal

23:45

basically energy from them , everything's

23:48

we're all just trying to harvest energy from our

23:50

environment and maintain our body . And

23:52

the endothelial cells in the lining of the artery

23:54

are the same way , and so when that energy

23:56

gets stolen it

23:59

creates damage . So what can steal

24:01

that energy ? Well , you

24:03

know , in the health space everybody throws around the term

24:05

like free radical or oxidative stress

24:07

or inflammation , and

24:10

all these things are kind of you know they're different processes

24:12

, a little bit that oxidative stress and inflammation , but

24:14

they're mostly the same thing . In my opinion

24:17

. They lead to the same kinds of

24:19

imbalances in the body . And

24:21

so just a kind of hit list of things

24:23

that can create oxidative

24:25

stress and damage the lining of

24:27

the artery . One psychological

24:30

stress can definitely do it . Toxin

24:33

exposure everything from plastics to

24:35

heavy metals to air pollution

24:38

, lots of different things like that have definitely been

24:40

shown to cause damage to the lining of the artery . Toxins

24:43

that happen when we get bacteria

24:45

that's in the body that

24:47

goes into the wrong place , so it's

24:49

in the gut or it's in the mouth or something and

24:51

it leaks into the bloodstream and it shouldn't be there and

24:53

the body tries to kill them and then releases endotoxins

24:56

. So that can happen for

24:58

dental health or gut health . Those

25:01

things lack

25:03

of , like I said , lack

25:05

of energy , so like lack of sunlight

25:08

or grounding or things like that , like decreasing

25:11

the amount of protection of the

25:13

lining of the artery and of the elements of blood

25:15

, all these things can contribute to this

25:17

eventual damage . And

25:19

then insulin resistance for

25:21

poor metabolic health , which is type 2

25:23

diabetes , like that's what leads

25:25

to type 2 diabetes , but

25:28

it can be present well before type 2 diabetes

25:30

happens . What

25:33

that plays a role ? Because when this damage happens

25:35

, the body can repair itself

25:37

. However , it's

25:39

really dependent on insulin signaling

25:41

for that repair to happen in the

25:43

endothelial cells . They

25:45

really dependent on that , and so if you become insulin

25:48

resistant , which is that precursor

25:50

to type 2 diabetes , and if you become full blown type

25:52

2 diabetic , then your cells

25:54

are not getting that signal to repair . So

25:57

the damage happens and the repair is

25:59

malfunctioning , and so that leads

26:01

to the body having to do something else

26:03

. To quote unquote

26:05

repair the tissue and

26:08

just like it would repair a

26:10

scratch on your arm with the clock , it

26:13

does the same thing on the lining of the artery . And

26:16

so those that can

26:18

happen gradually over time , and

26:20

it can happen on the lining of the artery , that clotting

26:22

material can form right there and that's what we call atherosclerosis

26:25

, and at first it's soft and it

26:27

gets there . If it's been there long enough it can form hard plaque

26:29

, and so that can happen gradually from kind of low grade

26:31

inflammation that

26:33

can be there chronically

26:36

for a long period of time and we can develop this atherosclerosis

26:38

. And it happens only

26:40

in arteries . We usually don't see it in veins

26:42

because the arteries are under more pressure , so

26:45

things are getting pushed up against the lining of the artery

26:47

more . We usually see in

26:49

lining areas of the artery where there's

26:51

a curve or where there's a bifurcation

26:53

of an artery , where they split , because those are areas

26:56

that are usually under more pressure and

26:59

the heart arteries happens the most

27:01

or it's

27:03

at the most risk for intense clotting

27:05

because those arteries are under the most pressure

27:08

of any arteries in the body , especially

27:11

the left anterior descending artery , and so , like

27:14

I said , that can happen gradually over time . Or

27:17

if you get yourself into a situation where

27:19

there's enough inflammation and

27:24

enough pressure , then

27:26

a clot can form . When this happens

27:28

, sometimes in people's legs , they call it a deep

27:31

vein thrombosis . It

27:33

can happen in lots of different areas , happens

27:36

in the brain , called strokes , and

27:39

so the theory is that

27:42

you get soft plaque and the soft plaque

27:44

rupture is causing a clot . But

27:47

there's many issues with that theory . We can talk about For

27:49

me , the fact that

27:51

I was under a lot of stress for about

27:53

eight months to a year before this

27:56

happened . And then

27:58

I received some very stressful news about

28:01

a family member a day and a half before it happened

28:03

. And I tried to do if

28:05

anybody knows anything about trying to manage blood sugars

28:07

when you're that stressed it's very difficult

28:10

. So my blood sugars were up and down a little

28:12

bit more than usual at that point and

28:14

then I did that workout and

28:16

I think that that , because it was like 15

28:18

minutes after , my blood flow kind of calmed

28:20

after the workout and then

28:23

I was just sitting there making some food

28:25

on the stove and then boom , clot

28:27

happened as soon as my blood flow got low enough . And

28:30

it all happened because I think I

28:32

created a situation , unfortunately

28:35

, that there was this

28:37

kind of maybe lower grade inflammation from

28:39

blood sugars that are always going to be higher than

28:42

the average person going

28:44

through that stress , having the acute stress , and it

28:46

was the stress . The stress affected me most because

28:48

it was the inability to do anything about the thing

28:50

that caused the stress . Me

28:53

or my family could not get to this person and help

28:55

them . So it was just kind of like

28:57

this waiting game we hope everything's okay and

29:00

so that was an issue . And

29:03

then I did the workout and inflamed

29:05

everything and as soon as the blood started

29:07

slowing down from the workout , the

29:09

clot formed in that most vulnerable

29:11

area , which is the left hand here descending artery

29:14

of the heart . And

29:16

there we are , and it was a big enough clot

29:18

that it blocked the whole artery

29:20

. Pretty much that's

29:23

what happened .

29:24

Yeah , very interesting , steven , and there's a couple of points

29:26

I want to make . And one is really

29:28

relevant to this issue , which

29:30

is Workhouse Triad . And this is

29:32

an old physiological kind of framework

29:35

of thinking about blood clotting and it

29:37

involves three factors and they

29:39

are endothelial injury

29:41

, hypercoagulability and

29:43

blood stasis . So those

29:46

three factors influence the likelihood

29:48

of forming a clot or not . And

29:51

if we think about what you've talked about , then

29:54

it makes sense when we're

29:57

considering what's going on here . Endothelial

29:59

injury is the blood

30:01

glucose dysregulation . It's

30:04

those factors that you mentioned

30:06

briefly before . Hypercoagulability

30:09

is the state that you get into when

30:11

we're insulin resistant or when we are

30:14

on that scale of metabolic dysfunction

30:16

, and there's blood

30:18

markers like fibrinogen which kind

30:21

of can give insight into that hypercoagulability

30:23

. And venous stasis , and

30:25

I think that that means or venous

30:28

arterial stasis is occurring

30:30

when , as you mentioned , there

30:32

could be some interruptions in flow , especially

30:34

around breakpoints

30:37

or branching in the

30:39

artery . So

30:41

that is a fundamental thing to think about in

30:43

terms of blood clotting , and the

30:45

person who I have read a lot about , who

30:47

has talked about this , was Dr Malcolm Kendrick

30:49

, and he has also given a really

30:51

good framework to think about the effect of stress on

30:54

vascular health and

30:57

the fact that you had that year of leading

30:59

up potential of stress in the background . One

31:02

of the mechanisms that he mentions

31:04

is that prolonged hyper , having

31:06

raised cortisol level related to stress

31:08

for a prolonged period of time , actually

31:10

inhibits the action

31:13

of vascular endothelial progenitor

31:15

cells . So your ability to heal

31:17

the background endothelial damage that's

31:19

occurring through maybe those blood

31:21

glucose swings or any of those other factors

31:24

, is impaired when you're stressed . So

31:26

perhaps you had a bit of a vulnerable

31:28

vessel wall in

31:30

this background because you've got this stressful

31:33

milieu and then bam , the

31:35

acute stress of exercise which is both

31:37

increased barotrauma because

31:39

of the demands of the exertion

31:42

and potentially

31:46

even temporarily higher blood glucose if it's

31:48

a really intense workout . That was enough

31:50

to bang pop off a

31:53

clot . The other interesting point which

31:55

is born out in long term studies

31:58

to do with the social determinants of health

32:00

and these observational studies showing that

32:02

lower socioeconomic people in Glasgow

32:04

, scotland , I believe , particularly

32:06

, were at high risk of getting heart disease

32:08

. And it goes to show what you're talking

32:10

about , or the impact

32:12

of hopelessness and that unresolving

32:15

, unrelenting , prolonged hyper

32:18

cortisol state that

32:20

we get from

32:22

hopeless type of stress . So

32:26

that's very interesting and I think that gives

32:28

us an explanation of why you had your event

32:30

. I just want to make

32:32

a point about the traditional risk

32:35

factors , because what we're going

32:37

to discuss next is very much beyond

32:39

the scope of the points

32:42

that . I was taught in medical

32:44

school that

32:46

my colleagues in both general

32:48

practice and cardiology approach

32:50

this idea of vascular

32:52

health and atherosclerotic cardiovascular

32:55

risk , these so-called

32:57

traditional risk factors , the main ones

32:59

being family history . So if you had found the history

33:01

of having heart attacks , high

33:04

blood cholesterol

33:06

, but that concept should

33:08

be atherosclerotic , sorry , should

33:10

be dyslipidemia , but it gets

33:13

confused with or lumped

33:15

in with isolated hypercholesterolemia

33:17

, smoking , diabetes and hypertension

33:19

. So those are the traditional risk factors , but

33:22

what you gave us a prelude to is

33:24

these kind of non-traditional factors that are also

33:26

going to be harming endothelial

33:28

health . So I just wanted to kind of put

33:30

that flag in the sand for people who are listening

33:32

, especially the doctors in the audience . So we're

33:35

not saying that the traditional factors don't play

33:37

a role , because they obviously do , but they are all

33:39

impacting the vascular

33:41

health in the context of clotting , which is a

33:44

point that I really want to make .

33:46

Exactly , and I'm glad you make that point , because

33:49

there are people out there that

33:51

well , first there's people out there that claim that

33:53

it was just high LDL and

33:55

that is what causes heart disease and

33:58

that's been the theory for a long time

34:00

, based on some more science and a whole history

34:02

of that . But then

34:04

there are also people that accept that that's not

34:06

the reality and that they're

34:09

still trying to analyze lipids

34:11

and get

34:13

the answer through this analysis of lipids . And

34:15

I think that , unfortunately , blood

34:18

lipids , while they may play a role in certain

34:20

situations , have become

34:22

a huge distraction to the actual causes

34:24

of vascular damage and

34:27

ultimately , you know , clotting

34:29

, instances

34:31

of clotting that can cause events and

34:34

so yeah , so that's kind of what I

34:36

had to discover on my own was

34:39

what are those risk factors

34:42

and how ? Usually the traditional

34:44

risk factors that they're looking at

34:46

, which there's actually a study

34:48

that came out that called the SMERFs , the

34:50

standard modifiable risk factors that

34:52

actually more of them , more cardiac

34:55

events are not being predicted by those

34:57

traditional , which are hypertension

34:59

, smoking , diabetes and cholesterol

35:02

, and so , in

35:04

addition , like those things and how

35:07

they're affecting , like you said , the clotting

35:09

, the likelihood that we will

35:11

see clotting , whether it's a minor

35:13

scale , on the line of an artery , or

35:15

it's a major scale and actually causes an event

35:17

like in my case . So very

35:20

, very important to make that distinction and

35:22

, I think , steer us away from

35:24

this very myopic view

35:28

of let's look at the lipids . They're going to give

35:30

us the answer , but just analyze them in the right way

35:32

. They're going to give us the answer , which I think they never

35:34

will . They may give us an indication of if

35:36

your lipids look like this , you're at more increased risk

35:38

. But why do the lipids look like that

35:40

? That's the more important question

35:42

.

35:43

Yeah , and my interpretation of lipid

35:46

panels just the standard lipid panel

35:48

is that it's simply a insight

35:50

into insulin resistance , particularly

35:52

the triglyceride to HDL ratio , and

35:55

, yes , it's predictive of different kind

35:58

of patterns of LDL , but

36:00

essentially it's giving us an idea

36:02

, another kind of window

36:04

into the same room , of insulin resistance . But

36:06

it is as you mentioned . It is fundamentally limited

36:09

in its predictive ability . And

36:11

the study that you quoted I believe it was

36:13

2012, . It

36:15

was a US study and they basically retrospectively

36:18

looked at the lipid panels post-admission

36:20

of over 100,000 people that

36:23

were admitted for various cardiovascular

36:27

pathologies and

36:29

yet more than 60% had LDLs

36:32

within the limit

36:34

, the reference range . And

36:37

the conclusion of the paper wasn't and

36:39

hang on , we're obviously using

36:41

a kind of a standard

36:44

, we're not using the best tool here . The conclusion

36:46

was we need to lower the lipid parameter

36:48

even further . So I mean

36:51

, you can't ? You know it's trying

36:54

to solve the problem with the same thinking that

36:56

created it . But let's talk about

36:58

this cholesterol , and I really want

37:00

to make a couple of distinctions

37:02

here , because I hear this getting discussed

37:05

and the lack of precision kind of annoys

37:07

me . I want to make the point

37:10

that cholesterol is a molecule , it's

37:12

a sterile and it's not

37:14

a fatty acid . It's actually sterile and

37:16

it is a component

37:19

of the cell membrane . It's component of red

37:21

blood cell membrane and that gets to the

37:23

point you were making , stephen , about the presence

37:25

of cholesterol in the plaque

37:27

is because it's gotten there through

37:30

the presence in red

37:32

blood cell membrane and then it is poured it around

37:34

the body in low density lipoprotein

37:36

, which is essentially a big ball that

37:39

has an apoby protein

37:41

or a different type of apolipoprotein

37:44

, and that allows these cholesterol

37:48

molecules to be soluble and to be transported

37:50

around the body . So I just want to

37:52

make that point , because people

37:54

say high cholesterol , but it can be a little bit

37:56

ambiguous . So why

37:58

is this ? With that background , why

38:01

is this problematic in terms of the explainability

38:03

of afterscolar

38:05

plaque formation ?

38:08

Why is the theory of high LDL

38:11

problematic ? Yeah yeah , yeah . Well

38:14

, I mean , first of all

38:16

, if you just back up in like big

38:18

picture , like wisdom

38:21

of the body , like if

38:23

the body is creating higher

38:25

LDL for a reason and

38:28

the person is not having this overt symptom

38:30

because of it , like obviously there's pathological reasons

38:32

why we could see imbalances in something , but

38:35

if it's happening and the person is experiencing good

38:37

health , then it must be doing it for a

38:39

reason . And

38:42

there are people that theorize that it's because

38:44

I mean , like in the case of a low carb

38:46

diet , that it's because more

38:48

energy needs to be delivered to the system

38:51

, which is lipids . We can use lipids

38:53

for energy , or it's one way

38:55

we can get energy , and

38:57

so your body puts more of it into the

39:01

bloodstream . There's

39:04

theories that when the

39:06

liver is on a low carb diet , the liver

39:08

is making more ketones , which you can also burn

39:11

for fuel . The process of making ketones

39:13

is very similar to the process of making cholesterol , so more

39:15

cholesterol gets made and it

39:17

ends up in the blood . Or

39:21

the liver shuts down

39:23

the absorption of

39:25

cholesterol because it's

39:28

wanting to leave more in the blood for energy

39:30

delivery , and so , instead of reabsorbing

39:32

cholesterol , it leaves more in the

39:34

blood and that's why it goes up , but there's always a reason

39:36

for it . There's some metabolic reason for it . There's

39:39

also circadian reasons why it could happen

39:41

too , because we're all

39:43

on this biological clock , and

39:45

so the point of being that there's

39:48

reasons why

39:50

LDL could fluctuate in the blood , just

39:52

like lots of things fluctuate , just like your blood

39:54

pressure is supposed to fluctuate . If

39:57

it goes elevated and stays elevated for a long time and

39:59

never comes down , that could be an issue that

40:01

could be an indication of pathology . But fluctuation

40:04

depending on when you measure , that

40:06

one snapshot in time is normal

40:08

. Even blood sugar is supposed

40:10

to fluctuate not as much as mine , because

40:13

I'm trying to control it as a type one but it's

40:15

supposed to go up when you eat something and

40:17

the ability of it to come back down , that's normal

40:19

, and so

40:22

it's that kind of mentality . Now the

40:24

other issue with the theory is

40:27

that when we look at atherosclerosis

40:30

and we measure that clotting material

40:32

, that's what it is . It's clotting material , and

40:34

very little of it is cholesterol

40:37

or lipoproteins or whatever

40:39

you want to say , which suggests

40:42

that the little

40:44

amounts of cholesterol that we do see in them is

40:47

just a byproduct of A . They're already there in

40:49

the endothelial cells or there just happens

40:52

to be some around whenever the clot forms and it

40:54

ends up being in there because

40:56

it kind of sucks in everything that's there . And

40:58

so there's these flaws in this theory . And

41:01

then

41:03

scientifically , if you want to go the scientific route

41:05

, there's lots of evidence that people

41:07

with higher cholesterol levels

41:09

, ldl levels , have

41:13

just as little or they

41:15

don't form atherosclerosis any more than people

41:17

with normal quote , unquote normal levels

41:19

. And there's

41:21

, you know , there's associational

41:25

studies that show kind of both , and

41:28

some of those associational studies are funded

41:30

by pharma and they push you in one direction

41:33

, others are not . But

41:35

what we do know is that , logically

41:39

, you

41:41

know , we have people with higher

41:44

cholesterol who have

41:47

lower all-cosmortality , they have

41:49

higher cognitive abilities , they have lower rates of

41:51

infection , lower rates of cancer , lower

41:53

rates of heart disease , associationally

41:56

. And so if something was that

41:58

bad for us or that causative on its own

42:00

of disease , why would these people

42:02

be having these other better health outcomes

42:05

, right , and not dying

42:07

more frequently ? And they've shown that with

42:09

people with familiar hyper-cholesterolemia , which is genetically

42:12

high LDL , they

42:14

don't live any shorter of a lifespan

42:16

than people with quote , unquote normal LDL . And

42:18

if they do , it's because of their

42:20

lifestyle habits , not because

42:22

of the high LDL . That's

42:25

literally what the researchers say when they look at those studies

42:27

. So anyway , you kind of slice

42:30

it up . There's

42:33

really no evidence for this theory that this

42:35

one molecule on

42:38

its own can be a driver of a whole disease

42:40

process which is fundamentally

42:42

flawed in general . Like the body is

42:44

a very complex biological ecosystem , it's never

42:46

like one thing is never gonna cause a whole

42:48

disease process . It's always gonna be

42:50

a combination of things , just like we're always a combination

42:53

of what happens to us in our environment . Yeah

42:56

, many , many flaws and holes in

42:58

that theory . But it's a very convenient

43:00

theory for pharmaceutical

43:03

companies Because if you can say

43:05

that a disease is caused by one molecule and you have a drug

43:07

to lower that molecule , then you

43:09

can sell more of that . If

43:11

your theory is that stenosis

43:14

of an artery is what causes heart attacks , then

43:16

you can make a lot of money doing stent and bypass

43:18

procedures which studies still don't work to

43:22

fix that stenosis . And it's very

43:24

profitable , very convenient for

43:26

that system to thrive . But

43:28

people are left with

43:30

poor results and in

43:32

higher rates of heart disease .

43:33

So yeah , and you're

43:36

specifically referring to the practice

43:38

of stenting . Asymptomatic people

43:40

who might have undergone a

43:43

angiogram , discovered to have a degree

43:45

of stenosis don't get exertional chest

43:47

pain or any other exertional symptoms and

43:49

then get stented . And there's not

43:51

good evidence that that is

43:53

benefit and there's lots of reasons for that , one

43:56

of which is the fact that the body develops collateral

43:58

flow if there's stenosis

44:00

that's occurring over a long period of time

44:03

. I wanna make a

44:05

comment about what you talked about

44:07

in terms of the LDL and the

44:09

lipid hypothesis , because I've

44:11

called this the original sin of having

44:13

apoby , and what

44:15

I mean by that is the way that

44:17

it's framed by mainstream

44:20

thinkers in the space , so particularly

44:22

Dr Thomas Dayspring , dr Peter Atia

44:25

, who are some of the

44:27

most fierce proponents of the

44:29

lipid hypothesis and the causal

44:31

role of apoby and LDL

44:34

cholesterol in atherosclerotic cardiovascular

44:36

disease is

44:38

that they would have you

44:40

reduce your apoby to

44:43

basically almost

44:45

undetectable . They and

44:48

I believe it's 70 , I think they want it under 70

44:50

as a kind of in

44:52

the US unit as a treatment

44:54

goal . And the why I call

44:56

this the original sin is because it's presuming that

44:58

the body made a mistake and it's presuming

45:00

that mother nature made a mistake in giving us

45:03

this LDL particle and it's huburistic

45:05

because it excludes this or

45:07

presumes that there is no other

45:09

reason for this molecule . Effectively

45:12

and it's not specifically what they've said

45:14

, but that's how it's interpreted is that there's

45:16

no other value for this molecule other than kind

45:19

of giving us atherosclerosis starting

45:21

at a very young age . But what I think

45:23

both of us are agreeing in what we're saying is it's

45:26

the context of which the this

45:29

particle exists in the body . It's the context

45:31

of the endothelial damage , it's the context

45:33

of the coagulating , the

45:35

pro-coagulant environment of the blood

45:37

vessel that , ashley , is gonna determine

45:40

the degree of pathology

45:43

or disease causing capability

45:46

of LDL . And

45:50

I think you make a really good point about

45:52

when there's a monomaniac or a

45:54

myopic focus on

45:56

one metric . It's because

45:58

that there is a medecatable endpoint

46:01

. And it's not a surprise

46:04

that we're not emphasizing triglycerides , because

46:06

the satin therapy doesn't do a lot for

46:08

hyperdrugless rightemia . What does

46:10

getting in the sun and cutting out

46:12

carbohydrates ? That's what gets you at

46:15

fixing metabolic health . So you

46:17

know , it's definitely a focus

46:19

of this paradigm because that

46:22

is kind of where we're

46:24

at . And in terms of the effect

46:26

modification , that's a concept that no one's talking

46:28

about . Is that the effect modification

46:31

of LDL and

46:33

having this apoB is metabolic health

46:35

, ill health and all these things

46:37

that are damaging in the lining of the blood vessel . So

46:40

maybe let's quickly talk about

46:42

the exclusion zone , because even

46:45

within metabolic

46:48

medicine and metabolic doctors who acknowledge

46:50

the presence of the glycocalyx , then I

46:52

don't believe they've got the full story , because we

46:54

do actually have a protective layer above

46:56

those glycoproteins that are sticking

46:58

out of the endothelial cells . And if you

47:00

wanna comment on anything else I've said , please go ahead .

47:03

Yeah , yeah

47:05

, so you know . I

47:08

think that , like you

47:10

said , we're over analyzing these lipids because

47:13

we're stuck on this idea that the lipids have

47:15

to be the answer . But

47:17

when you broaden your like , instead of asking do

47:20

lipids or what ratio of lipids

47:22

is more atherogenic , you're

47:24

gonna . We'll probably find a ratio

47:27

or a certain way that

47:29

the lipids are presenting themselves that

47:31

is indicative of more

47:33

atherosclerosis . But it's not the lipids driving

47:35

it , it's always the context of the

47:37

environment the lipids are in , and

47:40

so now we have to learn about this environment that the lipids are

47:42

in right . And one thing that has been completely

47:44

missed is the more

47:46

quantum biophysics side

47:49

of the cardiovascular system , and

47:52

that has to do with water and

47:54

basically it

47:56

has to do with your body's ability to hold

47:58

energy and use energy to create

48:00

structured water . So what is structured water ? So

48:04

we're all made of water . We're

48:06

all told we're 80 , 90%

48:09

water , whatever you wanna say , but

48:11

we're a large percentage water , and the

48:13

water in our bodies , most of it , is

48:16

in a structured state , meaning it's more

48:18

like a gel . It's not fluid , liquid , like

48:20

water , and it's not ice solid , it's in

48:23

the middle , it's more like a gel , like jello or

48:25

like the consistency of a raw egg yolk , like

48:27

it's kind of that gel , and

48:29

so most of the . That's why , if you can

48:31

touch your forearm , it feels like a gel . It kind of responds

48:34

and bounces back , and so structured

48:36

water forms . When there's a water-loving

48:38

surface which all biological

48:41

surfaces are water-loving and

48:43

you have water , obviously , and then you have

48:45

an energy source . There's

48:47

lots of different energy sources , but the main one is infrared

48:50

light . It's the most structuring

48:52

to water . When that happens , water will become

48:54

this . It'll form a layer

48:57

of this structured water on the biological

48:59

surface and the lining

49:01

of the artery . The endothelia , with glycochialis

49:03

on top , is one of these biological

49:05

surfaces , and in the lab of Dr

49:08

Geopolic they found that it does indeed form

49:10

on the lining of the arteries . Now the

49:12

thing about this structured water is

49:14

that it's got different names . It's

49:17

called fourth-phase water , but it's also called exclusion

49:19

zone water , and the reason that it's called exclusion

49:21

zone water is because the way that it forms it

49:23

becomes this nearly impenetrable

49:26

barrier . There are certain

49:28

very small hydrated ions of minerals

49:30

and certain metabolites that can

49:32

get through it for good reason . But

49:35

anything larger than those things , which

49:37

they're very small they're like fractions of a nanometer

49:39

cannot

49:42

get through there , and so red blood

49:44

cells are too big , bacteria is too big , all

49:46

the lipoproteins are way too big

49:49

, platelets are too big

49:51

, the protein albumin , which is the smallest protein

49:53

in the blood , is too

49:56

big . Nothing really gets in there if you have

49:58

this intact structured water there . And

50:00

so the thing is

50:02

that structured water is very electronegatively

50:05

charged , and so earlier , when I was talking

50:07

about all those that inflammation and oxidative

50:09

stress , those things can interfere

50:12

with and break down this barrier

50:14

of water that's protecting the lining of the artery , and

50:18

so eventually , if they break that down , then they damage

50:20

glycocalyx and they can damage the endothelia

50:22

, and then that leads us into this situation

50:24

that promotes clotting right

50:26

, this inflamed endothelia and

50:29

poor blood flow and aggregation . Now

50:32

, so we have this

50:34

water protecting the lining

50:36

of the artery , but the other thing is that structured water forms

50:38

on all biological surfaces . That includes

50:41

elements of blood , and so

50:43

red blood cells and lipoproteins

50:45

. They also have structured water on them

50:47

, and that gives them what's called a zeta potential . It

50:49

gives them this charge around it that

50:51

protects them . So you think of it like you

50:53

know , there's two lipoproteins next to each other

50:55

and they have the same charge , so they kind of

50:57

repel each other , but the water around

51:00

them is positively charged , so they kind of attracted

51:02

to that . So then they repel each other to get too close

51:04

. So it's just like this everything's evenly spaced in

51:07

the artery in the blood floating

51:09

in this water , evenly spaced but they're kind of hooked together

51:11

a little bit called electrostatically like

51:14

train cars hook together , and that keeps

51:16

everything evenly spaced , protects the lining of the

51:18

artery . And then the

51:20

last piece of it is that in Pollux Lab

51:22

they've shown that the formation of this water is

51:24

actually what creates blood flow . And

51:27

so here we are . We've

51:29

already predisposed everybody to

51:32

these three factors that generate

51:34

clotting . And that is damage to the lining of the artery

51:36

. It is aggregation of

51:39

elements of blood clumping together

51:41

and it is poor blood flow . And

51:44

I just told you that structured water is

51:46

responsible for protecting the lining of the artery so

51:48

that it doesn't get damaged , keeping

51:50

things evenly spaced in the blood , not

51:53

clumped together , and promoting

51:55

blood flow . And so if

51:57

we look at what atherosclerosis is , what

52:00

damage to the lining of the artery is , and

52:03

what clotting is , whether it's acute or

52:05

chronic clotting over long periods of time it's

52:08

basically an inability of your body to maintain

52:10

structured water in the few

52:12

places where water is still liquid

52:14

, and then structured water

52:16

onto elements of the blood

52:18

and lining of the artery within that liquid , and

52:21

that is lymphatic tissue , cerebrospinal

52:24

fluid and blood . And so

52:26

it's all about giving

52:28

your body enough charge and

52:31

water the raw material so

52:33

that it can do this and prevent

52:35

atherosclerosis . And so this is the

52:38

things that solidify this for me are

52:41

if you look at what

52:43

actual risk factors for heart

52:45

attack , heart failure , atherosclerosis

52:48

, stroke are , one of them is rithicite

52:50

sedimentation rate , which is measuring how

52:53

fast items

52:56

of blood clump together . Red blood cells clump together

52:58

. We don't want it to be that fast , we

53:01

want them to do that slowly , and

53:03

so you can measure this in how

53:05

, if they clump together

53:07

too fast , that's definitely

53:09

one of the best predictors for if you're

53:11

gonna have a clotting issue . Also

53:14

, poor blood flow has

53:16

definitely been associated with higher risk

53:18

of clotting , which makes sense . The

53:20

more stagnant something is , the more like it's gonna clot . Just

53:23

like if a river is always flowing

53:25

and beautiful , but you get an

53:27

area of the river that goes off to one side and kind

53:29

of eddies and it starts to treat this pool and

53:31

we always see things in it . We see the sticks and leaves

53:34

and stuff that can not get accumulated in it

53:36

and that's gonna increase clotting of

53:38

that area . If that was blood , which is why

53:40

we always see like vasodioid and

53:42

I've talked to cardiac surgeons about

53:45

this and the vasodioid at the time we

53:47

see clotting happen in areas

53:49

of a bend in the artery where

53:51

turbulence is supposed to happen , or if it's poor

53:53

blood flow , things can get stuck or

53:56

areas of bifurcation , things split and

53:59

so maintaining this water

54:01

is what keeps artery healthy . And

54:03

if you think about it like that , if

54:06

we are assessing lipids

54:08

and we see a lipids

54:10

present themselves in a way that

54:12

suggests that there's poor metabolic

54:15

health or inflammation or whatever

54:17

, it's all a reflection of how healthy

54:20

that structure of water is in your body . If that structure of

54:22

water is not there , it's because you have

54:25

poor metabolic health and it's

54:27

because you have high inflammation and oxidative stress

54:29

because you're not doing things to get energy into

54:31

your body to maintain that structure of water

54:33

. So I hope that makes sense . But it's kind of this overarching

54:36

thing that just looks at all

54:38

, takes all of it and says , oh , that's

54:40

what's going on , I don't need to overanalyze lipids

54:42

, this is the solution .

54:45

Yeah , thank you for such an excellent summary

54:47

, stephen , and I think what

54:49

you've just talked about and what you've described is so

54:51

fundamental and so pivotal and

54:54

so paradigm-shattering that it's almost

54:56

very it's difficult for me to overstate the importance

54:58

of what you've just said and I'm

55:01

gonna go over it again , and

55:03

really slowly , for

55:05

the doctors in the audience , because they

55:08

really need to understand this concept and

55:10

what you talked about

55:12

in terms of structured water . This isn't not

55:14

some woo-woo topic . This isn't

55:16

some kind of obscure

55:19

, esoteric concept not

55:21

based in scientific reality . This

55:25

, what Gerald Pollock described in his lab , who

55:28

is an electrical engineer

55:30

turned water researcher , is a fundamental

55:33

truth about the biophysical

55:35

properties of water that respond

55:37

to electromagnetic

55:40

radiation in the form of infrared light

55:42

. So the structure

55:45

, the actual molecular structure

55:47

of water is taking on a

55:49

completely different configuration

55:52

and confirmation under the influence

55:55

of infrared light

55:57

in biological systems , and

56:00

the power of structured

56:02

water to exclude solutes is

56:05

so great that this has

56:07

been looked into as technology to filter

56:09

water , meaning that if they

56:11

can harness the structured properties of

56:14

water by passing current through

56:16

it , by putting light on it , then

56:18

they can actually use it to filter

56:20

sea water , to filter all kinds of solutes

56:23

out of water . That is how powerful this is . So

56:26

what you've described and what makes sense is

56:28

that we have got this exclusion

56:30

zone structure water on the inside lining

56:32

of the blood vessel beyond the

56:35

glycocalyx , and this is our

56:37

force field barrier effectively . That

56:39

is , preventing contact of lipoproteins

56:42

and anything larger than potassium ion

56:44

which is what we talked about in your recent talk

56:46

from contacting the endothelial layer

56:49

. So what Peter Atia

56:51

and Thomas Dayspring and these

56:53

people don't understand

56:55

is that if

56:57

the body is healthy and there is

57:00

, the charge of the body is

57:02

within its physiological

57:04

optimal level , then there should not

57:06

be contact with the glycocalyx

57:09

, with the endothelial layer of any of these

57:11

contents of the blood from the lumen , because

57:13

that protective layer should be preventing

57:15

anything from effectively

57:17

contacting it . And whatever causes

57:20

the breakdown or the impediment

57:22

of the formation of structure water , as you've just

57:24

talked about , is therefore gonna cause damage

57:27

to the glycocalyx , is gonna cause those

57:29

microclots which over

57:32

time or suddenly , as we talked about in

57:34

your situation , form into

57:36

a full blown occlusion

57:39

of the vessel and you get acute myocardial

57:41

infarction . But I just really wanted to emphasize

57:43

that point because I think what you've just

57:45

described is simply paradigm

57:48

shattering for the entire field

57:50

of cardiology , preventative

57:52

cardiology , lipidology , and

57:55

it's groundbreaking

57:57

and I'm really struggling

57:59

to not overstate this , but I think it is that important

58:01

.

58:04

Well , first of all , just to your point too , like it's

58:06

not just Gerald Pollock he

58:09

is the one who has popularized fourth phase

58:11

water because of his book but Gilbert

58:13

Lane , albert St Georgie , who won the Nobel

58:15

Prize , jim Oshman

58:17

, may Wan Ho , james Clegg

58:19

, like there's so many scientists that are talking about

58:21

water . And

58:24

it's like , if

58:27

we talk about charge , like we all

58:29

know , we all learn in cellular physiology

58:31

that there's a net negative charge in the cell . Well

58:34

, guess where it comes from ? Structured water

58:36

. And if the charge of the cell is

58:38

altered , we know that that's a disease , cell

58:40

right , and that's because structured

58:42

water , whereas lost the capacity to hold

58:44

structured water into it . Structured water

58:46

is this net negative . And

58:49

, like you kind of mentioned there , like cellular physiology

58:51

, we know there's a separation of sodium potassium

58:53

inside and outside the cell and I just told

58:55

you that the , or you just told

58:58

us , based on my talk , that sodium

59:00

potassium is the cutoff . Sodium

59:02

is not allowed , potassium is allowed . So

59:04

structured water is playing a role in

59:07

this separation of charge . So this

59:09

is very well-established

59:12

physiology and there's tons

59:14

of literature on this . But

59:18

also it's kind of , like I said

59:20

, overshadows this whole lipid

59:23

theory , cause we're so focused on this

59:25

biochemistry and we step

59:28

back and we see that there's this biophysics

59:30

side to our body that makes all that biochemistry

59:32

. It changes the way we see it , it changes

59:35

the way we look at it and it's very , very simple . Like

59:37

heart disease and most

59:39

disease in general , is a result

59:41

of two things . One is

59:44

that in our modern way of life we

59:46

are exposed to things that interfere

59:48

with our body's charge , and

59:51

that is electromagnetic fields , it's

59:54

the wrong types of light , it's

59:56

all the toxin exposure

59:58

, the poor diet leading to poor metabolic

1:00:00

health , which is mitochondrial dysfunction

1:00:03

, Like all these things are decreasing

1:00:05

our body's ability to maintain that net

1:00:07

negative charge that we know as physicians

1:00:09

we would learn right . And

1:00:11

then it's also the second thing is a

1:00:13

lack of stimulus

1:00:16

of the things that increase that

1:00:18

charge , which is the sun and

1:00:21

contact with the earth and

1:00:23

movement . You just moving

1:00:26

your body , you create a piezoelectric effect that generates

1:00:28

electricity . So it's pretty much that simple

1:00:30

. Now all the details of different

1:00:32

disease processes and everything can get really complicated

1:00:34

, but it's really is that simple

1:00:37

. We've too much in contact with things that

1:00:39

interfere with our ability to get charged and we're not

1:00:41

in contact with things that maintain

1:00:43

our ability to get charged Like . That's what life is . It's

1:00:46

literally your

1:00:49

body . Define the second law of

1:00:51

thermodynamics , because the second law of thermodynamics

1:00:53

is things tend toward disorder . But

1:00:56

life has figured out a way to take energy

1:00:58

and create temporary order for

1:01:01

something to be alive , you

1:01:03

know , through its lifetime . And

1:01:05

if we lose the ability to take that energy

1:01:07

in and create order , we get disorder

1:01:09

. And that's what all disease processes

1:01:11

are . There's just a fundamental lack of energy

1:01:13

for your body to create that order , because it knows

1:01:15

how to create order . It's well designed

1:01:17

or evolved , however you want to say it , to create

1:01:20

order . And the lining of the arteries

1:01:22

is one of the first places we see

1:01:24

disorder , because it is kind of like the front lines

1:01:26

right , it's where what

1:01:28

your body is trying to send everything to process

1:01:31

or detox or metabolize

1:01:33

all the things . So it's , it's frontline in defense and

1:01:35

that's why we see it more common . That's why heart disease

1:01:38

is the number one killer , because in this state

1:01:40

where we're removed ourselves from energy and doing

1:01:42

things to damage energy , the blood

1:01:44

vessels see it first . So

1:01:47

it's when you look at it from that perspective

1:01:49

, it's very simplified . Even though the science

1:01:51

can be very complex , it's very simple

1:01:53

from that perspective .

1:01:55

Yeah , and it reminds me of that little

1:01:58

story of the two fish swimming in

1:02:00

the ocean . And you know they

1:02:02

, I think an older fish comes by

1:02:05

and is like you know , are you guys enjoying the

1:02:07

water ? Or something like this . And one fish

1:02:09

looks at the other fish and asks him you know , what

1:02:11

is water ? And that that

1:02:13

I feel like is is the lipid centric

1:02:15

model of looking at cardiovascular

1:02:18

disease , and it's , it's

1:02:20

it's physicians who aren't understanding

1:02:23

or realizing the context in which these

1:02:25

lipoproteins and these blood

1:02:27

constituents are really operating

1:02:30

in . But it makes all the difference and

1:02:32

it , as we've just talked about and

1:02:35

I think you know , in analyzing this , this

1:02:37

problem you really have , you've

1:02:39

got a couple of layers of it , because you've got biochemistry

1:02:43

, lipid analysis based

1:02:46

on pharmaceutical treatment and apoB lowering , which

1:02:48

is , you know , mainstream Western

1:02:50

medicine . Then you've got , and

1:02:53

still , a biochemical lens , but the

1:02:55

work of Dave Feldman , you

1:02:58

know Dr Paul Saldino and

1:03:00

all those looking at reducing

1:03:03

vascular risk through modifying

1:03:06

insulin resistance , which is effective

1:03:08

, and but I just think it's still

1:03:10

limited in a scope . And

1:03:12

the reason why I'm going to

1:03:14

emphasize this point is because if you

1:03:16

send a patient out or you send someone out

1:03:18

and they're eating a carnival

1:03:21

type diet . They're highly insulin sensitive

1:03:23

again , but they're working out into a blue

1:03:25

lit gym , they're sitting

1:03:27

next to the Wi-Fi router every day . They

1:03:29

get stressed and they pop off a heart attack . They

1:03:32

pop a clot off like you . Like you and

1:03:35

that biochemistry insulin resistance model

1:03:37

of atherosclerosis can't explain to that

1:03:39

person why they had that

1:03:41

event . And that is comes to this , jack

1:03:44

Ruz's idea of you know half truth always lose

1:03:46

these to a full lie . So to me

1:03:48

it's not satisfying enough . We need to go to this physics

1:03:50

level and what you talked about with charge

1:03:53

structured water makes elegant

1:03:55

sense in my mind and has

1:03:57

a much higher degree of explainability

1:04:00

of what is actually going on . And

1:04:03

you know Malcolm Kendrick made the point that you know

1:04:06

your theory . Someone's theory needs to be

1:04:08

able to fit , it needs to be modular , it

1:04:10

needs to be able to fit , you need to be able to test

1:04:12

it with different clinical scenarios

1:04:14

or different pathophysiological factors

1:04:17

and you need to be able to explain that in

1:04:19

your theory . And what you talked about , stephen , is

1:04:21

gives us amazing explainability of

1:04:23

all the factors that damage

1:04:26

the endothelium . But they're doing it through

1:04:28

these effect on charge . And

1:04:30

you know I listened to a podcast of Peter Ateer

1:04:32

and Alan Sniderman . And Sniderman

1:04:35

couldn't explain how smoking

1:04:37

has any effect on atheroscopic

1:04:40

or plaque formation , and

1:04:42

to me that shows that he's

1:04:44

so mired in this lipid

1:04:47

hypothesis that his

1:04:49

explainable theory of reality isn't

1:04:51

able to account for one of the most

1:04:53

damaging effects on cardiovascular

1:04:55

health , which is smoking . And we can

1:04:57

, you know , I think the listener can infer from

1:04:59

what we've just talked about for the past hour how

1:05:02

that might be the case . But it involves structural water , involves

1:05:04

the endothelium . So I want

1:05:06

to congratulate you for pulling these pieces together

1:05:08

and presenting them so

1:05:11

in such an explainable way , because what

1:05:13

you've just talked about and what you continue to

1:05:15

talk about , I think , is getting closest

1:05:17

to the truth . As I see it , as I can

1:05:19

interpret it .

1:05:21

Yeah , and like you know , like you were saying , like

1:05:23

you got the lipid

1:05:25

hypothesis people and then you got the people that are

1:05:28

disagreeing with that lipid hypothesis or

1:05:30

saying that there's holes in it , and they're showing

1:05:32

that it's more in the context of metabolic health and

1:05:34

that LDL is not the whole deal

1:05:37

. But , like you said , that's limited . That's only going

1:05:39

to get us so far . However , it is very

1:05:41

important because we need that data that they're creating

1:05:43

to prove that it's not LDL

1:05:45

. But once we prove that , we

1:05:47

have to take them somewhere Right . And

1:05:50

then we have to say , oh , it's not that and leave it

1:05:52

at that . We have to say we have to give them . Well

1:05:54

, this is what it is . This is what explains it

1:05:56

all . Here's the theory and that's what I

1:05:58

am more interested in . You know I'm not interested

1:06:01

in overanalyzing lipids to just prove

1:06:03

that theory . I think that's going to be done , regardless of what

1:06:05

I care about it or not . But

1:06:07

I want the next theory , like , where

1:06:09

is it going to take us ? Here's some more information

1:06:12

. Some of it makes the

1:06:14

most sense . But let's prove it , let's mess with

1:06:16

it , let's see if there's where's the reality , let's figure

1:06:18

it out Right . So that's what we have to take people

1:06:20

and it's not , I think the medical

1:06:23

establishment is going to be stuck in the lipid theory

1:06:25

as long as the power is held

1:06:27

over them by pharma . And

1:06:30

so it's really going to start with people . You

1:06:32

know like it's great if we take here's

1:06:35

the thing , so , like Dave Feldman's

1:06:37

group is doing great work and we're going to take

1:06:39

that to people , people are going to be like , oh , that

1:06:41

makes a lot of sense , you know , and that's

1:06:44

that's that makes way

1:06:46

more sense than what my cardiologist is telling

1:06:48

me . And so they're , ldl may skyrocket

1:06:50

and without

1:06:53

another theory , without another path

1:06:55

from that , they're

1:06:57

going to get scared and that fear

1:06:59

is going to shut down the decision and they're going to go right to taking

1:07:01

statins or that approach . And

1:07:03

I work with people day in and day out

1:07:05

guiding them through this information and

1:07:08

they're like I think I need to , I think I need to do the bypass

1:07:11

, I think I need to do this , I think I need to do that , and

1:07:13

I say , okay , well , here's what the data shows . I can't tell

1:07:15

you what to do , but here's what it shows . If

1:07:17

they don't have another path forward , they're

1:07:20

going to fall right back into that because of fear , and

1:07:22

we've seen what fear does people over the last three and a half years

1:07:24

, and so we

1:07:26

have to give them this other information

1:07:29

, this path forward that takes that fear away , gives

1:07:31

them the confidence I know I'm protecting my arteries

1:07:33

, because I'm doing this right

1:07:35

, and that's it's a critical piece . You

1:07:37

know they're all different pieces . What Dave Feldman's

1:07:39

group is doing is one piece , but we have to

1:07:42

give the other piece that really pushes everybody , because that's

1:07:44

how we're going to affect Western medicine is we're

1:07:46

going to take people away from it . And

1:07:48

if people end up in fear and go right back

1:07:50

to it , we have to give them another path , because a large

1:07:52

percentage of them will take that path rather than buying

1:07:55

into the fear .

1:07:56

Yeah , and I want to . I want to congratulate Dave

1:07:58

Feldman and his citizen science project because

1:08:00

, as you mentioned , Steven , he's doing incredible

1:08:02

work and especially with this concept

1:08:05

of the lean mass hyperexpondent , which is describing

1:08:07

what happens to to someone's

1:08:10

lipid , to apoB and LDL , and

1:08:12

particularly on a low carb diet and particularly in

1:08:14

those with low body weight or

1:08:16

normal BMI , and that that data came

1:08:18

out recently , a meta analysis

1:08:20

showing that it wasn't the saturated fat

1:08:22

intake but rather BMI that was the

1:08:25

greatest predictor of developing quite

1:08:28

high LDL on a low carb diet

1:08:30

. So what Dave Feldman's doing is

1:08:32

amazing work and again , his study that

1:08:34

on the lean mass hyperexpondent

1:08:36

, they're doing CT angiograms of

1:08:38

people and you

1:08:41

know yearly CT angiograms to look inside

1:08:44

the vessel , get an idea of plaque

1:08:46

formation on low carb and

1:08:48

they're not forming any , which is again

1:08:50

kind of as if , as if the

1:08:52

lipid hypothesis needed another nail . I mean

1:08:54

this is like the Rasputin of

1:08:57

theories , it like it's never

1:08:59

dying , but even even all this contrary

1:09:02

evidence , but it keeps piling up and

1:09:04

it's , it's exciting what he's doing

1:09:06

. And I think Nick Norowitz

1:09:08

did a recent N of one experiment

1:09:10

where he ate Oreos

1:09:12

and that was sufficient to drop his

1:09:14

, his LDL very acutely

1:09:16

again showing the ridiculousness

1:09:18

of and the holes in in in this whole

1:09:20

theory . But , like you said

1:09:22

we , it's not explainable enough and I really

1:09:25

invite Nick and Dave

1:09:27

and anyone else to start delving into the biophysics

1:09:29

of what's going on here . Try to understand

1:09:32

structured water , try to understand charge

1:09:34

, because I think it's closer to

1:09:36

the truth . Maybe a

1:09:38

good point now we can talk about sunlight , because

1:09:40

I had a recent conversation with

1:09:43

dermatologist Richard Weller and

1:09:45

he's done amazing work epidemiological

1:09:48

work showing reductions in cardiovascular

1:09:50

mortality and with greater

1:09:52

UV light exposure and and

1:09:54

non vitamin D mediated effects

1:09:56

. So talk to us about

1:09:59

how the importance of sun for

1:10:01

cardiovascular health , how you think about it and maybe also

1:10:04

how it relates to structured water and exclusion zone

1:10:06

water .

1:10:07

Yeah , definitely , um . Before

1:10:09

I get to that , I want to comment on something that you said , um

1:10:12

, and that is that you know , just

1:10:14

to kind of a big picture , look at this . You

1:10:16

know , when we determined what normal LDL

1:10:20

or lipids in the blood was , it was on a population

1:10:22

that was eating a process food diet

1:10:24

, right ? So what Nick

1:10:26

Norwood showed when he eats those Oreos

1:10:29

, it lowers cholesterol . Does

1:10:31

that mean that it's good or does that just mean

1:10:33

how we determine normal ? Right , but

1:10:35

what if ? How we determine normal was completely abnormal

1:10:37

for humans ? Right ? So what if

1:10:39

it's like ? It's like if we took a , you

1:10:42

know , a wild animal and we put it in the zoo

1:10:44

and we put it in a semi natural

1:10:46

environment , but then we fed it on that unnatural

1:10:48

diet , um , and we disrupted

1:10:51

it social network and whatever , and

1:10:53

then we sit , took it slow , but it said , okay , this is what's normal

1:10:55

for this wild animal . Like , it's the same kind

1:10:57

of idea . So if you think about it

1:10:59

like that , then what's normal , what's been determined

1:11:01

as normal , is completely wrong

1:11:03

. Based on what humans

1:11:06

, how humans lived , you know , millions

1:11:08

of years before , hundreds of thousands

1:11:10

of years , I guess , modern humans , um , before

1:11:12

we had these process foods . So think about it

1:11:14

in that context . And then you start to realize that when

1:11:17

someone eats a lower carb diet which would have been

1:11:19

, you know , traditionally what happened in humans

1:11:21

at least part of the year um

1:11:24

, then an LDO goes up . That could probably

1:11:26

be normal , right ? That's probably what's supposed to

1:11:28

happen . Um , you know , and they're trying

1:11:30

to prove that in the context of metabolic health , that's fine

1:11:32

, but I'm trying to tell you that that's probably just

1:11:34

the way it's been forever .

1:11:37

Yeah .

1:11:39

And one of those other natural

1:11:41

parts of of of life

1:11:43

for humans was being outside and being

1:11:45

in the sunlight . Um , and

1:11:48

so , to context this , all

1:11:51

life on earth is

1:11:53

in all energy . Energy on earth comes from

1:11:55

the sun , right , it's what's

1:11:58

driving everything . It's the only reason that life is here

1:12:00

, and it was only when life

1:12:02

figured out how to harvest that energy in

1:12:04

various ways . Um and

1:12:06

uh . Cells , you know

1:12:08

, initially harvest that energy in in various

1:12:11

ways , um , that cells could come together

1:12:13

and make multi-cellular things , and then evolution

1:12:15

kept happening . We had more complex

1:12:17

, um , multi-cellular organisms and

1:12:19

eventually , you know , plants , and then um

1:12:22

uh , fish , and then amphibians

1:12:24

, and then reptiles , and then humans Well

1:12:27

, mammals , and then humans , and so

1:12:29

they just kept going like that . And it was all of this ability

1:12:31

of life to use energy . And so

1:12:33

the idea

1:12:35

that the Sun is bad for us is it makes no sense

1:12:37

whatsoever . It's where all of our energy is coming from . Even

1:12:40

the food you eat . Yes , you get energy from that . The energy

1:12:42

that food came from the Sun , and

1:12:45

so when we look at our

1:12:48

ability to take

1:12:50

sunlight and make

1:12:52

energy from it , there's a few different ways we can do this

1:12:54

, because people talk to a long time

1:12:56

about vitamin D . That's what the Sun gives

1:12:59

us , that's why it's important , and that's UVB

1:13:01

light , which is midday light . But

1:13:04

we have other ways that we

1:13:06

can take energy from the Sun and use it to

1:13:08

make electricity in the form

1:13:11

of electrons to power the body

1:13:13

. One of them is the molecule

1:13:15

DHA , which

1:13:17

animals are made of . Dha

1:13:20

is a fatty acid , high

1:13:23

amounts in seafood , but you can also get it

1:13:25

, especially grass-fed forms of animals

1:13:27

, and

1:13:30

DHA literally takes the sunlight and has the ability

1:13:32

to take that sunlight and convert it into DC

1:13:34

current , electrical current , electricity

1:13:36

electrons that are transported throughout

1:13:38

the body , and most physicians listening

1:13:40

to this should know that we use electrons

1:13:43

to make energy , to make ATP

1:13:45

, or at least an

1:13:47

ATP molecule , which could be seen as energy , could

1:13:49

be seen as other things , but

1:13:52

so for the average traditionally

1:13:54

trained physician or anybody

1:13:56

familiar with solar physiology should know electrons

1:13:58

are important and DHA

1:14:00

can make that . Another one

1:14:03

is melanin . We're told that melanin is

1:14:05

this pigment in the skin that determines our skin color

1:14:07

, and that's pretty much what it does . But

1:14:10

actually melanin is concentrated in many different places

1:14:12

in the body in the nervous system , in the eye Lots

1:14:15

it's pretty much everywhere when light or

1:14:17

any energy form , like

1:14:20

sound or anything , hits

1:14:22

melanin , melanin can take that energy and

1:14:25

what they say dissociate the water molecule

1:14:28

breaks it open into

1:14:30

hydrogens , oxygens and electrons

1:14:33

. So it makes electrons and those

1:14:35

electrons can be used by

1:14:37

the body , especially mitochondria

1:14:40

at the beginning . So we can take the sun and

1:14:42

do that through melanin and DHA . Now

1:14:45

also , we've talked about this , we've alluded

1:14:47

to this infrared light is

1:14:50

the light that's most absorbed

1:14:52

by water , especially the 3000 nanomerewoven

1:14:54

, which is the far end of infrared

1:14:56

light , and

1:14:59

so 42% of the sun's rays are infrared

1:15:01

at all times . And

1:15:04

so we take that infrared light

1:15:06

and it energizes the water in our body so

1:15:08

that when it gets next to those biological surfaces

1:15:10

which is already next to it , builds

1:15:12

more structured water , and the structured

1:15:15

water is electronegatively charged , contributing

1:15:17

to our charge . It also

1:15:19

creates a battery situation

1:15:21

, because the electronegative area

1:15:23

is lined up right next to the positive area , because the

1:15:25

hydrogens are cleaved off and that leaves a line

1:15:28

of hydrogens , and so this is a

1:15:30

positive and a negative area which is a battery

1:15:32

, which is why you don't put batteries in your

1:15:34

remote control car or whatever , and that you have

1:15:36

to align the charges right , because

1:15:38

that's what creates the energy to move the car , and so that's

1:15:41

what happens in our body . It happens literally everywhere

1:15:43

, including the lining of the artery . So

1:15:47

sunlight does this . And so when

1:15:49

we talk about all those benefits

1:15:52

of structured water in the vascular system

1:15:55

to the vascular system and preventing clotting

1:15:57

and preventing damage , and

1:16:00

then we see that infrared light from the sun

1:16:02

is what's providing that , then we start to

1:16:04

see oh well , that's why the research shows

1:16:06

that when you do infrared sauna

1:16:08

or get infrared light from the sun , that you

1:16:10

get increased blood flow and you get

1:16:12

decreased risk of clotting and you get

1:16:14

lower incidence of all

1:16:17

kinds of heart disease , whether it's stroke

1:16:19

or atherosclerosis or

1:16:22

heart attack . And

1:16:25

it's not just the infrared , like the UVA and the UVB

1:16:28

also have benefits too . They've been associated with

1:16:30

health

1:16:33

benefits , cardiovascular health benefits

1:16:35

, and the research is very

1:16:37

robust on that that

1:16:40

this sunlight is what is charging

1:16:42

our bodies . And so when you use this

1:16:44

quantum lens and you see

1:16:46

how your

1:16:48

body takes sunlight and makes energy and you

1:16:51

understand that the body's job is really

1:16:53

just to make energy to maintain older in the tissues

1:16:55

, you see why the effect that is . It's not

1:16:57

some strange thing like oh , that's interesting , the

1:17:00

sun helps your vascular system

1:17:02

. It's like no , when you see it in this quantum lens , you're like that

1:17:04

makes complete sense . So

1:17:06

that's why we see that with sunlight .

1:17:09

Yeah , and I really want to make the point that

1:17:11

you mentioned , which is Pollux

1:17:13

work , which they found that the blood flow was

1:17:15

occurring on , basically

1:17:18

irrespective of or after

1:17:20

the heart was essentially

1:17:23

removed . The blood flow was potentiated

1:17:25

around the body with infrared

1:17:27

light . So when we're

1:17:29

in , naturally outdoors , that

1:17:32

to me is like we're

1:17:34

reducing the , you

1:17:37

know , we're reducing the strain on the heart . Effectively

1:17:39

, we're relieving the ventricles of their need

1:17:42

to pump blood because the blood

1:17:44

is simply being potentiated through

1:17:46

both the arterial and venous circulation by

1:17:48

infrared light . And if

1:17:50

we're inside all day then

1:17:52

we are not getting

1:17:55

that free boost of blood

1:17:57

pumping ability in addition to all those other benefits

1:17:59

that you mentioned from

1:18:02

simply being outside . And

1:18:05

there's to quickly make a point about

1:18:08

on the biochemical lens once more

1:18:10

, is that you're making nitric

1:18:13

oxide through UVA exposure

1:18:15

. So that is a very potent vasodilator

1:18:18

and it is helping

1:18:20

assist in that endothelial

1:18:22

health . There's also melanocortin receptors

1:18:25

inside the endothelium and they're having

1:18:27

an effect on the

1:18:31

on vascular health . And again , I

1:18:33

believe that that's mediated through nitric

1:18:36

oxide and there was some mouse models of

1:18:38

knocking out the

1:18:40

melanocortin one receptor in the vasodilator

1:18:42

endothelium and

1:18:44

those mice developed stiff arteries

1:18:47

and essentially endothelial dysfunction

1:18:49

. There's also photo

1:18:51

there's blue light mediated photo

1:18:53

relaxation effect of melanobsin

1:18:56

receptors in the endothelium . So being

1:18:59

outside in natural blue sunlight

1:19:02

, I bet , is having a

1:19:04

beneficial effect as well . And

1:19:07

possibly being under blue light all day artificially

1:19:10

and kind of wrecking those melanobsin

1:19:12

receptors or destroying them is probably

1:19:15

contributing to disease . But just to emphasize

1:19:17

the point that the benefits of

1:19:20

natural sunlight are so immense

1:19:22

in terms of cardiovascular health

1:19:24

that yeah , again , it's

1:19:26

hard to overstate .

1:19:28

Yeah , and here's the kicker is

1:19:30

that we talk about how this

1:19:33

is what's responsible for the blood flowing , and

1:19:35

you know , there's experiments and

1:19:37

studies back in the 40s and then repeated

1:19:39

in the 60s , that show that when they

1:19:41

stopped the heart beating

1:19:44

of dogs these studies

1:19:46

were done in dogs that the blood continued

1:19:48

to move for up to two hours . And

1:19:51

then in Pollux Lab they showed in a chick embryo

1:19:53

that if they euthanized the

1:19:56

embryo and the heart stopped , the

1:19:58

blood continued to flow . If they put infrared

1:20:00

energy to it , then it would continue

1:20:03

to flow indefinitely . So

1:20:05

these mechanisms definitely happened

1:20:07

, and so the real kicker is

1:20:09

, if you look at the research on infrared

1:20:11

sauna and heart failure , it

1:20:13

is absolutely phenomenal and

1:20:15

, like people with heart failure , it's not the heart that's

1:20:18

failing . The heart is a vortexing hydraulic

1:20:20

ram . It's not necessarily a pressure

1:20:22

propulsion pump that's supposed to be forcefully

1:20:24

pumping blood throughout the body , but

1:20:27

it's not Cardioid , just head explode . Yeah

1:20:29

, it's not failing . It's

1:20:32

being forced to do more pumping than it's supposed

1:20:34

to because the mechanisms of blood

1:20:36

moving are not up to par , and

1:20:38

that is poor energy . It's poor

1:20:40

mitochondrial function in the heart itself and

1:20:42

in the rest of the body and in its lack of structured

1:20:44

water of the vascular system . And so if you apply

1:20:47

this infrared light to the system

1:20:49

and they have enough raw material , which

1:20:51

is water , it's been shown to

1:20:53

A heal the lining of the artery

1:20:55

and increase nitric oxide production , endothelial

1:20:58

nitric oxide production . But

1:21:00

also in people with heart failure , it

1:21:03

increases blood flow , decreases edema

1:21:05

. It increases ejection fraction . There's

1:21:08

people with cardiomyopic hearts that come back

1:21:10

to normal size . Like it's just phenomenal

1:21:12

, Right this . So

1:21:14

I don't understand why there's not infrared sauna in every cardiac rehab

1:21:16

center everywhere in the world . But it's

1:21:19

not very profitable to do that . That's probably why

1:21:21

. But it's really just , it's really great

1:21:23

and it's not just . I mean just heating your

1:21:25

body in general is good , but infrared sauna has

1:21:27

specific benefits to the heart

1:21:29

and the reason that makes

1:21:31

sense is because 42% of the sun's rays

1:21:33

are infrared . That's why it works . But

1:21:36

infrared sauna is kind of this modern hack we can use

1:21:38

to help these people who have gotten themselves

1:21:40

in this situation .

1:21:41

Yeah , and what is happening

1:21:44

when someone has heart failure , either

1:21:46

heart failure with reduced ejection fraction

1:21:48

or heart failure with preserved

1:21:50

ejection fraction this is a problem that's occurring

1:21:52

over a matter of years , decades , and

1:21:55

you're getting hypertrophy of the cardiac , of

1:21:58

the cardiac , the

1:22:01

ventricles , the heart isn't lodging

1:22:03

. And just

1:22:05

as you hypertrophy your skeletal muscle if you do

1:22:07

lots of push-ups sorry or

1:22:10

bench press , if

1:22:12

you're asking your heart to take

1:22:14

up the role that

1:22:16

maybe infrared light was helping in terms

1:22:18

of vascular flow , then

1:22:21

it's not surprising to me that

1:22:23

hypertrophy of that cardiac muscle

1:22:26

is something that could happen . Yeah

1:22:28

, the point about infrared

1:22:30

in the cardiac ward that

1:22:32

makes so much sense , so

1:22:35

cheap , so efficient . Obviously

1:22:37

, if someone's acutely unwell they might not be able

1:22:39

to get in the sauna . But even

1:22:41

having a red light panel that

1:22:44

has infrared I

1:22:46

mean , I've been in cardiac care wards and there's

1:22:49

been it's pretty distressing a patient

1:22:51

going into acute pulmonary edema

1:22:53

right in front of you and everyone's . We're

1:22:56

scrambling , we're

1:22:58

scrambling getting the oxygen on . But

1:23:00

imagine if we had a full body panel

1:23:03

and simply just shining

1:23:05

infrared light on that patient . I

1:23:07

don't know , maybe some clinicians in the audience

1:23:09

can go to their CCU

1:23:11

and buy a panel

1:23:14

from Kyle at Midwest Red

1:23:16

Light Therapy and give it a rumble , but

1:23:19

what's the downside ? There isn't any . So

1:23:22

it's an amazing thought

1:23:24

about how we could revolutionize

1:23:26

cardiac care with the framework

1:23:29

that you've described and given us

1:23:31

, stephen . And

1:23:35

then grounding I mean let's feed

1:23:37

that into the mix , because you talked

1:23:40

about electrons and energy

1:23:42

, currency and charge . The

1:23:45

earth is a massive negatively

1:23:47

charged ball . Feynman

1:23:49

wrote about that early on , so

1:23:51

maybe just talk a little bit about grounding

1:23:53

and , as it relates to what we've talked about

1:23:55

, yeah .

1:23:57

So the evolutionary consistent

1:23:59

thing is that we would have been in contact with everybody

1:24:01

outside . We didn't have rubber sole shoes

1:24:04

. If anything , we were wearing something

1:24:06

natural like a mandrel skin shoe that was still

1:24:08

conductive . So the

1:24:10

earth is this big ball of energy

1:24:13

. Electrons , and it's because the

1:24:15

sun is . The solar rays from the

1:24:17

sun are being deposited and turned

1:24:19

into electrons in the ionosphere , in

1:24:22

the atmosphere , and every once in a while

1:24:25

well , actually more often than not , around

1:24:27

the world , very frequently that discharges

1:24:29

in the form of lightning to the earth . That's

1:24:32

why metal things that are conductive are

1:24:34

attracting lightning , right and

1:24:37

so because it's trying to find its way to the earth . And

1:24:39

so this earth is this huge reservoir of

1:24:41

electrons , and the law

1:24:43

of electrostatics tells us that when

1:24:45

two conductive surfaces are next to each other

1:24:47

, that the area that's more

1:24:49

concentrated in electrons will flow into

1:24:51

the area less concentrated . And

1:24:54

, try as we may , we're never going to be as concentrated as

1:24:56

electrons as the earth is . So

1:24:58

if we touch bearskin to

1:25:00

the earth , we conduct electrons through

1:25:03

the conductive , hydrated fashion

1:25:05

network of our body , and

1:25:07

they've shown this over and over again . This

1:25:10

happens if you put your feet on the earth and

1:25:12

you test the voltage of your body . You are like

1:25:14

your toes are like about 200 times

1:25:17

more electro negative

1:25:19

than your head right , because you're in contact

1:25:22

with that and you're soaking those electrons into your body and

1:25:25

so they've shown some

1:25:27

benefits in this . As far as the vascular system , in that you

1:25:29

remember that Zeta potential I talked about . As far

1:25:31

as the structured water that gives

1:25:33

this kind of net negative charge surrounding

1:25:36

elements of blood like red blood

1:25:38

cells , lipoproteins and everything . When

1:25:41

you ground you increase your Zeta

1:25:43

potential , which keeps everything nicely

1:25:45

spaced in the blood , which decreases

1:25:47

blood viscosity , which we know is a risk

1:25:50

factor for clotting , and keeps

1:25:52

things moving through the blood nice and evenly

1:25:54

. And so

1:25:57

that's , you know , one way that

1:25:59

grounding can help with that . But also we

1:26:01

know that if it forms structured water on those

1:26:05

elements of blood , it's forming structured

1:26:07

water elsewhere in the body because it's giving the body that

1:26:09

negative charge , that ability

1:26:11

, that energy for water

1:26:13

to structure itself onto that biological surface

1:26:15

. So it's like people

1:26:17

say , oh , putting your feet on the earth for hippies . You know

1:26:19

that's a woo-woo stuff , right , but there's actually

1:26:22

a lot of research on it . And

1:26:24

when you think about it from the perspective I just told

1:26:26

you about how the physics works from the energy from

1:26:28

the sun to the earth and into us , like it

1:26:30

makes sense , like it's really happening

1:26:32

, and it makes sense evolutionarily , because humans

1:26:35

would have been outside in the sun

1:26:37

with their feet on the earth or

1:26:39

in a natural body of water . That's an incredible

1:26:42

way to conduct that energy

1:26:44

from the earth , those types of things

1:26:46

, so definitely beneficial

1:26:48

.

1:26:49

Yeah , great , great answer . Maybe

1:26:51

some final thoughts . Have you looked

1:26:53

into the role of deuterium in terms

1:26:55

of mitochondrial health and specifically

1:26:58

with regard to cardiovascular

1:27:00

health ?

1:27:02

Yeah , so I mean again

1:27:04

, cardiovascular health is all about

1:27:07

maintaining this charge and

1:27:09

one of the ways that we do that . So if we think about

1:27:11

, you know at least the way we're traditionally

1:27:13

trained what mitochondria does . It's

1:27:15

job is to make ATP , right ? Well

1:27:17

, actually there's a lot of other

1:27:19

things we've learned that happened in the process of making

1:27:22

ATP through

1:27:24

that electron transport chain . You know , the

1:27:26

glycolysis and Krebs cycle is all just . You

1:27:29

know how can we take food and get electrons

1:27:32

from it , right , so we learn

1:27:34

about all those annoying , you know names

1:27:36

in medical school . But then

1:27:38

it's all about the electrons , and as the electrons are passed

1:27:40

, we get hydrogens pumped into the inner brim , brain

1:27:42

space , and those are used to

1:27:45

make ATP in complex

1:27:47

five in the mitochondria . However , the

1:27:49

mitochondria also generate heat in the

1:27:51

form of infrared light , and

1:27:54

they also produce carbon dioxide and

1:27:57

they produce water , and this is this perfect

1:27:59

energize to a . Construct yourself

1:28:02

water , right ? And

1:28:05

? But the other thing is is that so

1:28:07

you know , if you think about it in that way , mitochondria

1:28:10

are making all that we need . They just need electrons

1:28:12

to do it Right . They're

1:28:14

making the water , they're making

1:28:16

the heat that we need , which is why , if we put on

1:28:18

infrared goggles , someone will light up . You know we're making

1:28:20

infrared heat and then

1:28:22

they're making ATP . And ATP can

1:28:25

provide energy for some things . But it has another important

1:28:27

role . But the making of that ATP is dependent

1:28:29

on those hydrogens that are pumped into the inner membrane

1:28:31

space and those hydrogens are

1:28:34

specific . That form of hydrogen

1:28:37

, the isotope of hydrogen , is specific for

1:28:39

that and it's what can go through complex five and make ATP

1:28:41

. There are different isotopes

1:28:43

of hydrogen . One of them is deuterium , and

1:28:46

deuterium , you know

1:28:48

, largely comes from like eating

1:28:51

foods out of season . That's the

1:28:53

main way , Because if we're eating , you know , foods

1:28:55

that are higher in deuterium , like plant foods and stuff

1:28:57

in the summer , you

1:29:00

know , then the sunlight gives us the ability

1:29:02

to kind of process that deuterium

1:29:04

and get rid of them . However , if we're eating this in the

1:29:06

winter , out of season , because we ship foods around the world

1:29:09

, we concentrate the deuterium and

1:29:11

deuterium without the sunlight

1:29:13

that we would get in the summer , in

1:29:15

the winter they can get , we can get higher

1:29:17

amounts of it , and when we get higher amounts of it , that

1:29:20

deuterium is a

1:29:23

different isotope of hydrogen than when it goes through complex

1:29:25

five . So we make ATP kind of

1:29:27

jams up the system . It's too big

1:29:29

, it doesn't fit , but the body still tries

1:29:31

to use it and that kind of messes with complex five and then

1:29:33

we have mitochondria . They're

1:29:35

doing all these things and they can't get ATP at the

1:29:37

end of it . That can create

1:29:39

lots of issues . The main issue is that ATP

1:29:43

is responsible for unfolding

1:29:45

proteins , like cytoskeletal

1:29:48

proteins in

1:29:50

the cell , and those proteins are the hydrophilic

1:29:53

surface that water structures itself on

1:29:55

. So if those are not able to be unfolded

1:29:57

and creating surface area for water to structure

1:29:59

, the cells dysfunction

1:30:01

because we've got these tightly bound proteins , not

1:30:04

as much structure water can form . That interferes

1:30:06

with this negative charge of the

1:30:08

cell and interferes with cellular function

1:30:10

. We start to get dysfunctional cells , dysfunctional

1:30:12

mitochondria , and so that's this problem with deuterium

1:30:14

. And so , like I said

1:30:17

, deuterium can come from a lot of places tap waters

1:30:19

, unfortunately lots

1:30:23

of deuterium in it , and so the better forms of water

1:30:25

are like spring waters and glacial

1:30:27

milk waters and things like that . They're lower

1:30:29

in deuterium and , like I said , they're lower in deuterium . Some

1:30:32

might as well gives us the ability . Same with heavy metals , like

1:30:34

some might as well gives us the ability to

1:30:36

get rid of these things . And

1:30:39

if we're doing all these eating

1:30:41

or drinking you know this poor quality water

1:30:43

and eating these high-deterior foods

1:30:46

like plant foods in

1:30:48

the wrong season , then we really increase

1:30:51

the amount of this concentrated deuterium . So , like

1:30:53

lots of the reason that people on carnivore

1:30:55

diets see benefits , probably one

1:30:57

is that they're not eating plant foods out of season anymore

1:30:59

, which is not giving them different live information

1:31:01

, and the second is that they're

1:31:03

not concentrating this deuterium in their body at

1:31:06

the wrong times of year . So

1:31:08

they're starting to see these benefits because their mitochondrists are functioning better

1:31:10

and that's going to

1:31:12

help literally everything . So

1:31:14

that's kind of the story on deuterium .

1:31:17

Yeah , I really think the benefits of carnivore are

1:31:19

a low deuterium diet and

1:31:21

basically essentially helping

1:31:23

to deuterium to please yourself , and

1:31:25

that's having consequent effects on

1:31:27

beneficial effects on mitochondrial efficiency and therefore

1:31:30

energy and insulin resistance and

1:31:32

metabolic health . But

1:31:34

it all effectively comes

1:31:36

from that mitochondria function

1:31:41

functioning more properly

1:31:43

. Yeah

1:31:45

, thanks for that summary . I

1:31:48

mean this is such an interesting

1:31:50

and in-depth conversation and I

1:31:52

think we've touched on a range

1:31:54

of topics that mainstream

1:31:56

cardiology and preventative cardiology have no

1:31:58

concept of . I'm really

1:32:01

not optimistic that a lot of lipidologists

1:32:04

, conventionally trained , have any interest in kind

1:32:06

of learning about . But

1:32:08

I'm hoping that by having these conversations

1:32:10

and helping to educate people who are

1:32:12

interested individuals

1:32:14

, medical students , doctors

1:32:16

then we can slowly point

1:32:19

people's curiosity in the right direction and

1:32:21

they can make their own mind up about what they

1:32:23

want to do and what they think makes the

1:32:26

most sense for their health . So in

1:32:28

closing I just want to emphasize

1:32:30

one point myself and then I'll ask you , stephen

1:32:33

, to emphasize a point that you want to make For me

1:32:35

. One of the most kind

1:32:38

of mind-blowing parts of this interview was understanding

1:32:41

that Vercow's Triad , that

1:32:43

there's three components of blood clotting

1:32:45

, which are hypercoagulability

1:32:47

, endothelial damage

1:32:51

and stasis . That's simply a story of structured

1:32:53

water and exclusion zone water and the

1:32:55

way you describe that is so elegant and

1:32:58

it feels like a lock has kind of

1:33:00

been put into lock in my mind when

1:33:02

you put it that way . So

1:33:04

thank you for explaining that and I

1:33:07

really want people to take it at home and mull

1:33:09

over it because it's a critical

1:33:11

part of not only the atherosclerosis

1:33:13

cardiovascular disease story , but it's also

1:33:15

part of metastromboembolism

1:33:18

, part of a lot of autoimmune

1:33:20

disease , anytime where you've

1:33:22

got these blood clots happening

1:33:24

. So , yeah , any point you

1:33:26

want to emphasize , particularly before we sign off

1:33:29

.

1:33:30

I guess just more of like a practical

1:33:33

kind of guideline for people . We just

1:33:35

do a lot of information at

1:33:37

them and some of it can be paradigm shifting or

1:33:40

the first time they heard it or something like that . But

1:33:43

just advice for navigating

1:33:45

this world of health information that we have

1:33:47

, which can be very confusing . A

1:33:51

lot of the times when I work with clients online

1:33:53

, like in health consulting , it's what I end up doing

1:33:55

. Most of the time it's just helping them navigate the situation

1:33:58

. Well , this person said this and that person said

1:34:00

this Like who do I believe , and

1:34:02

I think that it's really important

1:34:05

to understand that

1:34:08

we live in this

1:34:10

world of hyper realities and hyper

1:34:12

reality is just something that we take

1:34:14

as more real than what's actually real . So

1:34:18

an example is like the weather channel and

1:34:20

how you can look at that green blob going across the

1:34:23

screen and you can say , oh , it's raining right there . And

1:34:26

I'll never forget the time I was driving in my

1:34:28

car and I had about two

1:34:30

, three hours to go and it was pouring rain . I was like man

1:34:32

, I wonder how long it's going to rain . So I pull up the weather

1:34:34

on my phone and it says it's not raining and

1:34:36

I was like it's pouring rain outside

1:34:38

. So , like this weather channel app , has become this hyper

1:34:41

reality that we tend to take as more real than

1:34:43

what's actually real . And , you

1:34:45

know , while things like

1:34:48

medical testing and medical

1:34:50

research and lots of different forms of research can

1:34:53

be helpful and they can help us clue

1:34:56

us into certain things , they are , to a certain level

1:34:58

, hyper realities that

1:35:00

we take as more real than what's actually

1:35:02

real . Which is what is real . Is us

1:35:05

Right ? What is what we feel day

1:35:07

in and day out ? And so , taking

1:35:09

that to the next level is , when you're trying to figure out what

1:35:11

to do to achieve health

1:35:13

, ask yourself what's real , what

1:35:16

is real ? Is the statin drug real ? No

1:35:19

, that's a man made thing . That's , you

1:35:21

know , totally defies this complex

1:35:24

biological exercise that affects one pathway in

1:35:26

the body . That's a hyper reality that this will

1:35:28

give you health , right ? Instead , focus on those real

1:35:30

things . What is real ? Real

1:35:32

light that's been present on the earth since

1:35:34

the earth's been here , real earth

1:35:36

, you know . Cut yourself to that real food

1:35:39

and the real way of eating food

1:35:41

, which is , which would only be available in your

1:35:43

local environment in season . Real

1:35:45

relationships , not artificial

1:35:48

ones or things that we think we know online

1:35:50

, like . Have those relationships that are actually

1:35:52

real and rely on those more

1:35:54

than artificial ones or ones that aren't serving you

1:35:56

. Maybe negative relationships , real

1:36:00

positive emotion , real gratitude . These real

1:36:02

things even feel real negative

1:36:04

emotions , but learn how to process them

1:36:06

in a healthy way , like these real

1:36:08

things are . Focusing on what's real

1:36:11

is way more

1:36:13

important than hyper realities

1:36:15

Like what does this medical research studies

1:36:17

say , which is fundamentally flawed from the beginning ? Because

1:36:20

the idea of

1:36:22

trying to eliminate every variable and

1:36:24

test if that's going to have an effect is a hyper reality , because

1:36:27

I've never exposed one variable at one time . So

1:36:30

what does that ? Does that really tell me anything about how my

1:36:32

body is going to react to something ? Probably not , but

1:36:35

it's informational . We can get information from it . So

1:36:37

, just , I always give people

1:36:39

that because it really helps them

1:36:41

navigate this world and think about the information

1:36:43

they're consuming . Is this real ? It's

1:36:45

a hyper reality . Should I get information from this

1:36:48

and use that to

1:36:50

to guide me a little bit , but never

1:36:52

take it as as in all be all ? It's

1:36:55

really important to have that context and I think

1:36:57

when I tell my clients that it's really

1:36:59

helpful for them for as far as navigating this

1:37:01

information they're just embarked with all the time these

1:37:03

days .

1:37:05

Great advice . Maybe

1:37:08

wake yourself up from the matrix of

1:37:10

health information and try and

1:37:12

understand what is real

1:37:14

. And yeah , that is a great advice . Thank you very

1:37:16

much , stephen . It's been

1:37:18

a pleasure speaking with you

1:37:20

and I think we've you've prevented

1:37:22

presented a lot of very important

1:37:24

information for everyone . So thanks

1:37:27

again and , yeah , we'll stay in touch , of

1:37:29

course .

1:37:30

Of course , thanks for having me .