4:19

welcome back to another episode of the

4:21

regenerative health podcast now

4:24

. I am very , very excited to be bringing

4:26

you this episode . It is with

4:28

dr michael wyman , who

4:30

I believe is one of the world's

4:32

leading decentralized cardiologists

4:35

. So , michael , thanks for coming on .

4:38

Thank you for the opportunity . It's going to be a fun one .

4:41

Great . Maybe we start with your credentials

4:43

and how you arrived at this

4:45

part of medicine .

4:48

So I'm a board-certified cardiologist

4:50

. I did all my invasive cardiology training

4:52

at St Louis University School of Medicine and

4:54

ended up staying in the area . So

4:56

I launched my own practice here about five years

4:58

ago , where now I just focus on the

5:01

prevention of heart attacks and strokes . I

5:03

took all my invasive skills and

5:05

didn't care really sick people in ICU and use

5:08

those to kind of reverse engineer

5:10

what you need to do so you don't end up in those situations

5:12

.

5:13

Yeah , reverse engineering . I love it and

5:16

that is what I try and do when I'm thinking about optimizing

5:19

people's health and trying to understand what

5:21

is going wrong so we can understand how

5:23

to prevent it from happening . So

5:26

maybe let's start with some definitions

5:28

, because ischemic heart disease and

5:31

heart disease is one of the biggest

5:33

, it is the biggest killer in

5:35

society . So let me

5:37

, or can you please , define

5:39

for our listeners what are the

5:41

exact meaning of atherosclerosis

5:44

, coronary artery disease , atherosclerotic

5:47

cardiovascular disease , ischemic heart disease all

5:49

these key , very important definitions

5:52

.

5:53

So for the majority of those that you just listed , they're basically

5:56

synonyms . Finishes so for the

5:58

majority of those that you just listed , they're basically synonyms

6:00

. But

6:04

you have nearly 60,000 miles of blood vessels . 99% of your blood vessels

6:06

are significantly smaller than the human hair . It's the microvascular system and as cardiologists

6:09

, we're mostly focusing on the large blood vessels

6:11

that you can see when you're doing procedures . But

6:14

it's really looking at what

6:16

is damaging the arteries and causing it to

6:18

get inflamed and then plaque

6:20

to build up . And when that plaque starts to develop

6:22

and calcify , that's when it first usually

6:24

starts getting picked up on some of these screening

6:27

tests and your now diagnosis having

6:29

atherosclerosis or coronary artery

6:31

disease .

6:33

Yeah , and the question

6:36

that I kind of get a lot and

6:38

I think a concern that people have

6:40

is one what

6:43

caused my plaque or

6:45

what caused the deposition of

6:47

calcium in the blood

6:49

vessels and maybe that's been picked up on

6:51

something like a coronary artery calcium score

6:54

or maybe it's been seen

6:56

more directly in something

6:58

like an angiogram . So can

7:00

you talk through the listener about

7:03

how you think about coronary

7:05

artery plaque and why it's developing

7:07

and how it's developing ?

7:09

So it takes a few explanations

7:12

. But it's mostly about the

7:14

lining of the arteries . There's a layer

7:16

called the endothelium and it's one cell

7:18

thick . If you took out

7:20

all your endothelium it'd be the surface area

7:22

of six tennis courts . So it's one of your largest

7:24

organs and one of its main

7:26

jobs is to release nitric oxide , which

7:29

is a very short-lived gas . That

7:31

gas causes the artery walls to

7:33

relax , so that keeps your blood pressure normal

7:35

. But that nitric oxide also keeps the

7:37

blood flowing well , so things don't stick

7:40

to the artery lining . But only

7:42

in past few years it was a little bit more recognized

7:45

that there's something that actually protects the endothelium

7:47

. That's known as the endothelial glycocalyx

7:50

. It's a protective gel coat

7:52

for the endothelium . So if you think of

7:54

taking a fish out of water and it's slimy , that's

7:56

essentially what the glycocalyx is , and I know

7:59

your audience is pretty well-versed in the quantum world

8:01

. Well , that glycocalyx is heavily

8:04

structured in water

8:06

and so that's kind of like

8:08

the beginning part is that if that

8:10

structured water collapses , then

8:12

the lipoproteins , the white blood cells , they

8:14

start aggregating or sticking to the artery lining

8:17

and then that may kick off that cascade

8:19

of where , if you don't stop it , plaque

8:21

will build up . But there's infinite insults

8:24

for that glycocalyx . But the body can

8:26

only respond with three responses and

8:28

this I learned from one of my mentors , dr Mark Kusin

8:30

, many years ago . Those three finite responses

8:33

are oxidative stress , inflammation

8:35

and autoimmune dysregulation . So

8:37

those are normal responses , but

8:39

they get dysregulated the longer they go on

8:41

and it's like a fire . If you don't shut the fire

8:44

off , then the plaques start really forming in

8:46

the arteries pretty significantly .

8:48

Yeah , that's a great explanation . And let's

8:51

really be clear about the physiology

8:53

of the blood vessel and the lining

8:56

of this blood vessel . Because , say

8:58

, we're taking a cross-section of an artery

9:00

and we've got the lumen or the inside

9:03

of the vessel where the blood is flowing , and

9:05

then if we progressively go down the

9:07

layers , then , as you mentioned , the

9:15

first thing that we'll get to is a layer of structured water

9:17

or exclusion zone water , and we've got this , uh , glycocalyx , which is

9:19

can be thought of , as you mentioned , is a slippery , slippery

9:21

, like almost fish like

9:23

substance , and I did some , I did

9:26

research in in mucins and as

9:28

they relate to the gastrointestinal

9:30

tract and they , these glyco

9:32

, the glycocalyx , can be thought as just a

9:34

bunch of mucus-like stalks

9:37

that are sticking out of the endothelium and providing

9:40

a very slippery surface

9:42

, and below that we've got the endothelial

9:45

layer which , as you mentioned , is only

9:47

one cell thick . So the question

9:50

is and maybe again

9:52

define this for everyone what is the difference

9:54

between these larger

9:56

blood vessels in the artery and

9:58

the venous system compared to the smaller as

10:01

we go down in size ?

10:04

So arteries are pretty much similar

10:06

, even getting down into the capillary side

10:09

, but on the venous side

10:11

there's no smooth muscle in it and

10:13

so they're much thinner , less rigid

10:16

vessels . So the

10:19

real key is that , like you know

10:21

, atherosclerosis is , you

10:24

know , it's mostly an

10:26

artery-facing disorder

10:29

. Now there is a possibility to develop plaque

10:31

in the veins , just not nearly as common , probably

10:34

due to , like , there's lower shear stress

10:36

going across the glycocalyx and the venous side

10:39

. But , as

10:41

you had already mentioned , there's a layer of the glycocalyx

10:43

, there's endothelium underneath

10:45

, that's the intima , then the media

10:47

, then adventitia . So if you think of an artery

10:50

as , like in cross-section , you're slicing

10:52

a garden hose in half , you're

10:55

mostly looking at what's going on in the wall of the artery

10:57

. Too often in conventional cardiology

10:59

they're just focusing on what's in the lumen , either

11:02

by looking at your blood or doing

11:04

an angiogram and saying like you don't got a lot of blockages

11:06

, so you don't get a stent , or you

11:08

get a lot of blockages , here's your stent .

11:10

Well , the stent relieves the obstruction , but it doesn't fix

11:12

why you developed those plaques in the first place and

11:20

fix why he developed those plaques in the first place and then you're just playing a game of

11:22

whack-a-mole , you're putting in short stints and you haven't really treated the 60,000

11:24

miles . Yeah

11:28

, yeah , exactly . And the question , therefore , that would seem logical step to

11:30

me is that , before we can even get to damaging the lining of the blood vessels

11:32

and , like you mentioned , damage

11:35

to that endothelial lining and the glycocalyx

11:37

seems to be the prerequisite for forming

11:39

plaque , requisite for any

11:41

blood contents , whether they're red blood

11:44

cells or lipoproteins

11:46

, to actually enter

11:58

the subintimal space

12:00

and actually form plaque .

12:03

So I think it's not you know a either

12:08

, or I think it's just more of a

12:11

case where the

12:13

more lipoproteins you have , the more glycocalyx

12:16

disruption and nithelial dysfunction you have

12:18

. The conditions are more likely

12:20

you will develop plaque . It's kind of

12:22

the quantum world . It's not a guarantee , it's

12:24

just probability . But

12:28

there are cases where lipoproteins

12:30

can get into the entomal space and you

12:32

still have a fully intact glycocalyx and nithelium

12:34

. There are different receptors in the glycocalyx

12:37

but it just tends to be more when intact

12:39

glycocalyx and endothelium and there are different

12:41

receptors in the glycocalyx but it just tends to be more when the glycocalyx

12:43

has been shed . And again , it's kind of like thinking about

12:45

seagrass at the bottom of a water source . Is that if that

12:47

seagrass gets shed then there's

12:50

different receptors that are kind of sticking

12:52

out and

12:57

then you know more of these lipoproteins and white blood cells and platelets start

12:59

aggregating and sticking to that endothelial surface and then are more likely to kind

13:01

of get in . I really don't like the term and you

13:03

may not either , but like leaky gut it's essentially

13:05

like leaky arteries . There's more gaps , more

13:08

places for the lipoproteins to get through .

13:11

Yeah , and I think the point that

13:13

you made is particularly relevant . Maybe we're

13:15

going to get to the difference between

13:17

people with an

13:20

actual pathological lipid

13:22

physiology , which is

13:24

people with mutations in various genes

13:27

, with related things like familial

13:29

hypercholesterolemia , compared to people with

13:32

intact lipid physiology , and

13:35

I guess the angle of the question was that to

13:38

me it seems like if we have an intact structured

13:42

water layer above our glycocalyx in

13:45

someone with a normal lipid physiology , then

13:47

it seems to me very difficult

13:50

for any type of glycocalyx

13:52

damage or clot or plaque

13:55

formation to be initiated and

13:57

therefore continue yes

14:00

, I mean the glycocalyx is , you know , continually

14:03

being shed and continually being rebuilt

14:05

, and it's one of the things

14:07

where it's like glycocalyx is heavily negatively

14:09

charged because of all the sulfur units

14:11

in it and the lipoproteins

14:14

, the red blood cells , they're all negatively charged

14:16

as well , and negative repels negative .

14:17

and so with my patient I talk about like kind of being like a , and the lipoproteins , the red blood cells

14:19

, they're all negatively charged as well , and negative

14:21

repels negative . And so with my patients I talk about like kind of being

14:23

like a maglev train . If your arteries have a very healthy layer of the glycocalyx , those

14:26

lipoproteins should be repelled from it and

14:28

slide on by . But there's something that's

14:30

going to damage the glycocalyx . And then it's a positive and a negative

14:33

. Things will attract , and then it's a positive and a negative .

14:37

Things will attract . Yeah , that's a fantastic analogy

14:39

. I really like that

14:41

. So say there is damage to this glycocalyx

14:43

, maybe explain what happens

14:45

next ? Because clotting

14:48

, I believe , is underlying

14:51

this whole process of both

14:53

acute plaque rupture

14:55

but also the chronic process of

14:57

plaque formation .

15:00

So inside the glycocalyx it's kind of like

15:02

another way to

15:04

think about . It is like think about a

15:06

marsh . There's different creatures that live

15:08

inside this marsh and then

15:11

some of these things are helpful at knocking

15:14

down oxy of stress . So there's superoxide

15:16

dismutase You're continuously

15:18

breathing oxygen to make energy

15:21

in your cells . That oxygen

15:23

can be toxic to the

15:25

arteries . So the superoxide dismutase

15:27

knocks down some of the reactive oxygen species

15:29

and there's different clotting factors

15:32

inside the glycocalyx . And

15:34

so think of it as kind of like something where , like

15:36

if it gets scratched , you want to be able

15:38

to clot as needed . But

15:40

there are certain things that will tend to really

15:43

kind of denude the

15:45

glycocalyx , and then that sets it up where you're more

15:47

likely to clot than you are to bleed , and

15:50

so it's going from a normal physiologic

15:52

process to a pathologic process when

15:54

the glycocalyx is severely shed

15:56

and you start becoming more hypercoagulable

15:58

.

16:01

And what are some of the factors that are

16:03

going to be contributing to this ? Again , to

16:05

disturb this structured water and then start

16:08

shearing or damaging this protective

16:10

seagrass layer .

16:12

Yeah , the biophysical is , you know , pressure

16:15

. So hypertension . You know , I often tell

16:17

people it's not necessarily a disease , but it's a marker

16:19

that you're not really having a healthy lining

16:21

of your artery . Your arteries probably have very low levels

16:23

of nitric oxide availability and the arteries are

16:25

very stiff . But the higher the

16:27

shear stress , the more that's going to damage that glycocalyx

16:30

layer . And then there's a whole host of biochemical

16:33

things , but dysregulated

16:35

insulin and glucose are high on the list

16:37

. More likely

16:39

the oxidized lipids are

16:41

going to damage it . Infections

16:44

, microplastics , heavy metals

16:47

, toxins like air pollution

16:49

there's numerous things

16:51

that can damage the glycocalyx and the body's

16:53

always trying to repair . But it's when

16:55

you kind of overwhelm that repair system

16:57

that you tend to go into points where the

16:59

person starts developing endothelial dysfunction , vascular

17:02

inflammation , soft plaque , hard plaque

17:04

and events . But you have many years

17:06

to intervene before they have those events .

17:10

Yeah , and explain to us what the difference

17:12

is between the soft

17:14

plaque and the hard plaque . And , as you

17:16

said , this is an exercise

17:19

in prevention and just like there's

17:22

steps along the way of detecting

17:25

insulin resistance before someone becomes fully

17:27

blown type 2 diabetic , there's

17:29

steps along the way that we can identify

17:32

the progression of atherosclerotic

17:34

cardiovascular disease before someone ends

17:37

up in the emergency department with acute

17:40

chest pain .

17:41

No , and that's a great kind of segue into

17:43

it is that in the United States , every

17:46

40 seconds somebody has a myocardial infarction

17:48

and often the first

17:51

time that they have a symptom is having

17:53

the heart attack . They had no warning sign . This was going

17:55

to happen , but it's been building up in them

17:57

for many years . Most likely it

17:59

sometimes starts in your teens and twenties , where

18:01

you first develop glycocalyx disruption

18:04

, endothelial dysfunction . Then

18:06

you start developing vascular inflammation

18:09

where the intima starts to swell . So

18:11

as more and more lipoproteins get

18:14

retained in the intima it starts to

18:16

swell , much like if you sprain your ankle it's

18:18

going to swell , or if you get a splinter it's going to swell

18:20

. The territory as the white blood cells come and

18:22

investigate why are these lipoproteins getting

18:25

retained in the entomoma ? And then

18:27

, like a game of Pac-Man , the monocytes

18:29

start gobbling it up . They became foam cells

18:31

and then this is the nidus to start developing

18:33

these quote soft plaques . The

18:36

soft plaques , the body's going to keep trying to take care of

18:38

it . It's going to put smooth muscle down over it

18:40

to kind of scar it over , and eventually

18:42

it will ossify it or calcify it . So

18:45

the body , if it calcifies it

18:47

, that's probably going to be a stable scar and it's

18:49

probably not going to cause you any symptoms

18:52

, unless that scar builds up to

18:54

a state where you have now a 70% or 80%

18:56

blockage or stenosis in your artery

18:58

and the lumen is not flowing

19:01

very well . So that

19:03

is one of the cases where that's really late to the

19:06

game and sometimes that's the first time that people end

19:08

up seeing a cardiologist is that they start having chest

19:10

pain with exercise or shortness of breath

19:12

or exercise intolerance , and then

19:14

they go get a stress test and it's abnormal and they're

19:16

like oh , you have severe coronary disease . You

19:18

know we're going to do an angiogram and they get

19:21

a stent and they think they're all fixed . But

19:23

that's just their introduction . You know you haven't

19:25

fixed their endothelial dysfunction , their vascular

19:27

inflammation or really talked about why

19:29

their lipoproteins might be damaging their arteries

19:31

. So

19:41

that's kind of conventional . But there are a whole host of testing you can do that looks at the health

19:43

of the lining of the arteries and then you can look for the degree of soft plaque with carotid

19:45

scans using ultrasound . You can use different CT scans to look at the softer , hard plaque

19:47

in the corneal arteries and you can really tell people hey

19:50

, you have advanced disease , even though you've not

19:52

had any symptoms . And then those are the people

19:54

that want to be more aggressive with pharmaceutical

19:56

agents , supplements and lifestyle interventions

19:58

.

20:00

Yeah , and I want to be really clear about

20:02

the exact pathophysiology

20:04

of what's happening when someone is having

20:07

, maybe chronic vessel

20:09

damage that's leading to plaque formation

20:12

, versus that acute event

20:14

that leads to occlusion

20:17

or obstruction of an

20:19

artery that leads again

20:21

to symptoms . So explain the difference

20:23

to us .

20:25

So in the first case that's going to be more stable

20:27

angina , where this plaque has been building up

20:29

over time . The body is forming

20:31

smooth muscle over this plaque and

20:34

then it calcifies it

20:36

. The lumen is where the blood is flowing . So

20:38

again , if you think about a garden hose and you slice

20:40

it in half until the lumen

20:42

is occluded 70% , most

20:45

people are not going to have any symptoms . You're getting enough

20:47

oxygen nutrients downstream , where the tissues can

20:49

continue to make energy from

20:51

the blood . But once you start going

20:54

above 70% , most of the time when

20:56

it's under physiological stress , either from

20:58

mental stress or exercise , the

21:00

person starts having symptoms . They may

21:02

feel a pressure , tightness

21:05

, squeezing in their chest . They're short of breath

21:07

or the exercise that they used to be able to do

21:09

, they just can't do it . They stop the activity

21:11

, the heart rate slows down , the cardiac

21:13

output goes down and then the symptoms

21:16

improve . But

21:18

every time they do that type of activity or get their heart rate back up , they

21:20

typically keep having those symptoms

21:22

. Now where it's

21:24

more concerning is when the person has

21:26

no symptoms . They may have only

21:28

a 30% plaque or blockage in one of their

21:30

arteries . They cannot feel that plaque and

21:33

these plaques can become unstable . Often

21:36

in this situation where there's a lot of inflammation

21:38

and oxidative stress , think of these

21:40

plaques as like pimples

21:43

on the wall of the artery . If it's a really

21:45

thin pimple and it's inflamed

21:47

, then that pimple could pop and

21:49

then all the oxidized , damaged cholesterol

21:52

, white blood cells and other cellular debris that's

21:54

in this plaque , which is kind of like an

21:56

abscess in the artery wall , it spills out into

21:58

the bloodstream and now the body basically

22:00

thinks it's bleeding and then all these coagulation

22:03

cascades kick in and form

22:05

a clot . It's a big platelet plug

22:07

and it seals that plaque rupture

22:09

but it acts as a dam to

22:12

all the tissues downstream so no oxygen nutrients

22:14

go downstream . So when these plaques rupture

22:16

in your heart , that's what we would call a heart attack

22:19

. If it's in your brain , it's a stroke . Now

22:21

there are other heart attacks where there's aortic you

22:24

know dissections tearing down into arteries , or the spontaneous

22:26

coronary you know dissections

22:29

. You know there are some ulcerated plaques that occasionally

22:31

rupture , but the majority of plaques

22:33

it's a . You're going along fine

22:35

and then when these plaques ruptures , the

22:37

blood clots , you start having your event

22:39

.

22:41

Yeah , and that's a really important point to make , because

22:43

the degree of disease

22:45

or maybe occlusion that

22:47

we might have detected on something like

22:50

a CT

22:52

coronary angiogram doesn't necessarily

22:54

correlate to

22:56

the probability of having

22:59

an acute myocardial infarction . And

23:01

that is what I'm presuming is because

23:04

the occlusive event is

23:06

a massive thrombus or blockage

23:08

of the artery from red blood cell accumulation

23:10

. And whether you have 30% stenosis

23:13

or 70% stenosis , it

23:15

is an individual process . But

23:17

equally , depending on the underlying vascular

23:20

inflammation , could those two situations lead

23:22

to an AMI and an emergency

23:25

presentation ?

23:26

Correct . Yeah , and that was always kind

23:28

of . The scary thing is that there's people who come in

23:30

and they had no symptoms and

23:32

often they had quote

23:34

normal cholesterol

23:36

and people are like , well , they just had bad luck . It's probably

23:38

genes and , yes , there's probably some genetic

23:40

role for some of these people , but

23:43

you know , it's really something in their life

23:45

disrupted their glycocalyx and their telium for

23:47

a long period of time and this cascade

23:49

happened . It does not generally

23:51

happen overnight , and so that's why

23:54

it's most cases where it's like if you start looking

23:56

earlier , you start finding those people

23:58

that , hey , they really low nitric oxide

24:00

, their arteries are stiff , they're

24:06

starting to have higher blood pressure . Check some biomarkers and they got high sensitivity to your

24:08

PLV . Okay , what's going on with this person ? And start trying to find out , well , before

24:10

they ever have their first symptom .

24:12

Yeah , and I think one case that really illustrates

24:16

this well is Stephen Hussey , who

24:18

I've interviewed and I'm sure you're aware of . He's talking

24:20

about the quantum and circadian implications

24:23

of heart disease and he had an

24:26

acute myocardial infarction and basically

24:28

occlusion of

24:30

his left anterior descending artery

24:33

artery

24:40

. But when they looked at his , when they did the angiogram , he had

24:42

no disease , he had no hard clot . So that is indicating that the process of his

24:44

heart attack was a spontaneous clot

24:46

and in the setting of those

24:48

inflammatory factors that we talked about

24:50

really briefly earlier .

24:53

Greg , yes , and it's one of the cases where you know you

24:55

don't always have , you know , a severe stenosis

24:57

when these people have heart attacks so

25:00

the goal needs to be keeping

25:02

that endothelium as stable

25:04

and as least inflamed

25:07

as possible in in my mind .

25:08

Would you agree with that ?

25:10

absolutely . Again , it's you know , it's the three finite

25:12

responses , it's the oxidation , the inflammation

25:15

and autoimmune dysregulation . If you can

25:17

keep at bay , you don't tend to keep

25:19

going down those pathways where these plaques build .

25:22

And maybe one more concept to delineate before

25:24

we go further is this idea of

25:26

Virchow's triad and as it relates

25:28

to blood clotting and coronary

25:30

artery disease and AMIs

25:33

.

25:34

Sure , and actually it had been a while since

25:36

actually I thought about the actual triad . But it's , you know

25:38

, you know , it's uh , you know , injury

25:41

, there's stasis , and then

25:43

there's this hypercoagulable response

25:45

. Um , and it fits in

25:47

the . The story of the glycocalyx is

25:49

that , you know , something damages the glycocalyx

25:52

, that sets off the case where

25:54

these hyperpochromic factors get released

25:57

and the blood's more likely to clot

25:59

. But what we call stasis

26:01

, well , I mean that would be

26:03

, you know , in the kind of quantum world , you

26:05

know it's low redox potential . You don't

26:07

have enough net negative charge

26:10

to have the blood flow , you

26:12

know , on its own , essentially over

26:14

the negatively charged glycocalyx , you

26:17

know . So that's where I would

26:19

try to think about it . Stasis is a lack of

26:21

electrons .

26:23

Yeah , and you can imagine that a

26:25

lack of electrons , from a lack of grounding and

26:27

a lack of negative charge , that is , repelling

26:30

those red blood cells away from each other and away from the

26:32

lipoproteins and away from the glycocalyx

26:35

, could potentially cause stasis

26:37

and the other two I

26:39

mean hypercoagulability in a state

26:41

of insulin resistance and , yeah

26:44

, I

26:46

mean vessel injury from whether that's

26:48

you know , just a decade

26:50

of smoking and those particulates are cleaving

26:52

and shaving off your glycocalyx

26:55

, cleaving

26:58

and shaving off your your glycocalyx . Maybe it's actually a good opportunity to talk

27:00

about briefly the perspective of cardiac

27:02

physiology that relates to

27:04

the , the microcirculation

27:06

and the fact that maybe the heart is

27:09

having not was not

27:11

the only source of propulsion on

27:13

flow in in blood vessels . What's your

27:15

perspective on this idea is the heart

27:18

is not a pump .

27:20

So I have read Dr Cohen's

27:22

book and I know some of Dr

27:25

Hussey's postings are talking

27:27

about this . It's an

27:29

interesting theory . I think it's

27:31

plausible , it

27:33

makes sense to me , but is

27:36

it something that I give a lot of credence

27:38

to ? No , I don't really think too much about it because

27:40

either

27:42

it is or it isn't , but it's the same

27:44

things I'm going to teach people . It's like I want them outside

27:47

grounding , I want them getting full spectrum sun

27:49

on their body , I want them to avoid

27:51

fluoride in their water . So all the things

27:53

that are going to improve their net negative charge is

27:55

going to improve the flow through

27:57

this 60,000

28:00

miles of blood vessels that you have . But

28:02

it is interesting that the heart

28:05

is one of the most energy-dense organs

28:07

but , even that being true , it

28:09

may not have enough force

28:12

to be able to truly pump blood through

28:14

that kind of a distance . And I know that there's been

28:17

some studies where they've just shined

28:19

infrared light on blood

28:22

vessels and the flow continues to go

28:24

. So that's an interesting

28:26

experiment

28:28

and , yeah , I think it's plausible

28:30

, but I don't spend too much time worrying

28:32

about it .

28:34

Yeah , and you're right . If the implications of

28:36

it are the same , then , yeah

28:38

, the practicalities is what matters

28:40

, and I think you're referring to Dr

28:42

Gerald Pollack's recent paper

28:45

on the driving of blood beyond

28:48

the heart , I think , and he showed in a chick embryo

28:50

the shining of infrared light was able

28:52

to potentiate blood flow . So , yeah

28:55

, it's a very interesting area of

28:57

development . So talk to us

29:00

now , michael , about what

29:02

are some of these indicators

29:04

that we might look into for

29:06

gauging our endothelial health , if we've accepted

29:09

what you and I have said for the first

29:12

20 minutes of this interview that inflammation

29:14

in our blood vessels is important , endothelial

29:16

dysfunction is important and the

29:19

health of those blood vessels are important so

29:21

how can we get an insight into their health ?

29:25

So with my patients I always talk about

29:27

that . There's two things we need to look at . We need to look at the biophysical

29:30

and we need to look at the biochemical , because

29:32

if you just look at one or the other you don't really

29:34

have the full picture . So I always just

29:36

start with you know what is actually going on with the arteries

29:39

, because that is really going

29:41

to tell you how aggressive to be with the things that you see

29:43

floating through your blood . So

29:45

the endothelium there's

29:47

a few things you can use to test it . You know , at home

29:49

it can just be as simple as is your blood pressure

29:51

less than 120 over 80 ? Good , that's

29:57

a good start . You know , if you're a man , do you have erectile dysfunction ? If you

29:59

do , you're probably going to have some microvascular disease . Now you got to figure out

30:01

, okay , why do you have microvascular disease ? You

30:04

know , in the office . You know there are tests you

30:06

can do where you can test your salivary nitric oxide

30:08

levels . It's like a little salivary sample

30:11

on this . You know , litmus paper type

30:14

, and the brighter red it is , the more

30:16

you can make nitric oxide through that salivary pathway

30:18

. There's devices that look

30:20

at pulse wave velocity . So

30:22

essentially , how elastic are your arteries . If your

30:24

arteries are really elastic like an accordion , they're

30:27

probably making good nitric oxide . If your arteries

30:29

are like a lead pipe , they're probably pretty sick

30:31

. There are tests that look at

30:33

your ability to release nitric oxide

30:35

when a vascular

30:38

stressor has been applied , and this would be

30:40

called the endopat test . It's a

30:42

15-minute non-invasive test where

30:44

you have a blood pressure cuff pumped up on your arm

30:46

, higher than your systolic blood pressure , and

30:48

you have probes on each of your fingers measuring the flow

30:51

. And then , after a five-minute occlusive

30:53

period , you open up the blood pressure cuff

30:55

, the blood rushes back down into your hand

30:57

and that blood's going to flow over the glycocalyx

30:59

that is transduced to the

31:02

underlying endothelium like hey , here comes a big slug

31:04

of blood and the nitric oxide gets released

31:06

. The smooth muscle in the artery relaxes

31:08

and the flow rushes back down to your hand and your

31:10

hand wakes up . And then with this system

31:13

we can calculate well , how much do arteries

31:15

dilate when there's this vascular stressor ? And

31:17

optimal your arteries should triple or quadruple

31:19

in size . But if your arteries

31:21

, you know the cutoff is 1.68

31:24

. So if your arteries don't dilate more

31:26

than 168% , then you have

31:29

endothelial dysfunction and you got to go

31:31

looking in through the biomarkers or their lifestyle

31:33

. Okay , what's driving

31:35

that ? So that's how you kind of test the endothelium , and

31:37

then on the biochemistry part of it , you

31:40

would look at labs such as homocysteine

31:42

uric acid , adma

31:51

, which stands for asymmetric dimethyl arginine . And then there's just that old school urine

31:53

microalbumin creatinine ratio . So if you're leaking protein

31:55

into your urine , that means you've damaged the glycocalyx

31:58

to the arteries in your kidney and you're leaking protein

32:00

. So those are kind of the starting points to tell

32:02

a person how healthy their arteries

32:04

are . And then we can get into talking about , like , okay

32:06

, once that has been broken down , what

32:10

can you expect with soft plaque , hard

32:12

plaque and what tests you should look for that ?

32:13

then Thanks

32:17

for that , michael . Yeah , and it's a good place to mention that . Nitric oxide

32:19

, this highly labile gas

32:22

that you mentioned , has an

32:24

incredibly important role in vasodilation

32:27

, or opening up those blood vessels

32:29

, and it

32:31

is essentially stimulated or

32:33

released , liberated when we get ultraviolet

32:36

light on our skin

32:38

. I think that's the key distinction

32:41

. Previous listeners of my podcast would

32:43

have heard the episode with Professor Richard Weller

32:45

, who was instrumental in discovering

32:48

that pathway and therefore

32:50

joining dots to show

32:53

that people with higher UV

32:55

light exposure have less cardiovascular

32:57

death , less cardiovascular mortality and

33:01

less cardiovascular disease . With

33:05

regard to those assessments of endothelial

33:08

dysfunction or health , do

33:11

you typically see , I'm guessing

33:13

you see people with type 2 diabetes who smoke

33:15

regularly ? I'm guessing you

33:17

see people with type 2 diabetes who smoke

33:19

regularly who have never grounded before ?

33:24

They have poorer endothelial health . On those metrics

33:26

they would , but I would say I probably have a more health-conscious-minded

33:30

practice at this point . So I

33:32

think I'm kind of on the hand of my . I have

33:35

nearly 900 patients . I

33:38

think less than five of them still actively smoke

33:40

. How many are actually truly type two diabetics

33:43

? Probably less than five

33:45

. As well , there's a lot of pre-diabetics and people with

33:47

early signs of resistance . But people who are frank

33:49

diabetic with A1Cs near 10 , like

33:51

I used to see all the time very , very few

33:53

. But those are the people that , yes , you're

33:56

basically probably going to be more secondary prevention

33:58

for those people . This isn't their first rodeo

34:01

. If you're smoking , that is like the number

34:03

one thing that's going to damage the glycocalyx

34:05

. It's not the nicotine , it's all the heavy metals

34:07

and other toxins and then combustible

34:10

cigarette . It's the delivery form . That's

34:12

the problem . That then shears off

34:14

your glycocalyx and now everything

34:16

else is going to be starting to stick there . Oh

34:19

, and you got an A1CF10 ? Okay

34:21

, well , great , You're never going to regrow that glycocalyx

34:23

and you're just going to have all this microvascular

34:25

disease . And that's what you see . These

34:27

patients go blind , they

34:29

lose their extremities , they

34:32

have kidney failure . Yes , they also

34:34

tend to develop some macrovascular

34:36

disease where they're getting stents . But it's

34:38

the microvascular system and those people that you really

34:41

see kind of go downhill quickly .

34:43

Well , it sounds like you've

34:45

selected for a very health-conscious

34:47

patient population . But I

34:50

love the analogy of the seagrass and

34:52

the grass because it actually reminds

34:54

me of regenerative farming , which is one

34:57

part of the optimal health puzzle that I like to talk about

34:59

with regard to food sourcing . But

35:01

I'm just imagining grass and if you're constantly

35:04

mowing it or you're constantly whippersnapping

35:07

it with a brush cutter and then you're not

35:09

letting it grow back , then maybe

35:11

you're spraying herbicides on it . That's

35:14

maybe an analogy for what's happening to the endothelial

35:17

glycocalyx when we're inhaling the

35:19

diesel particulate fumes and eating

35:21

drinking Mountain

35:24

Dew every day and that glycocalyx

35:26

is just getting hammered by the fluctuating blood

35:28

glucose and all those micro

35:31

particulate particles .

35:33

I think that's a perfect analogy . I often

35:35

use that one about seagrass . Is that ? Yeah

35:41

, because the glycogalix has these like little strands out there and it's

35:43

sensing the flowing blood and it's sending information to the underlying

35:45

endothelium and there

35:47

are certain things that will damage one

35:51

patient's glycogalix . That won't necessarily damage

35:53

others , but it's sometimes

35:55

. Thousands of micro cuts

35:57

is what's doing it and you have to go figure out like

35:59

hey , what are the major drivers for this person

36:01

? Unfortunately , there's a lot of things you can do

36:03

, even if you don't get to the absolute root cause

36:05

. You know we've talked about some of them . It's just like you know

36:08

proper sun exposure , grounding , you

36:10

know proper hydration that doesn't have fluoride in

36:12

it , like you're just trying to allow the body to have as many

36:14

kind of building blocks as it needs to

36:17

start regenerating the glycolysis , because the body

36:19

is pretty resilient if you get out of its way

36:21

. But

36:25

you know , I was recently on a podcast and they were asking about the microplastic situation . You

36:27

know there's a recent study that was talking about that about half the patients

36:29

that were getting carotid endodirectomy surgeries

36:31

. They were finding these microplastics inside

36:34

the plaque and it's presumed

36:36

that they're probably ingesting them . But they could also

36:38

be inhaling them . But the

36:40

more interesting thing wasn't that , like , there was these microplastics

36:43

in the plaque ? In my mind it's why

36:45

didn't all of them have it in their plaque ? What

36:47

was reducing the risk of some of those

36:49

people not getting it ? My suspicion

36:52

is that those people had bad

36:54

glycocalyxes , briefly , but they

36:56

were doing some more things that prevented the

36:58

microplastics from getting retained in there . So

37:01

, you know , that's how I kind of think about it . It's

37:03

like you know , what can you do to improve the

37:05

lining of the glycocalyx ? Well , you know , there

37:07

are some , you know

37:09

, patented nutraceuticals

37:12

that kind of give the building blocks to the glycocalyx

37:14

. But a lot of it is just trying to remove the insults

37:16

because we're all going to be exposed to things . It's just , you

37:18

know , everybody has a different threshold for when

37:21

those insults are going to really lead to the diseases

37:23

.

37:24

Yeah , great point . And that specific trial

37:26

or study was very interesting and

37:29

I'll just reiterate that it showed

37:31

when they took , essentially

37:33

reamed out the inside

37:35

of these carotid arteries in

37:37

people and they analyzed the plaque

37:40

that they removed and found microplastics . And

37:42

yeah , you're right , that is the right

37:44

question , which is why

37:46

did some people have this and others didn't ? And Dr

37:49

Jack Cruz made the point

37:51

that I mean melanin . If we've cultivated

37:53

our melanin and our quantum

37:55

point of view , our melanin is

37:57

acting like it's a heavy

37:59

metal complex or another form of antioxidant

38:02

, then that's one particular reason why

38:04

we could help to detoxify

38:06

or remove those types of substances

38:08

. And

38:11

the question I wanted to ask

38:14

you was specifically about homocysteine

38:16

, so you mentioned it . What degree

38:18

is a raised

38:21

homocysteine a risk

38:23

factor in the context of perhaps

38:26

no other

38:28

deranged blood markers , and how is

38:30

it having its effect on raising

38:32

the risk of atherosclerotic

38:34

cardiovascular disease ?

38:37

having its effect on raising the risk of atherosclerotic cardiovascular

38:39

disease . So

38:43

homocysteine is an amino acid that's supposed to get converted to methionine . I usually

38:45

like to see a level of homocysteine less than eight and often if

38:47

it's elevated the person may have chronic

38:50

kidney disease . That might be driving

38:52

it . It's just the detoxification

38:54

pathways don't work well in the people with renal failure

38:57

, but often it's a person who

38:59

has an MTHFR mutation

39:01

, either homozygous or

39:03

heterozygous , 677 or 1298

39:06

mutation and you need

39:08

to be able to methylate the

39:10

homocysteine to methionine . If

39:12

you build up high levels of homocysteine it

39:15

will often drive up the asymmetric dimetharginine

39:17

and asymmetric dimetharginine

39:20

competes with endothelial

39:22

nitric oxide synthase to produce nitric

39:24

oxide . So the higher ADMA

39:26

levels , the lower your nitric oxide . So

39:28

in patients who have high homocysteine and

39:31

then you discover that they have a methylation issue , then

39:33

often you will support them with

39:35

different methylated products . Drive the homocysteine

39:38

back down . You see the AD omega down

39:40

. Often they start making more nitric oxide

39:42

and it's all about keeping

39:44

nitric oxide high and available .

39:47

Interesting because the other things that can

39:49

drive up homocysteine are like a B12

39:51

, obviously a vitamin B12 deficiency , riboflavin

39:55

and a folate deficiency

39:57

as well , so it's tied into

40:00

cardiovascular risk via nitric oxide .

40:03

Correct . And yes , that's usually when I

40:05

say people have a methylation issue . They're often going to have

40:07

either low B12 or folate , or

40:09

likely both in some instances , and

40:12

then you give them a combination replacement

40:15

to get their levels of B12 and folate back

40:17

to optimal . Those are cofactors . There's

40:19

a few other things like biopterin

40:22

that then help this methyl

40:25

tetrahydrofolate reductase enzyme convert

40:27

the homocysteine back into methionine .

40:30

Okay , yeah , that's a little bit of a technical

40:32

but interesting point , thank

40:34

you , so say

40:36

we've done these , and

40:39

maybe one more that you could describe for us is

40:41

the high-sensitivity CRP , and C-reactive

40:43

protein is obviously cleaved

40:46

, produced by the liver and is

40:48

an indicator of inflammation , but how do you

40:50

look at high-sensitivity CRP

40:52

as a cardiovascular risk indicator ?

40:55

It's included in my panel that I check

40:58

for all new and established patients

41:00

. It is a quick check on

41:03

the inflammation system . I

41:06

tell patients it depends on if you're coming in and

41:09

this is pure on screening . Your HSCRP

41:11

should be normal , but if you recently

41:13

had an infection , surgery , musculoskeletal

41:15

injury , you should expect it to be slightly high

41:18

. It's not a problem if it's high and you have a ready explanation

41:20

. The problem is when it's you know two

41:23

, three , four for years and you don't know

41:25

why they have this high sensitivity to CRP elevated

41:27

. So then you got to start doing the detective

41:29

work . Now , often it's untreated

41:32

sleep apnea , it's insulin resistance , it's some

41:34

type of you know , sensitivity

41:36

to gluten . Possibly you know

41:38

there's something that's going to be driving it and

41:40

then you try to withdraw that and the CRP goes down

41:42

. But it's not

41:45

the be-all , end-all test . But

41:47

it's one of those cases where , like if you have high sensitivity

41:50

, crp high and lipoproteins

41:52

, you're much more worried about that person

41:54

. And then this is the kind

41:56

of idea of why

41:58

you know stans have this potential

42:00

pleiotropic effect at lowering inflammation

42:03

. That may be one of the reasons why they actually work

42:05

, not just lowering the lipoproteins

42:07

.

42:08

Yeah , okay . So we've looked at these specific

42:10

biomarkers and then we really get to the lipid

42:13

panel and there is so

42:15

much controversy over and

42:17

, I think , a lot of ambiguity as to what people

42:20

are talking about when they're referring to cholesterol

42:23

and these other blood

42:25

lipids . So maybe give us a quick overview

42:27

of what are the main

42:29

lipid components in a lipid panel . What do

42:31

you look at and to what degree are they

42:34

helping us predict

42:36

this disease ?

42:38

So in a traditional lipid panel there's

42:40

four things that you know mostly get reported

42:43

. You know there's total cholesterol , hdl

42:45

cholesterol , triglycerides and LDL

42:47

cholesterol , which sometimes is just calculated

42:49

. You really want to have at least a direct LDL-C

42:52

, but I'll get to that in a moment like that's

42:54

probably still not enough . So in

42:56

a traditional panel if the total

42:58

cholesterol is over 300 milligrams per deciliter

43:01

and the LDL cholesterol is over 190

43:03

milligrams per deciliter , then

43:05

the person may have familial

43:07

hyperlipidemia , which is a

43:09

genetic abnormality , often with the LDL

43:12

receptors , where the person just doesn't

43:14

clear lipoproteins very effectively from the bloodstream

43:16

, and then they have these higher levels of

43:19

total cholesterol and LDL cholesterol

43:21

. So I will always look at that in every

43:23

patient . But there are some patients who had

43:25

quote normal panels . They do one

43:27

of these kind of more restrictive

43:30

diets where they're full keto

43:32

or carnivore with high saturated fat

43:34

and they may see this panel happen even

43:36

though that they don't have FH . But

43:40

I don't put a lot of stock

43:42

in the traditional panel to predict risk because

43:44

again , half the people coming into the hospital

43:46

who have heart attacks have quote normal cholesterol

43:48

In the traditional panel . Yeah , I will

43:50

look at the triglycerides because it's often

43:52

a sign . Is the person insulin resistant or not

43:55

. I generally like to see the triglycerides less than 80

43:57

, but you'll see , some people are very fit

44:00

no evidence of insulin resistance and they

44:02

have high triglycerides . Now there's

44:04

certain genes that affect lipoprotein lipase at

44:06

times that raise the triglycerides . So it's not a perfect metric

44:08

but in many people it's a marker of

44:10

insulin resistance if it's high . And

44:12

then the HDL cholesterol . It's

44:15

anybody's guess at this time . Now

44:17

there's just actually a recent trial that

44:19

came out where they were infusing HDL

44:22

in patients having STL elevation MIs

44:25

and it showed no benefit for these

44:27

patients . So the HDL side

44:29

of the equation is still very , very murky

44:31

. I really

44:33

dislike the term good cholesterol . You

44:36

should almost basically not look at your HDL cholesterol

44:38

. Focus more on the LDL side of the equation

44:41

first , especially if you have plaque in your arteries

44:43

. So that's what I do when I look at the traditional

44:45

panel . But if anything

44:48

, patients are going to see me

44:50

, for they're going to be doing some of the advanced

44:52

lipoprotein analysis . So

44:54

we're doing themr analysis and

44:56

then checking an apob and then that's really where

44:58

you can get into , like you know , helping

45:00

people understand , like what the risk is yeah

45:04

, and maybe we won't specifically

45:06

go into the , the nuances of lipidology

45:08

.

45:09

Uh , this , this conversation , because I really do

45:11

want to get the rest of your thoughts on

45:13

a range of other topics and maybe we

45:15

can come back to it but say

45:17

you've assessed someone's risk based

45:21

on some blood work . Maybe

45:23

now explain to us what

45:25

you're going to do next and I think , before

45:28

we even go there , you can explain those three concepts

45:30

of primordial prevention , primary

45:32

prevention and secondary prevention .

45:35

So yeah , so start there . So , secondary

45:37

prevention you've already had a heart attack , you've

45:39

already had a stroke , you have stents in your arteries

45:41

, you've had bypass surgery . We're trying to prevent

45:44

you from having it again . And yes , I do

45:46

have some patients I've had prior events . Often

45:48

they're not under my care . They've had them

45:50

out in the real world and they come to see me to

45:52

try to not have it again . Little

45:55

in-depth duty at that point . You know that's

45:57

honestly where most cardiologists play

46:00

. You know they're only treating people who've had events

46:02

, and so that's why they're not going to talk about

46:04

a lot of things that I'm talking about , because , one , they've

46:06

never learned about it and two , these aren't the patients that

46:08

they're seeing . They're seeing the sick as the sick , and

46:10

so they're throwing the kitchen sink at these people . But

46:13

primary prevention in the classic

46:15

world is that you've not prior had

46:17

an event . But if you're

46:19

only using conventional tools , you're going

46:21

to miss things . And so if you

46:23

use a lot of these advanced testing , they're

46:25

probably not necessarily primary prevention

46:27

, they're probably like 1.5

46:30

. They're not one , they're not

46:32

two , but primordial means . Like

46:34

you're born , you have

46:36

perfectly healthy arteries . How do you stay

46:39

that way ? That is really really challenging

46:41

. There are certain tests that I do

46:43

a CT angiogram test which

46:46

uses AI to look at the arteries . It

46:48

looks for plaque . I've

46:50

screened a couple hundred

46:52

patients over the past three years . I've

46:54

only seen two women

46:56

with perfect scores . I've never seen

46:58

a man not have some degree of salt

47:00

plaque in their arteries . Now I'm starting to start

47:02

screening people less than 40 . That

47:05

is a caveat is that most I'm

47:07

screening patients over 40 , but

47:10

last year I saw a 36-year-old gentleman

47:12

who had a calcium score nearly 1400 . Ct

47:15

angio had severe right coronary stenosis and he

47:17

got stented before he came to see me and

47:19

then we were doing deep dive . Okay , how did you

47:21

end up with such serious disease at 36 years

47:23

old ? So I think primordial

47:25

prevention is the goal and we

47:28

really need to kind of keep teaching the primary

47:30

care doctors and even the pediatricians

47:32

what to be looking for , because this

47:34

is a disease that starts in your teens , twenties

47:37

, and a lot of your habits they're

47:39

set and not stone , but like

47:41

a lot of your nutritional habits are set when you're

47:43

a teenager and your exercise

47:46

patterns are set as a teenager . Those

47:48

are two big levers that people need to kind of

47:50

optimize as they move forward .

47:53

Great and I want to make the point of how

47:55

relevant this is in terms of

47:57

lifestyle and how our lifestyle

47:59

in this modern age right now , I

48:02

believe , is increasingly responsible

48:04

for the development of

48:06

atherosclerotic disease at younger and younger

48:09

ages . And I believe there

48:11

was an observational study done of a Catarvan

48:13

population who are

48:15

living a traditional lifestyle in

48:17

their island location

48:20

. They're eating

48:23

mainly coconut oil as a kind of a fat

48:25

source , they're eating fresh fish , they're obviously grounded

48:27

, they're getting a heap of sun and

48:30

I think they even smoke . They have a high rate of smoking

48:32

and the amount of coronary

48:35

disease that they have is is very , very

48:37

little . And whereas you're

48:39

you're talking about now the fact that

48:41

if everyone is doing everything wrong

48:43

with regard to these risk

48:45

factors that we've briefly talked about , then

48:47

you're gonna , we're gonna see a deposit

48:49

of deposition of plaque um earlier

48:52

and earlier , and younger and younger .

48:55

I definitely agree with that . I mean , you

48:57

know 80 , 90%

48:59

of this really could be prevented

49:01

with . You know the things that you

49:04

know you and your audience frequently would talk

49:06

about . You know it's setting your circadian rhythms

49:08

, it's grounding , it's , you know , avoiding

49:11

. You know toxins when you can . You

49:13

know it's improving your net

49:15

negative charge . Those things

49:17

make you more resilient for the infinite insults

49:19

you're going to see as you go forward . But

49:22

I think it's the story

49:25

of that . Our technology is great to be able to talk

49:27

across the world with each other , but

49:30

too many people get drawn inside

49:32

in front of these things all day long and

49:34

they never touch the ground outside . They never

49:37

see a sunrise , they never spend

49:39

more than three minutes outside in any one

49:41

day . They highly ultra processed

49:43

food and you know it's

49:45

. You know I sometimes get pigeonholed and think that you

49:47

know . People ask me like well , you don't have , you know

49:50

a diet to recommend every cardiac patient ? Like it's

49:52

individualized . You know . Like you know I

49:54

didn't know , like your maternal haplotype . Where

49:56

do you live in the world ? What are your goals ? Like

49:58

are you trying to lose weight ? Add weight , you

50:00

know , add muscle . Like there's going to be some nuance to it

50:02

. But food is

50:04

important . But you know , as Dr Cruz talks

50:06

about , you know , it's

50:12

maybe five , six , seven down on the list me . They

50:14

haven't even started to even think about that

50:16

as the big thing that they had been

50:18

missing in their life . Why are they showing up sicker

50:20

than they should be ? Nope , they have

50:22

not really slept well and the circadian rhythms

50:24

are way off .

50:26

How do you think about the sunlight

50:28

and the circadian rhythm as it

50:31

particularly pertains to the development

50:33

of atherosclerosis

50:35

?

50:44

I mean the body has different circadian timings in the heart . At nighttime your blood pressure is

50:46

dropping it should drop by at least 15% while you sleep and it starts

50:48

to increase in the morning as cortisol

50:50

starts to rise . This is why a

50:53

lot of times heart attacks happen between 3

50:55

am and 6 am , as cortisol is rising , your

50:57

blood's getting stickier , your blood pressure's going

50:59

up and

51:01

then there are reasons why that

51:04

if you don't have your circadian rhythms dialed in , you're

51:06

going to be more insulin resistant . So

51:08

it is all connected . But

51:11

I think you had said it earlier . It's like teaching

51:14

the person how to use the sun appropriately

51:16

. I'm not telling people to go outside 24-7

51:19

and bake . It's getting morning light

51:21

in your eyes . Set your circadian rhythms

51:23

Ideally expose more skin

51:25

so that your skin is preconditioned

51:27

for when UVA and UVB come out

51:29

later in the day . But the more infrared

51:32

A you can soak up , the more nitric oxide

51:34

is going to get liberated from your skin and keep

51:36

your blood pressure normal , keep your blood flowing

51:38

like red wine , not so much like ketchup

51:40

. So it's just teaching people the simple

51:43

ways to kind of rewild

51:45

themselves , just get back into nature .

51:47

Yeah , yeah , I love that . So let's talk

51:49

about screening

51:52

and maybe risk stratification , because

51:54

what type of

51:56

imaging would you suggest

51:58

for people at different

52:00

stages of this heart disease prevention

52:03

journey ?

52:05

And that's a good point is that I do recommend imaging

52:07

. I mean , there's a lot of different risk

52:09

calculators people can use and

52:12

they're good at a population level , but

52:14

you really want to know do you have plaque

52:16

? What do you need to do ? So

52:19

you need to go look at the arteries

52:21

. So , head to toe , there's

52:24

different scans you can do . If you've

52:26

had other scans for other reasons , you can always look

52:28

at the results and see if they ever mentioned that

52:30

you have any calcified plaques in

52:32

the brain or your abdomen . I've

52:36

seen some ones where people get panorexes

52:38

of their teeth and they see some plaque in their carotid

52:40

artery that's calcified . So

52:42

look at your old imaging if you have access to it . But

52:44

if you don't have those often , I

52:47

will start with patients getting a carotid

52:49

intramedial thickness ultrasound no

52:52

radiation , takes about five minutes . The

52:54

scan of the arteries on the side of the neck . It's

52:56

something that you can repeat generally

52:59

yearly . You have a baseline and

53:01

see what has changed . If

53:03

you're doing things right , things shouldn't

53:05

change year over year . Ideally you see

53:07

things getting better . If they already had intimal thickening

53:10

and you've got it improving . It

53:12

was Dr Thomas Sunderham in the

53:14

1600s . The famous saying a man

53:16

is as old as his arteries . So if your

53:18

vascular age is higher than your biologic age , you

53:21

got a problem . That

53:23

being said , you know there are other tests . You

53:25

know you really want to look at your

53:27

coronary arteries noninvasively . You

53:30

know , for somebody who's you know , probably

53:32

around the age of 40 , and this is kind of

53:34

in the primordial , primary prevention

53:36

a CT-coordinated calcium

53:38

scan is a good starting point . Often

53:41

joke it's kind of like a mammogram for the heart it's

53:44

going to put you in buckets . Are

53:46

you truly low risk and you have a calcium score of zero

53:48

? Or do you have a calcium score over 400

53:50

and you're high risk ? Now it's common

53:52

people will develop a positive calcium score

53:55

sometime in their life . But I've seen

53:57

people in their 80s and the scores have still been zero

53:59

. But I've seen a 36-year-old with

54:01

the score nearly 1400 . So just

54:03

looking at somebody from the outside , you have no idea what

54:05

the coronary arteries are going to look like unless you do one of these tests

54:08

. But the downside of

54:10

the calcium score test is that it will not see

54:12

any of the soft plaque . So

54:16

if the person has a strong family history of early cardiovascular disease or

54:18

they have quote scary blood work , then

54:21

maybe you would add on a CT-coordinated

54:23

angiogram . It's a little

54:25

bit more radiation , there's a

54:28

contrast risk , so

54:30

you have to have an IV , have normal kidney function

54:32

and there's a cost risk . It's probably a

54:34

factor of 10 to 15 times more expensive

54:36

to do a CT angiogram than it is a calcium score

54:38

test , but it's a more sensitive

54:41

test and will tell you with a high degree

54:43

of certainty how much stenosis you have

54:45

in your arteries . But it's more going to tell you about the soft

54:47

versus hard black in your arteries , and

54:49

so that's a good starting point for most people .

54:59

It's like do something that looks at your carotid arteries , do something that looks at your coronary

55:01

arteries . Yeah , and I've talked to radiologists about this problem and in the emerging field , which is

55:03

something that I'm trying to cultivate , of decentralized radiology

55:06

, there's a lamentation

55:08

that all this imaging is being done

55:10

for CT chests , for

55:13

abdominal MRI , abdominal CT , and

55:16

the biggest findings that

55:18

are relevant to the patient's long-term cardiovascular

55:20

metabolic health aren't even being reported

55:22

on , and that is the presence of

55:24

calcified hard plaque in

55:27

these arteries . There's an incidental

55:29

finding that the radiologist

55:31

might have made a note of it in their head

55:33

but they don't put it on the report

55:35

. And if they don't put it on the report , then no

55:37

one does anything about it and people can go for

55:39

10 years , 15 years , and then they

55:42

wind up in the emergency department and

55:44

I see them in the emergency room with

55:47

chest pain and maybe this could have been prevented

55:49

if the radiologist had made

55:51

a comment on it 15 years

55:53

ago .

55:55

No , that's a very good point and that's something I've been doing for many

55:57

years is just looking at any old imaging

55:59

and finding stuff . I'm like did you know that they reported

56:01

your coronary artery was calcified 10 years ago

56:03

? I'm like nobody ever told me that . I'm like well

56:06

, that's not surprising , it's unfortunate

56:08

, but I was recently at a conference

56:11

where they were talking about how they're using

56:13

AI to basically tackle

56:15

this . One problem is that they're going to

56:17

take old images and

56:19

they're going to feed it through the machine and

56:21

look for these cardiac

56:24

calcifications and images

56:26

that weren't designed to look for it . So

56:28

they're not going to be as precise

56:31

because they're not gated images , but it's

56:33

better than nothing and it's already basically

56:35

free data . It's already been done . So if

56:37

you can give some information to the patient that

56:40

, as something that they did five years ago , you might

56:42

kind of be able to help intervene well before

56:44

they're having symptoms still .

56:46

Yeah , exactly , and that's something I've been

56:48

in discussion with a cardiac radiologist

56:50

about . So if any radiologists are listening and

56:52

want to actually start

56:55

reporting the important metabolic

56:57

findings , then get in touch with me . But the

56:59

next question that I have for you , michael , is

57:01

when ? So you

57:03

mentioned that the calcium score is a

57:05

great start and it's cheap . In Australia

57:07

, I believe , it costs about it's about $150

57:10

from any kind of radiology practice

57:12

. You just get a request from your GP and

57:21

if you want to do a CT coronary angio

57:23

, that's a bit more involved and what

57:25

would be the indications

57:28

for you to step beyond those tests ? But

57:30

even what are the implications of some of the findings

57:33

of the calcium and the CT

57:35

coronary angio ?

57:38

So , starting

57:40

with , what would you normally see is

57:42

that most

57:44

general cardiologists

57:46

are not going to do this type of testing

57:48

. They're only going to do this testing

57:50

once you have symptoms and they're going to recommend

57:53

some type of stress test and stress tests

57:55

are useful if you're having symptoms . They're going to try to

57:57

recreate your symptoms in

57:59

this environment where they're

58:01

exercising you and see , like , oh , when you have

58:03

chest pain , it happens when you get to this heart

58:05

rate and then you have a wall motion abnormality

58:08

on echo or fusion defect on

58:10

nuclear imaging . But again , it's kind of a late

58:12

to the game type of finding so

58:14

often you know

58:17

the images that you find on a calcium score

58:19

, ct angio , you know you're

58:21

just helping risk stratify that person into

58:23

buckets . You know , like on the

58:25

CT angiogram , you know there's

58:28

a company in the States called Clearly that

58:31

uses AI and machine learning to

58:33

quantify the quality

58:35

of the plaque . That uses

58:37

AI and machine learning to quantify the quality of the plaque . They have a scoring

58:39

algorithm that's zero , one , two or three and it's kind

58:41

of like cancer screening . You know , are you kind of like

58:43

a local cancer or is it metastatic

58:46

? So the more plaque you have , the

58:48

higher cardiovascular events occur

58:51

, and so those are the

58:53

people that need much more intensive

58:55

occur

58:57

, and so those are the people that need much more intensive pharmaceutical supplement

58:59

and lifestyle interventions . And so you're often using these tests mainly

59:02

to risk stratify people like how aggressively

59:04

am I actually going to treat this person ?

59:06

Because that's such an important point ? Because

59:09

I've seen calcium scores done and

59:11

patients get referred to a cardiologist and

59:14

that is a indication

59:16

, or , dare

59:18

I say the word , excuse for

59:20

invasive angiography

59:23

, stenting and bipolar

59:25

surgery , maybe in someone that doesn't even have any

59:27

symptoms . So the

59:29

question that I want to know , and what you think

59:31

about , is to what degree is

59:34

collateral flow , a collateral

59:37

blood flow formation , play

59:39

a role and to what degree are we

59:41

potentially opening people up to over-servicing

59:44

if we're doing these images ?

59:47

No , and I've definitely seen it both ways

59:49

, where the calcium score test is kind

59:51

of an opening to

59:53

doing more stress testing and invasive testing . But

59:56

you're wanting to literally just risk

59:58

stratify the person . Now

1:00:02

, on the calcium score test a normal score is

1:00:04

zero but approximately 8%

1:00:06

of those people with

1:00:08

a calcium score of zero they can still have significant

1:00:11

plaque in their arteries . It's mostly soft plaque that

1:00:13

hasn't yet calcified . So symptoms

1:00:15

will always trump what you find on this imaging

1:00:17

. So , that being said

1:00:20

, on a calcium score test if your score

1:00:22

is over 400 , that's considered high

1:00:24

risk . Over 1,000 is very high

1:00:26

risk , high probability

1:00:28

one of your three corneal arteries is going to have a

1:00:30

moderate to severe amount of stenosis . But

1:00:32

highest scores I've ever seen seen

1:00:35

one that was over 7,000 . The other year Person

1:00:38

reported to be asymptomatic and

1:00:40

we did a stress test . They had a kind

1:00:42

of indeterminate stress test so we ended

1:00:45

up sending him for an invasive cath and

1:00:48

he had some moderate to severe disease and

1:00:50

he ended up getting a coronary intervention and he does

1:00:53

report his exercise tolerance is a little bit better

1:00:55

with it . So maybe he was a little bit minimizing

1:00:57

some of the symptoms and so exercise

1:00:59

tolerance improved . Okay , maybe that's a win for that gentleman

1:01:01

. But using the calcium

1:01:04

score test in people who have no symptoms

1:01:06

and it's high , that is somewhat

1:01:08

of a gray zone In my practice when

1:01:10

I was still doing invasive testing

1:01:12

. If the calcium score is over 400

1:01:14

, it's

1:01:17

reasonable to do a stress test to see can you provoke ischemia at peak activity

1:01:20

. But I didn't automatically recommend

1:01:22

cath unless people had symptoms . Now

1:01:24

if their score is over 1,000 , there

1:01:27

was kind of a push to kind of like automatically

1:01:30

cath people if it's over 1,000 . But

1:01:32

you can't make somebody who feels

1:01:34

normal better

1:01:37

by doing something to them . And

1:01:40

it was in my experience . Half

1:01:42

the time I'd get in there they had no appreciable

1:01:45

luminal stenosis . Their arteries look

1:01:47

like concrete pipes . They had big fat

1:01:49

arteries and the lumen's wide open and

1:01:52

people are like how's that possible ? Like well , it's Glasgow's

1:01:54

principle . Their artery got bigger and the plaque is

1:01:56

like an iceberg . Most of the plaque is still on the wall of the

1:01:58

artery . They're still very high risk of having cardiovascular

1:02:01

events but they're not needing a stent

1:02:03

today . They don't need to go off to bypass surgery

1:02:05

.

1:02:06

I think I want to really impress that point on the

1:02:08

listener and really reemphasize it again

1:02:10

which is just because someone has

1:02:12

had a high calcium score doesn't

1:02:14

necessarily mean that the lumen of

1:02:16

their coronary arteries is stenosed and

1:02:18

therefore the blood flow in

1:02:21

those coronary arteries is impaired . And

1:02:23

what you've just described and I've heard

1:02:25

the same thing which is a patient

1:02:27

goes for an invasive angiography

1:02:30

which , again for the listeners , is the

1:02:32

passage of

1:02:34

a wire through the radial artery

1:02:37

and then the injection of dye to visualize

1:02:40

directly using dye and

1:02:42

the openness

1:02:44

or the flow in those vessels

1:02:46

. So what she found

1:02:48

in this particular patient was that there was a massively

1:02:51

high calcium store , but exactly the same

1:02:53

as what you've mentioned , Michael , which is in

1:02:55

pristine flow . So it just shows

1:02:57

that the process of plaque

1:02:59

deposition was a a

1:03:01

what the body's response or a healing

1:03:03

process to deal with the

1:03:06

, the endothelial damage and the endothelial inflammation

1:03:08

dysfunction that had been happened because

1:03:10

they'd been again breathing

1:03:13

in diesel smoke or having high

1:03:15

uh fluctuating blood glucose

1:03:17

or running a marathon Maybe

1:03:19

they ran 300 miles in a row

1:03:21

, but it was the

1:03:24

body's response . So I think that point

1:03:26

that you made is so important and critical .

1:03:29

Yeah , and I was actually just recently at a

1:03:32

cardiology conference

1:03:34

and there was a debate , you know , between the

1:03:36

interventionalists and the kind of more

1:03:39

you know , non-invasive guys , and

1:03:41

it was really come down to where , like you

1:03:43

know , the imaging is important because

1:03:46

you know , irrespective of

1:03:48

the symptoms , that person's at higher

1:03:50

risk of having events . So treat that

1:03:52

person more aggressively with lipid

1:03:54

lowering therapies , blood pressure medications , if

1:03:56

lifestyle alone doesn't get them down . Those

1:03:59

are the people you're worried about , the people who are symptomatic

1:04:01

. Those are people pretty easy to treat . There's

1:04:03

various antigenals you can use and then

1:04:05

if the medications don't get them to be controlled

1:04:08

, then it's not unreasonable to offer

1:04:10

that person a coronary intervention to

1:04:12

help them feel better . But I always tell patients

1:04:14

like stents are tools . They'll

1:04:16

make you feel better sooner than waiting

1:04:18

for the medications . But unless you're having a

1:04:20

heart attack and the stent is used to stop

1:04:23

the heart attack , the stent is not reducing

1:04:25

risk of having a heart attack . The stent

1:04:27

isn't extending your lifespan . It's

1:04:29

spot welding a small area of stenosis

1:04:32

in your artery and you still have 60,000

1:04:34

other miles you have to treat hall

1:04:36

area of stenosis in your artery

1:04:38

and you still have 60,000

1:04:40

other miles you have to treat .

1:04:42

Yeah , and the reason is because I think so often when in conventional cardiology

1:04:45

, to the man with the hammer , everything

1:04:47

looks like a nail and if your job is an interventional cardiologist and you deploy stents into people's

1:04:49

arteries all day , I mean you're going to find reasons

1:04:51

to do that and there's

1:04:53

data that shows that that isn't a benefit

1:04:55

in people that don't have symptoms . And

1:04:58

yes , if you're having an

1:05:00

ST elevation , a myocardial infarction

1:05:02

, we rush you to the cath lab

1:05:04

and there's a benefit , but not in

1:05:06

a patient that you've just described

1:05:09

. So talk to this idea of collateral

1:05:11

flow . Why are they able to idea

1:05:18

of collateral flow ? Why are they able to deal with this depositional plaque

1:05:20

and maybe even stenosis of their arteries without developing symptoms

1:05:23

, and why are others simply not able to cope with that ?

1:05:26

No , it's a great question and it's . You know , something

1:05:28

that even in reverse , you sometimes see , is that

1:05:30

you know you do an invasive

1:05:32

angiogram in somebody , their three

1:05:34

corneal arteries are quote wide open . You're

1:05:37

like you're good to go , you don't need a stent , but they're

1:05:39

having classic angina . Well

1:05:41

, that microvascular disease you

1:05:43

know , and so that's something that's been recognized

1:05:46

for many years , at least in my practice . And

1:05:48

at this big conference they're starting to more and more

1:05:50

talk about this microcirculation . But

1:05:52

for those patients , if you're developing

1:05:55

plaque over time , the

1:05:57

body has an amazing ability to make

1:05:59

new blood vessels . You make your own bypasses

1:06:01

so that hypoxic kind of myelo causes the

1:06:04

stem cells to get activated . Hypoxic

1:06:06

kind of myelo causes the stem

1:06:08

cells to get activated . You start making

1:06:10

these bypasses and so oftentimes

1:06:13

you can get in there , find that

1:06:15

the person has a chronic total occlusion , their

1:06:23

artery is 100% blocked and they've had no symptoms and you see bypasses

1:06:25

, the arteries kind of help each other out . But the people who do worst are

1:06:27

the people who have no collateral flow . It's

1:06:29

they had this 30% blockage and

1:06:31

then boom , it clots . Now you have 100% blockage

1:06:34

. The other artists haven't had the time to build

1:06:36

collateral flow or build these natural bypasses

1:06:38

and those people tend to do worse at times

1:06:41

.

1:06:41

Yeah , and that's exactly what , circling back

1:06:43

to the beginning of the conversation , which is if

1:06:46

there's some certain factors that are causing an acute

1:06:48

damage to that endothelium and acute

1:06:50

disabling of your endothelial

1:06:53

healing process and you get a massive

1:06:55

denudation of your glycocalyx

1:06:58

and you form a big thrombus

1:07:01

and you just clot off , then there's

1:07:03

obviously no time to develop

1:07:05

collateral flow in that acute

1:07:07

setting . The other point that seems

1:07:09

reasonable to me is that if you're getting

1:07:12

things like regular sunlight , and you're getting

1:07:14

especially sunlight on the chest , and you're

1:07:16

building nitric oxide directly

1:07:19

in those vessels repeatedly

1:07:22

, that seems to be like a good strategy for

1:07:24

helping encourage angiogenesis

1:07:27

or the development of collateral blood flow .

1:07:30

No , definitely , and there was a very

1:07:32

fascinating trial done a few years ago . It was in

1:07:34

Israel . The patients were having ST elevation

1:07:37

of MIS . I believe there was only 12 patients

1:07:39

in the trial , so a very small

1:07:41

kind of like proof of concept trial . But

1:07:43

all the patients got standard of care . They got rushed

1:07:45

to the cath lab , they all got stented , all

1:07:47

the usual medications , but half

1:07:49

the group got photomodulation during

1:07:52

the cath a day later and three days later

1:07:54

, and they didn't directly treat the heart

1:07:56

, they treated the patient's tibia . So

1:07:58

they were activating mesenchymal stem cells with

1:08:01

the light therapy . And

1:08:07

so there are protocols where you can either use your shin or you can use your manubrium , your

1:08:09

sternum , and activate the stem cells there , and then the stem

1:08:11

cells can help activate some of the angiogenesis

1:08:14

.

1:08:14

Yeah , that's absolutely incredible . I talked to

1:08:16

Andrew Latour of Gemba Red

1:08:19

, who's a photobiomodulation company , and he's described

1:08:21

the same thing , which is this so-called absorble

1:08:24

effect , where you can treat one part of your

1:08:26

body and have a benefit

1:08:28

in a completely different organ

1:08:30

. But to me it

1:08:32

makes so much sense to use infrared light

1:08:34

for acute cardiovascular

1:08:37

care , whether that's an AMI

1:08:39

or acute pulmonary edema or

1:08:42

decompensated heart failure Because if

1:08:44

we assume that there is

1:08:46

infrared flow potentiating the

1:08:48

blood through the cardiovascular system at the microcirculation

1:08:51

level , then any bonus

1:08:53

to aid in in

1:08:56

in um cardiovascular flow

1:08:58

is going to be helpful . And whether

1:09:00

, yeah , so things like

1:09:02

photobiomodulation device , I mean you

1:09:04

get zero infrared light in in in

1:09:06

the cubicle of the er room

1:09:08

correct

1:09:11

and yeah , this is probably the whole reason

1:09:13

why you know sauna therapy actually has such

1:09:15

, you know , compelling data in it .

1:09:17

You know , and you know it's a lot of it's been

1:09:19

done in japan and like heart failure patients and

1:09:21

they're doing , you know , at least four sessions a week . You

1:09:23

know , you know in the quantum world that's

1:09:26

obviously helping structure the water and

1:09:28

so you know you get that , you know going

1:09:30

, you get the flow going improving

1:09:33

. You know you get all that benefit of , you know

1:09:35

, detoxing from heavy metals , sure , but

1:09:38

it's probably more . That structuring of the water is

1:09:40

probably the main benefit you're getting yeah , that

1:09:42

makes sense to me .

1:09:43

so say we've got all these

1:09:45

people and say we're classifying

1:09:48

people at different cardiovascular risk all

1:09:50

along the spectrum , and

1:09:53

that is from the person with absolutely

1:09:56

no disease young guy wants to just optimize his

1:09:58

heart health and endothelial health

1:10:00

all the way to the gentleman

1:10:02

who's had coronary artery bypass

1:10:04

grafting and is now getting

1:10:07

stable angina . So there's a massive spectrum

1:10:09

of patients and people , from the

1:10:11

most diseased to the

1:10:14

healthiest . But I think

1:10:16

the key point is that the

1:10:18

behaviors and the lifestyle that

1:10:20

we're going to recommend to everyone

1:10:22

is actually going to be the same

1:10:25

.

1:10:26

It's going to be very , very similar . I mean , I

1:10:28

often talk about being four lovers . You know , there's

1:10:30

nutrition , there's exercise yes , they're important

1:10:33

. But the other two that people sometimes don't

1:10:35

always dial in is , you know , the stress

1:10:37

that people are going to be exposed to . You know

1:10:39

, I tell people , you're always going to be exposed to stress , but

1:10:41

how do you manage or mitigate the stress , how

1:10:43

do you recover ? And then the fourth pillar

1:10:46

, which is actually probably the base of it , is

1:10:48

sleep . I

1:10:50

know that I did not sleep well during

1:10:53

my medical training , Every

1:10:58

third night sleeping in the hospital , working under artificial lights , not knowing any of this stuff

1:11:00

that I know now abusing yourself like crazy in your 20s . But

1:11:03

once I figured out this stuff , I

1:11:05

stepped out of the hospital , stopped doing the damage and

1:11:07

didn't take any major hits by doing

1:11:09

that . But it's

1:11:12

telling people that you have to figure out how

1:11:14

to sleep as best as you can , because if you don't sleep

1:11:16

well , you will not age well , and

1:11:18

it starts with your light environments and the timing

1:11:21

that your food comes in .

1:11:22

Yeah , and that's something that I've

1:11:25

talked about at length , and everyone who's

1:11:27

followed the podcast is really going to be kind

1:11:30

of up to speed with those type of interventions

1:11:32

. Maybe we can start now

1:11:34

by contrasting this decentralized

1:11:37

, holistic approach that you and I are

1:11:39

advocates of , compared

1:11:41

to this conventional approach , because to

1:11:44

me there's radically different strategies

1:11:47

for this primordial

1:11:49

primary and secondary prevention of heart disease

1:11:51

if you're a mainstream trained

1:11:54

cardiologist or family medicine doctor

1:11:56

, compared to someone

1:11:58

like you or I .

1:12:01

Yeah , and this is where I sometimes give

1:12:03

a lot of props to my conventional colleagues

1:12:05

. It's a hard road to

1:12:07

get to where they're at . It's 10 years of training

1:12:10

to be a cardiologist . You know

1:12:12

it's really hard to

1:12:14

take all that knowledge and run

1:12:16

out to practice and then say like I'm

1:12:19

going to abandon all this and I'm going to try to do it a different

1:12:21

way . That's it's going to be a kind of a gradual process

1:12:23

. You know I often joke that it's like the

1:12:25

matrix . You know you eventually step out of the matrix

1:12:27

and you don't necessarily want to go back in , but

1:12:30

you know that how you would need to if

1:12:32

you went back in . So

1:12:34

there's always going to be a place for conventional cardiologists

1:12:37

Until the world wakes up and does all these

1:12:39

lifestyle things that we're talking about . People

1:12:41

can keep having cardiac events that need hospitals

1:12:43

. Hopefully it decreases

1:12:46

in our lifespan , but I'm not holding

1:12:48

my breath for that just yet . But

1:12:51

the way to think about it is that , like you

1:12:54

know , you just want somebody who is curious

1:12:56

. You know , because if they're

1:12:58

not curious they're not going to progress

1:13:00

in their learning . You

1:13:05

know a lot of stuff I've learned in my training . I no longer recommend or

1:13:07

do , or I've heavily modified it . I don't abandon it all . Use the tool

1:13:09

that works . You know wise healer uses the

1:13:12

most effective tool with the least amount of side effects

1:13:14

. Sometimes that is conventional medications

1:13:16

, and I talked about the pre-op

1:13:18

. I guess you know sometimes you need to be able to reverse

1:13:20

engineer . If you don't do these things

1:13:22

, you're going to end up in cardiogenic shock in

1:13:24

the ICU . These are the things that can

1:13:26

mitigate that risk . But

1:13:30

the quantum world ? It's fascinating . But

1:13:33

one beef I have with the quantum world is that

1:13:35

sunlight and grounding is not

1:13:37

going to fix everything . It's a good start

1:13:39

for many , many things , but sometimes you

1:13:41

have to use more aggressive therapies

1:13:43

.

1:13:44

Yeah , and people on various

1:13:47

degrees of bought in to lifestyle . And I

1:13:49

like to say and a mentor of mine

1:13:51

you know he taught me he said it

1:13:54

only works if the patient does it and

1:13:56

it only works if you do it . So

1:13:58

, and you can recommend these

1:14:00

gold standard lifestyle interventions to

1:14:02

people , but if they don't do it , then

1:14:04

they're going to be at high risk and you need

1:14:07

to bring other options onto the table

1:14:09

. So

1:14:13

I mean , I'm completely on board with what you said , michael , and I agree

1:14:15

completely and I see myself as same as you , I'm guessing is

1:14:17

that I'm just here to provide options for

1:14:20

my patients and it's up to everyone what

1:14:22

they want to take and as long as they have informed

1:14:25

, explained , consent about the risks

1:14:27

and benefits of every option , whether that's

1:14:29

medication or lifestyle , then that

1:14:31

that's my job done oh

1:14:34

, very much .

1:14:34

So I mean my whole job now is just as an

1:14:36

educator . You know patients come in , you

1:14:38

know I basically you know , interpret

1:14:41

any of their prior testing from through a different lens

1:14:43

, talk about you know what their arteries

1:14:45

are doing right now and do

1:14:47

the advanced blood work and then have a conversation

1:14:49

. Okay , like this is your risk right now . These

1:14:52

are your options .

1:14:56

What risk do you feel comfortable taking at this

1:14:58

point ? Yeah , and it's such a holistic process that

1:15:01

we have to go through and

1:15:06

, as we mentioned , it starts when we're very young and there's

1:15:08

all these insults in our environment that are contributing to potentially building our plaque

1:15:10

and damaging our blood vessels . So

1:15:12

it's an ongoing battle for everyone and

1:15:14

it's understandable that some people go through a rougher

1:15:16

time where they can't prioritize their health or they

1:15:19

have a stressful period and we

1:15:21

didn't mention the mechanism , but Dr Malcolm

1:15:23

Kendrick talks about it a lot in his book the Clot Thickens

1:15:25

, which is high level

1:15:27

, is actually going to impair the function

1:15:30

of the vascular endothelial progenitor

1:15:32

cells . So your ability to repair

1:15:34

glycocalyx damage or endothelial

1:15:36

damage is stopped

1:15:39

or slowed or delayed or retarded when

1:15:41

you're acutely stressed , whether

1:15:43

that's someone dying , a family member

1:15:45

passes away , or you're about

1:15:47

to get fired for your job , or someone

1:15:50

breaks up with you , et cetera , et cetera . So

1:15:52

yeah , it's

1:15:54

a process .

1:15:57

No , and that's just a quick side note

1:15:59

, that's stress-induced cardiomyopathy

1:16:01

, that's Takotsubo syndrome . I definitely saw

1:16:03

many cases of that in my career . A patient

1:16:05

shows up after a stressful event

1:16:07

. The EKG looks

1:16:10

like a heart attack . They're having all the same symptoms

1:16:12

of the heart attack chest pain radiating up

1:16:14

to the neck or back , rushing to the cath lab

1:16:16

. Their coronary arteries are

1:16:18

wide open . You do a left ventricular

1:16:20

gram . The

1:16:22

base of the heart barely moves . The apex is

1:16:24

pounding away . It's a stress-induced

1:16:27

cardiomyopathy because that extremely high cortisol

1:16:29

and adrenaline vasoconstricts all

1:16:31

the microcirculation and then once the

1:16:33

acute stressor is kind of mitigated

1:16:35

, often use some beta blockers to kind of

1:16:37

knock down some of the adrenaline . That left

1:16:39

ventricular function improves back to normal . So

1:16:42

if it can happen acutely , it definitely

1:16:44

happens chronically for patients as well .

1:16:46

Yeah , and what is going to drive up

1:16:48

this cortisol level ? Maybe

1:16:50

subclinically over a long period of time ? And that

1:16:52

is blue light and being

1:16:54

exposed to artificial light at night and

1:16:56

dysregulating your cortisol

1:16:58

melatonin curve . That

1:17:00

is inherent or is critical

1:17:03

in your circadian rhythm

1:17:05

. So that's another mechanism

1:17:07

that the light stress could

1:17:09

contribute to the development of heart

1:17:11

disease . But let's talk about . Because

1:17:14

we're on the topic of conventional treatments

1:17:16

, let's talk about a

1:17:19

conventional doctor wants to

1:17:21

reduce someone's risk of heart

1:17:23

disease and look , let's say that they've addressed

1:17:25

these common traditional

1:17:27

risk factors . Addressed these common

1:17:29

traditional risk factors , and

1:17:34

by that I mean blood pressure , diabetes or insulin resistance . Obviously we can't do

1:17:36

too much about family history . You know

1:17:38

smoking . They've all addressed

1:17:41

those . So

1:17:47

we got to this last one , which is lipid level and cholesterol level . So what is their approach

1:17:49

and how do you agree or disagree with them

1:17:53

?

1:17:53

So let's say , in the conventional world you know they're

1:17:55

going to be thinking about anti-pliotherapy

1:17:57

, so aspirin , 81 milligrams for the

1:17:59

majority blood pressure control

1:18:02

, you know , ideally less than 120

1:18:04

over 80 . And they will often

1:18:06

use , you know , combination of

1:18:08

diuretics , beta blockers , calcium

1:18:11

channel blockers , ACE

1:18:18

inhibitors or anti-intensive receptor blockers . Of those I honestly prefer that they would use the ACE

1:18:20

ARBs or the calcium channel blockers because those actually lower central aortic

1:18:22

blood pressure . The diuretics and the beta blockers

1:18:24

make your blood pressure look pretty when

1:18:26

they check your arm but if you actually put a catheter back

1:18:28

up in their heart their pressures are not necessarily controlled

1:18:31

with those medicines . So I try to limit

1:18:33

those medicines to like third or fourth line . And

1:18:36

then they're going to use generally a high dose

1:18:38

statin , like it's going to be Lipitor

1:18:40

40 , 80 . It's going to be Crestor

1:18:43

20 or 40 . And those are the options

1:18:45

. You know I tend to use

1:18:47

a lot more low-dose statin

1:18:49

therapy if I'm going to use it and we use

1:18:51

the advanced testing to kind of you know , kind

1:18:53

of guide to say like , okay , well , is this person

1:18:55

likely a hyperproducer of sterols ? Or if they're

1:18:57

a hyperabsorber of sterols , well , maybe a zetamide is a

1:18:59

better option for this person . So

1:19:02

it's mostly , you know , statin

1:19:04

, aspirin and some type of blood pressure agent

1:19:07

is kind of the standard to care . But those

1:19:09

are good starting points but they don't really

1:19:11

improve nitric oxide availability

1:19:14

in the majority .

1:19:15

Yeah , and a quick mention about those blood pressure lowering

1:19:17

medications . I've just released

1:19:19

a course called the Solar Calus course and I'm

1:19:22

talking about medications that can increase our

1:19:24

photosensitivity or likelihood

1:19:26

of sunburning . And this is important because

1:19:28

if we're getting out into full spectrum

1:19:31

sunlight that includes ultraviolet light then

1:19:33

we don't want to be taking anything that's going to make

1:19:35

us sunburn . And it happens

1:19:37

that hydrochlorothiazide

1:19:39

, thiazide diuretics , fruzomide

1:19:42

, as well as medications like statins

1:19:44

and atorvastatin and amiodarone

1:19:47

are all responsible for increasing

1:19:49

our photosensitivity . So it's

1:19:51

a little bit of a catch-22 when we've

1:19:53

got a situation where we're trying to lower someone's

1:19:56

blood pressure by giving them a thiazide

1:19:58

diuretic that's perhaps

1:20:00

precluding them from getting full spectrum sunlight

1:20:02

, when the actual solution to their problem

1:20:05

is UVA light to promote

1:20:07

the nitric oxide , to essentially do

1:20:10

it in nature's way to reduce

1:20:12

their blood pressure in Mother Nature's way .

1:20:15

Right , yeah , the

1:20:18

pharmaceutical ways of doing things . They

1:20:20

work , but do

1:20:22

you have to pull them out all the time ? No

1:20:25

, I mean , somebody runs into your office and their blood

1:20:27

pressure is 200 over 110 . Well , you got to throw the kitchen

1:20:29

sink at them while you're trying to figure out . Why are they so dysregulated

1:20:31

. But one of my favorite

1:20:34

things to do is deprescribe medications

1:20:36

. Patients come in with a whole host of meds . You

1:20:38

start working on these lifestyle things . You just

1:20:40

start trying to peel all these medications back

1:20:42

whenever you can .

1:20:44

So I agree with that . That's

1:20:46

very satisfying , but let's talk about

1:20:49

this primary prevention in someone who hasn't

1:20:51

had a heart attack and

1:20:53

all they've got essentially

1:20:55

wrong is a high APOB

1:20:58

or LDL cholesterol , and they don't

1:21:00

have atherogenic dyslipidemia , which is

1:21:02

a medical speak for the high

1:21:04

risk panel

1:21:06

, which also includes a low HDL and

1:21:08

a high triglyceride . So let's just say

1:21:11

that they have a high LDL-ApoB

1:21:13

, which is typical or possible on

1:21:15

a low-carb or carnivore diet

1:21:17

not in everyone , but in some and

1:21:20

their conventional doctor prescribes them

1:21:22

a torvastatin . What's

1:21:24

your opinion on that ?

1:21:27

I mean I've seen a lot of those cases where patients

1:21:29

have had relatively normal lipid

1:21:31

panels . They go carnivore

1:21:33

, keto and they have these severe

1:21:36

dysregulated lipid panels

1:21:38

. And , yes , generally it is

1:21:40

that they do not have high

1:21:42

triglycerides or low HDL in the panel

1:21:44

. But that doesn't mean that those

1:21:46

particles are not necessarily atherogenic

1:21:48

. I've had some patients like you got to show me that you have

1:21:50

healthy nitric oxide levels , you

1:21:52

don't have vascular inflammation , and

1:21:54

a calcium score test is a good point . But

1:21:56

if you want a bonus , do a CT angio

1:21:59

and show me that you don't have a lot of salt plaque building up

1:22:01

. But not everybody

1:22:03

who eats those diets has that type of lipid

1:22:05

response . You know it's really maybe about

1:22:07

20% of the population has a pretty

1:22:09

significant response to higher saturated

1:22:12

fat in their diet . Sometimes

1:22:14

in these patients if they cut their saturated

1:22:16

fat to less than 8% of their total calories , eat

1:22:19

more fish , more olive oil , they

1:22:21

may not have significant

1:22:23

bumps in their ApoB particles . But

1:22:26

in my practice I typically will use the

1:22:28

Boston Heart Lab panel to look at not

1:22:30

only their ApoE status , because it's the ApoE4s

1:22:33

that tend to have this happen more often , but

1:22:35

the people who are hyperabsorbers

1:22:38

of sterols , especially the beta-cidesterol

1:22:40

. They tend to have this pattern more often

1:22:42

and the stans might

1:22:44

work . But if the person is not willing to change

1:22:47

their diet , then azadamide

1:22:49

would work better , prevent the sterols from being ripped

1:22:51

away from the gut and you generally get a significant

1:22:54

reduction in their lipoprotein burden

1:22:56

then .

1:22:57

Yeah , that's an interesting point that you made

1:22:59

and I think it's relevant because people sometimes

1:23:01

go on a carnivore type diet and

1:23:05

they have this high ApoB or LDL and

1:23:08

they're almost , you know , kind of say

1:23:11

, okay , I'm at low risk because I'm eating carnivore

1:23:13

, and my , my perspective

1:23:15

is that you're addressing perhaps

1:23:18

one of the contributors

1:23:20

to endothelial damage and and

1:23:22

poor vascular health , and that is insulin resistance

1:23:25

and perhaps fluctuating blood glucose . But if you're getting blue light , if you're blue

1:23:27

light toxic , if you're not grounding , um , if you're getting blue light

1:23:29

, if you're blue light toxic , if you're not grounding

1:23:31

, if you're doing other things that are disrupting

1:23:33

your structured water and

1:23:36

you have endothelial dysfunction , which is

1:23:38

what we've just talked about , then

1:23:41

there's no protection against that sudden

1:23:43

clotting event that

1:23:46

can occur and therefore your risk of

1:23:48

AMI is not zero

1:23:50

.

1:23:52

Right and I think that's

1:23:54

a nuanced approach to every patient . It's

1:23:56

that you know , can carnivore make

1:23:58

people's gut health better and their

1:24:01

joints feel better ? Of course it is . But you

1:24:03

know you still have to look at like , what

1:24:05

are the arteries doing with this lipoprotein

1:24:07

burden ? You know you're mimicking

1:24:10

familial hyperlipidemia . Now

1:24:12

there are people with FH who don't go on to have

1:24:14

severe disease and if you have a calcium square of zero

1:24:16

and you've had FH , good for you . That

1:24:18

means whatever you're doing means you have a healthy

1:24:20

glycocalyx . But not everybody who's

1:24:23

carnivore is necessarily going to be that same pattern

1:24:25

.

1:24:25

Yeah , so it really seems like we have to

1:24:28

focus on . Yeah

1:24:31

, so it really seems like we have to focus on the endothelial health first and , as you said I really

1:24:33

like your framing is that you have to the patient has to prove to you that their

1:24:36

blood vessels are healthy in order to

1:24:38

be able to tolerate or be able

1:24:40

to deal with that perhaps higher

1:24:42

lipoprotein burden and that not

1:24:44

necessarily contribute to the deposition

1:24:46

of plaque . I'm really

1:24:48

thinking about a lot lately , because there's almost

1:24:51

two armed camps that are polarizingly

1:24:53

assembling with

1:24:56

weapons raised on either side . On

1:24:58

one side is the strict

1:25:00

carnivore . Any type of

1:25:02

raised ApoB isn't an issue at

1:25:05

all . Obviously , the troglodytes

1:25:08

rides are low and the HDL is reasonable , reasonable

1:25:10

. But then the opposite side of the picture is guys

1:25:12

like dr muhammad alo , who has

1:25:14

made I mean , some of his calls have

1:25:16

been a little bit , have been well , they've been outlandish

1:25:19

and just patently false , but he's really

1:25:21

advocating for statin therapy for basically

1:25:23

anyone who has an apo b above

1:25:26

this arbitrary threshold

1:25:28

, which is , um , you know . So

1:25:30

I'm just wondering yeah , do

1:25:32

you have any more thoughts on those two kind of

1:25:34

polarizing opinions

1:25:36

and how to split the middle the most effectively

1:25:38

?

1:25:40

You know you're very much right . You know it is polarizing

1:25:42

. It's that you know the patient

1:25:45

is just trying to find out , like , what do they need to do

1:25:47

for themselves ? And you

1:25:49

know , like Stans , you know they're tools

1:25:51

, they should not be in the water where we're all taking them and

1:25:53

they're not horrible for everybody . You

1:25:56

know I often get the concerns

1:25:58

, you know , like , oh , it's a mitochondrial toxin

1:26:00

, it's going to give me diabetes , like it

1:26:02

doesn't take somebody who's not insulin resistant

1:26:05

and make them frank , diabetic . You know , is it

1:26:07

mitochondrial toxin ? A

1:26:13

little bit , but it's probably taking out the weak mitochondria so that you replace them

1:26:15

with better . And it's the . You know it's risk versus reward . You know , nothing is risk-free

1:26:18

for the most part , you know , but in the right selective population

1:26:20

. You know statins can be the right

1:26:22

tool for that person . But the

1:26:25

other side of the equation , you know , having an AOB

1:26:27

of 20 , that is not evolutionarily

1:26:30

feasible for

1:26:32

everybody . Are there people that

1:26:34

have low APOBs ? Yeah , my own father

1:26:36

has an APOB of 43 with no meds , but

1:26:39

he has a loss of function PCSK9

1:26:41

gene . His grandmother had that . She lived to 106

1:26:44

. So okay , but not everybody

1:26:46

has that pattern . Do we need

1:26:48

to use three pharmaceutical agents to drive everybody

1:26:50

down there ? I don't think so . It's

1:26:52

never been studied or shown that that's really

1:26:54

where we need to be targeting people for . So

1:26:57

I just really think that we've had a great conversation

1:26:59

. I was like what is the glycocalyx

1:27:01

doing ? How much can you support the structured

1:27:03

water in the body ? I often

1:27:05

talk about being like it's a force field . If your force field's

1:27:07

up , it's less likely that these

1:27:10

lipoproteins are kind of crashing the gates and getting through

1:27:12

. It's possible , but just not as likely

1:27:14

.

1:27:15

Yeah , no , that's great advice . I mean , I've delved

1:27:17

into the statin as mitochondrial toxin

1:27:20

issue as well , and there's a particular

1:27:22

paper that I have in mind I think it was published in 2017

1:27:25

. And

1:27:30

it details there's a number of mechanisms biochemically , and obviously

1:27:32

what is happening at the bench level or what we

1:27:34

find in the lab is

1:27:36

not always translatable

1:27:38

in vivo , but there was

1:27:40

mechanisms involving reduction of mitochondrial

1:27:42

membrane potential , there

1:27:47

was acceleration of apoptosis , there's

1:27:54

a range of mechanisms . So to me , uh , it doesn't seem like a drug that we need

1:27:56

to be . We should be throwing around willy-nilly

1:27:58

, and the rhetoric that you hear out

1:28:00

of so many conventional

1:28:02

, mainstream , uh , centralized cardiologists

1:28:05

is that this is a drug without side effects

1:28:07

, and that is the impression that you get

1:28:09

when you hear some of their rhetoric

1:28:12

.

1:28:14

Yeah , I mean they definitely have side effects and you know we talked

1:28:16

about some of them earlier . I mean the musculoskeletal

1:28:18

ones are real and the trials , you

1:28:21

know it's a few percentage points but in the real world

1:28:23

, you know a quarter of the patients might

1:28:25

have some symptoms who really queered them hard enough

1:28:27

. But

1:28:33

I do a pretty comprehensive screening in some way before I'm going to recommend these things . I want

1:28:35

to know what their ApoE genotype is . If they're an ApoE4 , I'm probably not going to push

1:28:37

it very hard on them . What is

1:28:39

their vitamin D status ? If you're vitamin D deficient

1:28:41

, you pretty much always get myelosis on statins

1:28:43

. If your CoQ10 is low at baseline

1:28:46

, well , you're just going to make it worse adding

1:28:48

the statin on board . If you're hypothyroid

1:28:50

, much more likely to have muscle

1:28:53

symptoms , and then in some instances

1:28:55

that people have already tried them and had a lot of issues

1:28:57

, you know . Then I'll do some genetics and there's a gene called

1:28:59

SLCL1B1 . If

1:29:02

you have an abnormal copy of that , you know you're two

1:29:04

, three , four times more likely to have muscle symptoms

1:29:07

with statin . So no , they're not

1:29:09

risk-free . But there's

1:29:11

patients that you can select that generally are going

1:29:13

to tolerate them . Well , and if they can't tolerate them

1:29:15

, or they just only say like hey , doc , I just

1:29:17

don't want to take this .

1:29:18

Okay , there's bimedoc acid

1:29:21

, there's red yeast rice , there's bergamot , there's berberine

1:29:23

there's

1:29:35

PCS9 inhibitors , zetamide , there's a whole host of other options if you're really going to go down the route of trying to help somebody lower

1:29:37

their lipoproteins . Yeah , and I think the one mechanism we haven't mentioned in terms of lipid lowering is the sun , and there

1:29:39

are multiple randomized control trials showing that sunlight

1:29:41

, uv light , lowers lipid

1:29:43

profiles , lowers , ldl lowers , apob lowers

1:29:45

, I believe triglycerides too . You

1:29:48

might ask okay , well , what is the effect size

1:29:50

? And maybe the effect size isn't

1:29:52

as dramatic as rapidly

1:29:55

changing the diet to

1:29:59

a low-carb or rapidly doing

1:30:01

those , but there is observational

1:30:04

and interventional evidence that sunlight reduces

1:30:06

ApoB . Can

1:30:08

you talk to this precaution of

1:30:10

these E4 carriers

1:30:13

and why you might not prescribe them as statin ?

1:30:17

So when you have an ApoE4 allele , it's

1:30:19

going to affect your LDL receptors

1:30:21

. Your LDL receptors are going to be

1:30:24

not as plentiful and they're probably not

1:30:26

going to be as functioning . So your LDL receptors

1:30:28

stand on the outside of the liver and they grab these

1:30:30

APB particles as they go by and pull

1:30:32

them into the liver . But the

1:30:35

APB4 carriers they're at increased

1:30:37

risk of diabetes . They're at increased

1:30:39

risk of Alzheimer's , which is likely

1:30:42

a form of insulin resistance in

1:30:44

the brain coupled with subclinical

1:30:47

or I should say more microvascular disease

1:30:49

. So the same things that are causing plaque in the coronary

1:30:51

arteries are the same thing that do it in the brain and

1:30:54

then when you hit enough neurons , then they're

1:30:56

going to call you Alzheimer's . But the

1:30:58

APU4 carriers they just tend to

1:31:00

have more side effects with

1:31:02

the high-dose statin . So often I'll just

1:31:05

use low-dose or sometimes even intermittent-dosed

1:31:07

resuvastatin in those people .

1:31:09

Yeah , and look , there's so many other areas

1:31:11

. I

1:31:16

believe Dr Malcolm Kendrick wrote a really good article in 2018

1:31:19

that's worth reading . That was looking

1:31:21

at the odds ratio of the development of Lou Gehrig's

1:31:23

disease , which is essentially , you lose

1:31:26

your motor neurons

1:31:28

basically voluntary

1:31:30

muscle contractions and

1:31:33

the odds ratio for statin use

1:31:35

is enormous and

1:31:37

, again , it's a rare disease . But

1:31:39

if you go on from

1:31:41

eight cases per 100,000 to 40 cases

1:31:44

per 100,000 , that's

1:31:46

a significant relative increase and those

1:31:48

are pretty compellingly linked

1:31:50

to to statin usage .

1:31:52

So I don't know if you've encountered that or

1:31:54

come or have an opinion on that I

1:31:57

haven't seen that uh , particular study

1:31:59

, but you know again , it's , you know nothing's

1:32:02

risk-free and so it's like you know if you've had

1:32:04

you know your grandmother die

1:32:06

at you know 59 and

1:32:08

you're 40 and you know stan's been recommended , maybe the you know 59 and you're

1:32:11

40 and you know Stan's been recommended , maybe then you know your risk of

1:32:13

atherosclerosis taking you out is higher than a

1:32:15

neurological . But if you're , you

1:32:17

know a 25-year-old woman with , quote

1:32:19

, high cholesterol , yeah , stan's

1:32:21

probably not the right tool for that person .

1:32:23

Yeah , look , it's such a good advice and it's

1:32:25

really hammering home the point that this needs to be

1:32:27

an individual decision and so many

1:32:29

, unfortunately , the way that

1:32:32

there's not a lot of access to for

1:32:34

people to get a nuanced opinion

1:32:37

like by a practitioner like yourself

1:32:39

, michael , so that people seem to be doing

1:32:42

a lot of self-decision , self-diagnosing

1:32:44

and self-treating based on what

1:32:46

they listen on the internet and really they

1:32:48

need someone to take into account

1:32:50

all their risk factors , their endothelial health and

1:32:53

everything that we've talked about to

1:32:55

make an individualized opinion . It's

1:32:57

hard , when this decentralized movement

1:33:00

is growing and there's so much contrasting

1:33:02

and conflicting information , for people to make

1:33:05

the right decision .

1:33:07

No , and I appreciate the opportunity

1:33:10

to come here and chat with you and your audience . I mean

1:33:12

, I think people probably should go back and listen to this one

1:33:14

. You know once or twice and you know they'll hear a lot of the

1:33:16

same themes . You know we're talking about nitric

1:33:19

oxide , endothelial function , the glycocalyx

1:33:21

, vascular inflammation . You

1:33:23

know it's all you know connected

1:33:26

. You know I tell patients , you know

1:33:28

sometimes these words are complicated

1:33:30

, but when you actually sit down and think about

1:33:32

what you need to do on a day-to-day basis to have healthy

1:33:35

arteries , it's really not that hard . It's

1:33:38

really just . Can you keep nitric oxide levels

1:33:40

high ? Can you keep inflammation low ? And

1:33:42

if you need to modulate lipoproteins

1:33:44

, figure out which best lifestyle supplement

1:33:47

medication you're going to be able to use to modulate

1:33:49

the lipoproteins in .

1:33:51

Yeah , great advice . Well , thank you so much

1:33:53

, michael , for coming on . Do you have any parting

1:33:55

thoughts that you want to share with the

1:33:57

listeners , or any topics or questions ? I didn't

1:33:59

ask you .

1:34:02

No , I just often tell patients that you

1:34:04

do have to be your own doctor , and your doctor

1:34:06

is supposed to be your guide . Be

1:34:10

your own doctor and your doctor , you know is supposed to be your guide

1:34:12

. You know your health is in your own hands and you know your lifestyle determines about 80

1:34:14

to 90% of what's going to happen with you

1:34:16

. So in your mind

1:34:19

, just try to set up . You know what an optimal day is for

1:34:21

you and try to win that day every day

1:34:23

. You know , it should start with seeing

1:34:25

morning light . It should be including

1:34:27

some amount of grounding outside

1:34:29

. Ideally , do some stress

1:34:32

management and then highly

1:34:34

prioritize your sleep . You should be sleeping

1:34:36

seven and a half eight hours every night

1:34:38

and feeling very well rested . If you're not sleeping

1:34:40

well , start there .

1:34:42

Yeah , fantastic advice , michael

1:34:44

Twyman , thank you so much for coming on the Regenerative

1:34:46

Health Podcast .

1:34:49

You're very welcome , thank you .

1:34:50

And where can people find you , follow you , even

1:34:53

employ your services if they're

1:34:55

interested ?

1:34:58

So my practice at Polycardiology is in

1:35:00

St Louis , missouri . We are still accepting patients

1:35:02

. Our patients always come to

1:35:04

us initially for their first visit . We

1:35:07

do a comprehensive head-to-toe cardiovascular

1:35:09

assessment . I call them

1:35:11

toys . We have all the toys in the office

1:35:13

to test your endothelial function , your vascular

1:35:15

health , and then all follow visits

1:35:17

can be done remotely . I'm

1:35:19

relatively active on social media

1:35:21

on Instagram . I have an IG Live

1:35:24

every Monday night 6 pm Central Time

1:35:26

. Right now I'm kind of doing more just

1:35:28

an Ask Me Anything type of format

1:35:30

. So potential

1:35:32

patients or just people who are interested in following me

1:35:35

. They submit questions ahead of time and

1:35:37

some of the questions are similar to tonight about

1:35:39

lipoproteins or grounding

1:35:41

or sauna or something

1:35:44

along those lines that benefit other people

1:35:46

. And then my

1:35:48

website lines

1:35:51

that benefit other people . And then my website , drdwimancom . You

1:35:53

have some links to my other podcast and people are interested in following

1:35:56

out where else I'm online . It'll be on drdwimancom

1:35:58

.

1:35:58

Great , fantastic . I'll include all that information

1:36:01

so the listeners can have ready Sure

1:36:04

, thank you you .