0:00

The breakthrough that's happened in the

0:02

field of genomics in the last

0:04

10 years is realizing that chronic

0:06

diseases, cognitive decline, heart disease, diabetes,

0:08

obesity, depression, anxiety, autism, they're not

0:10

because of one gene. You can

0:13

use your genomics to determine do

0:15

they have problems with getting enough

0:17

blood flow to the brain, and

0:19

even within that, is it because

0:21

they don't make enough nitric oxide,

0:24

or is it because they're hypercolagulable?

0:26

Do they have mitochondrial membrane issues?

0:28

Do they? have issues with transporting

0:30

coaling. Your DNA holds the blueprint

0:33

for your health and Dr. Sharon

0:35

Houseman Cohen is the scientist decoding

0:37

it. Harvard trained

0:39

physician, 25 years in integrative medicine,

0:41

co-founder and chief medical officer of

0:44

Intel XDNA, the precision genomics tool,

0:46

unlocking the future of personalized health.

0:48

This particular gene is involved in a couple

0:50

of things. These are the kinds of things

0:52

that you can learn about using Intel

0:55

XDNA. She's not just studying the

0:57

science, she's rewriting the playbook. From

0:59

cognitive decline to cardiometabolic disease, autism

1:01

to the so-called unsolvable cases. Her

1:03

work is helping top physicians crack

1:06

the code on root cause medicine. It

1:08

gives me a more targeted approach. We

1:10

are able to really get to the core

1:12

depth and the breadth of what Intelix DNA

1:14

provides. Intelix DNA isn't just a

1:16

tool, it's a revolution. Dr. Houseman

1:18

Cohen's research is fueling cutting-edge studies,

1:21

including those led by Dr. Dale

1:23

Brettison, proving that DNA-driven medicine isn't

1:25

the future. It's happening now. In

1:27

comparison to other genomics tools,

1:30

intellects is by far the

1:32

best. Longevity seekers, health disruptors,

1:34

the next frontier of medicine

1:37

is here, and Dr. Sharon

1:39

Hausman-Cohen is leading the way.

1:41

I've done gene therapy to

1:43

reduce my age by about

1:45

nine years. Why do you

1:48

think we can't change our

1:50

genetics? You're listening to the

1:52

human upgrade with Dave Asprey.

1:54

master's degree in

1:57

cell biology, and

1:59

your It seems like we've had

2:01

a genetics fetish over the past

2:03

30 years and we discovered DNA

2:05

and we got into all this

2:07

stuff and we all got our

2:09

genetics done and I got a

2:11

report back and it said your

2:13

0.1% strange Russian shamanic tribe and

2:16

you have a 10% increase in

2:18

risk of something that isn't a

2:20

very big risk anyway and it

2:22

was sort of a big yawn.

2:24

How useful are genetics for longevity?

2:26

I think you have to look

2:28

at the right things. And so

2:30

when genetics started, people started with

2:32

pharmacogenomics, people started with cancer genetics,

2:34

and then neutrogenomics came along, and

2:36

all of them had their place.

2:38

But if you're really wanting to

2:40

look at longevity, you have to

2:42

understand cognition. You know, what makes

2:44

up longevity? Heart, bones, brain. And

2:46

you can't just look at one

2:48

gene variant. So it's sort of

2:51

like the bucket of all of

2:53

your genes as useful for longevity?

2:55

Yes, and I think that looking

2:57

at some of the genes that

2:59

are less common, but clinically significant,

3:01

and that's another huge piece, is

3:03

if you just look at genes

3:05

and you're like, okay, I have

3:07

a copy of, I'm going to

3:09

pick on MTR because it's a

3:11

pretty pop gene, well, 45% of

3:13

people have a copy of MTR,

3:15

so how important could that be?

3:17

You know, yes, methylation is important,

3:19

but... If you have somebody that

3:21

has cognitive decline, you can use

3:23

your genomics to determine, do they

3:26

have problems with getting enough blood

3:28

flow to the brain? And even

3:30

within that, is it because they

3:32

don't make enough nitric oxide? Or

3:34

is it because they're hypercuagulable? Do

3:36

they have mitochondrial membrane issues? Do

3:38

they have... issues with transporting coalene

3:40

or but... Wait a minute. Do

3:42

you have my genetic profile? With

3:44

that list, literally I have nitrogoxide

3:46

genes, I have sulfation genes, I

3:48

have MTHFR, I have blood flow

3:50

issues to the brain, and there's

3:52

one other in there. So are

3:54

these common... problems or am I

3:56

just like am I fucked? Well

3:58

some of no no so so

4:00

I'm I'm pretty sure your brain's

4:03

working really quite well pretty happy

4:05

but I think that some of

4:07

them are common so the gene

4:09

that relates to Colleen for example

4:11

it does give you about a

4:13

60% increase risk of cognitive decline

4:15

and that one's fairly common that

4:17

one's like 40% of the population

4:19

but Some of them are common,

4:21

some of them are less common.

4:23

There are gene variants that, so

4:25

the one that relates to mitochondrial

4:27

membranes. It can give you more

4:29

than double the risk again of

4:31

dementia. It's 2.7 times the risk,

4:33

and that one's in like 25%.

4:35

But no one gene causes Alzheimer's.

4:38

And I think that the breakthrough

4:40

that's happened in the field of

4:42

genomics in the last 10 years

4:44

is realizing that chronic diseases... cognitive

4:46

decline, heart disease, diabetes, obesity, depression,

4:48

anxiety, autism, they're not because of

4:50

one gene. They're not sickle cell

4:52

or tasex. They're because of a

4:54

combination of gene variants interacting with

4:56

each other, but also with diet,

4:58

lifestyle, the environment, and together by

5:00

understanding the components, you can then

5:02

improve these specific things that may

5:04

run in your family or that

5:06

you're at risk for. I'm a

5:08

friend who's been on the show

5:10

and been an inspiration for me

5:13

is a Bruce Lipton. A cell

5:15

biologist turned biology of belief, epigenetics

5:17

guy, and some people have noted

5:19

that biohacking, when I first defined

5:21

the word, it's a restatement of

5:23

epigenetics, particularly around longevity, and epigenetics

5:25

being the environment, affects chains. Can

5:27

you separate epigenetics from genetics? I

5:29

think epigenetics is an answer to

5:31

genomics or genetics. And so if

5:33

you think of your, so genetic

5:35

diseases are ones that are inherited,

5:37

you know, mom has one copy,

5:39

dad has one copy, you get

5:41

it. But genomic issues are things

5:43

that are small changes in your

5:45

DNA that increase your risk for

5:48

something, but they're not what we

5:50

call pathogenic. They don't cause it.

5:52

And epigenetics is how we respond

5:54

to it. So let's take T&F

5:56

Alpha. So there's lots of different

5:58

kinds of inflammation. But T&F Alpha

6:00

causes leaky blood brain barriers. It

6:02

causes leaky blood gut barriers. And

6:04

some people make much more T&F

6:06

Alpha because they have an overactive

6:08

promoter. So if you have a

6:10

gene variant that makes that T&F

6:12

alpha promoter four to five times

6:14

more active, you can't change it.

6:16

Your promoter is kind of hyperactive.

6:18

But what you can do is

6:20

use things, diet and lifestyle, to

6:23

decrease the transcription and kind of

6:25

slow the transcription and the expression

6:27

of T&F alpha down, and you

6:29

might need that more than someone

6:31

else. So lion's main mushroom is

6:33

great for T&F alpha. even chili

6:35

peppers is really good for T&F

6:37

alpha, sulforaphane, and there's many different

6:39

things. And so the way that

6:41

I think of epigenetics is how

6:43

do we respond to our genome

6:45

to say, oh, nothing I can

6:47

do about it. Well, that's not

6:49

the biohacker way. It's like, let's

6:51

understand it and become empowered by

6:53

it because there's so many things

6:55

that can help your longevity and

6:58

how do you know which ones

7:00

are right for you? Rizzveritrol can

7:02

increase the expression of clotho, which

7:04

is an important longevity gene, but

7:06

if you're already the high clotho

7:08

type of genotype, that may not

7:10

be the most important thing for

7:12

you, even though it's important for

7:14

many people. So with genes, if

7:16

you have both alleles and it's

7:18

MHFR, you know that whatever environmental

7:20

things you do, you're not going

7:22

to turn off a gene when

7:24

it can't be turned off because

7:26

it's all you have, right, and

7:28

you can't turn on something that

7:30

isn't isn't isn't present. So epigenetics

7:33

has great power, but what you

7:35

can do and what I do

7:37

is, well, I know that my

7:39

body will over-produce this. or under

7:41

produce it. Therefore, I will block

7:43

it, right? And it becomes complex

7:45

at one level, but if you

7:47

look at symptoms, like I've, for

7:49

most of my life, I've had

7:51

really strong muscle tension between my

7:53

shoulder blades, upper back, to the

7:55

point in my 20s, it felt

7:57

like a candle burning there. And

7:59

it was a lot of pain,

8:01

like probably seven out of 10,

8:03

just all the time. And some

8:05

of this has to do with

8:08

liver and toxins, and I get

8:10

rid of those. But ultimately for

8:12

me, it's a catacolamine issue and

8:14

the way my body makes things

8:16

like adrenaline and cortisol and no

8:18

adrenaline. And I finally figured it

8:20

out and some of its genetic

8:22

and if I take the right

8:24

substances, I am golden. I have

8:26

no muscle tension and I have

8:28

no pain in my body. I

8:30

could have done that, you know,

8:32

geez, 40 years ago, had we

8:34

had the right genetic screening and

8:36

understood the pathways. Now we understand

8:38

those things. but I didn't do

8:40

it with genetics, I just did

8:43

it with symptoms. How far along

8:45

the path are we of using

8:47

genetics to be able to turn

8:49

off symptoms? Like are we a

8:51

third of the way? Are we

8:53

all the way? I think it

8:55

depends on what topic. We're making

8:57

great headways in certain fields. Because

8:59

I came from a neuroscience background,

9:01

we do a lot of neuroscience

9:03

with Intellix DNA, which is the

9:05

company where I had the research.

9:07

So we do a lot, we've

9:09

done a lot with cognition, a

9:11

lot with autism, a lot with

9:13

mental health. But we also, in

9:15

uncovering the foundations of all of

9:18

health, looking at the detox pathways

9:20

extensively and inflammation and many other

9:22

things, we actually have surprisingly been

9:24

able to help a lot with

9:26

pain. Patients where they're pain, you

9:28

can have three patients, your pain

9:30

maybe because you have all this

9:32

high adrenaline, different genes, and there's

9:34

a lot of different adrenergic receptors

9:36

and compte and such, but I

9:38

had a patient and she literally

9:40

was limping in and she was

9:42

a photographer and she said that

9:44

by the end of the day,

9:46

she would have to crawl. up

9:48

her stairs because she was in

9:50

so much pain. Wow. And in

9:53

her, and she really wasn't somebody

9:55

who wanted to do 20 things.

9:57

And in her genomics, it became

9:59

really clear that she had something

10:01

called factor two, which gives you

10:03

increased fibrinogen, which makes it so

10:05

you don't get enough blood flow.

10:07

Yep. I had that. She did

10:09

not transport B12 into her brain

10:11

or CSF well. And that's pretty

10:13

common. That's about 18% of the

10:15

population. TCN2, but then she also

10:17

had seven times the risk of

10:19

gluten intolerance. And she had a

10:21

few other things, but just by

10:23

having her get rid of gluten,

10:25

adding some picnogonol and lumbrokines to

10:28

address the vibranogen, and B12, in

10:30

four days, she was able to

10:32

literally run up the stairs, and

10:34

she hadn't done that for years.

10:36

But then there was another patient.

10:38

And she's a makeup artist and

10:40

she would get pain in her

10:42

arms and muscle cramps and dropping

10:44

things. And for her, the secret

10:46

was she couldn't make co-cutin, but

10:48

also couldn't recycle co-cutin to its

10:50

antioxidant form, to the UVQH form

10:52

or vitamin E. So for her,

10:54

getting rid of her pain was

10:56

vitamin E and UVQH. And again,

10:58

for you, it was things that

11:00

lower your cortisol. So I think

11:03

that... Oh, you had low cortisol.

11:05

Yeah, I had to increase nor

11:07

adrenaline. Oh, okay. So difficulty converting

11:09

like dopamine to nor padrennour adrenaline

11:11

or such. Yeah. And so there's

11:13

everybody is different. And so I

11:15

think that genomics can take us

11:17

a long way towards getting well,

11:19

but the science is still in

11:21

its infancy. So we have a

11:23

list of 100 different topics that

11:25

we're working on that actively, but

11:27

there's hundreds and hundreds and hundreds

11:29

more. It feels like to me

11:31

maybe we're 10% of the way

11:33

into this knowledge. I think that

11:35

that's reasonable. And so what we

11:38

do is we start with the

11:40

common things. I'm not going to

11:42

start, someone asked me if I

11:44

would work on, you know, it

11:46

was something that, oh, it was

11:48

a lipidemia. nothing wrong with helping

11:50

people with lipidemia, but it's not

11:52

common. And so I'm like, well,

11:54

we're still working on fertility and

11:56

heart disease and diabetes and cognitive

11:58

decline. And so we'll put it

12:00

on the list, but it's not

12:02

happening in tomorrow. You're a longevity

12:04

doctor and I don't know if

12:06

you read my longevity book or

12:08

not, but I said, look, there's

12:10

these big four killers and subsequent

12:13

books in the space have called

12:15

them the horsemen of the Apocalypse.

12:17

I didn't do that felt a

12:19

little bit too alarmist, but... It's

12:21

heart disease, it's cancer, it's Alzheimer's

12:23

and its diabetes. And if we

12:25

just handle those things, then you

12:27

get to the weird people like

12:29

me who have 18 different weird

12:31

genetic pathways. And I honestly think

12:33

I would be disabled. I bought

12:35

disability insurance when I was 26,

12:37

because I'm like, so many things

12:39

don't work and the doctors are

12:41

useless and maybe out of, I

12:43

don't like to hurt all the

12:45

time and feel dumb. I struggled

12:48

my way out of it and

12:50

I'm lucky that I made a

12:52

bunch of money in my 20s.

12:54

I lost it. But I managed

12:56

to figure out the combinations and

12:58

learn the pathways. I didn't do

13:00

it genetically. I did it via

13:02

systems biology and understanding this leads

13:04

to this, leads to this, and

13:06

there's a blockage here. And it

13:08

was a lot of work and

13:10

no one should ever have to

13:12

do that. A.I. is pretty good.

13:14

But now that we have the

13:16

type of work you're doing with

13:18

genetics, I have the ability to

13:20

say well. Here's the top three

13:23

things that make my life not

13:25

as good as I want it

13:27

to be. Maybe it's brain fog,

13:29

right? Maybe it's pain, and maybe

13:31

it's the arthritis I was diagnosed

13:33

with when I was 14, or

13:35

it's low energy, right? And when

13:37

people come through at upgrade labs

13:39

and they do a survey, so

13:41

well, what matters do you? Was

13:43

it cognitive function or longevity? You

13:45

got to pick one, and like,

13:47

why don't I want both? I

13:49

mean, yeah, do them, do them,

13:51

do them, and I do them,

13:53

and I want both. I want

13:55

both. Right, and I can say,

13:58

well, all right, I want to

14:00

look at this report through the

14:02

lens of let's not hurt anymore,

14:04

or I want my brain to

14:06

not keep forgetting words. And how

14:08

do you guide people? people though

14:10

and they get a report to

14:12

know like this is the one

14:14

that matters for you. Well that

14:16

was actually one of my goals

14:18

as well. So people would come

14:20

to me bringing their 23 and

14:22

me and say I've got a

14:24

family history of Alzheimer's or I've

14:26

got macular degeneration in my family

14:28

or heart disease or whatever it

14:30

was and there was no tool

14:33

out there that mapped out by

14:35

topics that we as human beings

14:37

as well as physicians want to

14:39

think about. So the way that

14:41

we use genomics is genomics is

14:43

in our cognition and memory report,

14:45

for example, we'll put together all

14:47

the gene variants that increase and

14:49

decrease the risk of Alzheimer's or

14:51

cognitive decline by at least 20%.

14:53

Some of them may be 200%,

14:55

some may be 80%. And then

14:57

we'll look at what does the

14:59

gene variant do, and then what

15:01

does, what can you do to

15:03

modulate that with diet, lifestyle, supplements,

15:05

medications, medications, but additionally, because I'm

15:08

a functional medicine physician, physician, physician,

15:10

physician, physician, detox, inflammation, extensive detox,

15:12

extensive inflammation, lots of pathways, nutrients,

15:14

GI, and usually if you address

15:16

those foundational gene variants and then

15:18

you look at the ones associated

15:20

with the specific diseases, you'll find

15:22

answers. But some of the people

15:24

who've been diagnosed with Alzheimer's, their

15:26

gene variants aren't in Alzheimer's pathways.

15:28

They're in brain ischemia pathways, things

15:30

that affect oxygen or in things

15:32

that affect the myelination of the

15:34

nerves. white matter changes. So we

15:36

went broad and then we started

15:38

using it with doctors, physicians across

15:40

the country, showed that we can

15:43

get results of improvement in cognition,

15:45

and then we went to the

15:47

next topic. And so we built

15:49

it by topic. And so that's

15:51

what we're saying. We now cover

15:53

a good 40 or 50 common

15:55

topics, but we don't cover. every

15:57

single esoteric disease state that someone

15:59

could have. And I think that's

16:01

okay because most people, even if

16:03

they feel really well, if you

16:05

dig in... They do have several

16:07

esoteric things. They just don't rise

16:09

to the level of importance that

16:11

it's worth dealing with. Well, and

16:13

also there's overlap. So I had

16:15

a colleague who has strong family

16:17

history of multi-systems atrophy. Scary. Yeah.

16:20

And but there's not, we hadn't

16:22

mapped that out. But when we

16:24

went into his genomics, he had

16:26

so many oxidative stress pathways that

16:28

I was then like, well, this

16:30

is a big part of what's

16:32

going on in your family. and

16:34

then people who have autoimmune pathways.

16:36

So there's different specific interleucans, inflammatory

16:38

molecules, as well as T&F Alpha,

16:40

that increase the risk for leaking

16:42

gut barriers and autoimmune disease. So

16:44

we're finding by using the principles

16:46

of functional medicine, we're optimizing the

16:48

human beings that even have issues

16:50

that we hadn't thought of, and

16:52

we'll continue to add more. I'm

16:55

actually really excited about this state

16:57

of what we can do with

16:59

DNA. Do you worry that if

17:01

you have a 23 in me

17:03

or something like that? Well, you're

17:05

not really getting the full human

17:07

genome. As far as I can

17:09

tell, I was one of the

17:11

first maybe thousand people to have

17:13

my full human genome mapped maybe

17:15

back in 2013 or something. And

17:17

it's just a big binder of

17:19

crap. I don't know what to

17:21

do with that. But how important

17:23

is a full sequencing? And what

17:25

are people actually getting when they

17:27

think they're getting them full sequencing?

17:30

That's a really great question. So

17:32

a lot of people have done

17:34

either whole genome sequencing or whole

17:36

exome sequencing, and then they get

17:38

the results and they're like, this

17:40

wasn't useful. So it's not about

17:42

quantity, it's about quality. Because most

17:44

of the whole genomic sequencing products,

17:46

they're using a tool that reports

17:48

on the pathogenic gene variants, because

17:50

they can't report on everything. There

17:52

are, you know, a few million

17:54

SNPS that have been associated it

17:56

with something in the literature. So

17:58

they're filtering for genes that have

18:00

been labeled by the NIH, National

18:02

Health Institute, as pathogenic. And that's

18:05

a problem because most of the

18:07

things that we care about, longevity,

18:09

again, all the chronic illnesses, those

18:11

aren't caused by pathogenic genes. So

18:13

I feel like they're not particularly

18:15

useful tools. And so with, again,

18:17

with the genomics that we are

18:19

doing, we don't report on a

18:21

million SNPS. What would you do with

18:23

it? We report on 700 SNPS,

18:26

but there are ones that have

18:28

been highly curated. to be very

18:30

highly clinically significant and associated with

18:32

these common things. Because what I

18:34

want to know when I'm working

18:37

with the patient is if they have

18:39

a family history or they have a high

18:41

blood sugar or a family history

18:43

of diabetes, tell me the five

18:45

biggest contributing factors. Do they not

18:47

make inkerton well? Well, then I'm

18:50

going to use the inkerton memetics,

18:52

the GLP ones, whether it's the

18:54

oral ones or the different injectable

18:56

ones. I'm going to give them

18:58

way protein because that helps you

19:01

make more inkerton. Or do they

19:03

have a channel that doesn't let

19:05

insulin in? Or do they have

19:07

a different regulator that affects their

19:09

mitochondrial biogenesis affects insulin? So on

19:12

and on and on, I want

19:14

something that's actionable. So even though

19:16

we've gotten to become a society

19:18

well more is better, I actually think

19:20

taking an intelligent approach to the

19:23

genomics and saying, let's... take the

19:25

most important things, address them first,

19:27

the most clinically significant, let's figure

19:29

out how to address them. And

19:31

that's been a lot of my

19:33

area of research is going, how

19:36

can we address them, and then

19:38

see what the results are. And we're

19:40

having, again, good results. So it's a

19:42

different approach. I bet we'll have to

19:44

do your genomics and you'll see the

19:47

difference. I'll come in. You're here in

19:49

Austin. So we should have done that

19:51

before and so we could talk about

19:53

my report. This is getting, I

19:55

would put this in the

19:57

realm of biohacking, it's just

19:59

exceptionally. focused and detailed and

20:01

I'm gonna look at like the

20:03

NIH genes for disease well avoiding

20:05

diseases is cool but how many

20:07

super power genes has NIH labeled?

20:09

No. That's not their goal. No,

20:12

that's not their goal. So you'll

20:14

find out you know if you're

20:16

a carrier for Duchane's muscular dystrophy

20:18

or cystic fibrosis and you'll find

20:20

out a lot of rare genes

20:22

but that's not their goal to

20:24

help the average person and so

20:26

if you're already 10 or 20

20:28

or 40 or you know, whatever

20:30

age you are, if you had

20:32

a pathogenic a pathogenic gene variant

20:34

causing a rare disease that was

20:36

like dominant where it was causing

20:38

it, you probably would have figured

20:41

that out. You know, if your

20:43

child is born and they're seizing

20:45

and there's all kinds of funny

20:47

things about them, that person needs

20:49

whole genomic sequencing and a geneticist.

20:51

If you are, you know... I've

20:53

done okay in life but my

20:55

brain's not as sharp as I

20:57

want it to be and my

20:59

blood sugar is still a little

21:01

bit high even though I try

21:03

to exercise and eat well and

21:05

there's a family history of heart

21:08

disease and I get depressed every

21:10

now and then are anxious. That's

21:12

genomics because genomics is the science

21:14

of small changes in your DNA

21:16

that by themselves are not disease

21:18

causing but together along with diet

21:20

lifestyle and the environment can be

21:22

and each other can be disease

21:24

contributing. and can be addressed. You've

21:26

probably heard that mitochondria make the

21:28

energy in your body that you

21:30

use to be yourself. And you

21:32

might have heard that damaged mitochondria

21:34

are a primary cause of aging.

21:36

In fact, I wrote a New

21:38

York Times best-selling book on longevity

21:41

about how I'm going to live

21:43

to at least 180 and mitochondria

21:45

are at the very, very center.

21:47

And I use something called urolithin

21:49

A in the form of timeline.

21:51

to support my goal to reach

21:53

at least 180 years. you and

21:55

I are going to live way

21:57

longer than anyone expects. And for

21:59

me, timeline is a part of

22:01

my strategy because I know that

22:03

if I have young mitochondria, I

22:05

will have the energy of youth

22:07

for as long as I want

22:09

it. This is something that is

22:11

our human birthright. So go to

22:13

timeline.com/Dave and get 10% off your

22:15

first order of mightopur. There's a

22:17

new technology for improving your performance,

22:19

improving how your cells work. And

22:21

it's pretty cool. It's working at

22:23

the quantum level. Now, I've had

22:25

all kinds of people send me

22:27

quantum ballpoint pens and all sorts

22:29

of nonsense because people abuse the

22:31

quantum word, but there is convincing

22:33

evidence that reality is based on

22:35

quantum systems. We know for a

22:37

fact that your brain is a

22:40

quantum system, and there's a few

22:42

studies that support that and all

22:44

kinds of science. So it makes

22:46

sense that you can use quantum

22:48

stuff. to affect biology, except that

22:50

sounds like a really hard thing

22:52

to do. Well, enter my friends

22:54

at Lila Quantum Tech. They make

22:56

biohacking tools that actually make waves

22:58

in scientific circles because you'd almost

23:00

think they couldn't work, except in

23:02

dozens of studies, they do work.

23:04

And they've got a range of

23:06

cool products, like necklaces that harmonize

23:08

the energy around you. I actually

23:10

brought those in for my employees

23:12

across all my companies, because I

23:14

think it's worth it. and the

23:16

Lila quantum block that you can

23:18

use to charge items with quantum

23:20

energy. In these randomized double blind

23:22

studies, which is the gold standard,

23:24

Lila's products improve blood quality and

23:26

heart rate variability, and heart rate

23:28

variability is also at the core

23:30

of biohacking because it's a sign

23:32

of how well your body recovered.

23:34

I use my Lila quantum tech

23:37

pretty much all the time in

23:39

one form or another, and I

23:41

can feel the difference. You can

23:43

get 10% off your order by

23:45

going to lilaq.com/Dave. I know it's

23:47

a big claim. to say that

23:49

something works by quantum, and I

23:51

love it that they back up

23:53

their claims with real world. results.

23:55

You have to believe it works,

23:57

you can measure it. I've done

23:59

gene therapy to increase my fallest

24:01

talent levels and reduce, for the

24:03

average person, reduce my age by

24:05

about nine years. It's great. I

24:07

want to change my genome to

24:09

be more highly functional. How soon

24:11

can I do it? Well, I

24:13

think there's two levels to that

24:15

question. So unless you have access

24:17

to crisper, you can't actually... change

24:19

your genome. Everyone has access. I

24:21

mean, Jay Zainer has been on

24:23

the show. I think I've known

24:25

Jay for a long time. I'm

24:27

one of the first people to

24:29

do CRISPR editing at home. A

24:31

very controversial. I mean, any of

24:34

us have CRISPR. But what you

24:36

can do, so I actually went

24:38

to college with Jennifer Doudna, so

24:40

I'm not going to try to

24:42

do home CRISPR. I'll let. I'm

24:44

not recommending that for anyone. For

24:46

real. But what we can do,

24:48

and that's really, some of this

24:50

work is really understanding that, yes,

24:52

you can't necessarily change your DNA,

24:54

but if you understand your DNA,

24:56

you can change transcription and expression.

24:58

So really what we're doing is

25:00

taking the knowledge of our DNA

25:02

to change how much of it

25:04

goes into proteins. When part of

25:06

how this work started, we were

25:08

working on, we were working already

25:10

on cognition and cardiac and kind

25:12

of adult neuroscience and lots of

25:14

other things. And I was at

25:16

a conference that PLMI that Jeff

25:18

Blent had hosted that was. Jeff,

25:20

he's been on the show. Yeah.

25:22

It was for thought leaders on

25:24

genetics and genomics and a colleague

25:26

of mine from Australia who had

25:28

her first degree molecular biology and

25:31

then got into genetics and nutrition

25:33

as her second PhD. was because

25:35

her child was born with autism.

25:37

And she was like, and the

25:39

child, well her child wasn't born

25:41

with autism. Her child developed autism

25:43

around age two and she's like,

25:45

well, if what we've been doing

25:47

in diet, environment, exposure to inflammation,

25:49

etc., could trigger this, then we

25:51

can figure out how to untrigger

25:53

it. I reverse my autism. It's

25:55

a hell of a lot of

25:57

work, but it's doable. Absolutely, we

25:59

have hundreds and a hundred, well

26:01

thousands at this point of children

26:03

that their score, their ATEC score.

26:05

has gone from the autistic range

26:07

back into the normal. Because why

26:09

would a disease go from one

26:11

out of every thousand or even

26:13

10,000 children to one out of

26:15

every 35 in one lifetime? Well,

26:17

it's because of the interactions. So

26:19

I don't think you can actually

26:21

change, you know, if you're swabbing

26:23

somebody, their DNA sequence will be

26:25

the same, but you can certainly

26:28

change their phenotype, how they feel.

26:30

They don't have to be depressed

26:32

anymore or have brain fog. Why

26:34

do you think we can't change

26:36

our genetics? Well, the actual DNA,

26:38

the code? Why not? Well, that's

26:40

kind of like, usually if you're

26:42

changing, how would you change the

26:44

DNA in every cell in your

26:46

body? I'm talking about changing the

26:48

code, not just the expression. Yeah,

26:50

I'm not changing the code, not

26:52

the expression. Well, every cell in

26:54

my body gets refreshed about every

26:56

seven years, right? Maybe some stuff

26:58

in the bones a little bit

27:00

longer than that. And some of

27:02

the cells turn over every 48

27:04

hours. So what's stopping us? I

27:06

think it's just a different, I

27:08

think that we're talking about similar

27:10

things, but a little different. I

27:12

do think we can change how

27:14

our DNA affects us, but I

27:16

think that if I were to

27:18

code... What's the law hanging through?

27:20

Let's put on our future as

27:22

half. Science fiction here. I think

27:24

that I think you would have

27:27

to figure out how to get

27:29

into every cell in the body,

27:31

or maybe you would just change

27:33

it with some kind of... I

27:35

mean, that's how viruses work, actually,

27:37

as they do change our DNA.

27:39

So I guess you're right, there

27:41

are things that can happen that

27:43

change your DNA. I'm not sure

27:45

that all of them are good.

27:47

No, I'm not sure. I'm not

27:49

sure they're all good either by

27:51

a long shot. We know a

27:53

lot of our non-coding DNA came

27:55

from viruses and there. Liz Paris

27:57

has been on the show and

27:59

I know a project she's working

28:01

on around using viral vectors to

28:03

introduce beneficial changes to our DNA,

28:05

by the way, with full informed

28:07

consent and not doing it to

28:09

people via mosquitoes and ticks and

28:11

all the weird shit that dark

28:13

people are thinking about. I'm actually

28:15

thinking it's possible and I've already

28:17

made temporary changes to my genetics

28:19

using a miniscircle technology where I've

28:21

instructed the cells in my body.

28:24

Use this new code to make

28:26

this longevity protein, but that's only

28:28

good for a couple years, right?

28:30

And then those cells die and

28:32

they don't pass it on. And

28:34

I'm thinking, all right, I know

28:36

that I have dysfunctional pathways here,

28:38

and maybe we get a signal

28:40

in, so only some of my

28:42

cells are better off than they

28:44

were before as they get refreshed.

28:46

Is this even in the realm

28:48

of possibility? I think that it

28:50

hasn't been something that I've worked

28:52

on. So my response, for example,

28:54

to something again, so like the

28:56

number one longevity proteins, clotho, Foxo3,

28:58

ApoE2 is actually a benefit for

29:00

longevity, so ApoE4 is kind of

29:02

negative, is to say, okay, if

29:04

we know, so you take the

29:06

person who feels like they're aging

29:08

too fast and you do their

29:10

genomics and you find out that

29:12

they have, they're in the 2%

29:14

of the population that's really low

29:16

clotho, Well, we can do things

29:18

to increase their expression of it,

29:21

even down to exercise. Aerobic exercise

29:23

is great for clotho, but anaerobic

29:25

is not. So weightlifting is not

29:27

good for those people. If they're

29:29

going to do it, they need

29:31

to sandwich it between aerobic. That's

29:33

where Rizveratrol works, to help, because

29:35

sertuents, clotho, clotho, and clotho interact.

29:37

I mean, even the people who

29:39

are kind of hacking longevity and

29:41

it won't work. So you want

29:43

to understand some of the foundations

29:45

for each person and I think

29:47

that your your interest in changing

29:49

And do they, it's very interesting,

29:51

I've been approaching it by going,

29:53

well, what do we know? I

29:55

mean, there's, you even, you know,

29:57

we know that clotho makes it

29:59

so people, it regulates all the

30:01

other anti-accident pathways. So talking to

30:03

someone about increasing spiralina in their

30:05

diet, if they are very low

30:07

clotho, so that they can have

30:09

more anti-accidants, decreasing oxidative stress, not

30:11

smoking's pretty obvious, so. It's fascinating.

30:13

I looked at cloth that was

30:15

one of the most important proteins

30:18

when I wrote my longevity book,

30:20

which is superhuman. And you couldn't

30:22

buy anything to do it. We

30:24

didn't know as much when I

30:26

wrote that, except there was one

30:28

probiotic that made a lot of

30:30

it. So I illegally imported that

30:32

from Japan. And I'm like, okay,

30:34

maybe that's the way. But now

30:36

we know a lot more. And

30:38

soon we'll be able to increase

30:40

clotho probably with some of these

30:42

gene therapies. Right. In the meantime,

30:44

like I'm saying, just change your

30:46

lifestyle. But if you don't know

30:48

you're weak, you wouldn't know. And

30:50

this is what your company does,

30:52

right? Right. Because again, you and

30:54

I, we could probably say supplement

30:56

Jeopardy and list a thousand different

30:58

supplements and how they work. But

31:00

what most people want to know,

31:02

some of bioheckers, they might be

31:04

willing to do 20 different things,

31:06

or people who really want to

31:08

optimize longevity or brain health. But

31:10

most people want to know. If

31:12

I'm going to do five things

31:15

or 10 things, what are the

31:17

top 10 of diet lifestyle supplements,

31:19

nutrients, nutrients? You mean they're not

31:21

the same for all of us?

31:23

Yeah. I would argue that probably

31:25

the top two are the same

31:27

for the vast majority of people.

31:29

It would be a broad spectrum

31:31

mineral supplementation just so your genes

31:33

could have the zinc and all

31:35

the other things they need to

31:37

do their thing and the fat

31:39

soluble vitamins. But even that some

31:41

people have a vitamin D blockade,

31:43

they need more or whatever, right.

31:45

Right, right. There could be very

31:47

different levels needed. So there's about

31:49

9% of the population that don't

31:51

make this carrier for vitamin D,

31:53

this GC protein, and they need

31:55

about 50,000 I use of vitamin

31:57

D a week to... their levels

31:59

in that 40 to 60, whereas

32:01

somebody else might only need 14,000

32:03

a week to keep it at

32:05

the same levels. And you can

32:07

test vitamin D levels, but when

32:09

you understand why someone needs more,

32:11

it just helps you come up

32:14

with a kind of a lifelong

32:16

plan, so that you're not going,

32:18

why am I needing so much? Or

32:20

some people, again, their peripheral thyroid levels

32:22

can look great. But it's a different

32:24

gene that converts T4 to T3 in

32:26

the brain than it is in the

32:28

periphery. So if you know that about

32:31

yourself, then, and your hypotheroid, or

32:33

even if you're just kind of

32:35

subclinical, you're going to want a

32:38

supplement or a prescription that has

32:40

T3 in it to keep your

32:42

brain optimal. But for somebody else,

32:45

they don't need that. It's so fascinating.

32:47

We just didn't understand this stuff for

32:49

so long. And you see people walking

32:51

around and their doctor says, oh, you

32:53

know, your vitamin D, you know, take

32:55

the US RDA. I had been one

32:58

of those in my early 20s and

33:00

I'm fortunate that I got

33:02

invited to run a non-profit

33:04

longevity group and suddenly Dr.

33:06

Cannell from the vitamin D research

33:08

institutes there, I got my blood tests.

33:10

Turns out I have the genetics, I

33:12

need 15,000 I use a day to

33:14

keep my levels at about 90. Yeah,

33:17

so you probably don't make it and

33:19

break it down more quickly and don't

33:21

have that carrier protein. And that can

33:23

be huge. You had said that when

33:25

you were younger, you had pain. That

33:27

is a huge factor for pain, because

33:30

vitamin D's job is to turn things

33:32

off. And so one of the things

33:34

that turns off is inflammation. It also

33:36

turns off auto-immunity. It also turns off

33:38

cells going rogue, which is why it's

33:41

so important for cancer. So every single,

33:43

there's so many pathways that are so

33:45

important to our overall longevity, our

33:47

overall health and well-being. I believe

33:49

that we all have a right to any

33:52

information about what's going on in our biology

33:54

and that nowhere in the Constitution does

33:56

it say that anyone has the right to

33:58

limit my access to that. information and I

34:00

didn't hire any regulators to do that or

34:03

even empower them to do that. It feels

34:05

like a power grasp. If you could provide

34:07

the reports direct to consumers right now without

34:09

somebody saying you're not allowed to do that

34:11

would you do it? Yes but we would

34:14

also provide training. Okay. But it would be

34:16

you know one of the things is even

34:18

Even our physicians, so Dr. Breton, which many

34:20

of your listeners probably know who don't Breton's.

34:23

He's been on the show, he's a friend.

34:25

Yeah, I love Dr. Breton's work. In their

34:27

research, they're using our report, our brain optimization

34:29

report, because it helps them get where they're

34:31

going for optimizing. But even the doctors who

34:34

are at the top of their game doing

34:36

research. we want to train them so that

34:38

they get the most out of the report

34:40

because most of us, whether it's a person

34:43

on the street that's a computer programmer or

34:45

a physician, we didn't get the study of

34:47

genomics in our education. So we can really

34:49

help by helping kind of get good education

34:51

as well. Yesterday I went to ChatGPT, the

34:54

latest model, and I said, hey, if I

34:56

upload my genomics report, can you... help me

34:58

out with mthf r and it said absolutely

35:00

i can identify all the snips and i

35:02

can tell you what's going on or what

35:05

to do about it Isn't that enough training?

35:07

Well, let me tell you, I was working

35:09

on where we are about to release our

35:11

women's health and fertility report. Oh, it's so

35:14

good. It's really exciting. It's very, very exciting.

35:16

Are you working on that? Are you working

35:18

with Anne Shippey on that? Yeah. Well, Anne

35:20

is writing a book on fertility, and we've

35:22

talked extensively about the genomics, so she can

35:25

include some of that in her book, and

35:27

she uses on genomics. But it is exciting.

35:29

We can talk about that we can talk

35:31

about that because we can talk about that,

35:34

because we can talk about that, because we

35:36

can talk about that, because we can talk

35:38

about that, because it, because it's the whole.

35:40

you know, assisted reproductive technology. That was my

35:42

first book was on fertility and Dr. Shipi's

35:45

been on the show close friend doing preconception.

35:47

I love it that you guys are working

35:49

together. Yeah, and oxidative. stress and coagulation and

35:51

so many things, nutrients all relate, but one

35:54

of the things is we were working on

35:56

using, we were talking about chatGPT, and so

35:58

I was working on that and I thought,

36:00

well what happens if I pop this gene

36:02

that's supposed to be relating to hormones and

36:05

hot flashes into, and I used one of

36:07

the tools that's supposed to be one of

36:09

the better ones for science for AI, and

36:11

It came up with completely wrong information that

36:14

thought it was a gene related to hypertension,

36:16

giving me all these things. Enough that I

36:18

was like, let me just go double check,

36:20

you know, making sure I didn't type the

36:22

number wrong. I didn't. So you do have

36:25

to be a little careful because it might

36:27

have a lot of information on common gene

36:29

variants, but it thought that this gene that

36:31

related to hormone transformation related to hypertension. And

36:34

I'm like, hmm, we're not quite there yet.

36:36

So that's my comment. We're not quite there.

36:38

I'm not ready to turn my health care

36:40

decisions over to CHATGPT yet. I'm 100% with

36:42

you. I find it's a better guide than

36:45

most Americans get in the three minutes they're

36:47

going to have with a GP. However, it's

36:49

not that good. And if you were to

36:51

train your own AI, which you're probably already

36:53

doing, so that you could better help the

36:56

physicians who you've trained. the next three years

36:58

of medicine is going to be your doctor

37:00

working with an AI that's trained on a

37:02

specific set of things so that the combination

37:05

of the healer and the data and the

37:07

analytics and the patient and the condition becomes

37:09

very different. Yes. So if we can and

37:11

I think that is where medicine is going

37:13

where we can filter what data set we

37:16

want the AI to learn from so that

37:18

we know that it's so again one of

37:20

the things we're proud of at italics DNA

37:22

is we have. 20,000 references in our report.

37:25

And so it's all evidence-based, actionable from what

37:27

this gene variant does to the interventions. Well,

37:29

if we can train a computer, of course,

37:31

to help keep all those references in mind

37:33

and keep the whole thing, yes, that'll make

37:36

it a lot. faster so

37:38

that somebody can be

37:40

like okay well kind

37:42

of help me go

37:45

through this report and

37:47

find everything that relates

37:49

to infertility or miscarriage

37:51

and you know count

37:53

me synthesize it and

37:56

I do think that's

37:58

the future of medicine

38:00

using personalized medicine tools

38:02

genomic tools labs and

38:05

using computers to help

38:07

us come to conclusions

38:09

a little faster than

38:11

our brains can work

38:13

or at least the

38:16

most of us can.

38:18

And then we use

38:20

the computer to 3d

38:22

print new DNA that

38:25

snort that goes in

38:27

and rewires all the

38:29

problems right? Maybe

38:31

in our great grandchildren's. We can

38:33

always hope. All right what about

38:35

mitochondrial DNA? What do you do

38:37

about that? So the mitochondria are

38:40

interesting and just in case most

38:42

of your listeners probably know that

38:44

mitochondria are that extra I call

38:46

it the backup power source so

38:48

you wouldn't plug an important computer

38:50

into a shoddy electricity source food

38:52

is a really shoddy energy source

38:54

for a human because evolutionarily you

38:57

might go a long time without

38:59

it. So mitochondria can take our

39:01

oxygen and you know different nutrients

39:03

and things and make energy. So

39:05

mitochondria have their own DNA they

39:07

don't have very many of many

39:09

genes in a mitochondria but there's

39:11

also genes in the human genome

39:14

that affect the mitochondria's DNA. And

39:17

we right now sequencing the actual

39:19

mitochondria's DNA is a little harder.

39:21

So we do a lot of

39:23

we have a few of the

39:25

mitochondrial genes we don't have all

39:27

of them but we do have

39:29

some of the important ones like

39:31

cox1 affects cognition and that's mitochondrial

39:34

but we also have things like

39:36

mitochondrial membrane gene variants that are

39:38

actually in the human genome. One

39:40

of the mitochondrial membrane gene variants

39:42

is kind of the neighbor to

39:44

APOE4 on chromosome 21 and so

39:46

you we have some of that

39:49

but I do think that mitochondrial

39:51

membrane mitochondrial medicine is a huge

39:53

topic not taught in medical school.

39:55

I had to learn it I

39:57

learned it when I started to

39:59

work with the autism world because

40:01

it's really important there. But it's important for

40:03

Parkinson's. It's important for people who have mold-related illness. So anything

40:06

chronic ultimately seems like metaconder

40:08

are at least involved, if not

40:10

causal. Absolutely, and I think that it's

40:12

because there are so many things that

40:15

damage your mitochondria. So I always tell

40:17

my patients that the big A's damage

40:19

your mitochondria. Antibiotics, which so many of

40:21

us get, aging and anesthesia. And

40:23

then in addition to it, we

40:25

know that mold doesn't start with

40:27

A, but it also is a

40:30

big mitochondrialochondrial insult causes insults, and

40:32

then there's many other things. So

40:34

I do think that we need

40:36

to pay attention to mitochondria, especially

40:38

people with anything brain or energy

40:40

related. I would totally agree that

40:42

it's been a big focus for

40:44

me. And one of the areas

40:47

that I believe that you'll end

40:49

up doing... is looking at the

40:51

mismatch of mitochondrial DNA and nuclear

40:53

DNA. And for listeners, nuclear DNA

40:55

is your DNA from your entire

40:58

cell. And then the mitochondrial DNA,

41:00

I think of it like the wiring of

41:02

the cell. So if you have the

41:04

building plans in your DNA for a

41:06

warehouse, but then you get the wiring

41:08

plan for a restaurant, like they don't

41:10

match very well. Is there anything where we're

41:12

going to be able to do about that?

41:15

Well, again, I think that what I'm

41:17

trying to do with my research. is,

41:19

and some of it's not using genomics,

41:22

some of it's using, there's other mitochondrial

41:24

tests, but help people understand where

41:26

is the fault. So if it

41:28

is, so if it's the p-par

41:31

pathways, which people think of as

41:33

diabetes pathways that relate to mitochondrial

41:35

biogenesis, that might be pushed by

41:37

alphilippoic acid, but if it's the

41:40

mitochondrial membrane proteins, that might be

41:42

benefited by giving things that the

41:44

membranes need to repair like phosphatatal

41:46

colon and... Ethnolomy, mine, different kinds

41:49

of things for different causes. And

41:51

so I like to say, what

41:53

can I do to get the

41:55

best understanding possible? Methylene blue can

41:58

help with Cox 1. CoQ10. can

42:00

help bypass some of the electron

42:02

chain. And I think that we used

42:04

to kind of take a disease state.

42:07

This was how medicine was. Take this

42:09

topic of depression or cognitive decline or

42:11

anything. And psychists very significantly does this.

42:14

Okay, we'll give the diagnosis and

42:16

then this is our first line. This

42:18

is our second line. This is our

42:20

third line. And when I'm trying to

42:23

do, whether it's mitochondrial or whether it's

42:25

again a disease state like depression, is

42:27

go, well, I don't care. about all

42:30

the components that we might address,

42:32

I want to know for this person

42:34

how important are these specific components. You

42:36

were talking about MTR and that is

42:39

important for depression because without it, it's

42:41

not just about turning genes off, it's

42:43

also about making serotonin, making norphinephrine, but

42:46

a lot of people don't realize

42:48

that there is a sister to MTR

42:50

called BH4, tetrahydrobyopterin. And for people, you

42:52

know, for the 4% of the population

42:55

who don't have, don't make enough tetrahydra

42:57

biopteran because of their genomics, you can't,

42:59

we've had people where their depression, anxiety,

43:02

ADHD, PMS, goes away after years

43:04

or decades because now they know how

43:06

to address it. And that's a supplement?

43:08

Mm-hmm. Yeah. What's it called? What's it

43:11

called? It's called pteridine-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T-T- D-I-N-Teridine-4 I think,

43:13

or Separopteran. I know that New Beginnings

43:15

is one company that has it. There's

43:18

sometimes the compounding pharmacies also can

43:20

make it, but then you need a

43:22

prescription. That's cool. Yeah. The tetra hydro

43:24

family, because we're getting a little nerdy

43:27

here, it seems like those quite often

43:29

aren't supplements. I've been particularly interested in

43:31

tetra hydrofolate. When I wrote that first

43:34

fertility book, I'm like, well, if

43:36

you don't want a kid with autism,

43:38

because I was concerned I had it

43:40

and didn't want to pass on to

43:43

my kids, said you might want to

43:45

supplement with phalanic acid. And it's different.

43:47

than methyl folate and it's different than

43:50

foli casa which I don't think

43:52

should be on our food supply and

43:54

shouldn't. We can talk about that. It's

43:56

actually a huge detriment but we'll go

43:59

on to the phalanic acid first. Right

44:01

and this is the only way you

44:03

can get it unless you're eating a

44:06

lot of liver or maybe a

44:08

lot of romaine lettuce. A lot of

44:10

romaine lettuce. So like what do you

44:13

do and the funny thing is When

44:15

people have a poor reaction to creating,

44:17

like they can't sleep, it's usually because

44:20

you didn't have enough of this. And

44:22

it's an unknown supplement. But if

44:24

you're pregnant or you have a brain

44:26

that just needs it, getting that form

44:29

of folates important. How you get to

44:31

know? Probably knowing your genetics would be

44:33

helpful, right? So yes. So in our

44:36

genomics, there is a gene, FOLR1, a

44:38

folate, and again, the thing is

44:40

that I don't have all the numbers

44:42

memorized. I can say a gene, but

44:45

they're particular variants. So you can't just

44:47

go, well, do I have this gene?

44:49

Everyone has every gene. I'm sorry. You

44:52

talk about cognitive function longevity, and you

44:54

haven't memorized all the numbers in

44:56

the entire human genome? Memorized all two

44:58

billion RSIDs. But there are about 11%

45:01

of the population that have a gene

45:03

variant in their folate receptor. And to

45:05

go, again, I'm going to take the

45:08

nerdiness and bring it, dial it

45:10

back. You can't take folic acid, which

45:12

is the artificial folate that they're putting

45:14

in breakfast cereals and flour, that actually

45:17

can't cross the blood brain barrier. In

45:19

fact, it can gum up the blood

45:21

brain barrier and make it so your

45:24

methylpholate and phalanic acid don't cross

45:26

well. Well, most people can use methylpholate,

45:28

and that's their best brain source for

45:30

making their serotonin and norphinephrine and all

45:33

of their neurotransmitters, but 11% of the

45:35

population... have a variant that makes them

45:37

not transport methyl folate well. It's a

45:40

smaller percentage, only about 2% that

45:42

have two copies of the FOLR1 variant.

45:44

They need phalanic acid because that uses

45:46

a different carrier. So there's a second

45:49

carrier called the reduced folate carrier and

45:51

the phalanic acid bypasses the... receptor, that

45:53

FLLR1 receptor and uses the other one.

45:56

So these are the kinds of

45:58

things why genomics is so exciting. So

46:00

having an FOLR1 receptor variant, even one

46:02

copy of it, more than doubles the

46:05

risk of autism because getting enough folic

46:07

acid, whether it's methylpholate or phalanic, because

46:09

they can switch back a little bit.

46:12

super important to the brain. And

46:14

in the autism world, one of the

46:16

most common things for children who are

46:18

not speaking, our non-verbal, is to give

46:21

them methyl B12 and phalanic acid, and

46:23

it can do wonders, because you can

46:26

also get an autoimmune brain disease, autoimmune

46:28

antibodies against the folate receptor that

46:30

creates the same kind of thing where

46:32

you have then a brain, a cerebral

46:35

folate deficiency. But yeah, there's so much

46:37

science. And when people ask me what

46:39

I do, I say, my job. is

46:42

to take everything out in the literature,

46:44

that all this different information in

46:46

the literature that is published and make

46:48

it accessible so people can use it

46:51

to improve their health. Because I'm like

46:53

you, I'm a nerd. It's super cool.

46:55

In fact, another guy's been on the

46:58

show, another Austin guy, you probably know,

47:00

Brandon Crawford. just posted something about,

47:02

look, I'm fighting phalanic acid is reversing

47:04

autism and a lot of the kids

47:07

and he makes the 528I laser, they'll

47:09

be at the Biohiking Conference in May

47:11

28th, Biohacking conference.com guys, 4,000 people filling

47:14

up the Fairmont here in town. And

47:16

I'm going, okay, this is really

47:18

interesting and I look at my own

47:20

history. I have spina bifida. A cultist,

47:23

which about 20% of people have, and

47:25

it sounds all fancy. And if you

47:27

remember that movie, you know, it's one

47:30

of the bifidas. Remember that? Was that

47:32

Ricky Bobby? Anyway, that made me

47:34

laugh. But spinnabifidas, when there's a folate

47:36

deficiency, I didn't know, that made me

47:39

laugh. But spinnabifidas, when there's a folate

47:41

deficiency, I didn't use whatever. No symptoms.

47:43

not a big deal, but it means

47:46

that I likely have the genetics. And

47:48

so for me, getting my levels

47:50

correct has been a bit of hidden

47:52

myths. I know I have the issue.

47:55

But what happens when someone takes an

47:57

excessive amount of methylfolate? Well, you know,

47:59

methylfolate has been studied in pretty high

48:02

doses. So again, I don't know, it

48:04

depends on, if you take a

48:06

lot of methylfolate and you don't have

48:08

enough B12. you may get symptoms because

48:11

you're kind of pulling from other pathways.

48:13

So that's kind of the methylfolate steel-type

48:15

issues. And so some people don't do

48:18

well when they get large amounts.

48:20

But then there were studies done using

48:22

15 milligrams of methylfolate and people with

48:24

depression, and not only were there no

48:27

side effects, it was very effective. I've

48:29

never really, you know, again in the

48:31

autism world where you have to first

48:34

address B12, you know, if you

48:36

have someone and you give them either

48:38

phalanic acid or methylphalate and they get

48:41

hyper or they don't do well, I

48:43

always say take it back and look

48:45

at some of the other nutrients, but

48:48

some of the genes that relate to

48:50

spina bifida, for example, their homocysteine

48:52

and methylation related genes, MTR, MTR, MTR,

48:54

MTR, MTHFAR, there's lots of M's and

48:57

T's. And so those people might need

48:59

more and they also might do better

49:01

decreasing the folate, the artificial folates in

49:04

their diet, not using those processed cereals

49:06

because again you want to get

49:08

it into the spinal cord, but they

49:10

also need some of the genes also

49:13

require them to have... more colon or

49:15

more betane. And so I think it's,

49:17

some of them have B6 as cofactors.

49:20

Some people need more rapidly than. Yeah.

49:22

Right. And knowing that about myself

49:24

has created huge improvements in longevity, cognition,

49:26

energy, health, and it's taken a lot

49:29

of time and a lot of trial

49:31

and error because we didn't know all

49:33

the pathways now. And I. Like if

49:36

I could go back in time, if

49:38

I could choose when to have

49:40

all the crap wrong with my biology,

49:42

if I was 19 years old today,

49:45

I'd be like, you know what? Mom,

49:47

dad, I need some help, you know,

49:49

it's gonna cost me a few thousand

49:52

dollars in diagnostics. And I'm gonna cost

49:54

me a few thousand dollars in

49:56

diagnostics. And I'm gonna cost me a

49:58

few thousand dollars in diagnostics. And I'm

50:01

going to figure a few thousand dollars

50:03

in diagnostics. And I'm going to cost

50:05

me a few thousand dollars in diagnostics,

50:08

in diagnostics, in diagnostics, diagnostics, in diagnostics,

50:10

in diagnostics, and diagnostics, and diagnostics,

50:12

and diagnostics, and diagnostics, and diagnostics, and

50:14

diagnostics, and diagnostics, and diagnostics, and diagnostics,

50:17

and diagnostics. Here in Austin at our

50:19

patient facing practice for resilient health, we've

50:21

swabed children as young as two or

50:24

three weeks. I mean, that's not common.

50:26

That's not our typical patient. But

50:28

we have patients where they've helped themselves.

50:30

We had a woman who had been

50:33

unable to get pregnant. She had a

50:35

bad AMH, which is a fertility score,

50:37

failed IVF twice. She had MS. She

50:40

hired a surrogate. Her surrogate got pregnant.

50:42

She actually, the surrogate ended up

50:44

miscaring, but meanwhile we optimized her genomics.

50:46

She now has two healthy children. But

50:49

those are many people, I think most

50:51

people's children are precious children, but she

50:54

then was like, I want you to

50:56

tell me the roadmap for how I

50:58

can raise these children to have

51:00

the lowest risk of autoimmune disease and

51:03

the best health. So we swabbed her

51:05

kids when they were little and then

51:07

came up with a plan. And I

51:10

think that it's ultimately, I think that

51:12

we can improve the health. of

51:14

any person, of any age, by understanding

51:16

some of the most important things for

51:19

them to address. Some people, again, have

51:21

very different needs than others. I am

51:23

somebody who needs more B12 than other

51:26

people, but I also, you said, you're

51:28

low cortisol. I'm a very high

51:30

cortisol person. You probably wouldn't have guessed.

51:32

You know, high energy, high adrenaline person.

51:35

So for me... I wish I had

51:37

Ashwaganda when I was going through high

51:39

school. Right. You know, it made a

51:42

huge difference to me as an adult

51:44

because it let me lower my

51:46

cortisol 30% but you can't do everything

51:48

with trial and error and so people.

51:51

they're getting diagnosed with ADHD, they're getting

51:53

diagnosed with anxiety, instead of labeling children

51:55

adults, let's look at what's going on

51:58

and just address it. There's always a

52:00

reason for it. It's funny, I

52:02

actually just take cortisol. But like, just

52:04

the way some people take thyroid, my

52:07

body literally makes very little cortisol and

52:09

knowing that about myself is just amazing.

52:11

But the genetics behind that are not

52:14

ones that normally get tested. It's most

52:16

likely in the RCCX thing. If

52:18

you looked at RCCX. So we have,

52:20

so that also can relate to mold

52:23

and we do have some early research

52:25

with that. It's not one that we

52:27

have odds ratios for yet. I don't

52:30

think anybody does. And I think that

52:32

that's one of the problems when

52:34

you're creating. We're trying to start with

52:36

the things, we do have like the

52:39

ability to kind of like a research

52:41

tool, but in our formal report, we

52:43

haven't put RCCX yet because we don't

52:46

have odds ratios yet. But we do

52:48

have it on our radar. And

52:50

for me, it was, oh my gosh,

52:52

I have this one gene that stops,

52:55

what was it, dehydration progesterone, from converting

52:57

to cortisol, my liver doesn't do that.

52:59

Like, oh, that explains a huge number

53:02

of things that happened in my life,

53:04

not to mention all the other

53:06

things. Now, if you're listening to this,

53:09

you're like, Dave, you sound like you're

53:11

a train wreck. Pretty much biologically, yes.

53:13

Which is why if I can extend

53:16

my life and I can be 5%

53:18

body fat with a highly functional brain

53:20

and do all the stuff I've

53:22

done as a 300 pound autistic, you

53:25

know, pretty broken human as a young

53:27

person, it should be easier for you.

53:29

And it should be a lot more

53:32

affordable for you. And now that we

53:34

have tools. Like the ones we're talking

53:36

about today, it's kind of the

53:38

golden age to have a chronic illness

53:41

because there are specific things you can

53:43

do because even 10 years ago, we

53:45

didn't know these pathways, did we? No,

53:48

no. And one of the things to

53:50

put it in perspective, the human genome

53:52

wasn't sequenced till 2000 and... And

53:54

I think the final was 2003, was

53:57

we got the human genome sequenced and

53:59

it was the cost of close to

54:01

$3 billion. And so even after it

54:04

was sequenced, it took a couple decades

54:06

because for these genes, like when

54:08

I was talking about the one that

54:10

relates to tetrahydrobyopterin, we're about to publish

54:13

a paper because we have enough cases

54:15

of people that have benefited from this.

54:17

That two copies is 4%. So how

54:20

many people would you have to screen?

54:22

Well, if it's going to cost

54:24

thousands and thousands and thousands of dollars

54:26

to run someone's genomics, doing studies on

54:29

the less common genes was cost prohibitive,

54:31

and that's why the literature is exploding

54:33

now. So we started out, I remember

54:36

teaching about MTH of R. 15 years

54:38

ago I was talking about it

54:40

to people with depression and all kinds

54:42

of things because it was easy to

54:45

find people who had it and it

54:47

was you know it was so common

54:49

but now the literature is exploding and

54:52

what I want to know is I

54:54

want to know some of those

54:56

gene variants that I have that are

54:58

only in 2% 5% 7% because sometimes

55:01

they're the most impactful and that's what's

55:03

so exciting about this decade is that

55:05

literature is is exploding. It's exploding and

55:08

I think AI is going to make

55:10

it take less time than we

55:12

all think it will in order to

55:14

find like that weird thing. And it

55:17

could be even worse. Saying, well, I

55:19

have the COMT gene and I have

55:22

an MTHFR gene, but the combination of

55:24

those two with this other thing that

55:26

no one ever thinks about, like

55:28

that gives you a third eyeball syndrome

55:31

or whatever. No one's ever going to

55:33

see that, but I think AI will.

55:35

Well, and that's some of what our

55:38

research has done. Now, AI helps our

55:40

research team now because we still have

55:42

to vet everything. But we started

55:44

in 2016, and we were the first.

55:47

tool that I know of that looked

55:49

at combinations. So let's talk about APOE4

55:51

combinations because that's huge. Oh yeah, I

55:54

want to go. Well first, what is

55:56

APO versus APO2, APO3, APO4? So, okay,

55:58

so APOE is the gene name.

56:00

APO-like approach. E. And it is a,

56:03

it's a lipid carrier, but it also

56:05

relates to amyloid processing, but the apoee

56:07

protein also interacts with 1,700 promoters. That's

56:10

a big deal, given that we only

56:12

have about 3,000 genes that have been

56:14

identified. This interacts with all these

56:16

other genes, genes that relate to your

56:19

BD&F brain drive, you know, what I

56:21

call the fertilizer for the brain. Genes

56:23

that relate to hormones. So people who

56:26

have APOE2, they're the lucky ones that

56:28

make more APOE, it's really a gene

56:30

that just kind of upregulates your

56:32

APOE production, and they're going to have

56:35

actually 40% lower risk of getting Alzheimer's

56:37

and cognitive decline. APOE3 is what most

56:39

of us have two copies of it,

56:42

and that's the normal amount of APOE.

56:44

And then apoee for individuals, their apoee

56:46

is funky and there's less of

56:48

it. So the apoee protein should look

56:51

like this because of this one molecule

56:53

that got, that one amino acid that

56:55

got changed, it gets a cross-link, so

56:58

it looks like an A instead. So

57:00

it doesn't work well. So it doesn't

57:02

turn on and off all the

57:04

genes that's supposed to. And it causes,

57:07

again, problems with longevity, with sertuens. It

57:09

causes problems with growth factors for the

57:11

brain, with inflammation with inflammation, with inflammation

57:14

for the brain, inflammation, inflammation. However, in

57:16

overall, if you look at all

57:18

APOE4s together, it gives about 3.2 times

57:20

the risk of Alzheimer's with one copy,

57:23

14 times the risk with two. What

57:25

is the normal risk of Alzheimer's? It's

57:27

a good question because it gets muddled

57:30

with so many other kinds of dementia.

57:32

But ultimately... it is the most

57:34

very common cause of death. Like 20%?

57:37

Yeah, about 20% of people will have

57:39

cognitive decline when they get into their

57:41

late 70s or 80s. 14 times 20%

57:44

is more than 100. How's that work?

57:46

No, 14 times the risk compared to

57:48

someone who's in April 3.3. Okay,

57:50

got it. So everybody, there's a lot

57:53

of people who... they learn they have

57:55

a boy four, they get all scared.

57:57

Well, that's what drove us to better

58:00

map out the combinations because if you

58:02

have a boy four and 75% of

58:04

people who have a boy four

58:06

also have the mitochondrial membrane issues, that

58:09

together gives part of the risk, but

58:11

then there's a gene, it's called beautical

58:13

in esterace, if you don't have that.

58:16

30% of people who have apoe4 don't

58:18

have that BCAG gene variant, then your

58:20

risk gets cut in half. So

58:22

it's really only, so it's really 1.7

58:25

times the risk instead. Well that's a

58:27

huge difference. And then there's ones, there's

58:29

a T&F alpha, there's things that relate

58:32

to detox, there's all kinds of genes

58:34

that interact, and one area of our

58:36

research is to empower apoe4 individuals.

58:38

to say, hey, I might have APOA-4,

58:41

but it's not only about APOA-4, what

58:43

do I have with it and what

58:45

do I not have? So they can

58:48

truly decide what makes sense to help

58:50

optimize their brain health. And I have

58:52

APOA-4-4 patients in my practice, one

58:54

who's 81 years old, who's still in

58:57

the 92nd percentile for cognition. And so

58:59

it doesn't have to be this, oh

59:01

my gosh, I'm going to not have

59:04

my brain when I'm 80. You just

59:06

have to work at it. She works

59:08

at it. So you know what

59:10

it is, and then you block all

59:13

the appropriate pathways. When people get a

59:15

blood test, and they say, oh, you

59:17

have high apolipo protein levels, that's dangerous,

59:20

it's a genetic thing, you should go

59:22

on drugs, what do you think about

59:24

that? So I think there's a

59:26

lot of different apoproteins, and I think

59:29

you're talking a lot about the lipidology

59:31

with cardiac and some of those as

59:33

well. And I think that we're getting

59:36

more knowledge than that. So it's not

59:38

just what your LDL is, whether or

59:40

not you have cardiac risk. It's

59:42

your LDL oxidized, what are the size

59:45

of your particles. And so I think

59:47

that we need to throw out... medicine

59:50

from 30 years ago? Oh yeah, all

59:52

that. And bring it into the current

59:54

century. Yeah, I'm going to look at

59:57

my levels really quick here and

59:59

we'll just talk about that. Because I

1:00:01

don't care about the cholesterol stuff unless

1:00:03

it's oxidized or there's evidence. And small

1:00:06

particles. And it also depends on what

1:00:08

quality your endothelium is in. And so

1:00:10

many other things. There are people

1:00:12

who get more vascular inflammation. There's people

1:00:15

who build up calcium. So again, with

1:00:17

heart disease, there's really like 10 things

1:00:19

I like to know at least. What

1:00:22

are they? I like to know if

1:00:24

somebody has like LP Little A because

1:00:26

it can affect microclotting. There are

1:00:28

gene variants that affect calcification. I think

1:00:31

that's really important because if calcium builds

1:00:33

up in your arteries that's that increases

1:00:35

your risk of abdominal aortic aneurysms but

1:00:38

also premature heart disease. I like to

1:00:40

know some of the couple of inflammatory

1:00:42

pathways that combined with each other

1:00:44

can make you have up to four

1:00:47

or five times the risk of heart

1:00:49

disease. I like to know Compte, actually,

1:00:51

because those people who have the slow

1:00:54

compte that get the high adrenaline, they

1:00:56

need to be a little bit careful

1:00:58

about the super high adrenaline if

1:01:00

they have other cardiac risks because they

1:01:03

have more sudden cardiac death. Those are

1:01:05

some of the ones. There's things that

1:01:07

relate to haptoglobin type, which is important

1:01:10

if you have sugar. Well, there's a

1:01:12

haptoglobin. I know a lot. That's a

1:01:14

new one on me. So haptoglobin

1:01:16

was first popularized. by a cardiologist and

1:01:19

another physician named Baylandonine. And they showed

1:01:21

that if you're this certain haptoglobin type,

1:01:23

2-2, and you have high blood sugar,

1:01:26

it gives you a dramatically higher risk

1:01:28

of heart disease. And the reason I

1:01:30

care about it is, one, keeping

1:01:32

those people's blood sugar is really important,

1:01:35

but vitamin C is super important for

1:01:37

people who have the more detrimental haptoglobin

1:01:39

type. So there's just so many fun

1:01:42

things. And even Apoee can affect cardiac

1:01:44

risk. There's a marker in blood that

1:01:46

just, they call it apolipo protein.

1:01:48

And it's, you want somewhere between like

1:01:51

50, it goes up to like 200.

1:01:53

You're talking about apolipoprotein B? Yeah. So

1:01:55

talk about that in the context of

1:01:58

risk, because there are people out there,

1:02:00

one person in particular I'm thinking of,

1:02:02

who says, you can't extend human

1:02:05

life, but I'm a longevity doctor. And

1:02:07

it's like, if you have that, you

1:02:09

have to go on drugs right away,

1:02:12

go on statins, go on statins. And

1:02:14

it, is that a risk factor? Or

1:02:16

is that a risk factor? Is it

1:02:19

causal or is it just there?

1:02:21

It's a marker for small protein, for

1:02:23

a small LDL. So I think of

1:02:25

our lining of our arteries, it's called

1:02:28

the endothelial lining, and there's a lot

1:02:30

of things that affect making it healthy.

1:02:32

But between the cells, because they're kind

1:02:35

of like pavers on a sidewalk,

1:02:37

there's cracks. And if you have lots

1:02:39

of small particles, especially if they're oxidized,

1:02:41

they can go between the cracks. So

1:02:44

if you have a very high apobe,

1:02:46

that means you've got lots of small

1:02:48

particles. a one cup measuring cup and

1:02:51

you have little teeny pebbles in

1:02:53

it versus marbles you can fit a

1:02:55

lot more pebbles it's more dangerous so

1:02:57

it's a marker that you might pay

1:03:00

more attention to your other cardiac risk

1:03:02

factors if and it's a gene variant

1:03:04

if you have the gene variant that

1:03:07

makes you have the smaller apo

1:03:09

bees and you and again there are

1:03:11

things you can do one of the

1:03:13

things is to keep your endothelial lining

1:03:16

healthy there's different things that you can

1:03:18

do so the cholesterol so the macrophages

1:03:20

don't take up the cholesterol that

1:03:22

have to do with inflammation and to

1:03:25

me it's just one piece of knowledge

1:03:27

I wouldn't have I wouldn't have thought

1:03:29

of that as someone's main cardiac risk

1:03:32

to be honest I wouldn't either and

1:03:34

Paul Saledino and I talked about it

1:03:36

when he was on the show

1:03:38

and and there's one person out there

1:03:41

who's like no you have to go

1:03:43

on stands right away if you have

1:03:45

that and it seems alarmist I think

1:03:48

that the more tools we give patients,

1:03:50

that we give clinicians, that we give

1:03:52

cardiologists, the less they'll focus on

1:03:54

cholesterol. There's a molecule that most people

1:03:57

have never had checked in their blood.

1:03:59

blood that's soluble ST2 and it's kind

1:04:01

of the anti-inflammatory marker for the heart

1:04:04

and I'm much more concerned about the

1:04:06

person who instead of having their anti-inflammatory

1:04:08

cardiac pathways attached to the heart

1:04:10

muscle has it floating that's due to

1:04:13

a gene we look at that I'm

1:04:15

more concerned about that than I am

1:04:18

about cholesterol typically because that's been associated

1:04:20

with 4.9 times the risk of heart

1:04:22

disease and heart failure and you're going

1:04:25

to work on it with inflammation.

1:04:27

So I think it's about, let's take

1:04:29

a personalized approach to human health and

1:04:31

longevity. You said something really important. I

1:04:34

take 150 supplements a day. I've disclosed

1:04:36

a bunch of stuff on myself. I've

1:04:38

had people offer me tens of thousands

1:04:41

of dollars to go into my

1:04:43

supplement. room where I have all the

1:04:45

shelves all stuff I take so they

1:04:47

can copy me. And I'm like, don't.

1:04:50

You'll probably get a headache and disaster

1:04:52

pants. This is carefully designed from my

1:04:54

biology with dozens of longevity doctors and

1:04:57

functional medicine doctors and years of

1:04:59

research. And it seems absurd to recommend

1:05:01

that. So you have to say, well,

1:05:03

what are your goals? What are the

1:05:06

problems you have? Do you want to

1:05:08

live a long time? Do you want

1:05:10

your brain to work better? you come

1:05:13

up with almost like a counterbalance.

1:05:15

It's a dance. So I see people

1:05:17

out there saying, well, here's my 55

1:05:19

ingredients and my longevity thing. And they're

1:05:22

not even targeted at one pathway. I

1:05:24

love multi-formulas that do one thing. But.

1:05:26

What do you think about this? Are

1:05:29

these... So when someone comes into

1:05:31

me on 100 supplements or 50 supplements

1:05:33

or even 25, I say, let's start

1:05:35

with your genomics. Yes. And let's get

1:05:38

a better understanding of you, let's get

1:05:40

an understanding of what things you've noticed

1:05:42

about yourself and your body, what is

1:05:45

in your family and your genomics,

1:05:47

and let's build a protocol starting from

1:05:49

scratch. Not that there aren't going to

1:05:51

be things that you're already on that

1:05:54

we would, but let's at least start

1:05:56

by going, what's the most important. That

1:05:58

way, and again, somebody who has, I

1:06:01

mean, I have some patients that

1:06:03

have, because we do a quite a

1:06:05

bit of brain in our practice, who

1:06:07

have pretty bad genomics for cognitive decline.

1:06:10

And I tell them, if you're in

1:06:12

APOE44 and you're already having some

1:06:14

memory problems, we can help you, but

1:06:16

we're not helping you with three supplements.

1:06:19

You are going to have to do

1:06:21

more with diet lifestyle and supplements.

1:06:23

But I think that depending on

1:06:25

someone's health, being able to prioritize... can

1:06:28

be very beneficial because you are a

1:06:30

very disciplined person. There are a lot

1:06:32

of people who are like, I'm happy

1:06:34

to do seven things, I'm happy to

1:06:37

do 12 things, I'm happy to do

1:06:39

20 things. There are very few that

1:06:41

can do 100, so I feel like genomics

1:06:43

as well as labs and history is

1:06:46

a tool that can help you say,

1:06:48

okay, what if I were only going

1:06:50

to take a certain number of things

1:06:52

and not just supplements? Also, what foods

1:06:54

should I add? I mean, there's definite,

1:06:56

as I mentioned, like, chili peppers are

1:06:58

really great for T&F Alpha, but

1:07:00

for someone who's got all this

1:07:03

oxidated stress pathways with catalase, then

1:07:05

we might be doing more of

1:07:07

the antioxidant foods with spiralingen and

1:07:09

the allergies. For somebody else, with

1:07:12

some of the detox pathways, some

1:07:14

of them you regulate with pomegranate

1:07:16

juice and some you regulate with

1:07:18

vitamin C. I tell people that

1:07:21

genomics can be really helpful as

1:07:23

somebody wants to optimize longevity because

1:07:25

it lets you take your desire

1:07:27

to optimize longevity and make

1:07:30

a more focused protocol. And

1:07:32

then you can use testing. There's

1:07:34

a lot of biomarkers that you

1:07:36

can use to look at your

1:07:38

overall health. You're, you know, whether

1:07:40

you use glycanage or telmer length

1:07:42

or on and on, there's so

1:07:44

many markers. I use a lot

1:07:46

of CNS vitals, which is a

1:07:48

cognition test that also looks at

1:07:50

processing speed, visual memory, verbal memory,

1:07:53

do a baseline, then let me

1:07:55

optimize your brain or work with

1:07:57

a doctor that can use genomics

1:07:59

to opt. your brain and see how

1:08:01

the numbers do. Let's get data. I

1:08:03

love looking at outcomes there. And I

1:08:06

just, I worry that you take a

1:08:08

50 plus ingredient, a blend of whatever.

1:08:10

It's too little of everything. It's too

1:08:12

little of everything. Or, you know, maybe

1:08:14

it's a couple scoops of it. Problem

1:08:17

is, like, oh, you don't handle that

1:08:19

supplement at all. Or this one is

1:08:21

not enough for you. So what I

1:08:23

find is most of the time, people

1:08:26

are getting... not the results expected because

1:08:28

at least one ingredient wasn't right for

1:08:30

them. The personalization is important. You could

1:08:32

do it with genetics, which is your

1:08:34

approach. You could also do it with

1:08:37

metabolomics. What's the difference between genetics and

1:08:39

metabolomics? How do you know what to

1:08:41

use? That's a great question. So one

1:08:43

of the issues with metabolomics is what

1:08:46

it is, is the idea that we're

1:08:48

looking at some genetic expression. So what

1:08:50

in your metabolism. The reason that the

1:08:52

area of weakness for metabolomics is brain

1:08:54

health. And again, I started out doing

1:08:57

my PhD in neuroscience, so I always

1:08:59

am thinking about the brain. Because the

1:09:01

blood brain barrier, I don't think metabolomics

1:09:03

helps as much with things that are

1:09:06

cognitive. Because you can have, like in,

1:09:08

they've shown this in autism studies, you

1:09:10

can have a child that has 45

1:09:12

times the normal amount of T&F alpha

1:09:14

in their cerebral spinal fluid. but their

1:09:17

blood levels might only be minimally high

1:09:19

because something got into their brain and

1:09:21

is inflaming their brain. So I think

1:09:23

that metabolomics has its place and a

1:09:26

lot of people say, oh, it's better

1:09:28

than genomics. Things aren't better or worse.

1:09:30

They have different purposes, but even for

1:09:32

something like osteoprosis, and I consider bone

1:09:34

health part of longevity, you can't get

1:09:37

at everything going on your bones with

1:09:39

your blood. So anything that's from a

1:09:41

blood draw. is kind of a blood

1:09:43

biopsy and there's limits to what it

1:09:46

can help. So it has its place.

1:09:48

I don't use it a lot in

1:09:50

my practice to be honest because I

1:09:52

find genomics more useful. I'm a huge

1:09:54

fan of... more data is better and

1:09:57

let the computer sort it out. I've

1:09:59

had great learnings from metabolomics especially in

1:10:01

combination with my gut bacteria. Yes, gut

1:10:03

bacteria is definitely one where you definitely

1:10:06

need not genomics because you're not talking

1:10:08

about your DNA, although there are genes

1:10:10

that make you more prone to getting

1:10:12

more colonized with yeast and getting more

1:10:14

and having a worse immune system and

1:10:17

your first kind of gut exposure. I

1:10:19

agree that there are definitely areas that

1:10:21

you need other data. Yeah, so just

1:10:23

if you're listening to this and like

1:10:26

I have lots of money and I

1:10:28

really want to live a long time

1:10:30

and I'm into this longevity thing, you

1:10:32

probably need to know what's going on

1:10:34

in your gut, right? That's important. You

1:10:37

need to have, I believe, a metabolomics

1:10:39

report, like a viome sort of thing

1:10:41

to know what's actually going on in

1:10:43

there. And then also you need a

1:10:46

full genomic genomic analysis so that like,

1:10:48

like, my genes are capable of. And

1:10:50

these are things that they're doing. And

1:10:52

if you have all of that data,

1:10:54

now you're as fully equipped as you

1:10:57

possibly could be. And you know, if

1:10:59

there's a weird plant virus in your

1:11:01

gut or something that's tweaking a gene

1:11:03

that you know you have. And it's

1:11:06

more than any brain, even yours, is

1:11:08

going to be able to do. But

1:11:10

you have all the tools that support

1:11:12

your brain. Right. And I think that

1:11:14

using different tools together. The genes that

1:11:17

relate to OCD, some of them also

1:11:19

relate to your ability to fight infections.

1:11:21

And that makes complete sense because infections

1:11:23

can, if you can't accurately fight an

1:11:26

infection, and you then get your gut

1:11:28

microbiome off, that creates inflammation and that

1:11:30

can, because the blood gut barrier affect

1:11:32

the brain. And so you said you

1:11:34

need your, you know, you need your,

1:11:37

your genome. I say we need. an

1:11:39

informed genomic tool. Yeah, you need an

1:11:41

analysis of your gene from just a

1:11:43

bunch of numbers won't do anything. Right,

1:11:46

we need something like, you know, and

1:11:48

one of the things with Intallix DNA

1:11:50

that I think helps our patients and

1:11:52

doctors get better outcomes as you were

1:11:54

talking about, like the person who gets

1:11:57

the supplement, and they're like, oh, I

1:11:59

need alphilippo acid, this has it, and

1:12:01

it has 20 milligrams. We actually have

1:12:03

information about what doses were used in

1:12:06

the different studies, so that if you're

1:12:08

looking at a brain report, or a

1:12:10

blood sugar report, what dose of Burberine

1:12:12

was used to improve blood sugars? Because

1:12:14

again, you can't just take a little

1:12:17

bit of something and think it's going

1:12:19

to have the same effect as two

1:12:21

grams. It's fun you mention OCD and

1:12:23

infection. When I was a kid, I

1:12:25

had tons of strep throat and sinus

1:12:28

infections because I lived in a base

1:12:30

in a toxic mold and that's a

1:12:32

symptom of toxic mold. But then when

1:12:34

you have a lot of strep, it

1:12:37

makes proteins that create antibodies and antibodies

1:12:39

to those proteins also go after parts

1:12:41

of the brain, which causes OCD and

1:12:43

ODD, which I had. And if you

1:12:45

guys don't know what ODDD is. Think

1:12:48

of the Rage Against the Machine song.

1:12:50

If you, I wouldn't do what you

1:12:52

told me. It just makes it normal

1:12:54

to do that. And yeah, I was

1:12:57

able to turn off the information. I

1:12:59

like unpacked all that. But my God,

1:13:01

there's a lot of, a lot of,

1:13:03

Dave was a bad child in my

1:13:05

seventh grade report. And thank God my

1:13:08

brain worked well enough to get good

1:13:10

enough grades. Because otherwise I'd probably be

1:13:12

in. prison or something. And what you're

1:13:14

talking about is the pants, which is

1:13:17

when you get psychiatric symptoms from neuroinclamation

1:13:19

from different infections, and we used to

1:13:21

think it was just strep, pandas. But

1:13:23

now we know that it's both things

1:13:25

like mold, yeast, lime, strep, all kinds

1:13:28

of infections. And environmental bacteria from water

1:13:30

damage buildings, right? Absolutely. But one of

1:13:32

the fun things about that people who

1:13:34

get kind of the OCD from infections

1:13:37

is they tend to either make too

1:13:39

much T&F alpha, which affects the blood

1:13:41

brain barrier and the blood gut barrier,

1:13:43

or they have problems with a pathway

1:13:45

that's called their manospining lexin pathway, which

1:13:48

is the first line of defense against,

1:13:50

they might have a normal... level if

1:13:52

you were to check their blood, but

1:13:54

it might be that the gene protein

1:13:57

is misformed and doesn't work, and that's

1:13:59

your first line of defense against yeast

1:14:01

and lots of bacteria and mold. And

1:14:03

so the people who get the kind

1:14:05

of OCD from mold, they often have

1:14:08

problems with their immune system. So this

1:14:10

is kind of why I get, you

1:14:12

know, I was a physician, a family

1:14:14

physician, integrated physician for 30 years, and

1:14:17

now I... love training physicians across the

1:14:19

world and leading the research team because

1:14:21

it's so much fun for me to

1:14:23

go hear these different cases and go,

1:14:25

oh, this makes complete sense, this makes

1:14:28

complete sense, let's publish this, let's talk

1:14:30

about this, because we're making sense of

1:14:32

why did this woman have such severe

1:14:34

PMDD, why did this person have such

1:14:37

severe depression, even starting as a little

1:14:39

kid, or this person have ADHD that

1:14:41

didn't respond to stimulants, well, because their

1:14:43

ADHD wasn't caused. by low norphinephrine, it

1:14:45

was caused by more of a connective

1:14:48

pathway. Wow. One of the things that

1:14:50

is, just as a patient that's coolest

1:14:52

about this, is that if you're listening

1:14:54

to the show, like something's wrong with

1:14:57

it, no, you just have a harder

1:14:59

problem. And it's so validating to see

1:15:01

your pathways and to see, oh, it's

1:15:03

no, but I'm not trying hard enough.

1:15:05

And this was my thing. I'm like

1:15:08

I'm feeling out of warden business school

1:15:10

and like no matter what I do.

1:15:12

No matter what I do. No matter

1:15:14

what I do. I do. I do.

1:15:17

I do. And all these things, and

1:15:19

I remember when I got Dr. Daniel

1:15:21

Amund's brain scan, it's like, you have

1:15:23

holes in your brain, not actual holes,

1:15:25

but areas of zero metabolic activity as

1:15:28

a result of chemical exposure from mold.

1:15:30

I'm like, oh God, I have a

1:15:32

hardware problem. And if there's things that

1:15:34

have tormented you in your life, and

1:15:37

then you get your genomics report, like,

1:15:39

oh my God, I just needed this

1:15:41

one supplement. And like you said, in

1:15:43

four days, some people like, I got

1:15:45

my life back. Absolutely, and not everybody

1:15:48

do we get well in four days.

1:15:50

Just want to put that disclaimer. But

1:15:52

actually our co-founder and CEO, one of

1:15:54

the reasons that she was so dedicated

1:15:57

to building Intellic's DNA was so So

1:15:59

many people, including she had been told

1:16:01

she's more of an Ellers-Danlos type person

1:16:03

and people get labeled, oh you're just

1:16:05

complaining about pain, you're just complaining about

1:16:08

this, you've got fibromyalgia, and she was

1:16:10

like we have to stop the labeling

1:16:12

in medicine when people go to a

1:16:14

physician and they get labeled or the

1:16:17

person who's depressed, we'll just get over

1:16:19

it. Well if we can instead look

1:16:21

at the root cause or blaming a

1:16:23

child or a parent or a parent

1:16:25

because the child has ADHD, look at

1:16:28

the root cause and stop blaming people

1:16:30

and labeling and instead say we now

1:16:32

are in a time when we can

1:16:34

have the technology to understand and address

1:16:37

what's going on. And there's an epidemic

1:16:39

of physicians who don't have enough time

1:16:41

to deal with patients, so they just

1:16:43

make a really quick assessment. I remember

1:16:45

very well when I went into a

1:16:48

psychiatrist when I'm failing out of school.

1:16:50

And he looks at me, he looks

1:16:52

at me, you can tell what this

1:16:54

skeptical thing on the company, these supplements,

1:16:57

things don't work, but I'm feeling out

1:16:59

of class, so it's just not working.

1:17:01

And he's like, tech bro wants Adderall,

1:17:03

classical Palo Alto thing. And like, I

1:17:05

didn't even want Adderall, I wanted Modafino,

1:17:08

because I'd done my research. And it

1:17:10

was an awful label used for ADHD

1:17:12

back then, and it's one of the

1:17:14

most potent pharmaceuticalicals for cognitive enhancement that

1:17:17

isn't addictive like Adderall is. When I

1:17:19

came back and he saw my data,

1:17:21

which wasn't even genomics back then, we

1:17:23

didn't have the ability to do that,

1:17:25

he was like, inside your brain is

1:17:28

total chaos. I don't know how you're

1:17:30

standing here in front of me, you

1:17:32

have the best camouflage I've ever seen.

1:17:34

And I was like, I just relaxed,

1:17:37

I think God, someone believes me for

1:17:39

like the first time. And with a

1:17:41

genomics report like this, it's like, oh,

1:17:43

you're not crazy. There's nothing wrong with

1:17:45

you. It's just you're riding around in

1:17:48

a meat suit with dysfunctions. You have

1:17:50

a flat tire in your car. Well,

1:17:52

if you change your oil, it's not

1:17:54

going to fix it. But you put

1:17:57

air in the tire, you might like

1:17:59

it. And like, we're almost there for

1:18:01

humans, aren't we? Yeah. like now is

1:18:03

leaps and bounds beyond what it was

1:18:05

10 years ago, and I think it's

1:18:08

gonna continue to improve. And it's a

1:18:10

really exciting time to be a human

1:18:12

because you can, yeah, I don't yet

1:18:14

believe that we're gonna get to, for

1:18:17

most people, to 130, 140, but I

1:18:19

think what we can do is make

1:18:21

our years on this planet much healthier

1:18:23

so that we. are having a brain

1:18:25

that works. We're having the energy to

1:18:28

exercise and enjoy life and feel vital.

1:18:30

And so, you know, feel calm. And

1:18:32

so I think that it's a really

1:18:34

exciting time to be a human. It

1:18:37

is. And you said one important thing

1:18:39

for most people. And if we can

1:18:41

take one person... and we can do

1:18:43

10 years better than our current best.

1:18:45

We've meaningfully extended human life. And if

1:18:48

everyone else is working towards the goal

1:18:50

of extending their life as a side

1:18:52

effect, they just have a great health

1:18:54

span. I'm like, that's great. It kind

1:18:57

of makes me sad though, and people

1:18:59

say, our goal is health span. I'm

1:19:01

like. I want health span for twice

1:19:03

as long, thank you very much, and

1:19:05

I'll just take whatever I can get.

1:19:08

Right. Right. So it's just a difference

1:19:10

of framing of the longevity movement. Are

1:19:12

you on the health span until you

1:19:14

die at the average age, or are

1:19:17

you on the health span for extended

1:19:19

time? Right. And I think that you're

1:19:21

absolutely right. I think that if we

1:19:23

get the average lifespan extended... Five years

1:19:25

seven years ten years. That's huge long

1:19:28

as we take care of our world

1:19:30

along with it That's a side effect

1:19:32

of believing you're going to live longer

1:19:34

than you're supposed to you You're not

1:19:37

going to throw the plastic in the

1:19:39

ocean because you know you'll eat it

1:19:41

and you're not going to drink things

1:19:43

with plastic because they're you know hormone

1:19:45

disruptors and you understand how they affect

1:19:48

your they're big effects on epigenetics if

1:19:50

I am successful living to at least

1:19:52

180 and I eight unlimited microplastics. I

1:19:54

would be made out of Tupperware by

1:19:57

the time I'm 150. I don't want

1:19:59

that. Sharon, it's been a great pleasure.

1:20:01

Thanks for your just incredibly complex and

1:20:03

interesting work both. as a clinician, as

1:20:05

a researcher, I'm really excited to see

1:20:08

how genetics went from, you know, almost

1:20:10

useless at the very beginning of this

1:20:12

to something that has meaningful predictive power

1:20:14

for what you can do today. So

1:20:17

thank you. Thanks for having me. And

1:20:19

if there are any of your listeners

1:20:21

that want an Intellic's DNA report, they

1:20:23

can go to our website and you

1:20:25

can actually, we put in a special

1:20:28

thing for you guys where they can

1:20:30

click that what they're looking for is

1:20:32

a human upgrade consults, a longevity consult,

1:20:34

and that way they will find clinicians

1:20:37

that feel comfortable working with biohackers on

1:20:39

the topic of longevity. and doing an

1:20:41

initial one-hour consult to get them going

1:20:43

and then giving you the report and

1:20:45

the tools you need to continue to

1:20:48

explore and if you want to do

1:20:50

more you can but the one thing

1:20:52

is it does two L's and two

1:20:54

X's, I-N-T-E-L-L-X DNA because it's an intelligent

1:20:57

approach to DNA and my co-founder and

1:20:59

myself are both women so that's the

1:21:01

two X's. Awesome. Thanks for having me.

1:21:03

See you next time on the human

1:21:05

upgrade podcast. The

1:21:10

human upgrade, formerly bulletproof radio, was created and

1:21:12

is hosted by Dave Aspery. The information contained

1:21:14

in this podcast is provided for informational purposes

1:21:17

only and is not intended for the purposes

1:21:19

of diagnosing, treating, curing, or preventing any disease.

1:21:21

Before using any products referenced on the podcast,

1:21:23

consult with your health care provider, carefully read

1:21:25

all labels and heed all directions and cautions

1:21:28

that accompany the products. Information found or received

1:21:30

through the podcast should not be used in

1:21:32

place of a consultation or advice from a

1:21:34

health care provider. If you suspect you have

1:21:36

a medical problem or should you have any

1:21:39

health care questions, please promptly call or see

1:21:41

your health care provider. This podcast, including Dave

1:21:43

Asbury and the producers, disclaim responsibility for any

1:21:45

possible adverse effects from the use of information

1:21:47

contained herein. Opinions of guests are their own

1:21:50

and this podcast does not endorse or accept

1:21:52

responsibility for statements made by endorsements

1:21:54

and advertisements for products

1:21:56

or services. Individuals on

1:21:59

this podcast may have

1:22:01

a direct or indirect

1:22:03

financial interest in products

1:22:05

or services referred to in

1:22:07

products or services referred podcast is

1:22:10

owned by owned by Bulletproof Media.