0:07

Hey there, this is Ari. Welcome

0:09

back to the Energy Blueprint Podcast.

0:11

With me today is one of

0:13

the absolute creme de la creme

0:16

of gut health and microbiome experts

0:18

in the world. This is someone

0:20

who is my go-to expert for

0:22

all things related to the gut

0:24

and the microbiome. I've

0:26

had the pleasure of taking one of his

0:29

courses. He's a professor at multiple

0:31

universities who teaches on gut health and

0:33

the microbiome. He's also

0:35

the head of research at

0:37

probioticadvisor.com, which is basically an

0:39

encyclopedic reference and kind

0:41

of search engine where you can put

0:43

in either specific

0:46

strains of probiotics and find all

0:48

the research on what the scientific

0:51

evidence has shown those strains to be beneficial

0:54

for. It's a reverse where

0:56

you put in the specific symptom or

0:58

condition and it will immediately

1:00

pump out a whole list

1:02

of all the specific studies showing

1:04

what strains of specific bacteria,

1:07

probiotics have been shown to

1:09

be beneficial in the context

1:11

of treating that symptom or condition.

1:14

This is an extremely

1:16

valuable resource, particularly for

1:18

practitioners and not enough

1:21

practitioners and clinicians actually know about

1:24

this. Part of what

1:26

I want to do this podcast for is just to

1:28

help people know this literature more because

1:30

having taken a course with Dr.

1:33

Harlack, it's clear to me that

1:35

there are levels of knowledge around

1:37

the microbiome and around things like

1:40

probiotics. He

1:42

is just levels above most people in

1:44

this area. His

1:46

passion for gastrointestinal health and

1:49

the microbiome and probiotics

1:51

was ignited his final year of undergraduate

1:53

training in 1999. He

1:56

went on to do his honors, first

1:58

class and PhD. degrees in

2:01

the areas of gastrointestinal microbiota,

2:04

irritable bowel syndrome, and the clinical

2:06

applications of pre and probiotics. He's

2:08

written extensively in the medical literature

2:10

on these topics in

2:13

scientific papers as well as including

2:16

20 clinical textbook chapters. Again,

2:18

in my opinion, the

2:22

top 0.0001% of gut health

2:25

experts out there, absolutely brilliant at what

2:27

he does and my personal

2:30

go-to expert for whenever I have

2:32

questions about anything related to gut

2:34

health and the microbiome. So with

2:36

no further ado, enjoy this wonderful

2:38

podcast with the brilliant Dr. Jason

2:41

Harlack. Dr. Harlack, welcome.

2:43

It's such a pleasure to have you.

2:45

Thank you for taking the time to

2:47

do this. I think it's very important

2:49

for people to hear from you and

2:51

to understand this piece of the puzzle

2:53

of the importance of the gut microbiome

2:55

and its relationship really to

2:57

everything in the body as more and

3:00

more research is confirming. But this

3:02

piece of that story around the connection between

3:04

the gut and mitochondria in particular is what

3:06

we're going to be focused on here. So

3:08

thank you so much for doing this. You're

3:11

very welcome. It's lovely to be here and always great to

3:13

chat to you too. Alright, and anytime

3:16

I get a chance to talk to the wonders

3:18

of microbiome, I will take

3:20

it as someone who's an avid fan

3:23

in love. I've gotten a gut microbiome.

3:25

I'm just really thankful I chose it

3:27

as a research showing for my PhD

3:29

back in the year 2000. I

3:32

don't know what I'll be doing now. I'm not sure if

3:35

I'm doing this. So

3:39

speaking from personal experience, it's not often that

3:41

I can say for one of the speakers

3:43

or people that I'm interviewing that I've actually

3:45

taken a lengthy course with. But

3:48

in this case, it's true. I've taken

3:50

one of your courses on gut health

3:52

in the microbiome and

3:54

I've interviewed many, many,

3:56

many gut health experts over the years

3:58

and I can say for everybody

4:00

listening that Dr. Harlach is la creme

4:03

de la creme. He is really among

4:05

the best of the best microbiome experts

4:07

in the world. So what

4:10

I want to ask of you, given

4:12

that, is for you to give people

4:14

a picture of

4:16

the importance of gut health and

4:18

the microbiome in

4:21

overall health. Like, how would you go

4:23

about explaining that from sort of like,

4:25

what's your paradigm for understanding the role

4:27

of the gut, the microbiome and human

4:29

health? Yeah, I

4:31

mean, I think... I'm

4:34

lucky enough to have been doing this for

4:36

20 some years. It's been interesting seeing the evolution

4:38

and the amount of research that has bloomed

4:40

over that time too. And that you go back

4:42

to when I started writing my thesis on

4:44

how wonderful the microbiome was, because I

4:46

was essentially a child through my thesis,

4:49

was looking at, OK, what

4:51

do we know at that time? And we knew that

4:53

the... Even from research in

4:55

the 1950s and 60s was telling us that it was

4:57

really important for immune system functionality, that if we gave

5:00

mice or rats a megadose of antibiotics

5:02

and then locked them in sterile cages

5:04

and gave them sterile food, essentially

5:07

their immune system would dip

5:09

dramatically. Their thymus gland would shrink, their

5:12

spleen would shrink. Their ability of their

5:14

white blood cells to actually attack invaders

5:16

would decrease dramatically. The number of...

5:20

Cybacteri G8 producing cells would decrease by

5:22

90%. This is

5:24

actually huge. And then they could

5:26

essentially expose them to poo. And

5:29

also all these... The thymus

5:31

gland would grow again and the spleen would grow

5:33

and the immune system would start functioning normally again.

5:35

So some of that aspect of it was known,

5:37

but not really that widely talked about outside, probably

5:39

microbiota research. Yes, it's important

5:42

for gut diseases, and that was

5:44

what we talked about for a while, like how altered

5:46

thorac and regionarval bowel syndrome were in flamper bowel disease.

5:49

Those things have been known for a fair while too. Its

5:52

ability to involve with digestive processes, to make vitamin

5:54

K, make some B vitamins for us, some of

5:56

those things were known at that time too. And

5:59

its capacity to... The

6:01

ecosystem would protect us against foreign invaders.

6:03

So if we have exposed a salmonella

6:05

or giardia, early research found that

6:08

if we – let's

6:10

say if we gave a course of antibiotics to

6:12

some people and then we could give them

6:14

salmonella or giardia, and they actually did these

6:17

studies. Typically an imprisoned inmate, I would point

6:19

out, probably without their consent, but

6:21

they did these studies and showed that, hey, they

6:24

could give one-tenth the amount of invading pathogen when

6:26

there's an eosidant disruption and get these people sick.

6:28

And they could take it for longer. So we knew it

6:31

was important for that aspect too, but what's been amazing to

6:33

see is all this stuff that's come out around. Actually,

6:37

microbiome and how

6:39

our nervous system is working, how our brain is functioning, how

6:42

our mitochondria work, how

6:45

we age, our level of inflammation,

6:47

our body. And I think that it's been

6:49

that shift from here are some microbes that

6:51

probably aren't that important in the gut that

6:54

we can just kill with antibiotics if they

6:56

don't matter, to actually know these are important.

6:58

Maybe we should start thinking of these microbes.

7:01

Like a microorgan, like we started back in the early

7:03

2000s, there were people talking, this is the microorgan. We

7:05

have to start taking seriously. It's really

7:08

important. We can't just be killing

7:10

it willy-nilly with different interventions. And so I think it

7:12

has consequences, and those consequences are much greater than that.

7:16

But I think even what's shifted in the

7:18

last 20 years is that that conception's gone

7:20

from here's an important organ in the body,

7:22

like the liver, to actually, you are a

7:25

being that's made out of microbe cells and

7:27

non-microbe cells. And we are still

7:29

debating what the ratio of that might be. We've

7:31

got 100 trillion bacteria in our guts, and

7:34

some people would argue that we're 90% bacteria.

7:38

Some people would argue we're two-thirds bacteria, one-third, not bacteria,

7:40

but either way, we are mostly bacteria.

7:43

And that what

7:46

they do for us is super important and

7:48

integral to what makes us human and how

7:50

everything else works. And I think what you

7:52

alluded to before is, it's correct that every

7:54

single year that comes out, we're going, oh,

7:57

this is connected to the microbe. This

8:00

is connecting the market bottom. That is what's been

8:02

the most lasting last 20 years. And you go

8:04

back to the one people paper published in 2006.

8:08

It was the first one that showed that kind of what

8:11

we could do, we could essentially we could pass on obesity.

8:13

You know, amazing study

8:15

because they essentially took poo

8:17

from obese rats and gave it to these little thin

8:19

rats. And they

8:21

were able, they essentially went obese despite no

8:24

change in caloric input or caloric output. They

8:26

weren't exercising less. They weren't eating more. Essentially,

8:29

the change in the microbiota is all it

8:31

took to induce substantial obesity in these animals.

8:33

And I think that was the paper that

8:35

really shifted people's brains. Like, oh my God,

8:38

it's not just gut. It's actually, we can

8:40

influence things like that. Who

8:42

knows what that was? We can influence anything really. And I think

8:44

that's what's coming out of it too. There's now

8:46

research showing that high blood pressure, we can take

8:48

in a poo from people with high blood pressure

8:50

and give it to rats. And

8:53

they will develop high blood pressure. And firstly, we can take,

8:55

fecal transplant wise, we can take poo from people with

8:58

normal blood pressure, give people high blood pressure, and their

9:00

blood pressure will normalize for a period of time. You

9:02

know, and you never would have thought of high blood

9:04

pressure being associated with the gut market by the competition.

9:06

It is. As

9:10

well as things like depression

9:13

and anxiety and

9:15

obesity and time-to-dibedies, I can number

9:17

different conditions now. And

9:20

more than that, too, eating the corporate heart

9:22

disease has a cancer.

9:28

And other pre-cancer conditions often have a

9:31

microbiota component, too. And even

9:33

more fascinating, I think, in some respects,

9:36

is there's now research showing that people

9:38

who have certain eating conditions will respond

9:40

differently to cancer, like treatments, like chemotherapy

9:42

or radiotherapy. If you have a certain

9:44

microbiota feature, you have a better, much better outcome. And

9:47

it's only been the last 12 months that

9:49

I've actually started working with cancer patients to

9:51

optimize the microbiota to get the best outcome

9:53

for their conventional cancer treatments. And again, that

9:55

would not have been something that was on

9:57

the inverse radar in even five or ten years.

10:00

So that aspect has been absolutely amazing to

10:02

see. I

10:05

have a broad question for you. I

10:07

spoke with another gut specialist,

10:10

friend of mine, Dr.

10:12

Vincent Pedre. I don't know if you're familiar with

10:14

his work. He just came out with a new

10:16

book called, I think, The Gut Smart Protocol. And

10:21

several months ago, I think

10:23

for the process of writing the book, he traveled to

10:26

Tanzania, to Africa, to

10:29

see the Hadza

10:32

tribe. And they did

10:34

some microbiome testing of some

10:36

of the members of the tribe there. And

10:38

they found some interesting and surprising results. I

10:40

know one of the things that's sort of

10:42

previously known from those kinds of studies was

10:45

enormous amounts of diversity of microbes,

10:48

along with many species that are considered

10:51

pathogenic. But in that context,

10:54

don't seem to cause any problems. But

10:57

he also said, and I

10:59

believe I'm getting this right, I

11:02

think he said that there was almost no

11:04

Bifidobacteria, or maybe actually no

11:07

presence of Bifidobacteria in the microbiomes

11:09

of that population. Have

11:12

you heard anything like that? Does that make any

11:14

sense to you? And the reason I bring this

11:16

up is to ask the question, on

11:24

a scale of 1 to 10, what

11:28

do you think is our overall

11:30

understanding of the microbiome? How

11:33

completely do you think we understand this?

11:35

Maybe as a bit of context, I think there's a

11:37

famous quote from 1920 or 1930, somebody who

11:41

was a clerk in the US Patent Office,

11:45

who pronounced in 1930, all things that can be invented have

11:52

already been invented. We're done. We've

11:54

figured everything out. There

11:56

will be no more inventions from here. We

11:58

understand everything we've invented. did all possible things

12:01

and kind of understanding the role of human

12:03

hubris. Do you think we're in

12:06

the infancy in the adolescents and the teenage

12:08

years of understanding the microbiome or do you

12:10

think we've got it all

12:12

figured out? Where would you sort of grade our current

12:14

understanding? Definitely not all figured out,

12:17

no. I don't think

12:19

we're in infancy either. I think probably adolescence, I

12:22

think might be the better way of describing it.

12:24

And I think it also depends when you come

12:26

into this too, because I will hear people that

12:28

– maybe new commerce is the wrong term, but

12:30

people that have nothing to the microbiome into a

12:32

couple of years ago, and they're like, oh, I

12:34

haven't found the microbiome. I want to start looking

12:36

at it. And then you see

12:39

those people often go, oh, we're in infancy. We

12:41

don't know anything yet. And it's like, well, for

12:43

them it's true. They don't, because they only spent

12:45

a couple of years looking a bit at browsing

12:47

at the edges. But I would say that

12:49

people that have spent 20, 30-plus years looking at the

12:52

stuff, we'd go, no, actually we know

12:54

a fair bit, and we're always learning more.

12:56

There's certainly enough here to actually implant the change of

12:58

those lives. And I think that's probably the most painful

13:00

point, because there'll be other – some of those people

13:02

who are browsing the slides and this is all news,

13:05

and we're like, oh, we don't know enough. We can't

13:07

change it. I hope you wouldn't do anything yet with

13:09

the information we've got. And I want the people are

13:12

missing out on optimal health and

13:14

continuing with disease states for thinking like that to be

13:16

huge, because as

13:19

a clinician too, I mean, I'm a research scientist.

13:21

I'm a clinician educator. I mean, I actually have

13:23

a chance to work with patients and implement things

13:25

that we come up with in research. And, okay,

13:27

we're discussing around how we can encourage – well,

13:32

let's say P-ray production through the

13:34

implementation of something like Partridge-Weehad-July's-Gore-Gum, reading

13:37

that in 2015. I came across

13:39

some research around that and said, okay, we'll start

13:41

drawing this thing on patients, and you start seeing

13:43

it works. You change someone's

13:45

microbiome composition, and you can

13:47

change almost everything. It's not

13:50

always super

13:52

quick, and it's not always like

13:54

this straightforward line of here to there. It

13:57

can be a bumpy journey, but I'm just always amazed at how

13:59

much you're doing. which we can change

14:01

from energy levels to carbon

14:03

capacity to disease state that

14:06

Crohn's disease are also kaleidos,

14:08

which associate with blood and

14:10

diarrhea and mucus, like quite a level

14:12

of information about here we can change

14:15

the micro-biotic composition. And boom,

14:17

that stops. And yeah,

14:20

and I work with, I think I just see it work on

14:22

a weekly basis for patients that

14:25

mark the modification and optimization changes

14:27

lives and changes the process of

14:29

those so many different disease states. So I

14:31

can't understand or even think properly

14:33

seriously of people who say we can't do

14:35

anything yet, we don't know enough because it's like,

14:37

yeah, we do. Does it mean that

14:39

what I do 15 years ago is what

14:41

I do now? No, because

14:44

we're always learning and we should be learning and

14:46

changing things and evolving as the research evolves and

14:48

our clinical experience evolves too, is we get better

14:50

at doing what we're doing and modifying things. We

14:52

have better tools now to assist the micro-biotic than

14:54

we did before. But I

14:56

mean, going back to the bifidobacterium

14:59

one, you're right, there were some other research scientists

15:01

years ago showing that the adult HADSA don't

15:03

seem to have bifidobacteria. And equally enough, it's still

15:05

in the babies, the ones who are breastfed

15:07

do have bifidobacterium. So it's obviously there in the

15:09

lower mounds, so I think it can't get

15:11

passed on to the next generation. It

15:14

just doesn't seem as though the diet of the

15:16

HADSA, even though it is immensely

15:18

rich in fiber, it's like 150 different

15:21

grams of fiber per day on

15:23

average, I believe. It's

15:26

pretty good at nurturing bifidobacteria, but it does

15:28

nurture a hell of a lot of different

15:30

bacterial species, more than what we have, a

15:33

lot more. And it might be that

15:36

there's just so much more competition. More

15:39

plant compounds in that

15:41

gut, so it gets split over water and things.

15:44

And for every reason, they've got your donut. But they

15:46

are there in the breastfed infants, so we know

15:48

that they are still playing that key role in

15:50

that time point in which

15:52

the arguably the immune system is being trained

15:54

and have to function properly is in that early

15:56

window and having live bifidobacterium is immensely important

15:58

at that time point. that time window.

16:01

And there's still I do think in Western

16:03

populations, it is immensely important microbe to have

16:06

and in a more off the level and

16:08

people who can be very clear, you bump

16:10

up the factory and then a bunch of

16:12

things to follow the place health wise for

16:14

them. But it may not be the case

16:16

for heads up. That

16:18

is a key integral component of the adult

16:20

ecosystem. Although I would say that if you

16:22

started giving those kids formula and breast milk

16:25

and you didn't feed the bacteria, that it's

16:27

going to be a lot of consequences, right?

16:29

To have that population disease

16:31

states that they develop as a consequence. And

16:33

just to clarify for the listener, the reason

16:36

that I ask this question

16:38

is because we have so much sort

16:40

of modern scientific literature that's emphasizing

16:42

the importance of Bifidobacteria species in

16:45

the microbiome. And then we went

16:47

out and found, you know, this population of

16:49

humans that has very

16:52

healthy guts, and doesn't

16:54

have most or maybe you

16:56

could say even all are close to

16:58

all of the gut problems

17:00

that are typical of Western populations. And

17:02

yet they don't have a

17:05

predominance of this Bifidobacteria species that are that

17:07

are very emphasized in the literature as being

17:09

important. So kind of gets at this question

17:11

of, well, how much how much do we

17:13

really know? Are we, you

17:15

know, you mentioned breast formula there. When

17:19

my wife was born in the in

17:21

the Chile in Chile in the 1970s,

17:23

all the doctors at that time were

17:25

telling mothers, new mothers, you

17:28

know, don't don't breastfeed your your

17:30

infants, because, you know, we

17:32

were, you know, we've, through

17:35

our science, we've got it all figured out.

17:37

And according to the

17:39

science, you know, we've perfected what babies

17:42

really need for nutrition. And our,

17:44

our very sciencey formula, baby

17:47

formula is much healthier and much better for

17:49

your baby than breastfeeding them, which is very

17:51

primitive and, you know, and that sort of

17:53

thing. And of course, we know now

17:55

that this was very, very

17:58

much based on on hubris. hubris and

18:00

ignorance and that we're very smarter

18:05

than nature most of the time I would say.

18:08

I concur. Yeah. Yeah.

18:10

And that wasn't just Chile. I grew up in 1970s

18:12

in Canada and the doctors were saying

18:14

the same thing so I was never given any

18:17

breath for that reason too. It was like I

18:19

was born with so much bitter. Right. No. Okay

18:21

so here's another dimension to this question

18:24

that I think is important. After

18:28

taking your course out of

18:30

curiosity I decided to do my own microbiome

18:32

testing and I've shared the results

18:35

with you and what was

18:37

interesting is because

18:40

I know that not

18:42

all tests are that

18:45

accurate or valid or

18:47

reproducible. Yeah. The practitioner was

18:49

ordering the test for me said you know

18:51

let's do this test. This is the test I like.

18:54

I said okay fine but I also want to order

18:56

this other one because I want to cross-check it so

18:58

we can validate whatever things show

19:00

up. I want to validate with another test with

19:02

a different technology to see if it's also showing

19:04

the same pattern. And

19:07

as you know those two tests

19:09

produce very different results and

19:12

so then you said hey based on this

19:14

we can't really draw firm conclusions. Let's do

19:16

another test, a test that you really like

19:19

and we did that test and then we

19:21

had now three microbiome tests and

19:24

there were still some patterns that were

19:26

hard to discern and you know

19:28

certain things that were you know

19:31

in one test I'm super high on butyrate, another

19:33

test I'm very low, another test says I'm very

19:35

high in bifidobacteria, another test is very low.

19:37

I mean there were things that were that were

19:39

very off. So

19:41

again speaking to this question of

19:44

kind of whether we're in the

19:46

the infancy or the adolescence or the adult

19:48

years of our understanding of the microbiome, looking

19:51

at this dimension of microbiome testing

19:54

and now all the different testing technologies

19:56

that are out there and things like

19:58

for example biome, u-biome and and biome

20:00

where they're saying, we've got this, the

20:03

microbiome holds the future to understanding your

20:05

risk of various diseases and

20:08

they'll test your microbiome and say, I've seen the

20:10

results of some of these things that they give

20:12

to people and they say, based

20:14

on your microbiome, you shouldn't eat

20:16

broccoli and you should,

20:18

like literally you shouldn't eat broccoli. Yeah.

20:22

And you should eat these foods and these foods and not

20:24

beat this food and this food and that food. And

20:27

avocados and broccoli are foods that

20:29

you should avoid, for example. Okay,

20:35

I won't give any further context, but what

20:37

do you think of this realm of testing

20:39

and how much, a

20:42

lot of it appears very sciency. What

20:44

should people know about this realm of microbiome

20:47

testing? I would say

20:49

that some of those specifics around diet, I

20:51

can't imagine they're all that super evidence-based. Yeah,

20:54

as someone who's been in the field for

20:56

ages and I look for microbiome food in

20:58

trackers all the time because we're changing microbiomes

21:00

through dietary needs. I mean, technically, to do

21:02

so that getting into specifics like that, I

21:04

think is beyond where we're

21:06

currently at. And I think they're probably just using computer

21:09

algorithms to help postulate

21:12

things based on some known

21:14

biochemical pathways of bacterial species. Because there

21:16

are tests which one of them uses

21:18

like shotgun metagenomic sequencing, which is arguably

21:20

the best way of assessing the microbiota

21:22

accomplishments in its entirety. We can look

21:25

at all the different DNA that's there

21:27

and we can look at it with

21:29

bacteria, we can look at protozoa, we

21:31

can look at the fungi. I

21:33

still think the tests are a little bit limited in

21:35

their fungal libraries. I don't know if you can tell

21:37

us too much about that, but eventually that'll catch up

21:40

on board. There's some viruses and

21:42

they can look at genetic pathways of those bacteria in

21:44

the gut. And I think there's

21:47

a lot of useful information that comes from that.

21:49

And I think they're very useful tests, but I

21:51

do think that they might be extrapolating, in

21:53

my opinion, too much. Those

21:55

pathways to lead to advice like that. I

21:57

do think that it can be helpful. guide

22:00

practice and I think

22:02

we can get a...

22:05

listen it's

22:07

a good question around the test yeah

22:09

and I think the challenge here is

22:11

like what's real almost

22:13

is what it comes down to because we used

22:15

to think culturing where we would take two samples

22:17

out and we'd grow them in peachy dishes which

22:20

gave us a true representation of what was there. Does

22:23

it? You know because we tend to

22:25

what we grow it on like if we grow that

22:27

kind of that back tree on one type of media

22:29

it grows really well and grows really politically. Another

22:32

media it won't grow at all. Another media

22:34

will grow a little bit and it's like have

22:36

we chosen the right media to accurately represent what's

22:39

there? We don't know. You know that's just what

22:41

we've done and we're making assumptions around that and

22:43

then now we're looking at that the proportion of

22:45

DNA which I think is a much better idea

22:48

around context going okay

22:50

well how much bacterial DNA is there? What

22:52

does it belong to? And we get proportional

22:54

representation of what's there so okay

22:56

well it's 2% bifidobacterium

23:00

20% bacteroides and we can piece it together

23:02

that way and to me that I

23:04

think is a much better idea or gives

23:07

a much better accurate representation of what the

23:09

organism actually is like and then we have

23:11

tests that are like PCR based which are

23:13

also using DNA bits so I think more

23:16

much more accurate than the old culturing type

23:18

approach but and

23:20

it's been a nice to try to quantify things too

23:22

and I just know clinically that I've just seen results

23:25

which has just seen a bit bizarre in some

23:27

of those those keep it quite a

23:29

PCR microbiome tests so

23:32

and they're not used that much in

23:34

the research world. I mean really the

23:36

vast majority of studies that are trying

23:38

to define the microbiome, expand our knowledge

23:40

and understanding of the microbiome what it

23:42

does is using unshowed kind of photogenic

23:45

sequencing or 6-TENUS or RNA which is

23:47

also DNA based thing that gives a

23:50

picture of its entirety. I think what we

23:52

have to do though is try to stick

23:55

within ecosystems from testing because if

23:57

you compare up 6-TENUS with a shotgun

24:00

The percentages for them things will match up. Other things

24:03

will not so much, but if

24:05

you've been looking at enough of them, you can still

24:07

get an idea of what's a normal level of lift-back

24:09

tray on a 16S versus a normal level on a

24:12

shotgun. So you can kind of see whether people

24:14

are higher or lower, but I

24:16

think it's important to stay within –

24:18

to really just compare within that ecosystem.

24:21

It gets more tricky when you start comparing between different

24:23

test types, as you saw. And I experienced, too, the

24:25

same thing when I sent in a 5. You

24:28

still have about six different labs, and

24:30

the results you got them were just like so

24:33

different in so many ways, but some

24:35

things, thankfully, were consistent, like some functional

24:38

markers, like digestive markers and flammage markers

24:40

were thankfully consistent. But in terms of

24:42

my computer composition, that differed a lot.

24:44

And I use culturing labs. I use

24:46

PCR labs, and I use them at

24:48

DNA-based ones, too, for my experiment. And

24:52

I just want to point out that there's

24:55

a broader principle

24:57

here that applies beyond the microbiome that

24:59

a lot of tests – I

25:02

think people assume – people

25:04

in the general population assume, hey, if

25:06

a test exists, it

25:08

must have lots of research validating it,

25:11

supporting that it's accurate, that it's valid,

25:13

that the results are reproducible. And

25:16

I just want to point out

25:18

to listeners, there are many –

25:20

the tests are coming from private,

25:22

for-profit companies. There is an industry

25:24

there. They are in pursuit of

25:27

creating new products, meaning new tests,

25:29

to bring to market constantly that

25:31

help make them money. And

25:34

those financial incentives often drive new

25:36

tests entering the market that aren't necessarily

25:39

valid or accurate or meaningful data or

25:41

even reproducible, meaning do the same test

25:43

twice, you get totally different results. And

25:46

that issue is pervasive across a lot

25:49

of testing, not only microbiome testing. Yeah,

25:52

no, I fully concur, and it is always amazing seeing

25:54

some of the tests that are offered in the sort

25:56

of un-comedicine field that have never been

25:58

validated against any sort of – gold standard

26:00

and we know that's kind of basic slow

26:03

crafter doesn't work at least as well as our current

26:06

tests are. And

26:09

with that, and this is really meaningful to understand

26:11

because let's say in my case I did just

26:13

the one test this practitioner wanted to order for

26:16

me. Based on

26:18

that test there were certain things

26:20

present that the practitioner was saying

26:22

well let's do this supplement that's

26:24

an anti-microbial supplement to cleanse

26:26

your microbiome and get rid of these

26:29

bad bacterial species but then I did

26:31

another test that didn't show the same

26:33

abnormalities as the first one showed

26:36

that he wanted to treat me for. So

26:39

these are differences that are very

26:43

consequential and I

26:45

highly recommend people cross check results

26:47

or use really smart high integrity

26:49

trusted practitioners who really know what

26:51

they're doing as far as accuracy

26:54

of tests. Okay

26:56

so looping back

26:58

to the first thing the connection of

27:00

gut health and the microbiome to health

27:02

more broadly we know we've got

27:04

you know as you said there's like all

27:07

these emerging layers to the story constantly the

27:09

gut brain axis, the gut skin axis, the

27:11

gut immune axis, the gut lung axis, the

27:13

gut liver axis on and on and on

27:16

and of course we know there's

27:18

a gut mitochondria axis. So what's

27:21

the connection between the gut and

27:23

mitochondria? Yeah and this

27:25

is one of those newer areas and

27:27

I think we're getting greater clarity all the time and

27:29

if we ask this question five years from now we'll

27:31

have so much more understanding because I really think it's

27:34

probably only been allowed ten years that people even thought

27:36

of this at all because again people really

27:38

just saw who was in the gut but I think now

27:41

we're looking at I think that to

27:43

me the mitochondria of microbiota axis is

27:46

needed for a few different things and

27:48

looking at primarily bacterial metabolites and I

27:50

think it can be been beneficially modified

27:52

by things like the production of beetrate

27:55

for example which is the short-term fatty acid and

27:58

then and also some polyphenol trans- products

28:01

and then also detrimentally impacted by

28:03

things like the release of endotoxin

28:06

in the gut. Those are probably

28:08

the three main ways in which

28:10

the microbiota can modify what her

28:12

systemically found by the chondria are

28:14

actually doing and how they function.

28:17

So let's talk about the lipopolysaccharide

28:20

aspect of the story. So what

28:22

are they first of all and

28:24

how are they getting into mitochondria

28:26

where they're causing damage at that

28:28

level? Yeah so

28:30

lipopolysaccharide might just say LPS for short

28:32

also known as endotoxin which I think

28:34

people might connect a bit better with

28:36

okay it's something that causes it to

28:38

function. But interestingly enough it's not grown

28:40

by the bacteria as a toxin. There

28:42

are bacterial toxins called exotoxins that the

28:44

bacteria are releasing in essentially to make

28:46

you unwell or to do some sort

28:48

of targeted thing. Endotoxin some

28:51

bacteria in your gut grow just like we

28:53

grow nails we go hair it grows endotoxin

28:55

and these bacteria called gram negative bacteria and

28:58

most people be familiar at least vaguely with

29:00

gram positive gram negative gram negative means they just

29:02

don't take on stains a color

29:04

stain by a banded by a guy called gram. That's

29:07

essentially what it was the stain thing something

29:09

took it out something that didn't and the

29:11

ones that didn't essentially have lipopolysaccharide in their

29:13

cell wall and it can make up about

29:16

80% of the cell wall so a lot

29:18

of that is LPS. Just

29:21

turns out that this stuff is immensely pro-inflammatory.

29:25

We know it can actually damage the lining

29:27

itself and cause like a leaky gut.

29:29

We know it enriches the circulation it

29:31

actually causes inflammation everywhere. We know it

29:34

can impact negatively blood sugar regulation and

29:36

it damages the blood-brain barrier. We

29:39

know it can change what neurotransmitters

29:41

our brain produces because of neurological

29:44

inflation induced and we know it's

29:46

a key driver of neurodegenerative conditions

29:48

like Alzheimer's and cognitive decline. That's

29:50

really come to the fore recently

29:52

and they can do all top teas

29:54

of people with Alzheimer's brain and it's

29:57

full of LPS. to

30:00

the healthy controls of the same age. It's like

30:02

really pivotal. What's interesting there

30:04

was that people's, the

30:06

amount of LPS-containing bacteria in the gut

30:09

dramatically differs per person, depending on

30:11

the composition of their ecosystem. So,

30:14

and even within that, there are

30:16

really pro-inflammatory types of LPS and

30:18

less inflammatory. So let's focus primarily

30:20

on the pro-inflammatory sort that we

30:22

get from a group of bacteria

30:24

we call protobacteria. And

30:27

people may not know that term, but I would have

30:29

heard of E. coli before, or

30:32

probably Salmonella or Shigella or

30:34

Campylobacter, Hulcobacter, I

30:38

think you lost- I think you lost E. coli and

30:40

Salmonella. Okay, I might have. Those

30:44

are all protobacteria anyway. So you kind of know

30:46

some of the more familiar ones. Those

30:49

ones, their endotoxin is just immensely

30:51

pro-inflammatory, immensely so. And then we

30:53

have other bacteria that we might,

30:56

some of you may have heard of like

30:58

Bacteroides or Allostytese, who are also gram negative.

31:00

They have lipocholus saccharide, but it's maybe 100th

31:02

or 1000th as

31:05

potent as an inflammatory agent. So

31:07

we're gonna focus on that on the protobacteria. Now,

31:09

as I was saying, it differs. How much

31:12

is in people's guts? Too typical for a

31:14

Westerner, it's like four, 5%. It's

31:17

far less in a lot of

31:20

nutritional cultures and people eating, I

31:22

would say more fiber-enhanced, plant-rich

31:24

diets, but you get some patients that I

31:26

see, I've seen it at 50%, 55% of

31:29

the ecosystem. And

31:31

I've seen it in 0.2%. It

31:34

gives a new spectrum of where that can be. And that difference

31:37

is dramatic. So in terms of the

31:39

amount of this pro-inflammatory compound that's being

31:41

released, so again, it's not really

31:43

seeing an intentional system. Bacteria are constantly living

31:45

and dying, living and dying. So

31:48

when they're dying, that endotoxin's released in your gut. And

31:51

your body can deal with that endotoxin, it's

31:53

fine. Your intestinal cells would detoxify it. Then

31:55

it gets to your bloodstream, your liver will

31:57

detoxify, and you get very little, generally. If

32:00

you're eating really well, your gut integrity

32:02

is good. Your bowel transit time is good.

32:04

Your ecosystem composition is good. You get very

32:06

little endotoxin flicking on your bloodstream, but that's

32:08

just not the reality of Western life. We

32:11

think we have poor integrity. We're ingesting

32:14

lots of alcohol. We're taking non-thral anti-inflammatory medications

32:16

for pain relief. And we know like alcohol

32:18

and ended cause gut leakiness. And we know

32:20

that other aspects of our diet and lifestyle

32:22

might cause gut leakiness, too, so we get

32:24

more of that endotoxin coming in. But

32:27

that Western diet and lifestyle also leads

32:29

to essentially increased numbers of negative

32:33

prony bacteria in our gut, increased proportion.

32:36

So you get this combination of a lot

32:38

of endotoxin in your beliefs in the gut.

32:40

You've got a leaky or small bowel, but

32:42

typically for Westerners too, they have a slow

32:44

transit time. So that essentially means that that

32:46

endotoxin, rather than being pooed out, you know,

32:48

12 hours later is maybe

32:50

if you're lucky, pooed out two, three,

32:53

four, five, six plus days later. And the

32:55

problem is it's not really much. It's pooed

32:57

out by then because it's absorbed. It

32:59

doesn't just sit there. It will be absorbed and get into

33:01

your bloodstream. And as I said before, your liver can deal

33:04

with a little bit of it, but you get above that

33:06

point, it reaches, it goes beyond

33:08

that. And we know that the LPS is

33:10

the main driver of liver damage in alcoholics.

33:12

LPS is the main driver of liver damage

33:14

in fatty liver. It's not, it's

33:16

just the LPS from bacteria that cause the

33:18

damage. So it can directly damage that. And

33:20

we know that it works essentially as a

33:22

mitochondrial poison. It can actually cause mitochondrial inflammation

33:25

and mitochondrial dysfunction. And

33:27

it's doing that in the liver and it's

33:29

doing that everywhere in your system, including in

33:31

your neurological system to enhance leads to all

33:33

these nervous

33:35

system conditions that proceed more and

33:37

more commonly in Western nations. And

33:40

for anybody listening, I would encourage you to spend

33:42

a little time going on PubMed or Google Scholar

33:45

and just typing in endotoxemia and

33:47

any disease you can think of.

33:50

And there's probably some research on

33:52

it. There's research on

33:54

it linked with chronic fatigue syndrome and

33:56

fibromyalgia, linked with neurodegenerative diseases, linked with

33:59

heart disease, linked with diabetes, linked

34:01

with obesity, non-alcoholic fatty

34:03

liver disease, on and on and on. I

34:06

mean, pretty much any chronic disease of

34:08

civilization, which is 80%

34:11

of the disease burden is gonna have

34:13

a link there. There's one other

34:15

layer to this that I wanna emphasize. I

34:17

think there is a tendency

34:19

for people to think that there are

34:21

certain things that cause leaky gut. It's

34:24

like when I take antibiotics, or

34:27

when I take alcohol, or when I do

34:29

this thing, then

34:31

I'm causing leaky gut, or

34:34

I do this combination of things and I have

34:36

leaky gut. This

34:38

layer to the story that you're talking about here is the

34:41

ecosystem of microbes themselves that's in

34:43

the gut, if there is a

34:46

big imbalance in the direction, a

34:48

shift in the direction towards a

34:50

predominance of these gram-negative bacteria, and

34:53

especially as you emphasized, the slow bowel

34:55

transit time, if you don't poo very

34:57

often, basically. I know that's not totally

35:00

accurate to measure bowel transit time, but

35:02

people who are maybe taking

35:04

one poo every three days, or something like that.

35:10

The presence of these bacteria themselves

35:13

are producing this

35:16

endotoxin that is itself driving

35:19

gut permeability in leaky gut. Yeah,

35:21

very much so. Even recently,

35:24

we've been looking into the C.Lacto-3,

35:27

Lutorture 2, and it's now being linked to, it's

35:30

not just gluten, it's gluten with lots

35:32

of proteobacteria that's changed anything to result

35:34

in the gut damage, and it seems

35:36

to be a core prerequisite

35:38

for C.Lacto-3 to developing people with

35:40

the right genetics, it's not just

35:43

eating gluten. Actually, you'd have a

35:45

dysbiotic small bowel ecosystem with these

35:47

proteobacteria present, which leads to the

35:49

gut damage in the C.Lacto-3 develop.

35:51

So yes, it is really a key thing

35:53

that the composition of the gut and remembering

35:56

that it's that balanced level

35:58

of proteobacteria to determine. Even

36:02

in other conditions like alcohol, we

36:04

know that. And even we can

36:06

look at non-sterolantic phlegm like ibuprofen.

36:09

We know, okay, yes, these cause gut damage, but

36:12

they don't cause gut damage in

36:14

germ-free mice and rats.

36:17

So if you've got mice and rats with no

36:19

bacteria present in their guts, you can mega dose

36:21

them of NSAIDs and they make no gut damage.

36:25

But if they have negative bacteria there, you

36:27

can give them a tiny dose and they

36:29

get severe damage. So it is, even as

36:31

agents we see as being gut damaging, it's

36:33

still mediated a lot through the microbiota too.

36:36

So you could think of that almost as like the

36:39

resilience of the gut to

36:42

insults, to chemical

36:45

or environmental insults, stresses.

36:49

The ecosystem itself is going to

36:51

influence whether a particular insult,

36:54

whether it be alcohol or NSAIDs

36:56

or gluten or something like that

36:58

is going to cause gut permeability

37:00

or not. Yes, which

37:02

I think is fascinating. And I think you're right, it's

37:04

not on people's radar. I bet

37:07

it's that. It's just a huge thing.

37:09

And I think even like, again, I've

37:11

been looking at the research on SIBO

37:13

literature too and even that thinking of

37:15

being too much bacteria growing in the

37:17

small bowel is actually changing to being

37:19

the wrong type of bacteria overgrowing the

37:21

small bowel. Again, it's coming to mostly

37:23

around proteobacteria. So you feel that's

37:26

a shift in the thinking, the paradigm around SIBO?

37:29

Yeah, I don't know if it's tooled for that yet, but

37:31

if you start looking at the research around it, it seems

37:33

like, okay, you can have higher levels of some bacteria, it

37:35

doesn't seem to be problematic, but there's definitely things

37:37

to be associated with symptoms and gut

37:40

damage when you have more gram negative

37:42

bacteria in your presence and it's

37:44

around diversity and also explains why there

37:46

was a study where they gave fecal

37:48

transplant in capsule form to treat SIBO

37:51

and they had amazingly successful rates of

37:53

treating SIBO for like six months afterwards,

37:57

cured and vast majority of people kept giving it fecal.

38:00

transplant by capsule and the thinking was

38:02

let's change we know that the existence

38:04

in the small bowel people see that

38:06

was less diverse and there's more proteobacteria

38:08

let's see if we can introduce more

38:10

diversity and healthy system and one study

38:12

so far but I think it was

38:14

just pivotal in shifting people's thinking about

38:16

the condition or starting to anyway. Very

38:19

interesting. Okay so there's a couple other

38:21

layers to the story of the gut

38:23

mitochondria connection that you mentioned and

38:28

you go where you want to take

38:30

this there's you know as we talked

38:32

about before before we started recording there's

38:34

the the the illagic acid and urolithin

38:36

A part of the story

38:39

there's the polyamines part of the story and

38:41

then there's the short chain fatty acid so

38:43

tell us what what kind of some of

38:45

the other layers of the gut mitochondria connection.

38:48

Yeah I think I think B-rate makes

38:51

sense to go to next because I think this is a key thing

38:55

and and it's one of the things that our our

38:57

each and can make force you know I think this

39:00

is also people to know

39:02

too that that and maybe just stepping back to

39:04

short chain fatty acids what are they so when

39:06

we consume foods present probably fibers but even I

39:09

would say to some degree you know protein a

39:11

she's foods to reproduce these things

39:13

cold short-term or bacteria ferment them or

39:16

future father I'm turning on with this

39:18

protein or fiber carbohydrate compounds to short-chain

39:20

fatty acids predominantly as the main in

39:23

product yeah and there's three main ones

39:25

there's acetate there's propionate and then there's

39:27

butyrate majority of people which

39:30

mostly acetate that they produce and then

39:32

here relative difference in proportion of the

39:35

planet and and be right and people don't make much

39:37

be great at all and this is there's a couple

39:39

of factors that can determine that one the

39:43

levels of be they producing bacteria you have in your

39:45

gut and to what you eat and that's probably the

39:48

people think that determines number one anyway for the

39:50

most part and again looking at

39:52

at what proportion of your ecosystem might

39:55

be be composed of

39:57

be great producing species in

39:59

the lowest I've seen is none, absolutely

40:01

zero, which is

40:04

someone who hasn't been a long-term antibiotic.

40:06

They call vancomycin, where it just completely,

40:08

there was just no growth, to 70%. I

40:12

thought you could just decompose a B-ray-preceding bacteria, but it's

40:14

probably a far extreme end of that. Most people would

40:17

fit in a sort of 10 to 25% sort of

40:19

mark. And I think this group

40:23

of bacteria is starting to get more

40:25

acknowledgement, but I think in terms of

40:27

what the names that people are familiar

40:29

with, probably not so much, because we're

40:31

talking about, I think one of the

40:33

key ones is fecalibacterium, fecalibacterium prostitii, which

40:36

starting to get a bit

40:38

of a name, outside research

40:41

circles or medical circles, but

40:43

there's other ones like roseburia

40:45

and eubacterium and subgilligranulum, anaerocytides

40:47

and tystinebacter ruminococci

40:50

that most people are, you

40:52

know, know nothing, have never heard of them before and have

40:55

no idea that they're actually really important. You

40:57

should really focus on feeding these

40:59

guys because you've got the capacity

41:01

to have these amazing B-ray-preceding factories

41:03

in your gut. They're functioning and

41:05

working for you, they're sitting idle.

41:08

And it kind of depends on what you're feeding and not going, we

41:10

can feed them up to, it might only be 2% now or 10%,

41:13

but a lot of work I'm doing with patients is okay, let's go

41:16

from that 10% up to 40%. So

41:18

you're actually increasing the proportion fourfold,

41:20

increasing that of B-ray-preceded or fourfold.

41:23

Yeah, so B-rate is an

41:25

amazing substance. So we know it's immensely

41:27

important for your intestinal integrity. So if

41:29

you want to protect yourself against leaky

41:31

colon, leaky small bowel is ensuring that

41:33

you're having enough B-rate being produced. It

41:37

makes up, I think, 70% of the energy needs

41:39

in your colon cells is from B-rates. If you

41:41

don't make a not B-rate, your colon cells don't

41:43

function properly and don't regenerate properly. And

41:46

that also puts persecto on it too because if you're making

41:48

a small amount of B-rate, every

41:50

little bit of that is being consumed

41:52

essentially by your colon cells. You

41:55

have to produce enough to feed

41:57

your colon cells and more so you can

41:59

actually get some into your circulation where you

42:01

start getting the systemic benefits of butyrate

42:03

and this is where it's helpful for

42:05

mitochondrial support. So that the bucket is

42:07

overflowing enough. There's excess after the colonocytes

42:09

have used their portion. Now it's overflowing

42:11

and now you've got this butyrate going

42:13

into the bloodstream where it can reach

42:16

the brain and reach the mitochondria throughout

42:18

the body. That's right because if

42:20

you don't get that and you don't have enough, just

42:22

enough to feed your colon cells, you don't get the

42:24

systemic benefits that were after for mitochondrial. So what does

42:26

it do once it reaches? It's

42:30

mitochondria and the brain systemically. Well,

42:32

we know it can actually help heal the

42:34

blood-brain barrier and it actually can decrease neurological

42:36

inflammation. And I just remember in

42:39

2016, I paper in a like

42:41

mainstream neurology neurology journal talking about

42:44

eating a high-fibre diet for brain health. It was

42:46

just like, it

42:49

was just mind-blowing because that would not have been something

42:51

that was discussed 10

42:54

years ago even, let alone longer in the past.

42:56

No one would have any connection of neurological conditions

42:58

and not or eating fiber and it's not like

43:00

this, eat more fiber. If you beat rate-preaching species,

43:02

it was just like, it was just great to

43:04

see that there. Because

43:07

we know it's actually decreased neurological inflammation,

43:09

help regenerate neurogenesis,

43:12

brain drive, neurotraffic factors is up

43:15

regulated with beat rate. It

43:17

decreases and improves and influences to these actually

43:20

improves blood sugar regulation as well. But

43:22

also improves mitochondrial function. It produces, I

43:25

think it enhances capacity to generate ATP, enhances

43:29

mitochondrial biogenesis and it can actually reduce

43:31

the amount of reactive oxygen species that

43:34

are developed as well. So you've got

43:36

this amazing thing that your

43:38

gut can produce for you if you can nurture

43:40

those species and encourage them to

43:42

make beat rate for you. Fascinating.

43:45

I love that. Yeah. There's

43:49

an interesting layer of the story that was

43:51

that Dr. Vincent Pedro mentioned to me about

43:53

the Hadza as well. He said that they

43:56

found, I hope I get

43:58

this right, but I'm pretty sure he... said that

44:01

they found not such high

44:03

butyrate levels, but they found

44:05

very high propionate levels. Interesting.

44:10

I think that they speculated that

44:13

it has to do with

44:15

either the amount of fasting

44:18

they do, or I think especially the amount, this

44:20

is what it was, it was the amount of

44:22

activity, physical activity that they do. And

44:24

they found that for some

44:26

reason, I don't know the biochemistry,

44:28

but propionate was

44:30

particularly beneficial for them

44:33

as they're out on a hunt all

44:35

day, as compared to high-dudurate levels. Something

44:37

to that effect. Maybe it's used, I

44:40

think it's that it's used in energetic pathways

44:44

more efficiently, like to help

44:46

support high levels of physiological or

44:48

physical activity or to suppress hunger

44:50

or something to that effect. Yeah,

44:53

interesting. Yeah, okay. I mean, I know a bit

44:55

about propionate too, but not a huge amount of

44:57

it in terms of, I know that really high

44:59

levels can be neurologically toxic because, I

45:01

mean, the models they use are animal models where they

45:03

kind of inject propionate into the brain and they go,

45:05

oh look, they start developing autism behavior.

45:07

So it's a bit of a false model, but I

45:10

have had kids on the spectrum that

45:12

I've worked with that have had really hyperplionate

45:14

producing species in their gut and it has

45:16

been issued for them and it can decrease

45:18

propionate levels and it does actually improve cognitive

45:20

capacity and awareness and it gets more and

45:22

more present in here now. So I think

45:24

that they can perform at large amounts, but

45:26

I don't think the answer. I

45:29

can kind of, I can actually improve

45:31

cognitively using bacteria in their gut. Okay,

45:35

so before we get to practical stuff, can

45:38

you tell us a little bit

45:40

about the urolithin A aspect of

45:42

the story and how that relates

45:44

to the gut mitochondria connection? Yeah,

45:47

and maybe we can take it a step

45:49

further back this round polyphenols first. And polyphenols

45:52

are the rightly colored compounds we found in

45:54

plant foods, natural foods, not the red food

45:56

dye or blue food dyes that you can

45:58

buy in processed foods. but blueberries,

46:01

eggplants, you know raspberries, red

46:03

rice, black rice, those

46:07

compounds of polyphenols are

46:11

pretty ubiquitous amongst the plant foods,

46:13

vegetables, grains, whole grains, whole grains,

46:16

vegetables, fruits, leggings, nuts, seeds, all

46:19

in their whole form have got a varying

46:21

amount and type of polyphenols. The interesting thing

46:23

about the polyphenols is 90 to 95 percent

46:26

are completely indigestible and

46:29

unadorable to us. So they're

46:32

there and if you

46:34

didn't have the gut bacteria and the right gut bacteria you

46:36

would just poo them straight out and they would do nothing

46:38

for us because they're too big. The

46:40

molecules are too big that we can't digest them. We

46:43

don't have the digestive arms to deal with them but

46:45

our gut bacteria do. Yeah and they can

46:47

actually they're really important for this conversion

46:50

of these polyphenols into smaller molecules which

46:52

we then absorb and in that process

46:54

they get food from it. So it's

46:56

like a win-win situation. So we're eating

46:58

the polyphenols from blueberries which taste good

47:00

to us, that's a win. Those polyphenols

47:02

reach the colon, oh let's do this

47:04

to these pomegranate. Let's say

47:06

pomegranate is a food, delicious food,

47:08

full of specific polyphenols

47:11

called the lagi tannins. Lagi

47:13

tannins aren't broken down by us. They're too big

47:15

to be absorbed by us. Even if they were

47:18

in our bloodstream we go oh it's an antioxidant,

47:20

it's great but we can't get it because it's

47:22

too big. It reaches the colon

47:24

and there it gets actually impacted by

47:26

gut bacteria and they convert that lagi

47:28

tannin, they eat it and

47:30

break it down to something else. They get

47:32

energy so their populations increase but they release

47:34

a breakdown product which then is there between

47:37

active and absorbable. And we

47:39

know that all these plant foods that have

47:41

these polyphenols were often entirely dependent on this

47:43

micro-biotic conversion to get the health

47:45

benefit. And I

47:47

think that's fascinating too but the one

47:50

is specific with the lagi tannins in

47:52

polygravate, you'll get them in walnuts and

47:55

pecans too. Chestnuts,

47:57

I love the study to find the

47:59

food. richest in it. It

48:02

was chest or water chestnuts

48:04

or something like that. The

48:09

big ones that are soft, I'm

48:12

pretty sure they're called chestnuts. Yeah,

48:15

the ones that they tend to roast, I

48:17

would think of those old English stories of

48:20

a roasting chef for Christmas time, sort of.

48:22

Yeah. They've got a very brown husk on

48:24

them, I reckon that's probably high in that

48:26

particular polyphenol. Yes. So yeah,

48:28

it's interesting. I

48:32

always hear people talk about pomegranate.

48:34

Nobody mentions chestnut, but chestnut

48:37

is actually, I think even slightly

48:39

richer than pomegranate. Interesting.

48:42

Okay. I think I love

48:44

pomegranate because I'm a herbalist and I use pomegranate.

48:47

The husk, the skin, which is actually much

48:49

higher, I must say, in Alagi tannins than

48:51

the fruit anyway. So if you're after a

48:53

really hefty dose, the skin would have give

48:55

you a hell lot more. You eat the

48:57

full peel with it? Yeah. Really? Yeah.

49:00

I mean, it doesn't taste good. So I mean, I

49:02

think the idea to sit down

49:04

and just tune on a whole is like not

49:06

remotely appealing. I mean, I've made a pomegranate husk

49:08

tincture for years, but now you can buy it

49:11

in powder form. And not to dissension,

49:13

it'll be capsules. When it's in the pomegranate,

49:15

you're like, ah, there's actually more Alagi tannins

49:17

in the skin than there is in the

49:19

fruit, but it's not particularly tasty. So you

49:21

know, I have patience in mixing those smoothies

49:23

and with other things that can be masked

49:25

over okay, but just like chewing on is

49:27

just not an option that you're going to

49:29

enjoy. It's really, really strong tasting. But

49:32

it's much higher in that compound. Yeah.

49:35

You think these

49:37

polyphenols and flavonoids and things should be

49:39

put in the category of prebiotics? I

49:41

know they're not generally considered to be

49:43

that, but based on the mechanism you

49:45

just described, it sounds like they essentially

49:47

are. Yeah. It probably depends

49:50

a bit on how narrowly

49:52

we define the term prebiotic. Yeah. And I

49:54

would probably put them in more into the

49:56

colonic food type category that it feeds a

49:58

wide diversity of micro. like

50:00

you put the random fibers in there that you can

50:02

see a number of things go up. There might be

50:04

some and I put pomegranate in this category actually where

50:07

you tend to get increased in bifidobacteria. So

50:09

there are like a much more standardized

50:12

response to it. You get degrees

50:14

level of the pathogenic bacteria, increased

50:17

B-ray producing species, increased bifidobacteria is

50:19

something we see with pomegranate house

50:21

congestion. So it's like that to me

50:24

would be that but I think would

50:26

be a different scenario if we were

50:28

talking around other types of polyphenols and would

50:30

feed other species like slakia

50:32

or gordonobacter or others which are very

50:34

important. Polyphenate transforming is a similar species

50:36

but we're not sure exactly if they're

50:39

a broader role in health enough to

50:41

say yeah that would be defined as

50:43

a prebiotic but I'm being a bit

50:45

picky with definitions. Okay

50:47

did I get distracted or I just want to

50:50

make sure we completed this part

50:52

of the story of how these flavonoids and

50:54

how the elagitanans are then

50:56

being converted by gut microbiome and how

50:58

this then influences mitochondria. Did you complete

51:00

that? Yeah we didn't quite get there.

51:02

We got to the conversion spots so

51:05

the polyphenols we just took the colon there that are

51:07

consumed and they're absorbed. So in the case of eli-tanins

51:10

for example from pomegranate or other

51:12

foods, some

51:14

people, not everybody converts it to

51:17

eurobecin A and I think

51:19

that is one of the most researched on because

51:21

there's also a B variety and some people just

51:23

that it doesn't get converted through depending on what

51:25

species are actually present. And this

51:28

is the nuanced bit of everyone's microbiome being

51:30

completely unique and unlike anybody else's is that

51:32

some people will have different pathways to see

51:34

which that will go through depending on the

51:36

ratio rate or number of bacteria

51:38

present. But I think we can

51:40

also work to encourage that too. Like I think

51:43

there's one study I read that initially at baseline

51:45

12% of people were produced the A

51:48

baroque variant but

51:50

then after ingestion for a while was actually up

51:52

to 40% of people were

51:55

and I think the research suggests with the elitin A

51:57

it's… And

52:00

other things like if you just eat

52:02

polyphenols consistently daily for long enough, you

52:05

will encourage the species that are there in lower numbers

52:07

to become more prominent. So you might not be a

52:09

urelief in a producer now, but

52:12

you might be after six months of

52:14

consumption. That's a possibility too. And

52:17

especially those people that don't

52:19

make either urelief in when it

52:21

comes to magic head. That's my experience.

52:23

And I was trying to delve into, can

52:25

we use other polybronics to help that? And

52:27

that's an interesting conception that thing hasn't been

52:29

delved into too much detail yet. But we

52:32

needed to find what species actually consume the

52:34

compound and we can work out or

52:36

essentially convert the alley-cannon to your reason

52:39

A. What species do that? I

52:41

mean, some research is suggesting it's a

52:43

bug called Gordonebacter as being particularly important

52:46

in this. So

52:48

it's like, how do we encourage that? Well, we don't know besides feeding

52:50

these canons that they like

52:52

eating, which is kind of

52:55

like, you encourage them if they're there, if

52:57

you give them food, they will grow. And

53:00

that comes the same with B-ray producing species too. It's like, they're

53:02

there, you feed them, their populations go up and you don't feed

53:04

them, they go down. You know, so by keeping a pet fish

53:06

or something, if you don't feed it, it will eventually die. And

53:08

if you feed it, it will grow. The

53:11

concept is pretty similar with our gut bacteria.

53:13

It's just some bacteria are pretty diverse with

53:15

their food sources, others less so. And Gordonebacter

53:17

I think is pretty diverse with its source

53:19

of polyphenols. So it wouldn't have to be

53:22

only that one. I think if you're eating a

53:24

wide variety, you probably have a better chance. I

53:26

can probably plant-based lots of polyphenols, lots of colorful

53:28

foods, the chance of having Gordonebacter there is far

53:31

greater than someone eating McDonald's and

53:33

Cacophage chicken, there. Yeah,

53:36

the circular sort of bidirectional nature

53:38

of the body in this regard is

53:40

always fascinating to me. And I grew

53:42

up as an athlete and

53:44

in the bodybuilding space. So my background

53:47

in health wasn't just theoretical, it wasn't

53:49

just studying concepts, it was self experimentation.

53:51

So the idea is like, it's

53:54

amazing how obvious and sort of

53:56

common sense it is for people who have that background

53:59

and self experience. but who

54:02

only study this in theory, it's not necessarily

54:04

obvious. But for me, it's like someone

54:08

saying, well, how do I get my

54:10

biceps stronger so that I can lift

54:12

weights? It's like, well, you

54:14

practice lifting weights. Yeah.

54:17

So then it's stimulated to grow stronger. And,

54:19

you know, the same is true here. If

54:21

you want to grow more of those species

54:24

that do a particular thing, you got

54:26

to feed them the thing that those

54:28

species like. Yeah. Yeah.

54:31

It's very much that way. And I think that's something too

54:33

about being, because some researchers aren't clinicians, and they just can't

54:36

take that final leap. How

54:39

do you convert this into something practically and

54:41

relevant and helpful for people? And it often

54:44

takes too early to do that, where it's

54:46

like, okay, well, no, we just

54:48

feed those bugs up and their populations will go

54:51

up. Right. And they should get that benefit.

54:53

Yeah. And I think that's what I think with

54:55

an A is its capacity to work as a mitophagy

54:57

inducer. And that's because

54:59

I think there's a lot of other polyphenols

55:01

that seem to be good at enhancing pyogenesis

55:03

or the creation of more mitochondria, which is

55:05

obviously really important too. But

55:08

I think what's really cool is we can

55:10

get research around the capacity of those dysfunctional, not

55:13

particularly well-energy-producing

55:15

mitochondria that are just slightly chugging along. Well,

55:17

here we can induce them to die. Try

55:21

taking this and be replaced by a

55:23

proper, well-functioning mitochondria, and then you get

55:25

all the flow and benefits that come

55:27

from that. So I think that's exciting

55:29

that we're teasing those things out. Because

55:31

I think we would have looked at

55:33

epidemiological studies would have shown that people that are eating lots

55:35

of polyphenol-rich foods have got lower rates of

55:38

neurojective diseases and cancers and heart disease and

55:40

all these things. And now we're just kind

55:42

of teasing out the whys in

55:44

more detail. And then we can obviously

55:47

apply it differently too, because people with

55:49

conifant T syndrome or fibromyalgia or other

55:51

neurodegenerative conditions that are associated with mitochondrial

55:53

dysfunction are like, okay, well, it's not

55:55

just including longevity for eating these polyphenols.

55:58

It's actually, we can start targeting. that

56:00

we can try to target things more

56:02

specifically by potentially using pomegranate skin as

56:04

a supplement, for example, where I think

56:06

they're coming out or that have come

56:08

out with an A as a preformed

56:10

supplement as a way of trying to

56:12

directly target those dysfunctional mitochondria. Right, yeah,

56:14

with the idea that roughly

56:17

30% of people don't have,

56:19

they say that they don't have

56:21

the species, again,

56:24

with the nuance of what you just described, that

56:26

if you consume that for a period of time,

56:28

maybe you will have the species, but the idea

56:30

is they say 30% of the people don't

56:33

have the species to take elagitanans

56:35

and create urolithin A, therefore,

56:38

implementing directly with urolithin A, this

56:41

postbiotic product of the bacteria

56:43

will be beneficial. And

56:46

there are studies to support, of course, that

56:48

it is beneficial. I'm actually personally looking to

56:52

create a supplement formula that has that compound in

56:55

it because there's so much positive research around it.

56:58

It's exciting to delve into that more recently, kind

57:00

of like, oh, look at that. And I just

57:02

love it because the Pupin Pupin Pumagrant has the

57:04

skin which is high in these compounds to a

57:06

lot of, to thousands of patients over the years.

57:08

And that's the unintended benefit that I had no

57:10

idea what was going on was actually this

57:12

urolithin A and at least in the decent

57:14

proportions of these people. Because I think, yeah,

57:16

going back to what we were saying before,

57:18

if you do not have any gordonobacter or

57:20

any of those species, then you can't feed

57:22

them up. It's just that if they're in

57:24

tiny amounts, you can revive that population. And

57:26

this is what, again, I've worked the

57:29

last decade doing this. Oh,

57:33

your sound cut out. The levels. Jason,

57:35

can you repeat that? Your sound cut out briefly there. Oh,

57:38

yeah, yeah. Can you hear me now? Yeah.

57:40

Okay. Yeah, so working with other

57:42

sort of bacterial populations where it's below detectable

57:44

level in stool test, you're like, okay, well,

57:46

let's see if it's extinct or whether it's

57:48

recoverable. Let's feed it. And that's

57:50

a clear way of seeing it. And you do a

57:53

post-test and go, has it actually come up or not?

57:55

And whether it's extinct. And I think thankfully for a

57:57

lot of people, these species that we see is below

57:59

detectable. aren't actually extinct. They're

58:01

just below the capacity of our technology

58:03

to see. And then if we continually

58:05

feed and feed and feed, fast forward

58:07

two months or four months, it's there.

58:10

And I can say that with things like Acromancy

58:13

or Biftebacter or Lactobacilli or different bean ray producing

58:15

species, I've seen that over the last decade of

58:17

practice very clearly. And that's going to be the

58:19

same thing. With Gornibacter II, we have to have

58:22

a test that can tell us that it's there.

58:24

And I'll tell you that shotgun tests

58:26

can do that. And

58:29

then you'd go, OK, well, let's eat this pomegranate

58:31

and let's see if we can get you there.

58:33

And then you might go, OK, no, you're going

58:35

to be the person who has to take your

58:37

Lusinee in his preformed amount. And

58:40

then there's always going to be discussion around the

58:42

amount that gets there too versus how much pomegranate

58:44

is required to get the same serum levels as

58:47

taking a capsule of your Lusinee that will

58:50

be some nice meaty side too. OK,

58:53

Dr. Harlach, do you have

58:55

10 more minutes to spare? I know

58:57

we're going to be a little

58:59

annoyed with me, but

59:03

I'm going to ask you a question

59:05

or two that I know you could spend five

59:07

or 10 hours answering, and I'm going to ask

59:09

you to answer it in a few minutes. OK,

59:12

I'll do my best. Let's

59:15

talk about some practical

59:17

specifics on how to optimize the

59:19

microbiome ecosystem, how to reduce levels

59:22

of LPS, and how to increase

59:24

levels of, you mentioned already kind

59:26

of in this case

59:29

of polyphenols and urolithin A, how

59:31

to optimize that, consume

59:33

more of the polyphenols that

59:35

feed those microbes that produce

59:37

those postbiotic metabolites. But how

59:40

do we reduce levels of LPS and

59:43

how do we increase levels of butyrate

59:45

producing species, which, as you emphasize, is

59:47

very important? Yeah, and

59:49

I think that's probably the

59:52

biggest takeaway is eat mostly plants,

59:55

high fiber, nothing processed, unprocessed

59:58

whole foods that can. a

1:00:00

wide diversity of fiber types and

1:00:03

colors of a polyphenols. We can

1:00:05

do all of that. With a

1:00:07

diet like that, you'll feed bead rate producing species, you'll

1:00:09

lower LPS, producing levels in the gut,

1:00:12

and you will have enough polyphenols to

1:00:14

nurture those species. That's like the big

1:00:16

answer. I think there are

1:00:18

some specific things like with similar

1:00:22

ideas here, though, because one of the key

1:00:24

bead rate producing species is fecalobacterium. It

1:00:27

likes eating polyphenols as well. Also,

1:00:33

frugalogus saccharides or inulin, which

1:00:36

we find in things like onions and garlic. It

1:00:39

also likes eating all the saccharides and legumes. We've

1:00:42

got legumes, onions, garlic, other foods that

1:00:44

contain frugalogus saccharides, including things like yakon

1:00:47

tubers, which are less commonly available but

1:00:49

really rich, asparagus,

1:00:51

globe artichokes, frugalogus. These

1:00:54

are just some of the foods that are

1:00:56

quite high in those compounds, which will feed

1:00:58

fecalobacterium. Then you have the resistant starches, which

1:01:00

are starches that are resistant to our digestive

1:01:03

processes, so they reach the colon intact. They

1:01:05

are there, can be consumed by those bugs that

1:01:07

have the right machinery to do so, and we

1:01:09

tend to get more bead rate, big produce at

1:01:12

the constants of that. So, resistant starches we find

1:01:14

again in whole grains that aren't milled really finely.

1:01:16

So, a chunky meal is going to be quite

1:01:18

different in terms of a fine meal. You find

1:01:21

them high in legumes. And also

1:01:23

what we call retrograde starch, which is

1:01:25

the cooked and cooled variety. So, say

1:01:27

you bake a potato and

1:01:29

you eat it cold the next day, you're going to

1:01:31

get a tremendous amount of resistant starch out of

1:01:33

it versus eating it. Or

1:01:35

particularly if you compare it to like a boiled potato. Boiled

1:01:38

potato, very little resistant starch. Steamed a little

1:01:40

bit more, baked. And then, if you're eating

1:01:42

hot, you're going to get a decent amount of resistant starch. But

1:01:45

if you even let that cool, you get a substantive increase in that. So,

1:01:48

I will often eat cooked and cooled rice. For example,

1:01:50

you eat rice the second day, you'll get more resistant

1:01:52

starch. Those refried beans,

1:01:54

you'll get – because you don't heat them up

1:01:56

too much just a second go, you'll get more

1:01:59

resistant starch in there. them too. So we can,

1:02:01

you know, those broader principles of what to eat,

1:02:03

but then the specific things, the new tricks we

1:02:05

can do to enhance resistance starch capacity and

1:02:08

encourage a greater amount of B-rate should be produced

1:02:10

in the gut. Okay, I have to ask

1:02:12

this. There is certain, there's

1:02:15

a, there's

1:02:17

always the latest dietary fad

1:02:21

trends that are emerging. And

1:02:23

you know, there's the low fat, there's

1:02:25

the low carb, there's the vegan, and

1:02:28

there's the paleo and there's the keto.

1:02:30

And now we're in a trend where

1:02:32

the opposite of vegan

1:02:35

has emerged. I think at

1:02:37

this point, all foods other than everything

1:02:39

other than water has been demonized by one

1:02:41

group or another. Incur.

1:02:45

And, and so we've got everything

1:02:47

from veganism that all animal foods

1:02:49

are trying to kill you to

1:02:52

the opposite, that literally there are there

1:02:54

are diet gurus now claiming that, hey,

1:02:56

you know, animals can can run away

1:02:58

from you. That's their defense mechanism, but

1:03:01

plants they can't run away. So what

1:03:03

they evolved is they evolved

1:03:05

these plant toxins, which are

1:03:07

really poisons that are designed

1:03:09

to make anything consuming them

1:03:12

ill. And therefore, all

1:03:14

these polyphenols and phytochemicals and things

1:03:16

of this nature are really plant

1:03:18

toxins that are trying to kill

1:03:20

us and therefore they're bad and

1:03:22

therefore you should avoid plants and

1:03:24

eat mostly or nothing but meat.

1:03:27

Yeah, from the perspective of

1:03:30

being one of the leading

1:03:32

gut microbiome experts in the world

1:03:34

and having value having spent decades

1:03:36

evaluating that literature, what

1:03:38

is your take on those claims and

1:03:40

that dietary approach as far as the

1:03:43

gut microbiome? We

1:03:45

got microbiome respective is, how to

1:03:47

put it, immensely detrimental

1:03:49

might be the nice way of saying

1:03:51

it. It

1:03:54

comes back to what are you feeding? What are you

1:03:56

not feeding? So all you're eating

1:03:59

is meat and fat. What do you feed

1:04:01

in the micro world microbes that eat eating

1:04:03

protein and bile? Alright, and if

1:04:05

you look at the metal of byproducts of those ones

1:04:07

and they didn't they listen to be gram negative bacteria

1:04:10

number one To you tend

1:04:12

to blooms in proteobacteria on that

1:04:14

diet number two three blooms in

1:04:16

hydrogen sulfide gas producers specifically because

1:04:19

they eat Amino

1:04:21

acids and they eat so

1:04:23

they're like they're gorging. They're not having a great

1:04:25

time of it And how do

1:04:27

you sulfide gas causes gut leakiness as

1:04:30

well and in large amounts to be a

1:04:32

mitochondrial toxin to we know in small amounts

1:04:34

It's actually good for us But in large

1:04:36

amount is we problematic and that diet just

1:04:38

encourages overgrowth of those those species And

1:04:40

then the people that I mentioned before that with like

1:04:43

low levels of B-rate producers Those

1:04:45

are people following diets like that Like

1:04:47

I had one woman who's just eating chicken Just

1:04:50

chicken nothing else and her beaker producers were

1:04:52

2% and I was even like somewhat thankful

1:04:54

There's any there at all to be honest

1:04:57

and maybe she just had chickens to last six months Only

1:04:59

meat because I do well I think based

1:05:02

on animal research you can eventually starve them

1:05:04

out to extinction and then you just you

1:05:06

can't bring them back bar of fecal transplant.

1:05:08

Yeah and certainly patients I've

1:05:10

seen post carnivore similar

1:05:12

type diets where it's been Almost

1:05:15

no plant foods is their ecosystem is so

1:05:17

low in the standard consumers and so low

1:05:19

in B-rate producers and so high in pathogenic

1:05:22

bacteria and and those sort of negative

1:05:24

pathobionts that I mentioned before so Certainly

1:05:27

not from mitochondrial perspective like not getting the

1:05:29

not B-rate being produced at all Not even

1:05:31

remotely enough for your colon cells even let

1:05:33

alone for anything You know systemic benefits that

1:05:36

might come from it and you get you

1:05:38

flooding yourself with endotoxin and we know that

1:05:41

particularly saturated fat from Lard

1:05:43

or butter or ghee or animal products because

1:05:45

sometimes they'll drink he took house milk to and those

1:05:48

kind of rationale

1:05:53

for it anyway We

1:05:55

know the saturated fat binds endotoxin and

1:05:57

increases its absorption that is very clear

1:06:00

the data. So not only are you encouraging

1:06:02

an environment that's full of bacteria, full of

1:06:04

endotoxin, you're

1:06:06

encouraging its absorption into your bloodstream at

1:06:09

the same time with that dietary approach.

1:06:11

Because what stops endotoxin being absorbed is

1:06:13

fiber. That's

1:06:16

clear. We've got data showing that. We can give people

1:06:18

a McDonald's breakfast meal

1:06:22

and their bloodstream fills up with endotoxin. But

1:06:24

if they take some fruit with that McDonald's

1:06:26

meal, they don't get that. It's

1:06:28

a lot of endotoxin at the consequence. We

1:06:30

can very clearly show that. That it's the

1:06:32

fruit, you know, the fruit and the polyphenols,

1:06:34

the fibers that bind to endotoxins and help

1:06:36

prevent them being absorbed even when they are

1:06:38

there in the gut. Whereas saturated fat encourages

1:06:40

their absorption through. So, and those patients that

1:06:42

are full of that diet, at a very

1:06:44

late time, are by far the hardest ones

1:06:46

to get better. And I want to

1:06:49

put that out there because I think in the

1:06:51

short term, you can have a reduction of gas-weighted

1:06:53

symptoms of bloating and distention. That's

1:06:55

what I wanted to say because there

1:06:58

are a number of anecdotal stories you hear from

1:07:00

people who I think

1:07:02

generally are starting with a lot of

1:07:04

dysbiosis and a lot of bad

1:07:07

ecosystem. When they then follow

1:07:09

recommendations like the ones you're giving to eat

1:07:11

more plant foods and a bigger diversity of

1:07:14

plant foods and fibers, they feel bloating, they

1:07:16

feel gas, they have pain, they

1:07:18

have diarrhea, they have problems. Then

1:07:21

they might try a carnivore diet, they get rid of

1:07:23

all the plant foods, they feel better,

1:07:25

they get rid of all those GI symptoms

1:07:27

and then they conclude, oh, this must be

1:07:29

the healthy approach, this must be the best

1:07:31

human diet. Yeah. And

1:07:34

that's exactly what happens in that situation. But I

1:07:36

just know that, yeah, it does reduce symptoms

1:07:38

for some of these people in the short term. It

1:07:40

does. But having seen people the longer term,

1:07:42

because all you're doing is increasing hydrogen sulfide

1:07:45

gas production, which actually worsens nerve inflammation in

1:07:47

your gut. Yeah, so it gets worse and

1:07:49

worse. And this woman that was just like

1:07:51

the, eating a couple of chickens, she

1:07:53

tried, she tried to go back onto

1:07:55

fiber after a few months off. And the thing she

1:07:57

used to tolerate, she did not tolerate now. even

1:08:00

the tiniest amount of intestinal gas being produced

1:08:02

because that doesn't, protein putrefaction doesn't produce much

1:08:04

in the way of hydrogen gas. So you

1:08:06

don't get much bulk that comes with it

1:08:09

and any of the hydrogen gaskets shunted to

1:08:11

hydrogen sulfide gas production would do to all

1:08:13

the amino acids and sulfur from

1:08:15

the bile that's around in that luminance. Any

1:08:17

hydrogen gaskets shunted away and hydrogen is a

1:08:19

big bulky gas. So not much is produced

1:08:21

anyway through protein putrefaction and what is produced

1:08:23

is shunted to hydrogen sulfide. So

1:08:26

you don't get bloated, you don't get distended

1:08:28

from it and hydrogen sulfide gas can speed

1:08:30

up your transit time too. So maybe your

1:08:32

health station goes from this process after the

1:08:34

first week or two of your ecosystem adapting

1:08:36

and all of a sudden lots of H2S

1:08:38

being produced which is hydrogen sulfide, transit time

1:08:40

is better, loading dissension is gone, pain is

1:08:42

going like oh my god that's fantastic and

1:08:44

systematically it is. I wouldn't argue with that

1:08:46

it's just that there the negative consequences of

1:08:48

that for the long, moderate to long term

1:08:50

are immense and the patients that have the

1:08:52

hardest time trying to get back are the

1:08:54

ones that who's essentially done that for long

1:08:56

enough that they're in level information that

1:08:58

God is so great and the

1:09:01

level and so the intolerance to anything

1:09:03

that that produces gas is so great

1:09:05

as a consequence. So how do you

1:09:07

feed the species that are just hanging in there

1:09:09

the edge of extinction? Because

1:09:12

I just want to emphasize

1:09:14

this because of visceral hypersensitivity

1:09:16

because the nerve cells

1:09:18

that sense gas and distension

1:09:20

in the intestines become hypersensitive

1:09:24

and therefore those people then

1:09:26

become hypersensitive and very reactive

1:09:28

to the gas and

1:09:30

to the signals that are then produced when they

1:09:32

reintroduce the plants and the fiber. That's

1:09:35

right and most of them had that to a certain degree

1:09:37

beforehand and so they had general symptoms that they tried the

1:09:39

plant-based diet. It was like all right you already got that

1:09:41

going on you might also have slow transit time and I

1:09:43

methane levels which split out in your gut and a bunch

1:09:46

of other things that very despotic got in a few different

1:09:48

ways that if you came to good practitioner beforehand they could

1:09:50

probably address those things and you have to go to my

1:09:52

path. But in

1:09:55

this case they have and you're right it's

1:09:57

essentially that hydrosulfide gas worsens and

1:09:59

worsens. and worsens that visceral hypergence to

1:10:01

be. So it gets excruciating at the point when

1:10:03

they have a small bit of plant food, they

1:10:05

get excruciating pain. So it's really hard

1:10:08

to come back, and it's hard to feed their beauty

1:10:10

producers when there's 2% or 1% and

1:10:12

the other healthful species from that, and I do

1:10:15

think at some point they will go extinct from

1:10:17

that process. I'm

1:10:20

grateful for the extra time that you took to

1:10:22

spend with me here. I wanna

1:10:24

be respectful of your time. Are there any final

1:10:26

words that you wanna leave people with? And maybe

1:10:28

final piece of advice is, I know you gave

1:10:30

a lot of nutrition

1:10:33

advice. I know that from learning

1:10:35

from you and other contexts and

1:10:37

having conversations with you, you also

1:10:39

talk about other lifestyle elements and

1:10:43

other dimensions beyond nutrition that influence the

1:10:45

microbiome. Anything else you wanna mention to

1:10:47

wrap up? Well,

1:10:49

I think the key takeaway I can

1:10:51

give one is love your microbiome. I

1:10:54

think that is key, and work to

1:10:56

nurture their cells as you would

1:10:58

a loved one or a pet. I think

1:11:01

people often make benefit because of their pet than

1:11:03

they do, and probably that's ignorance because they don't

1:11:05

know how important it is or how to do

1:11:07

it, but I think it's trying to shift that

1:11:09

narrative, and getting this, those microbes are immensely important

1:11:11

to you and your health, and I think just

1:11:13

keeping that in mind when making any kind

1:11:15

of dietary decision or lifestyle decision or medication

1:11:17

decision is

1:11:19

imperative for you in your

1:11:21

long-term health. I was just reading some

1:11:25

research on antibiotics, and

1:11:27

they were looking at cognitive function, and they found that

1:11:30

two months of cumulative antibiotic use

1:11:32

in your 50s, it's aged

1:11:34

your brain by three to four years. And

1:11:37

I thought that was fascinating, just

1:11:40

showing how, and yes, there's a time and

1:11:42

place where antibiotics are necessary. I totally agree,

1:11:44

but so many people are popping in for

1:11:46

viral infection and just trying to make a

1:11:49

list, trying an antibiotic, because what else to

1:11:51

do? There are consequences from a

1:11:53

microbiome perspective, and there are consequences that flow

1:11:55

on from that, because antibiotics are also seen

1:11:57

as mitochondrial toxins too, because what are mitochondrial

1:11:59

toxins? the central bay, we've all bits

1:12:01

of bacteria that's joined with

1:12:03

us. So yeah, so I think people being aware

1:12:06

of those things too when it comes to medication

1:12:08

choices too, that sometimes there's a choice. You don't

1:12:10

need to take water for viral infection. You

1:12:13

know, yes, for life-threatening bacterial infection,

1:12:16

no doubt, but just keeping that in mind

1:12:18

too, of always putting

1:12:20

the importance of the microbiota at the

1:12:22

forefront of your health decisions. Thank

1:12:25

you so much, Dr. Harlach, and let people know where

1:12:27

they can follow your work or get in touch with

1:12:30

you if they want to work with you. Ah,

1:12:33

I'll let you know. What's

1:12:36

that? Sorry, do you want me to let you know, or

1:12:38

you'll let them know? No, you let people know where they

1:12:40

can follow your work or get in touch with you if

1:12:42

they want to work with you and

1:12:45

as a patient of yours. Yeah,

1:12:47

so I've got a few different areas,

1:12:50

but I'm a clinician via Gould's

1:12:52

National Medicine in Hobart, Australia,

1:12:55

but I do see virtually patients from all

1:12:57

over the world, and I run courses to

1:13:00

both through my probiotic advisor site where we

1:13:02

have a, essentially, a

1:13:04

lot of material around

1:13:06

optimizing the microbiota and using probiotics

1:13:09

appropriately in an evidence-based manner, and

1:13:11

through my new site, the Microbiome

1:13:13

Restoration Center as well, where we're

1:13:15

teaching clinicians to essentially optimize the

1:13:18

microbiota and to treat gastrointestinal conditions

1:13:20

with the microbiome at the forefront.

1:13:22

You know, there's always choices. Path

1:13:26

A will damage your microbiota, Path B won't,

1:13:29

and we're essentially going through a range of gut conditions, like,

1:13:31

you know, very similar to the course that you did and

1:13:33

trying to focus on, okay, we can treat this, but in

1:13:35

a way that actually is gut-friendly and

1:13:38

prioritizes the health of the microbiota, so

1:13:41

you get the best long-term health outcome out of any

1:13:43

microbiota. Stay healthy through the treatment approach that we're doing.

1:13:46

Beautiful. Thank you so much for

1:13:48

doing this, my friend. It is always a

1:13:50

pleasure chatting with you. I always come out

1:13:52

with new layers of knowledge, and I really

1:13:54

appreciate your time and you sharing your wisdom

1:13:56

with our audience. You're

1:13:58

welcome. Always a pleasure chatting to you. Thank you. Hey

1:14:05

there, this is Ari. Again,

1:14:09

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1:14:11

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