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1:05

Hello, welcome to 5 Live Science. I'm

1:07

Chris Smith from The Naked Scientists.

1:10

And in this week's programme, scientists

1:12

give mice a rat's sense of

1:14

smell. Also, we find out

1:16

why some of China's biggest cities are sinking.

1:19

And 14 years after disaster struck

1:21

in the Gulf of Mexico, my

1:23

laser-treated cork will be able

1:25

to help us to clean up oil spills in

1:27

future. Plus... There is never

1:29

a time that the thought gets

1:31

to the end of the thought

1:33

because all of the other thoughts

1:35

have barged their way in uninvited

1:38

mostly. We're looking at ADHD, that's

1:40

Attention Deficit Hyperactivity Disorder, to find

1:42

out what it is, who's got it,

1:44

and how science can help us

1:46

to better manage it. The Naked

1:48

Scientists on 5 Live. First

1:52

this week in a landmark in

1:54

brain repair, scientists have used stem

1:56

cells to regrow a missing part

1:58

of the mouse brain. Two

2:00

studies published in the journal Cell

2:03

document how rat stem cells added

2:05

to embryonic mice engineered to lack

2:07

the normal smell circuitry made their

2:09

way to the brain and turned

2:11

into the right sorts of nerve

2:13

cells and successfully wired themselves in,

2:15

restoring the missing sense of smell.

2:18

The study has important implications for how

2:20

we might go about repairing damaged or

2:22

diseased human brains in the future. Kristin

2:25

Baldwin is Professor of Genetics and Development

2:27

at Columbia University Irving Medical Centre and

2:30

she's also one of the corresponding authors

2:32

on one of the two papers. Fixing

2:35

a brain that isn't working is probably

2:37

the most difficult task that

2:39

we have to face in medicine and we would

2:42

like to be able to understand how to

2:44

replace parts of the brain that aren't working

2:47

with other parts that do work. The goal

2:49

of this study was to test that. When

2:52

I was little I watched a programme,

2:54

Anders Bjorkland was the guy

2:56

from Norway and they were doing studies

2:58

on human patients where they were putting

3:00

in embryonic tissue to try to help

3:03

people with Parkinson's disease. Is

3:05

that the sort of thing you're talking about

3:08

getting better at? Cell-based therapy is not

3:10

necessarily with embryonic tissue but with cells

3:12

that are capable of moving

3:14

through the brain and turning into new cells

3:16

to fix things? Exactly,

3:19

we're trying to find the best way

3:21

to get cells to go into a

3:23

brain and actually help it function. So

3:26

how did you do it? We were

3:28

able to take what

3:31

are called early embryos in the mouse

3:33

or blastocysts which are balls of cells,

3:36

a couple hundred cells and we can

3:38

sneak into them about six cells from

3:40

another species, a rat, that are early

3:42

stem cells into that and then they

3:45

will co-develop in a mouse and become

3:47

a whole mouse rat

3:49

chimera where the rat cells are

3:52

peppered throughout the mouse's body and

3:54

we can see them Either

3:56

because they cause different fur color or because

3:58

we educate them. the near them to glow

4:01

in the dark red or green and the

4:03

mouse cells you not so we can look

4:05

under a microscope and see flow in the

4:07

dark red rats cells in the brain all

4:09

over the brain and also in the other

4:12

tissues. And how does this

4:14

address? Your question is seeing how we can

4:16

six bits of the brain that we want

4:18

to put cells into in the future. The

4:20

first question is. Are. There places

4:23

rat South Sam though in the brain

4:25

and places they can not and we

4:27

were able to clear the whole brain

4:29

and look through it with a microscope

4:31

and say. Basically. The

4:33

Raza seem to be very good at going

4:35

almost anywhere in the whole brain. That says

4:37

this kind of approach. The brain has flexibility

4:40

throughout the whole brain right now. If he

4:42

wanted to fix a broken brain, me at

4:44

least think we can do it in a

4:46

lot of different places. Question.

4:49

To that is well if there was something

4:51

wrong with the brain that the rat cells

4:53

go in and rescue it and fix it.

4:55

If the mouse his brain have a disease.

4:57

Or have been injured. And how did you

5:00

test that? So be tested

5:02

that. By using genetic

5:04

tracks we made. A mouse.

5:07

Brains that were missing. Important sells

5:09

for the mouse including those that

5:11

are important. For their sense of

5:13

smell. So in one case, we. Killed

5:16

those cells and ask for the

5:18

rats have come in and restore

5:20

that part of their nose and

5:22

in other cases instead of killing

5:24

them we just made them very

5:26

bad. At. Talking to the rest of the

5:28

brain so that animal couldn't smell, but

5:30

the cells were still there. And those

5:32

are sort of similar to things that

5:34

happened to humans either. They had a

5:36

disease we lose. The neurons are you

5:38

have the disease where they're just not

5:40

working very well. On

5:43

the question is you do this to the

5:45

mouse. And. Then see if the

5:47

rat cells come in a make good.

5:49

So before we think about whether they

5:51

world to, they actually go to the

5:53

right place and restore what's missing. That

5:56

was remarkable that they actually go

5:58

to the right place and. The

6:00

right kind of cells are they are. They

6:02

are adapting to that environment. They're born at

6:04

the right time and they become the right

6:06

size com and shape to sit into the

6:09

mouse brain, which is quite a bit smaller

6:11

than the rat. Brain so that is

6:13

already great news and her that

6:15

they can. Look like they're in the

6:17

right place and be the right kind of

6:19

neuron and that was one of the most

6:21

exciting early findings We out how to the

6:23

red cells. Know. We're.

6:26

The problem is in the mouse brain that

6:28

you've caused. And. Therefore, how to fix

6:30

and also to look like mouse cells when the

6:32

doing it. Right?

6:34

So all the cells go through

6:37

the stages of development and they

6:39

become. Something called. A Brains

6:41

and this our neural stem cell and

6:43

at that stage. They start to

6:46

listen to their environment which

6:48

tells them. Depending on where they're

6:50

sitting, what kind of brain cell? kind?

6:52

Of neuron of the com so if they happen

6:54

to be in the nose region.com The kind of

6:56

neurons that are important for smell as they happened

6:59

to be and an ice they might become the

7:01

kind of neurons. Is that are important. So

7:05

you get the smell system recapitulate is

7:07

obe it built by rat cells in

7:09

these mice. Exactly.

7:11

And that was a. Wonderful result

7:13

to see. Indeed to the

7:15

kind of argues if we did this

7:18

in human with human cells the might

7:20

work even better. Boots they should be

7:22

instruction sets there to guide the cells

7:24

to become the right thing. But the

7:26

key question must be do they work?

7:28

So if you test the smell system

7:30

in the mice that allow got a

7:32

rat sense of smell do they seem

7:34

to be smelling. That. Was the

7:36

big experiment when we found that being

7:39

in the right place at the right

7:41

time can build a rat nose and

7:43

mouth and would that. Mouse be able

7:45

to use that knows to do with it

7:47

like city which assigned a hidden cookies and

7:49

so we use this test for a mouse

7:51

in a cage where a many Oreo is

7:54

hidden and ask does it find it how

7:56

long as it takes and the mice that

7:58

we had. disrupted their

8:00

smile system wouldn't find the

8:02

cookie. And when we put the rat cells into

8:04

a mouse that had no mouse cells that could

8:07

do this, the mice were able to

8:09

find a cookie using a rat's nose. In the

8:11

other hand, this is not just plug

8:14

and play because if the mouse cells

8:16

were there but quiet or silent, in

8:19

that case, the mouse couldn't use the rat cells.

8:22

So we learned already that there are rules to

8:25

how well your brain can take

8:27

in different signals or signals

8:29

for a circuit that has been

8:31

hurt and is now being repaired. That

8:34

sounds like it might be a stumbling block then. So if

8:36

you have cells that are already there and

8:38

they're not working properly, they can get in

8:40

the way and frustrate the repair process. That

8:44

is one possibility suggested by the

8:46

work and something that we'd

8:48

like to investigate further because that's very important

8:50

to design appropriate cell therapies for

8:53

humans. I have to

8:55

ask you the question, are there things that mice like the

8:57

smell of that rats don't and when you test your mice,

9:00

you find that there are things that they've developed

9:02

a rat preference for that a mouse never would?

9:05

Well, that's my favorite experiment and we are gearing

9:07

up to try to do that. It takes

9:11

a few more tricks but one

9:13

thing is that mice actually smell

9:15

a rat, a cat or even a

9:17

snake and are instantly afraid they'll freeze.

9:20

Rats are not afraid of rats so what we'd really

9:22

like to do is see if that mouse with a

9:24

rat nose is no longer afraid of a rat. Very

9:27

exciting. Christine Baldwin there at Columbia

9:29

University in New York. China

9:32

is home to around one and a

9:34

half billion people which is more than

9:36

a sixth of the world's entire population

9:39

and the country's rapid urbanization

9:41

in recent years has seen

9:43

skyscrapers thrown up and groundwater

9:45

extracted at massive rates to

9:47

meet people's needs. But now

9:50

a new report published in the

9:52

journal Science has found that this

9:54

expansion is causing many of China's

9:56

biggest cities to literally sink into

9:58

the ground. out more

10:00

we put in a call to Robert Nichols,

10:02

who's director of the Tyndall Center for Climate

10:05

Change Research at the University of East Anglia.

10:07

He authored a commentary on the research. One

10:10

of the Chinese scientists, a very large group

10:12

of Chinese scientists, studied 82 cities

10:16

around China, the biggest cities, and

10:20

they used satellites to

10:22

measure how fast the land in

10:24

these cities is sinking or rising

10:27

and they found that many of

10:29

them are sinking sometimes

10:31

quite rapidly, more than a centimeter

10:33

per year. Oh goodness, that

10:35

is a lot. Absolutely, I mean it's

10:37

a substantial change and when you add

10:40

it up it can have quite big

10:42

sort of consequences if that continues. Why

10:44

do they think it's happening? Several reasons

10:46

but probably the biggest one is

10:49

groundwater withdrawal. These cities are

10:51

expanding very rapidly and when

10:53

you have increasing demand for

10:56

groundwater you pump it out

10:58

and actually the soils beneath

11:00

these cities when the geology's right,

11:02

doesn't happen for every city, you

11:04

get consolidation. The land literally falls

11:07

as the water is taken out.

11:10

Lots of cities though rely on

11:12

groundwater for their supplies.

11:14

Perth, Western Australia has seen

11:16

its groundwater levels drop considerably.

11:18

Cape Town in South Africa

11:20

relies very heavily. America,

11:22

also parts of America, lots and lots

11:24

of groundwater extraction. So is this likely

11:27

to be happening everywhere and it's just

11:29

that the Chinese have spotted it or

11:31

is this a uniquely Chinese problem? It's

11:34

not happening everywhere because many areas that

11:36

contain water on the ground like limestone,

11:38

when you take the water out they

11:41

don't drop. I mean, inside of England

11:43

we take water as a chalk and

11:46

that doesn't consolidate. In the case

11:48

of China it's the geology. They've

11:50

got sands, mud,

11:52

plays that are geologically

11:54

recent and they're very

11:56

old compared to you and I but they're

11:58

geologically recent. And when you

12:01

take the water out, the actual density

12:03

of the sediment increases. It's called consolidation,

12:05

and that causes the land to sink.

12:07

But it's not only happening in China.

12:10

Deltas are particularly prone to this. And

12:13

there are many, many deltas in

12:15

Asia, particularly around the Himalayan plateau.

12:18

What's the natural evolution of this, then? Does

12:20

it mean that, because of what

12:22

you've just said, these buildings will

12:24

settle eventually, and the retreat will

12:26

stop? Or are they going to

12:28

continue for the foreseeable to sink

12:30

like this? They won't

12:33

sink forever. So if you keep

12:35

on pumping groundwater, eventually all

12:37

the potential to settle has been used

12:39

up. Tokyo, for example,

12:42

subsided up to five meters in

12:44

the 20th century. So

12:46

you can get very large changes. Parts

12:48

of the central valley of California have

12:51

gone down more than 10 meters.

12:53

That's not in an urban area. So

12:55

you can get very large changes. Why

12:58

is it damaging? Well, it's

13:00

not normally uniform. So

13:03

you find that buildings will

13:05

literally fall down. Or

13:08

in the central area of a city where

13:10

maybe the demand for groundwater is highest, will

13:13

become a bowl, and it

13:15

will flood much

13:17

more frequently. So it will mess up the hydrology.

13:20

And if you're near the coast, if

13:22

the land sinks, the sea will flood it.

13:25

Just as if the sea level rose, the

13:27

land sinking will have the same effect. So

13:30

what can China do about it? Should they

13:32

be looking for other sources of water? Do

13:35

they need to be building their buildings differently? What's

13:37

the solution? First of all, it's

13:40

important to recognize this is happening. And

13:42

then you ask, what can we do about it? One

13:45

solution is to try and

13:47

provide other sources of water so that

13:50

they don't exploit the groundwater. That,

13:52

however, may not be possible. So

13:55

the first thing is, can we stop

13:57

removing groundwater? If not, can

13:59

we... adapt to these changes. But then

14:01

at least you're not being surprised by them

14:03

and back to your point maybe you can

14:06

build buildings that won't fall over if they

14:08

subside. Or on the coast maybe you have

14:10

to build dikes to keep the sea out

14:12

or maybe you have to move. I think

14:15

multiple solutions and it will vary from place

14:17

to place. It sounds expensive. I

14:19

think it is costly. Without doubt. Often

14:22

this problem is seen as a very

14:24

local problem and I think one of

14:26

the arguments we make in our piece

14:28

is that it's a big

14:31

problem and as you say it's

14:33

costly. Recognising it is going

14:35

to lower the cost because you're going to start

14:37

to plan proactively. Robert Nichols,

14:40

Director of the Tyndall Centre for Climate Change

14:42

Research at the University of East Anglia. You're

14:45

listening to 5 Live Science with me Chris

14:47

Smith. Still to come we're going to be

14:49

looking at ADHD, Attention Deficit Hyperactivity Disorder to

14:51

find out what it is and how science

14:53

can help us to better deal with the

14:55

disorder. Before that though,

14:58

to Cambridge University where researchers have

15:00

developed a way to use low

15:02

cost copper based semiconductors to produce

15:04

photovoltaic or solar panels that capture

15:07

the sun's energy but then also

15:10

use it to drive chemical

15:12

reactions on their surfaces. Effectively

15:14

it's an all in one chemical factory

15:16

that could produce simple fuels like hydrogen

15:18

or even more complex carbon based molecules

15:21

in the future. It's the

15:23

brainchild of physicist Sam Stranks. So

15:26

generally what we're trying to do is

15:28

harvest sunlight and convert that sunlight to

15:30

useful energy to do chemistry. And so

15:32

here we're splitting water to produce hydrogen

15:34

which could be used as a fuel.

15:37

So what is the actual problem we're trying to

15:39

solve? One of them

15:42

is how efficient we can harvest the sunlight and

15:44

convert it to energised electrons. Typically

15:46

this is done with silicon, it's a very

15:48

good material that can do this very very

15:50

efficiently but silicon is quite expensive to produce

15:52

so we've been using copper based materials which

15:54

are at the moment very inefficient, we've been

15:56

making them more efficient. These are cheap to

15:58

make and cheap to use. If

16:01

you can pull this off, what sort of improvement do you

16:03

think you're going to get? It's really

16:05

a step change in what we can do with sunlight. So

16:08

rather than just thinking about producing electricity,

16:10

we can start making very interesting materials

16:12

and making green fuels. So

16:14

this is, for example, carbon-based fuels

16:17

that could be used either in energy applications

16:20

or in materials developments as well. So

16:22

this is all done by green solar

16:24

power. And why have you

16:26

picked on copper? So copper is earth abundant. That's

16:28

a very important thing. We want, with these sorts

16:31

of applications, we want to be able to scale

16:33

them up in a very large way. So we

16:35

need materials that are readily available and can be

16:37

easily resourced. Copper is one of those. It's

16:40

also a very good material that does harvest

16:42

light quite well and can energise those electrons

16:44

to do the chemistry that we want to

16:46

do. So talk us

16:48

through actually how you make it, what you end

16:50

up with. If you had a physical lump of

16:52

this in front of us that we could see,

16:54

what would I be looking at? What

16:57

does it look like? And how does it actually work? Yeah,

16:59

so we make these through a process

17:01

that's called electrode deposition. So we use

17:03

chemicals dissolved in solution that can then

17:06

be converted to a solid crystal film

17:08

that will look relatively dark

17:10

and absorbing because it's absorbing the sunlight

17:12

quite well. And then we

17:14

have electrodes on them as well so we can

17:16

wire them up and measure the current, for example,

17:19

that we're getting from these devices. To all

17:21

intents and purposes then, does it work just like a

17:23

solar panel I would put on my roof? It

17:26

very much so, it does. So we have in the

17:28

same ways a solar cell has

17:30

an absorbent material that absorbs the

17:32

light and then the energised electrons are collected. It's current,

17:34

we have that in the same way in this

17:37

material. But the difference is that we have

17:39

catalysts on the surface that when the electrons

17:41

reach that catalyst then they can do some

17:43

chemistry to be able to reduce water to

17:45

hydrogen. And what was

17:48

stopping people doing this before then? So

17:50

the concept's been around for a while.

17:52

On the copper-based materials they've been limiting

17:54

because there's defects in these materials where

17:56

these electrons lose their energy to heat,

17:58

for example. So what we've really

18:01

done is being able to grow very, very

18:03

high quality crystals with fewer defects that mean

18:05

those energised electrons can travel a lot further.

18:08

And is it literally just electricity comes

18:10

out of wires and then you do

18:12

something with the electricity or is the

18:14

step here that you're doing something on

18:16

the surface of the material, so you're

18:18

doing sort of two jobs in one,

18:20

it's capturing the light, converting it into

18:22

useful energy, electricity or whatever, and then

18:24

you're doing chemistry and other exciting things

18:26

in situ there and then, fewer losses.

18:29

Exactly, it's integrated on the chip all

18:31

in one. So here, that's the advantage that

18:33

we don't have to wire it up and

18:35

then have a separate, what's called an electrolyser,

18:37

where the water splitting can happen separately. This

18:39

is all integrated into one, so it's a

18:42

very elegant solution and in principle could be

18:44

very efficient because you've got the absorber itself

18:46

energised electrons and then the chemistry is done on

18:49

the surface of that absorber. I'm

18:51

just trying to visualise that. So would you have it

18:53

sitting underwater then or do you have a thin film

18:55

of water or have you got little channels so the

18:57

water or the solution or whatever it is runs across

19:00

the surface, how do you do that? So

19:02

it is immersed in water and typically in our cells

19:04

that we make in the lab, we have a little,

19:06

essentially a little beaker that's soaking in. That

19:09

will be a challenge when we think about scaling it up

19:11

and there's different solutions for that, but that's for future work.

19:14

So the ultimate goal is it will produce

19:16

electricity which will split water into hydrogen and

19:19

oxygen. What you then tap off the hydrogen

19:21

and use that, how do you fit this

19:23

into a sort of production line? Right,

19:26

so it's extracting out the hydrogen in particular in this case

19:28

and that's something that then the hydrogen could be stored and

19:30

it could be used in applications

19:32

either on-site or off-site. So

19:34

thinking about things like green steel for example,

19:36

you could use hydrogen to produce that. But

19:40

there's also some exciting applications beyond

19:42

just hydrogen, so these materials particularly

19:45

that go beyond silicon in terms of the voltage

19:47

they can reduce, you can start to do interesting

19:49

chemistry on higher order

19:51

chemistry, so thinking about making carbon molecules,

19:53

multi carbon molecules as well and particularly

19:55

when we can start getting to these

19:57

high voltages that materials like copper oxide.

20:00

or other related materials can enable that

20:02

silicon can't at the moment. So we

20:04

can start to think about, for example,

20:06

reducing carbon dioxide to produce carbon molecules.

20:09

It's really that the holy grail of this solar

20:11

fuel world is to get to the C2 and

20:13

above carbon chemistries. C2

20:16

as in two carbons linked together? Exactly right, yep. So

20:20

very exciting. Sam Strank's there from the University

20:22

of Cambridge. It

20:24

was 14 years ago this week

20:27

that the Deepwater Horizon disaster spilled over 130

20:29

million gallons of oil into the Gulf

20:31

of Mexico. It

20:33

was the largest such spill in history.

20:36

Since then, scientists have been working on the

20:38

best way to contain disasters like this. One

20:42

problem, though, is that the chemical dispersants

20:44

that are often used to break down

20:46

oil can actually increase the toxicity in

20:48

the process. But researchers

20:50

in Israel and China say they've

20:52

come up with a clever way

20:55

around it, which involves using laser

20:57

treated cork. To find

20:59

out more, I've been speaking with

21:01

chemistry world's Philip Broadwyth and also

21:03

Boston University biologist Robinson Wally Forwiler,

21:06

who carried out the research on the environmental

21:08

impact of the disaster in the Louisiana wetlands

21:11

earlier in her career. So

21:13

it was this really intense environment, as you

21:15

would imagine, because there was all

21:17

of a sudden a huge influx of people trying

21:19

to work on this problem. We were

21:21

in and out of boats on salt marshes trying to look

21:23

for where the oil was coming up on the salt marsh.

21:26

And so it was really horrifying to

21:28

see this like, ooky substance,

21:30

for lack of a better word,

21:33

all over marsh surfaces and beach surfaces and things

21:35

like that. Many people look

21:37

at the big animals like birds, and that's

21:39

devastating when they get coated. But you were

21:42

very interested as well in the other things

21:44

in the environment that often get overlooked. What

21:46

were you looking at? We were really

21:48

interested in trying to understand how the

21:50

microbes that live in salt marshes that

21:53

do this process of nitrogen removal. It's

21:55

an ecosystem service or benefit that salt marshes provide,

21:58

and we were really interested in the process. trying

22:00

to figure out what could happen

22:02

when the salt marsh surface was covered with

22:04

oil and how that would change those microbial

22:06

dynamics. And did it? It did. And

22:09

I think some of the neatest work that's

22:11

come out of this, if you could say

22:13

like a silver lining of this awful, awful

22:15

event, is how much interesting work scientists have

22:18

done on the microbial communities, that sort of

22:20

the biodiversity of those microbial communities that are

22:22

in the environment and how they respond to

22:24

such an event. It was a huge

22:26

amount of oil that ended up in the sea, wasn't

22:28

it, Philip? How did they actually try and deal with

22:31

it at the time? Yeah, it was

22:33

huge. It was bigger than any of the sort

22:35

of spells that we'd seen before. And

22:37

it's coming up from very deep under

22:40

the water as well. There are various

22:42

ways that you can try to contain

22:44

that. You can put physical barriers in

22:46

the way, but you can also, if

22:48

you get there in time and under

22:50

the right conditions, you can apply chemical

22:52

dispersants. It's a bit like your kind

22:55

of fairy liquid. It's a surfactant. It's

22:57

breaking up the oil into smaller droplets.

23:00

And those would be applied at the surface

23:02

to try and disperse the oil over a

23:04

bigger area, so it can

23:06

disperse more quickly. But

23:08

in deep water horizon, they also

23:10

do this underwater as well. And

23:13

that changes the composition of the oil

23:15

as it comes up towards the surface,

23:18

means it's in smaller droplets, changes

23:21

the way some

23:23

of the different components of the oil go

23:25

into the atmosphere. So one

23:27

of the things that was kind of

23:29

reported later was that there were less

23:31

volatile things like benzene

23:35

in the air above the water

23:38

than there might have been had they not used

23:40

these dispersants underneath.

23:42

But the kind of flip side of

23:45

that is that then the dispersed oil

23:47

is a mixture of the oil and

23:49

the dispersants. The dispersants themselves have some

23:52

toxicity. And the mixture itself has a

23:54

different toxicological properties as well. So there

23:56

can be issues associated with the dispersed

23:58

oil. are different to if

24:01

the oil had just been kind of left on

24:04

its own. It will then bred out over a

24:06

larger volume of the sea and dispersing the oil

24:08

doesn't change its chemical composition at all. It's still

24:10

oil. The only way we kind of eventually get

24:13

rid of the oil is to have something

24:15

break it down and that's usually the

24:18

bacteria, similar to what Wally was talking

24:20

about. There's bacteria in the ocean that

24:22

will eventually break down the compounds in

24:25

oil and transport it to the seabed.

24:28

This new paper that's coming out they

24:30

say that they've got possibly something

24:32

else to bring to the party. What

24:34

are they proposing? It's taking cork, the

24:37

wood of cork trees, and they are

24:39

essentially charring it with a laser. It's

24:41

black which means it heats up in

24:44

the sun. That helps to warm it

24:46

up and make the oil a bit

24:49

runnier so that it can go into the pores

24:51

of the material. It's also

24:53

porous. It also repels water so it

24:55

can separate the oil from the water

24:57

and that makes it easier to deal

25:00

with. Sounds like you need a huge

25:02

amount though, Philip, and you're back to

25:04

sort of the problem you were saying

25:06

where you still got to go somewhere.

25:08

My interpretation is that you would have

25:10

it contained in some kind of matrix

25:12

material, some kind of blanket. There is

25:14

a similar material called oleosponge. It

25:17

is essentially like a mattress of

25:19

polyurethane mattress sponge that

25:21

then has a coating of titanium

25:23

oxide on it which does the same

25:25

thing. It makes it attract oil and

25:27

repel water and they kind of

25:30

fashion that into these mats which you can wring

25:32

the oil out of. You can put it under

25:34

the water on the top of the water. It

25:36

will absorb the oil. You

25:38

can take that off. You can physically remove the

25:41

oil by squeezing it out of the pores like

25:43

a sponge and then you can just go back

25:45

in and get some Wally

25:47

Fullwiler at Boston University and Phil

25:50

Broadwith from Chemistry World. The paper

25:52

on lasered cork has just come

25:54

out in applied physics letters. Right

25:57

now though it's time for the news and sport. Don't go away though, we're

25:59

going to be back. straight afterwards to

26:01

talk about ADHD, that's Attention

26:03

Deficit Hyperactivity Disorder, including

26:05

what it is, how many people have it, and

26:07

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26:51

Hiring for your small business, If you're

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27:26

back to 5 Live Science from

27:28

The Naked Scientists. With me, Chris

27:30

Smith. And in this half hour,

27:33

we're focusing on ADHD, that's Attention

27:35

Deficit Hyperactivity Disorder. The

27:37

Naked Scientists on 5 Live. Globally,

27:40

it's estimated around 5% of

27:43

children and adolescents, as well as adults in

27:45

fact, are affected by ADHD. But those numbers

27:47

do vary from country to country and, as

27:49

we'll find out a bit later on, diagnoses

27:52

appear to be on the rise. So

27:54

what's it like to live with ADHD?

27:56

Well, Nicola Jane Little is a social

27:59

entrepreneur who's We set up the

28:01

ADHD support group Celebrate Difference

28:03

and Tanya Martin works with

28:05

organisations around neuro-inclusion. They've both

28:07

recently been diagnosed with the

28:09

condition. We begin with Nicola

28:11

describing what ADHD is like

28:13

for her. It's like

28:16

three billion thoughts

28:18

all at the same time

28:21

and never been able to

28:23

get to the end of any

28:25

of them whilst tripping down the

28:28

stairs and not being

28:30

able to find your keys. Do

28:32

you mean as in you've got so many

28:34

things you feel you want to do, need

28:36

to do, have to think about that it's

28:39

hard to prioritise? Absolutely. And there is

28:41

never a time that the thought gets to

28:43

the end of the thought because all of

28:45

the other thoughts have barged their way in

28:47

uninvited mostly and knocked the thing I was

28:49

thinking about in the first place. And that

28:52

could be anything. It could be what am

28:54

I going to have for tea? And

28:56

then all of a sudden I'm painting a wall.

28:59

There is never a time for me where one

29:01

thing smoothly leads to a

29:03

conclusion. Your experience, Tanya, same?

29:05

Yeah, very similar. I describe it as I've

29:08

got a million little trampolines in my head

29:10

and thoughts bouncing off these little trampolines. And

29:12

they can go in all sorts of random

29:14

directions. And I never really know how I

29:17

sometimes end up where I end up in

29:19

terms of what comes after my mouth. And the

29:21

other thing for me is that I really struggle

29:23

with time and a sense of time. So

29:26

I don't really understand what time means.

29:28

So five minutes to me could mean

29:30

an hour in real life for somebody

29:33

else. Is that because you

29:35

get sidetracked by things and then sort of go

29:37

down a rabbit hole, almost like YouTube videos where

29:39

you get sucked from one thing into the next,

29:41

into the next, and you lose sense of time?

29:43

Or is it just that you have no sense

29:45

of I need to hurry, I need to be

29:47

somewhere and this is how long it's going to

29:49

take? It's the latter. I have

29:51

no sense of time. So if somebody says

29:53

to me, I'll meet you downstairs in 10

29:55

minutes. If I don't see what

29:57

the time is on a clock, I won't.

30:00

know how long 10 minutes has been. So

30:02

it means for me that I spend a lot of

30:04

time staring at the clock and staring at

30:06

the diary to make sure I'm where I need to be

30:08

at the right time. Have you noticed Nicola?

30:10

We've been on this interview for an

30:12

hour now and Tanya hasn't noticed. I

30:14

mean it could be us, it could be...

30:17

But being serious

30:19

again, Nicola when

30:22

did you realise that life was

30:24

not like that for everybody? You're describing sort

30:26

of tripping down the cognitive staircase all the

30:28

time and having and Tanya's got a hundred

30:30

million trampolines in her head. Was that always

30:32

the case and when did you realise that

30:34

that might not be the norm? So

30:37

I remember feeling different when I was

30:39

9 or 10. To feel different is

30:41

my norm and then subsequently

30:44

through my teens and twenties I

30:47

knew that the way I

30:49

perceived things and the way then I reacted

30:51

to things whether that's at work or outside

30:53

of work wasn't quite the way I thought

30:55

everybody else was doing it. I

30:58

had this feeling that I was never quite

31:00

getting there. I was never quite achieving my

31:02

potential but I didn't understand why. So most

31:05

of my life has been why does

31:07

this keep happening and I

31:09

had to ask me dad, dad why

31:11

do I keep ending up in these

31:14

situations? And then at 45

31:16

I read something I'd been scrolling

31:19

around and somebody had

31:22

put a list, this list of

31:25

problems and challenges that she'd had and

31:28

if you just took her name out and pop

31:30

my name in that was my list, that was

31:32

my life. She literally summed up

31:34

in a paragraph 30 years of

31:37

my questions. It was the most bizarre

31:39

moment of my life. Tanya did anyone

31:41

hold up a mirror to you like

31:43

that? I actually found out about

31:45

my own ADHD when I was

31:48

upskilling myself in my role

31:50

so I was having to learn

31:52

about neurodiversity which is that broad

31:54

umbrella term that includes ADHD, autism,

31:56

dyslexia, dyspraxia etc. doing

32:00

it, I was going down the list and I was

32:02

like, tick, tick, tick, tick, that's me. It was like

32:04

a bit of a light bulb moment for me. I've

32:07

also known for most of my life

32:09

that there's been something that hasn't quite

32:11

fitted and in fact I was actually

32:14

diagnosed with anxiety and depression at the

32:16

age of 13 and

32:18

I have spent my whole life trying

32:20

to fix the anxiety and depression because

32:22

as I mentioned I have a lot

32:25

of thoughts. If those thoughts aren't good

32:27

thoughts that can then manifest itself in

32:30

potentially anxious and not

32:33

so happy circumstances. So

32:35

the ADHD diagnosis for me was a

32:37

light bulb moment that shone a light

32:39

on why I have

32:41

struggled, as Nicola said, to fit

32:44

in. You feel different. And

32:46

Nicola, why did you decide to actually

32:48

formalise your diagnosis? You read that list

32:50

and you thought, yeah that's me. A

32:52

lot of adults would probably have said,

32:54

well that explains a few

32:56

things but life goes on. So why did

32:58

you actually decide to go and make this

33:00

formal? For me to get

33:03

a diagnosis that gave me an

33:05

explanation and a reason, not excuses,

33:07

an explanation and a reason for why

33:10

my patterns of behaviour as they are,

33:12

gives me half a chance to do something about

33:15

that. But if you're always guessing

33:17

or never quite certain for

33:19

me and this is probably my autistic

33:21

self, I can't see how you can

33:23

do anything positive with that. I

33:26

had to have my diagnosis because until

33:28

it was rubber stunk and

33:30

someone told me for sure it

33:33

wasn't or it may not be real. Nicola

33:36

Jane Little and Tanya Martin there and we'll

33:38

hear how Nicola and Tanya attempt to manage

33:40

their symptoms a bit later on. But

33:44

first, what exactly do we know

33:46

about ADHD? Well here's Jo Steer.

33:48

She's a consultant clinical psychologist and

33:50

author of My Unique ADHD World.

33:53

She's also the editor of Understanding

33:55

ADHD in Girls and Women. Broadly

33:57

speaking, we talk about ADHD as a... neurodevelopmental

34:00

condition or disorder and what

34:03

that means is it's lifelong

34:05

and it impacts on your

34:07

brain, it's the way your brain functions and

34:10

this means that if you're a

34:12

child and you are identified as

34:14

having ADHD you're very likely to

34:17

continue to have that into adulthood.

34:19

It might look differently and impact

34:21

differently in your adult life or

34:23

even throughout your childhood. Those symptoms

34:25

can shift and change slightly depending

34:27

on the demands that are being

34:29

made on you but also

34:32

depending on the support that's around to help

34:34

you with the difficulties you

34:36

struggle with. So it can look

34:38

different at different points, it's really

34:40

important to remember that and

34:42

what's also of note is that

34:45

we're finding more and more adults

34:47

are now coming forward and identifying

34:49

that they need an assessment for

34:51

ADHD and they weren't

34:53

identified in childhood and potentially

34:56

they have had those difficulties all the

34:58

way through their life. That's part

35:00

of the criteria, we need to see

35:03

evidence that these difficulties were there

35:05

before the age of 12 years and

35:08

many of these adults can tell

35:10

us in lots of detail that

35:13

they've had lifelong concerns around attention

35:15

and hyperactivity and impulsivity but they're

35:17

only now coming forward for an

35:20

assessment, perhaps just

35:22

learning about ADHD for the first time

35:24

or feeling confident enough to ask for

35:26

that assessment even though they might have

35:28

actually been struggling throughout the whole of

35:30

their childhood adolescence and into their

35:33

adult lives. Do

35:35

we know anything about risk factors? Is

35:37

it more common in families? Is one

35:39

gender more likely to have this than

35:41

the other? What do we know about

35:43

that aspect? We definitely know that

35:45

it runs in families. We do

35:47

see a genetic link so we

35:50

do see children who their

35:53

parents have symptoms perhaps they

35:55

may not have been diagnosed but certainly have

35:57

some of some of the symptoms or even

36:00

where more than one sibling

36:02

have the difficulties. Sometimes it

36:05

might not be the immediate family

36:07

that all have ADHD

36:09

or a number of people have

36:11

ADHD but a more extended family

36:13

so if you look out to

36:15

cousins or aunties and uncles but

36:17

it is really common and it's

36:19

definitely a risk factor that someone

36:21

in the family may be neurodiverse

36:23

and have ADHD. However there are also

36:25

times when I assess children

36:27

and adults and they come and

36:30

they can't identify anybody within their

36:32

family that has similar difficulties whether

36:34

they've been diagnosed or not. So

36:36

it's not a given and I

36:38

always say to young people and

36:41

adults that just because you have ADHD

36:43

doesn't mean that you will go on

36:45

to have a child who has ADHD

36:47

but it does increase the risk absolutely.

36:50

There can be

36:52

other factors that increase the risk

36:54

as well but nothing is causal

36:56

so there isn't one thing that

36:58

we know if this

37:01

happens this definitely causes ADHD.

37:03

So children

37:05

that are born prematurely, babies that

37:07

are born prematurely have an increased

37:09

risk of ADHD but not all

37:11

babies that are born prematurely will

37:14

have ADHD. So there are factors

37:16

like that that can play into

37:19

the situation but are not

37:21

causal. What about imaging

37:23

studies if we put people in brain

37:25

scanners does anything leap out? We

37:27

do know that there are differences

37:29

in the brains of people who

37:32

have ADHD and people who don't

37:34

and those differences can be in

37:36

the structure of the brain as

37:38

well as the neurochemistry of the

37:40

brain. Now what's really interesting is

37:42

at the moment where we're at

37:44

we can't pop someone in a

37:47

brain's camera and do the neuroimaging

37:49

and say right we can see

37:51

you've got ADHD so it's not

37:53

visible on an individual basis but

37:55

when we analyze groups so

37:58

a group of people who

38:00

have ADHD and their brain scans and

38:02

a group of people who don't, that's

38:04

when those differences do show up. I

38:07

hope in years to come, we may

38:09

progress and find that we are able

38:11

to use those brain scanners to help

38:13

us identify these differences more clearly in

38:15

an individual basis. But what we're seeing

38:18

is we know that

38:21

there are some key neurotransmitters

38:23

and what a neurotransmitter is,

38:25

is the body's chemical in

38:27

the brain that helps us

38:29

move messages around our brain.

38:31

And there are two key neurotransmitters

38:33

that we know are implicated within

38:36

the ADHD. So one of them

38:38

is called dopamine and the other

38:40

one is called noradrenaline. And we

38:42

know both of those are what

38:44

we might call dysregulated or different

38:46

in the brain of people who

38:48

have ADHD. To

38:51

what extent though, is a person with ADHD a

38:54

normal person? And what we've done is

38:57

to medicalise an extreme

38:59

of normality. Because if we think about the

39:01

population as a range of different traits

39:03

and personalities and behaviours and

39:06

characteristics, and there are

39:08

always extremes in a normal range and some

39:10

people might be at one end of that

39:12

range. And are we not in danger of

39:15

giving people a label when there isn't anything wrong

39:17

with them? It's just the way they are. I

39:20

think that's a really important question

39:22

and a really hot topic, absolutely.

39:24

And I think one of the

39:26

things that's really important to remember

39:29

about ADHD is that

39:31

you need to go for an

39:33

assessment with a qualified medical professional

39:35

to be diagnosed with ADHD. And

39:37

part of that process is to

39:40

assess and understand the impact of

39:42

the difficulties on somebody's life. So

39:44

the impact on school, the impact

39:47

on home or in the workplace,

39:49

depending on where someone's

39:51

at in their lifetime really.

39:53

And there has to be

39:55

a significant impact of their

39:57

symptoms of inattention, hyperactivity and

39:59

impulse. positivity on their daily

40:01

living and that's part of the criteria

40:03

to meet the threshold for

40:07

an ADHD diagnosis. Joe

40:10

Steer there. Now as Joe was just telling us,

40:12

the only way to find out if you have

40:14

ADHD is to get a diagnosis. But

40:16

there's been a huge uptick in referrals

40:19

in many nations with one prominent health

40:21

think tank here in the UK saying

40:23

that demand has overtaken the capacity to

40:25

meet it. I've been speaking with Thea

40:27

Stein who's the Chief Executive of the

40:29

Knuffield Trust. Interestingly, the data isn't collected

40:32

at a national level in terms

40:34

of the waiting list data. So

40:37

whilst I've got really good waiting

40:39

list data for assessment for autism,

40:41

there actually isn't the similar figure

40:44

for ADHD. What

40:46

we did though was use a proxy,

40:48

something to help us understand

40:51

that which was prescribing data

40:53

for ADHD medication. And

40:55

what we could see there between 2019-20 to 2022-23, so those

40:57

years between that, we had

41:02

a 51% increase

41:05

in the prescription medication for

41:07

ADHD. So

41:09

we know that something

41:11

is going on by looking at that

41:14

because a lot of people, children and

41:16

adults who have ADHD do

41:18

get a prescription for medication. And

41:20

so we thought by looking at that would give

41:22

us some idea of the scale of what was

41:25

happening. We also know through

41:27

a petitions committee that there are a

41:29

lot of people who are waiting really,

41:31

really long periods of time. And

41:34

at least 10% of

41:36

adults and children are waiting between two

41:38

and three years. Knuffield Trust

41:40

Chief Executive Thea Stein. Now Thea was

41:42

just explaining that the number of people

41:45

being prescribed ADHD medication has been used

41:47

to determine the extent of the condition.

41:50

It doesn't of course tell us the whole story

41:52

though. How does that medication affect

41:54

the people who take it? Here's

41:56

Nicola J. Little and Tanya Martin again.

42:00

with you. One of the reasons why

42:02

I wanted to gain a diagnosis was

42:04

because I wanted to try medication. For

42:06

most of my life I've been in

42:08

these bouts of depression and anxiety and

42:10

I wanted something to fix my brain.

42:12

I went to my GP, had a

42:14

conversation with her, she was

42:16

incredibly supportive and

42:20

I got a diagnosis quite quickly after

42:22

that. You mentioned

42:24

managing your symptoms and wanting to try

42:26

medication. What did you use? We

42:31

actually didn't get on with it very

42:33

well. I tried both stimulant and non-stimulant

42:35

medications. Unfortunately

42:38

I'm not medicated now because

42:41

whilst they helped some

42:44

of the symptoms, they made other

42:46

symptoms worse for me personally. Was

42:48

that your experience Nicola or have you just

42:50

gone down the behavioural route knowing the problem

42:53

and grappling with it that way? I

42:55

know I'm fully medicated up to my eyeballs. It's

42:58

the best decision I ever made is to

43:00

try stimulants.

43:03

For someone with ADHD and

43:06

again the narrative is really misunderstood,

43:08

a stimulant for me that might

43:10

stimulate someone else to make them

43:12

high I suppose is the term

43:14

for me. The stimulants let

43:16

me think in a straight line. So instead of

43:18

the plate of mad spaghetti that I can never

43:20

get control of, I have a

43:23

better opportunity to start a thought and get to

43:25

the end of the thought, to start a

43:27

task and get to the end of a task,

43:30

to be able to rationalise in

43:32

a different way. The meds for me

43:34

have changed my life in a positive

43:37

way. That's not to say

43:39

I always wanted to take them or

43:41

wanted to take them but in doing

43:43

so has fundamentally changed my life. I

43:47

also caught up with Barbara Sahakian. She's

43:50

the Professor of Clinical Psychology at the

43:52

University of Cambridge. This is one of

43:54

her specialisms and we talked about what

43:57

types of treatment people with ADHD are

43:59

currently prescribed. Methylphenidate.

44:01

Is also known as Ritalin. This

44:03

one of the most effective treatments

44:05

for a D H D and

44:07

it is really the first line

44:09

treatment that is offered to people

44:11

if you have moderate to severe

44:13

symptoms as he sees his symptoms

44:15

and mild they can be managed

44:17

was more psychological treatments such as

44:19

cognitive behavioral treatments and sort of

44:21

stuttering your activities and helping you

44:23

plan and that sort of thanks

44:25

Er Visits are more moderate to

44:27

severe. you may need a drug

44:29

treatment and and methylphenidate. Is you see

44:31

the first choice? What sort? Of a difference

44:34

does that might do? We have an in

44:36

quantitative for objective numbers we can put on

44:38

this. Has been said to be

44:40

about seventy percent effective and it seems

44:42

to work. And most people of

44:44

course no drugs work for everybody and

44:46

some people may have como abilities,

44:48

which means that you know they might

44:51

have anxiety or depression along with the

44:53

A D H D. and that may

44:55

be that the drugs doesn't work

44:58

quite so well in some other groups

45:00

with these com morbidities. What we

45:02

understand. About what the drug is actually

45:04

doing. In. The brain of someone with

45:06

a D H D to get them that

45:08

benefit. So. The chemicals on the

45:10

brain dopamine and noradrenaline a both

45:13

increase by muscles on a date

45:15

and what happens has saved We

45:17

take a sexy blocked so there's

45:19

more in the synaptic cleft so

45:21

that basically booths dopamine. And noradrenaline in

45:24

the brain? Do people who have a D

45:26

H D have a deficit in those chemicals

45:28

to start with? Or is there something else

45:30

roman boost in the levels of help to

45:32

solve another problem? well what we do

45:34

know is that can be changes in

45:37

the brains of people with a d

45:39

h d and that actually when they're

45:41

on drugs chronically like methylphenidate especially if

45:43

their children when they stop these drugs

45:46

they can actually mitigate the effects that

45:48

you see in the brain cells they

45:50

do do that but also are we

45:52

do know that mess of senate eight

45:55

is what we might call a cognitive

45:57

enhancing drugs so for anybody who has

45:59

some problems with attention, it will

46:01

improve attention, or for impulsivity,

46:04

it will do that as well.

46:06

So it is a sort of

46:09

general cognitive enhancer. And in

46:11

our study that we published in Brain with

46:13

Natalia Del Campo and other people, we showed

46:16

that the drug is not actually acting in a

46:18

different way in the brain of people with ADHD.

46:20

It's the same as it would in a control

46:23

group of people without ADHD. That's

46:25

part of the issue because people

46:27

have been suspicious sometimes and

46:30

the Care Quality Commission has said, you

46:32

know, the reason for increases in prescription

46:34

is because ADHD is being

46:37

identified and diagnosed more in children,

46:39

which is good, and now

46:41

in adults too, which is also good,

46:43

but there may be also circumstances where

46:45

people are using it more as a

46:47

cognitive enhancing drug and perhaps don't really

46:49

need the drug, but want to use

46:51

it because it helps with their attention

46:53

as well. And the issues. Nicola

46:56

said that it helped her

46:58

quite a bit. Tanya, on the

47:00

other hand, said she just couldn't get on

47:02

with it. Is that normal? Well,

47:05

there'll always be some people that the drug

47:07

doesn't work for. I mean, I think the

47:09

first person, you know, benefited from it and

47:12

most people will benefit from it. But

47:14

if you have some comorbidities, so for

47:16

instance, one of the side effects, sometimes

47:19

people can get a bit more nervousness

47:21

or, and so if you've got anxiety,

47:23

it might be it may exacerbate that,

47:25

for instance. And there's other

47:28

conditions where, you know, if you have a

47:30

sort of bipolar disorder, it might

47:32

exacerbate your mania, for instance. So

47:35

you have to be careful when

47:37

there's comorbidity involved. But in somebody

47:39

who has only the ADHD disorder,

47:42

then it should work out reasonably

47:44

well for treatment. One of the

47:47

paradoxes about this is that people with ADHD

47:49

struggle to stay on task and focused on

47:51

doing one thing, they want to be on

47:53

to the next thing before they finish the

47:56

first thing. And the

47:58

drugs that we're exploring to try to

48:00

help them are actually sometimes abused

48:02

because people want more energy and

48:04

want to be more impulsive. And it

48:06

seems a bit weird that we

48:08

treat a condition of impulsivity with a drug

48:11

that can make people impulsive. Yeah,

48:13

I mean, I first started to study the

48:15

drug because I was fascinated by the fact

48:18

why would you give a stimulant drug to

48:20

somebody who was hyperactive. But

48:22

actually the evidence is that it helps

48:24

control the behavior. There

48:27

is this idea that there's an inverted

48:29

U-shaped function with the arousal level so

48:31

that if you're under aroused, the drug

48:33

will bring you out to an optimal

48:35

level of arousal. If you're over aroused,

48:37

it will bring you down again. So

48:40

it may well be that it's working

48:42

to get the right optimal

48:44

level of arousal for whatever your

48:46

behavioral circumstances might be or your

48:48

cognitive circumstances as the case in

48:50

schools and universities. The University

48:52

of Cambridge is Barbara Sahakian. Well,

48:54

finally today, we're going to look at the new

48:57

and innovative ways that scientists are trying to help

48:59

people who have ADHD. Ellie Domet

49:01

is a professor of neuroscience at King's

49:03

College London where she leads their ADHD

49:06

research lab. We know from our

49:08

own research that individuals with

49:10

ADHD often end up exercising

49:12

as a way that they

49:14

recognize if self-managing the symptoms.

49:18

Changes in diet have been looked

49:20

at in various different ways. So

49:22

there's no recommendation, for example, to

49:24

do things like remove food for

49:26

the room, which is an area

49:28

that received quite a lot of

49:30

media coverage previously. The longest study

49:32

that's looked at diet has determined

49:34

something with a few foods to

49:36

do it. So that's

49:38

where you sort of remove lots of food and then

49:40

gradually reintroduce them and examine what happens to symptoms. And

49:43

that's probably the one that's received the

49:45

most attention, but it is also showing

49:47

very small effects. So whilst it could

49:49

be beneficial, those effects are quite small.

49:52

But while it's looking at diet

49:54

and exercise, there is research looking

49:56

into things like mindfulness and mindfulness

49:58

study into ADHD. have

50:00

seen some improvements. One

50:03

of the challenges to all treatments for

50:06

ADHD is that ADHD rarely

50:09

occurs by itself. It's a condition

50:11

that is often co-occurring or comorbid

50:13

to use in the medical term,

50:16

co-occurring with other conditions. And in

50:18

adults, it's particularly common, for example,

50:21

to see ADHD alongside depression or

50:23

anxiety or weight of these. Now,

50:26

mindfulness may be beneficial,

50:28

but what we're not clear on yet is,

50:30

is it beneficial to the

50:33

ADHD or does it reduce some

50:35

of the symptoms of depression and

50:37

anxiety so the person feels better,

50:39

even though their ADHD symptoms have

50:41

remained. So there's various lifestyle approaches

50:43

that are being taken to look

50:46

at how we could

50:48

improve the experiences of somebody with ADHD.

50:50

And then there's also behavioral

50:53

type treatments that are more

50:56

novel and innovative, so ones that are not

50:58

yet currently recommended, but people are looking in

51:01

search. So we're doing some work,

51:03

for example, on eye movement training

51:05

and whether that could be beneficial

51:07

to individuals with ADHD. We're particularly

51:10

looking at adults. So there's a

51:12

range of different approaches that are being

51:14

investigated. And that's a really important thing

51:16

because when a condition is as diverse

51:18

as ADHD, you will

51:21

not get a one-size-fits-all solution. How

51:23

might the way you move

51:25

your eyes affect your ADHD experience?

51:28

So the hypothesis that we're working with, and

51:30

it is very much still a hypothesis, which

51:32

means we're trying to test this idea out

51:34

so we haven't got definitive proof, but

51:37

our hypothesis relates to the fact that we

51:39

produce tiny eye movements all the time. And

51:41

these are ones that we're not even aware

51:43

we're making. And when we

51:45

make those eye movements, they're like rucicates.

51:48

They're very, very tiny. Those

51:50

eye movements are controlled by a very

51:52

small region in the middle of the

51:54

brain called the superior colliculus. The

51:57

superior colliculus is responsible

51:59

controlling those eye movements and the

52:02

movements correlate very strongly with

52:04

symptoms of ADHD. The

52:06

superior colliculus itself has been implicated in

52:09

the brain basis of ADHD in a range

52:11

of studies. What's

52:13

interesting and what offers the possibility

52:16

of a treatmental intervention is

52:18

that eye movements can be trained. So we

52:20

know that by doing various tasks to control

52:22

where we look with our eyes, we

52:25

can alter the movements that we make. And

52:27

in order to make the alteration of course,

52:29

we're actually altering the brain activity in the

52:31

area that controls the movements. So

52:34

if we can control our

52:36

eye movements by altering activity in that

52:38

area, and that area is also responsible

52:41

for some of the symptoms of ADHD,

52:43

then that may in turn improve

52:45

the symptoms. So this

52:47

is a very experimental idea, but

52:49

it just demonstrates this need

52:52

to look outside of traditional medication

52:54

treatments for ADHD and also recognises

52:57

the fact that we

52:59

still don't have a brilliant understanding of what's changing in

53:02

the brain with ADHD. So

53:04

we need to be constantly exploring

53:06

possibilities. Ellie Domet

53:08

from King's College London there. Well,

53:11

that is it for this week, but 5 Live

53:13

Sciences back at the same time next Sunday when

53:15

life in space is what we're going to be

53:17

looking at. Can we grow food? And

53:19

what does it do to our bodies to be

53:21

in space for long periods of time? We

53:24

will find out. If you'd like to get in touch in the meantime, 5livescience

53:26

at bbc.co.uk is the email address.

53:29

Until next time, from me, Chris

53:31

Smith, thank you for listening and

53:33

goodbye. BBC

53:35

Sound, Music, Radio, Podcast.

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