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2:16

Hey everybody, Chris Kresser here.

2:18

Way back in 2008, I wrote

2:20

an article called the chemical imbalance

2:22

myth, which challenged the dominant

2:26

idea that depression is caused by

2:28

chemical imbalance in the brain and changes

2:30

in serotonin levels. As

2:33

you can imagine, it was a pretty

2:35

controversial article, probably

2:38

received more comments than

2:40

just about anything else I've ever written, along

2:43

with quite a lot of hate mail and

2:46

pretty strong attacks, despite

2:49

the fact that the article was very well

2:51

referenced and included

2:53

many links to peer-reviewed evidence.

2:57

And since then, that theory

2:59

has only fallen apart

3:01

further. Most recently,

3:04

with a landmark paper that was published

3:06

by Dr. Joanna Moncrief

3:09

and colleagues, it

3:11

was a meta-analysis.

3:13

So it was a review of meta-analyses

3:16

that have been published on this topic, and

3:19

it just systematically debunked

3:22

the

3:24

idea that

3:26

depression is caused by

3:28

a chemical imbalance and changes

3:30

in serotonin levels.

3:32

So that's the topic of this show, and

3:35

I'm really excited to welcome Dr.

3:37

Joanna Moncrief as my guest. She's

3:39

a professor of critical and social psychiatry

3:42

at University College London and

3:44

works as a consultant psychiatrist in

3:46

the NHS. And she has

3:48

been researching and writing about the overuse

3:50

and misrepresentation of psychiatric drugs

3:53

and about the history, politics, and philosophy

3:55

of psychiatry for many,

3:58

many years. came

4:00

across her work in the early 2000s,

4:03

which is what led to me writing that series of articles

4:06

starting in around 2007 or 2008. And

4:09

since then I have followed

4:12

her work for all of that time and

4:15

continue to be just blown

4:17

away by how persistent

4:20

this myth is in the

4:22

complete absence of evidence to support

4:25

it. So I just want

4:27

to warn listeners that

4:29

this episode could be provocative

4:32

if you're currently taking an antidepressant and

4:35

if you if this is

4:37

news to you that this theory

4:39

of chemical imbalance is not

4:42

supported by the evidence. I

4:44

just want to gently invite you to

4:47

listen to this with an open mind, to not

4:49

take it personally, to

4:52

understand that there are forces at

4:54

work that namely

4:57

pharmaceutical companies that

4:59

have invested tens

5:01

if not hundreds of millions

5:03

or even billions of dollars in perpetuating

5:05

this hypothesis, which

5:09

that's even a generous term to use

5:11

a hypothesis. It's really more of a marketing

5:13

campaign that has been used

5:16

to sell more antidepressant

5:18

drugs. And again, this

5:21

this could be disturbing. I want

5:23

to give you fair warning, but I also

5:26

hope that you can

5:28

listen to it and take in some

5:30

of the information because ultimately I believe

5:33

it's incredibly empowering to

5:35

learn that depression

5:38

is not some

5:40

permanent thing that we can't

5:42

change, some flaw

5:44

in our brain that can only be addressed by taking

5:47

a psychiatric drug, and

5:49

that we actually have quite a bit of agency

5:53

over our own mental health and the

5:55

ability to make progress

5:57

without

5:58

taking these drugs. in many cases.

6:01

So I realize that's a longer

6:03

intro than normal, but this is I think

6:06

a very important episode. I really

6:10

enjoyed this conversation with Dr. Moncrief

6:13

and I have the deepest respect for

6:15

her work and her persistence

6:18

in the face of great opposition, not

6:20

opposition to the science, which nobody

6:23

really seems to be able to challenge, but

6:25

just to the general idea because

6:28

as Upton Sinclair once said, it's

6:31

difficult to get a man to understand something

6:33

when his salary is dependent on him not understanding

6:35

it. And I think that's largely

6:38

what's going on here with this particular theory.

6:40

There are just too many, too much

6:42

money invested in perpetuating

6:45

it and also, you

6:46

know, probably lots of careers and reputations

6:49

on top of that. So

6:51

my hope is that as Dr.

6:55

Moncrief and others who

6:57

are publishing, you

6:59

know, very, very detailed

7:02

and complete

7:04

analyses that debunk this theory

7:06

that over time the public perception

7:09

will shift. That's my hope. And

7:12

I hope that this podcast can play some small

7:14

role in that happening. So

7:18

without further ado, let's dive in.

7:21

Dr. Joanna Moncrief, thank you for

7:23

being here. It's such a pleasure to have you on the show.

7:26

Thank you for having me. Looking forward

7:29

to our conversation. So,

7:31

yes, I've been really looking forward to this because

7:33

as we were chatting before the recording started,

7:36

I've followed your work for at least 15 years.

7:38

I've been writing about the chemical imbalance

7:41

theory of depression since

7:43

then and over those many years

7:45

and other researchers like Dr. Elliott

7:47

Ballenstein.

7:49

And I think I'd like

7:51

to just start with the history here. How

7:54

did this idea that

7:56

depression is caused by a chemical imbalance

7:59

and particularly

7:59

serotonin depletion or serotonin

8:02

imbalance get started in the

8:04

first place because it became widespread

8:06

and pretty much anyone you would ask on the street

8:09

would say that that's

8:11

what causes depression. But how did this even

8:13

start?

8:15

So that's a good question. So it

8:17

starts in the medical community,

8:20

it starts in the 1960s

8:23

when

8:24

drugs, certain drugs

8:26

start to be proposed to have antidepressant

8:29

properties and people are

8:31

starting to think, oh, you know, maybe

8:33

depression might have

8:36

a chemical basis. And so

8:38

they start to speculate about how these different

8:41

drugs that they're using might be affecting

8:44

people's moods. And first

8:46

of all, the focus

8:48

is on noradrenaline and actually

8:51

for many years the main focus was on noradrenaline,

8:54

that was thought to be the key brain

8:56

chemical involved in mood. But

8:59

serotonin was also proposed to be important

9:02

in the 1960s. And

9:05

that is that idea is picked up

9:07

in the 1980s

9:09

when the SSRIs

9:12

start to come onto the market.

9:15

Now,

9:16

the other thing to say is that the

9:18

medical profession, particularly psychiatrists,

9:21

are keen on the idea of depression

9:25

having a biological basis all

9:28

the way through from the 1960s onwards.

9:31

But the pharmaceutical industry

9:34

are not interested in antidepressants

9:37

or depression until

9:39

the 1980s because

9:41

before that they are busy making

9:44

a lot of money selling vast, vast

9:46

quantities of benzodiazepines. Those

9:49

are the big sellers in the 1970s

9:52

and

9:53

very large numbers of Americans

9:55

and Europeans were taking benzodiazepines

9:57

at that time. And then in the 1980s, is

10:00

there's a real crisis concerning

10:03

benzodiazepines. It becomes apparent that

10:05

they are, in fact, addictive

10:08

even though they'd been marketed as being a non-addictive

10:10

alternative to

10:12

barbiturates. And

10:14

it becomes apparent that they've been doled out

10:18

like sweets to people who

10:20

have social and circumstantial

10:22

problems. So they

10:24

start to get a really bad press.

10:26

It becomes very difficult to market a

10:28

drug for anxiety.

10:30

And the pharmaceutical industry switch

10:32

to depression.

10:34

And they also realize

10:37

when they do that, when they start to

10:39

launch these new SSRI antidepressants

10:42

like Prozac, of course, is the first one, or

10:45

the first one that becomes successful,

10:47

launched in 1987. They

10:50

also realize because the scandal

10:52

about the benzodiazepine situation

10:55

is still in the

10:55

air at that time, they realize

10:58

that they've got to sell these drugs with a

11:00

different sort of story.

11:02

Now benzodiazepines were

11:04

quite clearly drugs that alter

11:07

someone's normal mental state that

11:11

produce their mind-altering substances.

11:14

And they basically replace

11:16

people's underlying

11:18

feelings with a drug-induced

11:20

state. And that was clearly

11:23

apparent to everyone. And

11:26

that had, because the benzodiazepines

11:28

had got

11:28

such a bad press, that had brought the whole

11:30

process of

11:32

giving people drugs to essentially numb

11:35

their emotions and numb them and

11:37

distract them from their social

11:39

problems

11:41

into disrepute. It had brought that whole activity

11:44

a

11:44

bad name. And so the pharmaceutical

11:47

industry, I believe,

11:49

realized that they had to tell a different story.

11:51

And that's when the pharmaceutical industry

11:53

really got behind the idea of depression

11:56

being a chemical imbalance and started

11:58

to very widely promote. that

12:00

idea.

12:01

That makes a lot of sense to me knowing the history

12:04

of the pharmaceutical industry and

12:06

other drugs that they've been involved

12:09

with with similar kind of

12:11

marketing based introductions.

12:14

But let me ask two

12:17

questions as a follow-up and we can

12:19

tackle the first one to begin

12:21

with and then move on to the second one. I

12:24

assume this wasn't just pulled

12:26

out of thin air. That there was at least some

12:28

early evidence or some

12:30

even if it was later proven to be false

12:33

or incomplete that

12:35

led them in the direction of this chemical imbalance

12:38

theory. You mentioned early on

12:40

in the 50s there was some, I

12:42

believe there was a bacteriologist

12:45

named Albert Zeller found that a

12:48

drug that was the

12:50

first monoamine oxidase inhibitor

12:52

and there were some other sort of indications

12:57

that these changes in chemicals in the

12:59

brain were at least possibly contributing

13:01

to depression. So is

13:04

that kind of, did they just take a little

13:06

bit of evidence that existed even though it was fragmentary

13:09

and incomplete and blow that up or

13:11

was there more going on at that

13:14

point that justified that approach?

13:16

So really this idea comes

13:19

from the fact that

13:21

certain drugs were noticed to alter mood.

13:24

There was never really any

13:27

convincing evidence independent

13:30

from the drug effects that there were abnormalities

13:33

in brain chemicals either

13:35

serotonin or noradrenaline or

13:37

anything else. So it really

13:40

was, it was an

13:42

assumption, there was an assumption made

13:44

that if you're able to change mood by giving

13:46

a chemical

13:48

therefore

13:49

depression must and depression and mood states

13:52

must

13:52

have a biological origin.

13:55

So that's really

13:58

what happens.

15:54

very

16:00

odd observation and almost certainly

16:03

not down to the emipramine. And I think that just shows

16:05

you how enthusiastic people were

16:07

about these drugs and how that coloured

16:09

their perceptions of what they were doing.

16:12

Yeah, it seems to me that this is a human

16:15

bias overall. We prefer

16:17

to know rather than to not know

16:19

and I think particularly prevalent in

16:21

medicine. There's a quote

16:24

I came across, I think it

16:26

was from Elliot Ballasting in his book,

16:28

he said, a theory that is wrong

16:30

is considered preferable to admitting our ignorance.

16:33

Yeah, yeah.

16:34

It seems like that had something to do with it.

16:36

It's, you know, we didn't know what caused depression.

16:39

It was affecting a lot of people. We didn't have a

16:41

clear solution or treatment.

16:43

And as soon as there was something that seemed like

16:45

it could be a

16:47

theory that would lead to particularly

16:49

pharmaceutical treatment that

16:52

it was off to the races after that.

16:54

Yeah,

16:55

I slightly dispute

16:57

that. I think we did have a theory of depression.

17:00

We just didn't have a biological theory

17:02

of depression. You know, there was

17:05

the old DSM defines

17:07

depression, it defines all mental disorders

17:09

as reactions to

17:12

circumstances, to live circumstances,

17:14

they're all called depression, it

17:16

is a depressive reaction formation.

17:19

That's how, you know, so they

17:22

are regarded as in a different way

17:24

than we regard mental health problems today.

17:27

And

17:28

ordinary people, I think, have always

17:32

held that view that emotional states

17:34

like depression are, consist

17:37

of a reaction to circumstances, obviously,

17:40

colored, you know, obviously with individual

17:42

differences, you

17:43

know, individual, the way that individuals

17:45

react to their circumstances is colored

17:47

by their upbringing, by

17:49

their history, and to some extent by

17:51

their genetic makeup. So it's not that biology

17:54

is completely irrelevant, but

17:57

it's not causing the emotion

17:59

in the image. immediate term in the sense

18:01

that biological theories of depression

18:04

want to suggest that it is. And

18:06

this came out to me when I was looking at

18:10

the material from

18:12

the defeat depression campaign, which was a

18:14

depression awareness campaign run in

18:16

the UK in the early 1990s,

18:19

partly funded by the

18:21

pharmaceutical industry, particularly Eli Lilly,

18:23

the makers of Prozac.

18:25

And the people who

18:27

were running that campaign commissioned a survey

18:31

before they got the campaign running. And

18:34

the survey uncovered that most

18:36

people believe that depression was caused

18:38

by

18:39

unemployment, marriage

18:41

breakdown,

18:42

poverty.

18:44

That was people's view of depression. They did

18:46

not feel that it was caused by a chemical

18:49

imbalance or a

18:50

brain problem. That

18:54

view was a view that that

18:56

campaign and the pharmaceutical industry

18:59

deliberately set out to change

19:01

and to override

19:03

so that they could instill in

19:05

people

19:06

views that would be conducive to

19:08

them taking antidepressants.

19:12

That's so fascinating. I want to come back

19:14

to other

19:15

potential biological contributors

19:17

to depression later in the conversation that have

19:19

been more recently studied and get your take

19:21

on those. But I want to continue this

19:24

conversation because that's the main focus

19:27

of this interview. So we've

19:29

we've established that there was never really

19:32

solid evidence to support the chemical

19:34

imbalance theory of depression. And

19:36

now I want to ask you about evidence

19:39

that contradicts directly that

19:41

theory. And maybe

19:43

I can just ask you a few questions and

19:45

you can tell me if these

19:48

are true or not or false. So

19:51

does

19:52

reducing

19:54

levels of norepinephrine, serotonin

19:57

or dopamine produce depression?

20:00

in humans.

20:02

So I'll answer your question in a minute,

20:04

but first of all I'll say it's very

20:06

difficult to prove a negative.

20:09

Okay. So

20:11

I don't think it's the case that we have

20:14

definitely, you know, we have

20:16

evidence that depression is definitely not a biological

20:18

condition and we probably never will have that evidence

20:21

because you'd have to have

20:23

massive, massive studies for every

20:25

area to be, you know, quite

20:27

sure that it's been disapproved.

20:31

What I think we can say confidently is

20:33

that we have not proved that there is a biological

20:36

basis to depression and that was

20:38

what people have, that is

20:40

what people have been led to believe. So

20:43

can you cause depression by reducing

20:46

levels

20:47

of brain chemicals in people

20:50

who don't have depression to begin with?

20:51

And the answer is no. For

20:53

example, looking at serotonin,

20:56

there have been several studies

20:58

which have used an experimental

21:01

mixture of amino acids which

21:03

lack the amino

21:04

acid that serotonin

21:07

is made out of, that's called tryptophan. And

21:10

if you give people this mixture of amino acids

21:12

without the tryptophan, in

21:14

order to make proteins, the

21:17

body has to use up all

21:19

the tryptophan that's available already,

21:22

and therefore there's not much available

21:24

tryptophan to make serotonin and to cross

21:26

into the brain to make serotonin in the brain. It's

21:29

probably not a perfect procedure, it's probably

21:31

doing other things as well, to be honest,

21:34

but it does reliably

21:36

reduce tryptophan

21:38

levels and is thought

21:40

to reduce serotonin levels. Anyway,

21:44

that has been compared with giving people

21:46

a drink of amino acids containing

21:48

tryptophan, and basically there's

21:50

no evidence that that produces

21:52

depression in people who

21:55

don't have depression to begin with. There

21:58

are some studies that show that that it might

22:01

make people's depression worse or bring

22:03

on a temporary

22:05

recurrence of symptoms in people who have

22:07

had prior depression.

22:10

But there are a number of problems with that. The first is that the

22:12

number of people in those studies is very small.

22:15

The ones that have been looked at

22:17

in a meta-analysis.

22:19

No one's done a recent meta-analysis and

22:21

the only studies that we found of that

22:23

sort that had been done recently actually didn't

22:25

show that,

22:26

didn't show any effect

22:27

in people with a history of depression. And

22:30

then the other consideration is that these people

22:33

have been exposed to, or are very

22:35

likely to have been exposed to antidepressant

22:37

drugs, which we know interfere with the serotonin

22:40

system in some way and therefore may confound

22:44

the results

22:44

of those experiments. So

22:47

basically from those, what are called tryptophan

22:49

depletion studies, there is no

22:51

evidence that reducing

22:54

serotonin

22:54

produces depression.

22:57

What about the flip side of that? Do

23:00

drugs that raise serotonin and norepinephrine

23:02

like amphetamines or cocaine alleviate

23:05

depression reliably?

23:07

That's a good question. So

23:09

amphetamine, I think people don't realize

23:12

actually how

23:15

little we really know about

23:17

what drugs do. So

23:19

SSRIs

23:21

are meant to increase

23:23

levels of serotonin, but actually

23:25

we found some evidence and it turns out there is

23:27

quite a lot of evidence out there that certainly

23:29

in the long-term, they probably reduced

23:31

levels of serotonin.

23:33

And they may well, some of them at

23:35

least have effects on other

23:37

neurochemicals that haven't really

23:39

been very well researched or understood. Now

23:42

amphetamine is a drug that affects

23:45

numerous brain chemicals. And

23:47

we're not sure which ones

23:49

are the

23:51

key chemicals, but

23:53

probably its main effects are produced

23:56

by its effects on noradrenaline,

23:58

which is a...

23:59

associated with arousal

24:02

and probably to some extent dopamine

24:05

as well, which is also associated with arousal.

24:08

It also does

24:10

seem to increase levels of serotonin.

24:13

Does amphetamine

24:15

relieve depression? Well,

24:17

amphetamine makes people

24:20

feel good, as other

24:22

stimulants do, as cocaine does

24:24

while people are taking it.

24:26

Does that mean it's curing depression? In

24:28

my view, no, it has the same effect

24:31

in anyone, whether you've got depression or not.

24:33

It has effects in animals,

24:36

behavioural effects in animals that are consistent with its

24:38

effects in humans. But

24:41

if you give it to people with depression, there are some

24:43

studies that show that amphetamine is

24:46

an effective antidepressant, that

24:48

it reduces depression rating

24:50

scale scores better than a placebo

24:53

or as well as other antidepressants,

24:55

which shouldn't surprise us given

24:57

what we know about its profile of

24:59

effects.

25:01

Right. And the question though, as

25:03

you pointed out, is that a valid

25:05

ongoing treatment for depression,

25:09

considering the whole range of effects, side

25:11

effects, et cetera.

25:13

On a related note,

25:16

I don't know that there's ever been a

25:18

great explanation for why antidepressant

25:21

drugs like SSRIs take so long

25:23

to produce an elevation of mood.

25:26

From

25:27

my understanding, please correct me if I'm

25:29

wrong, they produce their maximum elevation

25:31

of serotonin

25:33

in only a day or two and noradrenaline

25:35

or norepinephrine, but it takes often several

25:37

weeks for people to

25:39

experience a full effect.

25:42

Is that also an argument against

25:44

the chemical imbalance theory in your mind or is

25:47

there some other explanation

25:49

for why that

25:50

is? So let's come

25:52

on to what antidepressants do. So

25:56

in my view, antidepressants do

25:58

not have

25:59

worthwhile effects on depression.

26:02

If you look at placebo controlled trials

26:05

of antidepressants, the difference

26:07

between an antidepressant and a placebo

26:09

is miniscule.

26:11

It's really, really small. It's

26:13

two points on

26:16

the 53 or 54 point commonly

26:19

used Hamilton rating scale of depression. And

26:21

if I could just interject, is that, Joanna,

26:24

for mild, moderate and severe depression

26:26

or are there differences across the intensity

26:29

of depression?

26:30

Some studies seem

26:32

to find slightly higher differences

26:35

in people with severe depression, but some studies don't.

26:37

I

26:37

would say the jury is still out on that and

26:39

the average difference is

26:42

very small. And moreover,

26:44

I think there are other

26:46

explanations other than the pharmacological

26:49

effects of the drug that may account

26:51

for those differences, particularly

26:53

the fact that people

26:56

often know whether they're taking the

26:58

antidepressant or the placebo, especially

27:00

if they've taken antidepressants before, which many

27:02

people in these trials have done. And

27:05

we know they're

27:06

not truly blinded. So they're

27:08

not truly blinded. They're meant to be double

27:10

blind trials, but they're not. And we

27:12

know that the expectations

27:15

that people have about what they're

27:17

getting, about whether they're getting the drug or the placebo,

27:20

have a very profound impact

27:22

on the outcome of a study. So there's a very

27:25

interesting study

27:26

that compared sertraline,

27:29

an SSRI antidepressant,

27:31

with

27:32

St. John's Wort

27:34

and a placebo. Now in this study,

27:36

people couldn't guess what they were on. And this

27:38

was a negative study. There was no difference

27:40

between the two drugs and the placebo.

27:43

But when you asked people to

27:46

guess what they were taking, the

27:48

people who thought they were taking either

27:50

St. John's Wort or sertraline

27:53

did much better than people on the placebo.

27:55

And the difference is around five

27:57

to eight points difference, much

27:59

bigger.

27:59

than the normal difference you would see between a drug

28:02

and a placebo in a randomized controlled

28:04

trial. So what that says

28:06

to me is that we know there are some

28:08

studies where people can guess correctly what

28:11

they're taking and

28:14

if they can guess they are going to,

28:16

you're going to see this expectation effect

28:18

influence the outcome of the study

28:20

as if it were the real,

28:22

you know, a real, a true

28:24

outcome of a true drug effect.

28:27

Sorry, to come back to your question, so my

28:29

view is that antidepressants

28:31

actually are no better than placebo

28:34

and that what the reason

28:36

why we have this idea that antidepressants

28:39

take two weeks to work is that

28:41

placebo takes two weeks to work.

28:44

It takes two weeks

28:45

for people to, for people's hope,

28:47

the hope that people have and the good

28:50

feeling people have from having been listened

28:52

to and feeling that something's been done and

28:54

something's going to help them

28:56

to translate into an actual improvement

28:59

in mood. And also I think

29:01

it takes two weeks for people to,

29:04

often to get out of the situation

29:06

they're in

29:07

that has made them depressed. Not everyone,

29:10

of course, for everyone it takes much longer, for many people

29:12

it takes much longer, but for some people two

29:14

weeks is an amount of time where actually

29:17

they

29:18

can stand back, they can think, okay, maybe

29:20

I was feeling awful because of this and I

29:22

could do this about it.

29:24

Right, it's got nothing to do with serotonin,

29:26

you know, brain chemicals and how long they're taking

29:28

to increase or anything like that. It's, it's,

29:31

it's, that's how long it takes for

29:33

the treatment effect that's caused

29:35

by placebo

29:36

to actually happen.

29:39

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29:41

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29:43

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31:51

Two things here. First,

31:54

I completely agree and would say that I

31:56

think the average person is not

31:58

well-informed. about the extent

32:01

to which placebo plays a role

32:04

in certainly antidepressant research,

32:06

but just in research in general. And this has

32:08

been a fascination of mine for many years.

32:11

And I've written a lot about this too. Ted Capchuk,

32:14

for example, who's now at Harvard, but

32:17

started his career as an acupuncture, his very

32:20

interesting career trajectory, and

32:22

then ended up studying the effects

32:24

of placebo in antidepressant

32:27

medications in many other contexts as well.

32:29

But I remember a paper he published in 2009 in

32:32

Plus One, which found that

32:36

the

32:39

extent of placebo response is

32:41

large regardless of the intervention and

32:43

is mostly associated with the

32:46

steady population and size. So

32:48

that the greater the steady population

32:50

size, the greater

32:52

the placebo effect, I think.

32:55

What would you say? Because what happens

32:57

from, whenever I write articles about this,

32:59

and I do want to be sensitive to people who are listening

33:02

as well, I get

33:04

sometimes vitriolic hate

33:06

mail from individuals

33:08

who insist that they have been helped

33:11

by antidepressants who know

33:13

beyond a shadow of a doubt in their bones

33:16

that it was the medication and not a placebo

33:18

effect that helped them

33:21

and that take great offense

33:23

to the suggestion that the

33:25

drug that didn't have an effect and

33:28

that

33:28

depression is not biological because

33:31

their

33:33

interpretation of that often,

33:35

I

33:36

think, is that means depression

33:38

is my fault, that there's something

33:40

wrong with me, that I'm to blame for

33:42

what's going on. This is all on my shoulders.

33:45

And if I could, if only I was a better person

33:48

or could live my life better, then

33:50

I would not be depressed. And

33:53

that story is pretty

33:56

heavy for most people to take on and

33:59

not preferable.

33:59

to the idea that

34:02

depression is caused by a chemical imbalance

34:04

that the medication could fix. I

34:07

imagine you've encountered this as well,

34:10

whether from patients or other researchers

34:13

or professionals in the field. So I'm just curious

34:16

how you approach that,

34:18

how you respond to that.

34:20

Yeah, yeah, no, that's a really good point. I

34:23

mean,

34:24

the first point I'd like to make is,

34:27

it seems to me, I'm not trying to say that

34:31

people are gullible.

34:32

When people are really

34:35

depressed and really distressed and hopeless,

34:37

it is not at all surprising that

34:39

being offered something that

34:42

they are told might help them, gives

34:45

them hope

34:46

and therefore helps them. So I

34:48

don't think,

34:49

I'm really not trying

34:51

to say that people are gullible. I think it's a very

34:54

normal human response. So

34:56

that's one point to make.

34:58

The second point is, I'm

35:01

not trying to stop people taking

35:03

antidepressants, but I am trying

35:05

to make sure that people are informed and

35:08

that they are not misinformed

35:11

and misled. And it is

35:13

a fact that people have been misled

35:15

into believing that

35:17

there is a proven

35:19

chemical abnormality in the brain.

35:22

And that is not a fact,

35:26

nothing of the sort has been proven. The

35:28

evidence is

35:30

completely inconsistent

35:33

and very weak.

35:34

But the trouble is of course, that because

35:37

of this campaign that we were talking about earlier

35:39

that was started by the pharmaceutical industry

35:41

with the support of the medical

35:44

profession, many people have

35:46

been persuaded that that is the case

35:48

and have come to develop

35:51

an identity that they have something

35:53

wrong with their brain and that they need

35:56

a drug or some other

35:58

physical intervention to put that right.

35:59

And so

36:02

of course it's very challenging,

36:04

you know, when someone comes along and says actually that

36:06

identity is found is not

36:09

founded on fact, it's not founded

36:11

on evidence.

36:12

Of course that is very challenging. But

36:15

on the other hand,

36:18

it's not a good thing to have a

36:20

brain problem. And being

36:22

told that actually your brain is normal

36:25

and your emotional responses are

36:27

normal

36:28

is a good thing in the long run.

36:30

It may be difficult to absorb because

36:33

you've

36:34

been persuaded to adopt this

36:36

identity that's been sold to you. But

36:40

actually it

36:41

is a good thing to know that there's nothing

36:43

wrong with your brain.

36:44

Yes, it does give

36:47

us some responsibility for our

36:49

moods, but that is also a good thing

36:51

because that also,

36:53

the flip side of

36:55

having some responsibility is that

36:57

there is something that we can do to help ourselves

37:00

recover. We do

37:02

have some agency. And

37:05

I also think

37:07

we all have emotional difficulties

37:09

from time to time and some more

37:11

than others. I'm not, you know, as I said, there are

37:13

individual differences and there are some people

37:16

for lots of different reasons,

37:19

but often commonly because of terrible

37:22

things that have happened to them in their past

37:24

lives struggle with their

37:26

emotions more than others.

37:28

And people like that deserve sympathy

37:30

and support. It's not blame,

37:32

not you're responsible,

37:34

get on with it. We're washing our hands

37:36

with you. People deserve support. You

37:38

don't have to have a, I don't think

37:41

that, you know, people

37:43

have to have a

37:44

biological problem or a brain

37:47

chemical problem in order to merit

37:50

support from

37:51

health or social services to

37:53

get through a difficult time.

37:57

Right. And what, you know,

37:59

maybe an unintended.

37:59

intended or intended, I'm not sure, effect

38:02

of this chemical imbalance theory

38:04

is that they may be less likely to get that

38:07

support than they would be otherwise

38:09

if depression was looked at in a more

38:11

holistic frame. In other words, if

38:14

everyone is just bought into the theory that

38:16

it's chemical imbalance and someone goes to

38:18

the doctor

38:20

complaining of depression, chances are

38:22

they're just going to be prescribed an antidepressant

38:24

and there's not going to be a referral to a psychologist

38:27

or another mental health care provider or psychiatrist.

38:30

Even if they do go to the psychiatrist, nowadays

38:34

that has largely become a pharmacological

38:37

interaction where it's just a question of what

38:39

drug is going to be prescribed. Not

38:41

many psychiatrists are not doing psychotherapy

38:45

or providing that kind of support anymore, largely

38:47

because of this notion

38:50

has

38:50

taken such a deep hold in our culture.

38:55

Yes, I think you're

38:57

right.

38:59

Certainly in the UK, a lot of people

39:01

do get therapy. We do now have

39:03

a therapy service on the National

39:06

Health Service that is offered to everyone.

39:09

But

39:10

certainly in the past, the option

39:12

of offering people an antidepressant, I think, has

39:15

made

39:16

it less likely that people

39:18

will get other sorts of help. I also think

39:22

this

39:23

whole idea that depression

39:25

is a biological brain-based problem

39:28

actually means that

39:30

doctors, psychologists, everyone

39:32

who's trying to help people with their problems

39:35

is not really necessarily listening

39:37

to the problem.

39:39

Because what they're doing is saying, oh,

39:41

you're someone with depression. They're

39:44

dealing with a label

39:46

rather than with an individual with

39:48

a unique set of problems.

39:51

And that's, in my view, that

39:53

is how we need to help people with depression.

39:55

We need to see them as unique people who

39:58

have their own unique set of problems.

39:59

that they need support with and

40:02

it will be different for each individual. So

40:04

this idea that there is such a thing as

40:06

depression that has a single

40:09

sort of treatment or a single collection

40:11

of treatments is nonsensical

40:14

to begin with.

40:16

I think that's such an important point. And

40:19

going back to what you said before about how,

40:21

yes, when you take this information in,

40:23

it

40:24

can be difficult at first because it

40:26

challenges an idea that

40:29

may have had and that actually

40:32

that idea in some, at

40:34

least at first glance, may in

40:36

some way

40:37

make things easier, at least if

40:39

someone is interpreting

40:41

depression as being their fault, it removes

40:43

that blame from their shoulders. And

40:46

so there is a kind of a way that

40:48

I could see that that

40:50

makes it easier. And I'm

40:53

speaking personally as someone who's separate from depression

40:55

in my life. So I know what it feels

40:58

like. And I know, you know,

41:00

I've been through this myself. So

41:02

I'm not at all lacking

41:04

an empathy for people who struggle

41:07

with depression because I've been through

41:09

some pretty dark places personally.

41:12

But I've also experienced the difference

41:15

in interpreting

41:18

that depression as something that is

41:21

transitory

41:22

or at least potentially transitory,

41:25

that is not a fundamental characteristic

41:27

of who I am, that doesn't define me, like

41:29

you said, that isn't a problem

41:31

in my brain that is only fixable

41:34

by taking a pharmaceutical drug.

41:37

And one of the things that actually really

41:39

empowered me was your work and

41:41

the work of other people who debunked

41:43

this theory. And

41:44

anger was actually something

41:47

that helped me to get through this anger at

41:49

pharmaceutical companies for perpetuating

41:51

this story and

41:53

then realizing that

41:55

I was a victim of that

41:57

marketing push, basically.

41:59

that I took on this whole idea

42:03

of what caused depression. And for me,

42:05

it was short-lived because

42:07

I

42:08

got exposed to your work and the work of others that

42:10

disabused me of that myth.

42:14

But I think that

42:17

anger can be actually a powerful

42:19

motivating force in that situation where

42:21

people realize that they've been willfully

42:23

taken advantage of in order to be a

42:25

profit center for these pharmaceutical

42:28

companies who want to sell more drugs.

42:30

And there's very little accountability for those

42:33

companies, for things like this, which is a

42:35

whole nother conversation and we won't go down

42:37

that road. But it seems

42:40

to me that awareness is key.

42:43

It's the starting point to a different

42:45

way of dealing with depression,

42:48

whatever that might be for each individual. But

42:50

without awareness, you can't even take

42:52

that next step.

42:54

Yeah, absolutely. I mean,

42:57

I've met several people in the

42:59

same sort of situation since

43:01

the publication of the serotonin paper

43:03

and many people contact me

43:06

saying exactly what you're saying and really

43:09

feeling very disturbed and very

43:12

angry about what had happened.

43:14

Yeah. So,

43:17

a good segue to the next question. What

43:20

is the reaction? You know, when

43:22

I read your paper, my first thought was, oh,

43:24

boy, this is like, I

43:27

hope Johanna is doing okay.

43:31

What has the response been like

43:33

from your peers in your

43:36

field and just the public at large?

43:39

You know,

43:40

what's it been like

43:42

to publish that paper?

43:44

So, the response from my peers, from

43:47

the psychiatric profession, has been

43:50

basically to try and shut down

43:52

the debate

43:54

and to divert

43:57

it

43:57

and to do anything.

43:59

to stop people questioning the

44:02

benefits of antidepressants and

44:04

to stop people questioning the idea that

44:06

they work by targeting some sort

44:08

of biological abnormality.

44:10

You know, so the tactic has been, oh

44:12

yeah, of course we all knew that, you know,

44:14

the serotonin theory was wrong, but it's

44:17

more complicated than that. It's more complicated,

44:19

of course, you know, serotonin is involved in

44:21

some way and so is this and so

44:24

is glutamate and so is dopamine and so is

44:26

neuroinflammation and,

44:29

you know, just to throw everything

44:31

at it to give the impression

44:34

that there is, you know, good research,

44:37

that depression has a biological basis.

44:39

And I think most crucially to say,

44:42

don't worry about antidepressants, carry on

44:44

regardless. This doesn't change anything.

44:47

Wow, that's incredibly disappointing.

44:50

I'm sure for you much more than me, but

44:52

even for me as a bystander,

44:54

that's,

44:55

you know, it's wild to

44:57

me that as

44:59

professionals who, you know, are trying to learn

45:02

as much as we can about how to support our patients

45:05

and make progress.

45:07

I mean, I understand intellectually why

45:09

there would be so much resistance. When you invest

45:12

deeply in a theory and you become

45:14

identified with that as a clinician and

45:16

it's defined the way that you've treated

45:18

patients perhaps for

45:20

five, 10, 20, 30 years, I

45:23

get on a human level that that can

45:25

be hard to pivot from because then what

45:27

do you, you know, have I been wrong for

45:29

all these years and what am I gonna do?

45:32

And it's still very disappointing that that

45:34

is the response to what

45:36

I view as pretty much incontrovertible

45:39

evidence that you presented in that paper

45:42

and that they're not actually challenging the evidence.

45:44

They're just, like you said, diverting and obfuscating

45:47

rather than actually critiquing the arguments

45:49

you made in the paper.

45:51

I think it's extremely disappointing. And I

45:54

am also feeling very angry

45:56

because I do feel that actually

45:58

there

45:59

are... people who in the profession who do

46:01

not want the public to actually

46:03

have access to

46:05

the facts and don't

46:08

want the public to be able to appreciate

46:11

the debate and discussion that exists

46:14

around antidepressants. Yeah,

46:17

I think that, you know, and I think

46:19

the bottom line is that they

46:22

really, really don't want people to, well,

46:25

first of all, to question the idea that the depression

46:27

is a, you know, at root a biological

46:29

problem. And secondly, to

46:32

understand antidepressants in the way that

46:34

we used to understand benzodiazepines,

46:36

to understand them as a, you know,

46:38

emotion, nummer, something that just,

46:41

you know,

46:42

changes anyone's mental state.

46:45

Because people naturally would question

46:47

whether that's a good idea. And when you start talking

46:49

about drugs, you know, if

46:52

you acknowledge that these drugs are not correcting

46:54

a chemical imbalance, but they are

46:56

drugs, they're not placebo tablets, you

46:59

have to acknowledge that actually they're creating

47:01

a chemical imbalance, they're actually changing

47:04

our normal brain chemistry.

47:06

And I think the profession really don't want

47:09

people to hear that statement.

47:12

Because people will then rightly

47:15

worry about what changing your normal

47:17

brain chemistry might do to you, to

47:19

your brain, particularly if you

47:21

keep taking these drugs that are causing

47:24

these changes day in, day out

47:26

for months and years on end.

47:29

And we do have some evidence that

47:31

long term use of antidepressants can do some

47:34

really harmful and damaging

47:35

things to the brain. Thankfully,

47:37

not in everyone, not saying this is, you know,

47:40

a universal

47:42

experience, but they can.

47:43

They can cause really severe

47:46

and difficult withdrawal symptoms.

47:48

And they can cause sexual dysfunction, which

47:50

in some people appears to persist

47:53

after people have stopped taking the

47:55

medication. Yeah, along with specific

47:57

populations like teenagers, which I'm particularly interested in.

47:59

concerned about and before

48:03

we do that I just want to ask one more question that

48:06

I got did a lot when I read about this

48:08

topic

48:09

which is

48:10

this okay so maybe

48:13

antidepressants don't

48:15

work by addressing chemical

48:17

imbalance or serotonin you know shifting

48:19

serotonin levels

48:21

maybe they have pleiotropic effects like

48:23

statin drugs for example that have you

48:26

know maybe their main when it

48:28

was revealed that there might be some issues with

48:31

like you know statins are working in when cholesterol

48:33

levels aren't changing as much as you would think they are

48:36

that they have these other pleiotropic

48:38

effects which you know for

48:40

people who are listening or effects that are different

48:42

than maybe the primary effect it

48:45

was intended with the drug I

48:47

know you've kind of already answered this question

48:49

when you explain that antidepressants

48:52

don't work better than placebo on

48:54

the global level but what would you say to this

48:57

argument or this idea that their antidepressants

48:59

might help some people because of a pleiotropic

49:02

effect

49:03

since we published the serotonin theory there

49:05

seems to be you know more and more emphasis on other

49:07

possible biological theories of

49:10

what antidepressants might be doing and one

49:12

of the popular ones which

49:14

also ties into the use of psychedelics

49:16

that are becoming very fashionable now is

49:19

the idea that they stimulate neurogenesis

49:21

and that there's some deficiency of neurogenesis

49:23

in depression

49:25

there is no evidence for this there

49:27

are there are some

49:29

some mostly animal

49:31

studies showing possible increase

49:34

in markers of neurogenesis but there are many explanations

49:37

for that and one explanation is

49:39

that if you damage the brain you

49:42

the brain naturally produces

49:45

you

49:45

know neurogenesis to compensate for the damage

49:48

so actually finding indicators of neurogenesis

49:50

is not necessarily a good thing it might

49:52

indicate that the drugs are damaging the brain but

49:55

actually the majority of evidence comes from

49:58

studies looking at the size of the hip

49:59

campus. Some studies

50:02

suggest that the hippocampus is

50:05

reduced in people with depression.

50:07

Some studies don't. None of these

50:09

studies have effectively ruled out drug treatment

50:12

as a possible cause. And

50:14

that's basically what the evidence comes down to.

50:16

So this is,

50:18

I think calling this a theory is actually

50:22

doing it more respect

50:24

and justice than it deserves. It's a speculation,

50:26

along with many other speculations, which

50:30

has much weaker evidence

50:34

than there was for the serotonin theory, and that didn't

50:36

stack up. And the evidence for all these

50:38

theories is very unlikely to stack up. And

50:41

in a way, the

50:42

people putting these theories forward, I think many

50:45

of them probably know that and they don't care. They

50:47

just know that if they put something out there,

50:49

then they can keep on convincing people that

50:52

depression is biological and that they need to

50:54

take a drug to deal with it. And

50:56

that's

50:57

the main function of the theory, not

51:00

actually really to

51:03

explain anything.

51:04

Right. Even if that's not

51:06

what people intend, that is certainly

51:08

the effect of putting all these

51:11

ideas out there.

51:13

If one were cynical, one could say it's

51:15

more of a marketing campaign than

51:18

a legitimate scientific theory

51:20

that's based in published peer-reviewed

51:22

evidence.

51:24

Let's talk a little bit about

51:26

some of the possible long-term

51:28

negative effects of SSRIs, because

51:31

I at least want to spend a few minutes

51:33

on this, because as you pointed out, a

51:35

lot of people are under the mistaken impression that

51:37

these drugs are completely safe. They've

51:40

been used for decades. Every

51:42

doctor in every practice prescribes

51:44

them. So how could it be possible that

51:47

they would have serious long-term

51:49

side effects and risk? And if you could

51:51

address any general population

51:53

and then any specific populations that are of

51:55

particular concern, like teenagers,

51:58

that would be great. Yeah.

51:59

So antidepressants

52:01

have a range of side effects or adverse

52:03

effects like any drug. And

52:06

immediately speaking, they

52:09

probably, they're probably less,

52:12

less impairing to take than some

52:14

other drugs prescribed for mental health

52:16

problems such as antipsychotics, which are

52:19

more immediately noticeable, slow

52:22

you down and,

52:23

and have lots

52:25

of function impairing

52:27

effects. And modern antidepressants,

52:30

I guess, SRI's at least

52:33

produce less of that sort of effect, but nevertheless,

52:35

they do have immediate effects. And

52:38

one of the very well recognized immediate effects

52:40

they have is sexual dysfunction.

52:42

And they interfere with sexual

52:44

function

52:44

in almost

52:46

every way that you could think of. They

52:49

cause impotence, delayed ejaculation,

52:52

and reduce genital sensitivity.

52:54

And this seems to probably

52:56

correlate with their ability to cause emotional

52:59

blunting as well.

53:00

So they are drugs that reduce sensitivity

53:03

both physically and emotionally.

53:06

So it's well recognized that they have these sexual

53:08

effects in a very

53:10

large proportion of people who take them 60%, it

53:14

says

53:14

in a few studies

53:16

in the SSRIs, the particular culprits

53:18

here, other other antidepressants

53:21

are

53:22

have less impact on sexual functioning, although they do

53:24

have some,

53:24

most of them. So so

53:27

we recognize that they have these effects in the short

53:29

term. And what has been been

53:32

coming out over the last few years is

53:34

that in some people, these

53:36

effects do not go away

53:38

when you stop taking the drug and

53:41

seem to go

53:42

on for years in some

53:44

cases,

53:46

possibly getting better gradually

53:48

over the years, but we just don't

53:51

know we don't have enough really sort of long term

53:53

follow up evidence. So obviously,

53:56

obviously, this is a real worry with lots of

53:58

young people and teenagers.

53:59

teenagers taking these drugs. And

54:02

I suspect that very, very few

54:04

doctors are telling people about this. I think very

54:07

few doctors are actually aware of it. And

54:09

I think that's partly because

54:12

there does seem to be in the medical literature,

54:14

you know, an inclination to publish all these, you

54:16

know, rosy figures and lots of studies

54:19

about the benefits of drugs and a

54:21

much greater reluctance to

54:23

publish anything that shows negative effects

54:26

of drugs, or to fund

54:28

research that looks at negative effects

54:30

of drugs. So often these effects start with,

54:32

you know, we only find out about

54:34

them

54:35

sometimes years down the line when people are

54:38

reporting, you know, start reporting them.

54:40

As well as the sexual side effects I mentioned earlier

54:43

that

54:44

it

54:45

is now well-recognized again that antidepressants

54:48

cause withdrawal effects. And

54:50

in many people, these will not be problematic,

54:52

but in some people they are problematic.

54:56

And really can make it very

54:58

difficult to come off the drugs. And

55:01

in some people, these effects, even

55:03

when they come off the drugs, and even when they come off

55:05

the drugs

55:06

quite slowly, in some cases, these

55:08

effects can go on for months

55:10

and sometimes years. And I think

55:12

both of these things just highlight that

55:15

the brain is a very delicate organ.

55:17

And we really should not have been messing around

55:20

with it, with drugs, you know,

55:22

whose long-term effects we had not properly

55:25

tested. And people really

55:27

need to know this information, you know, they need

55:29

to

55:30

be very, very careful before they take

55:33

drugs that change the normal state

55:35

of our brain chemistry and the normal

55:37

state of our brain functioning.

55:39

Would you argue that that's particularly

55:41

true for the developing brain in teenagers

55:45

and that that population is even

55:47

more susceptible to these impacts?

55:50

Absolutely. I don't know whether we

55:52

have evidence about

55:54

antidepressant side effects

55:56

in young people, but we certainly have evidence

55:59

on anticyclons.

55:59

that

56:01

there, that side effects and young

56:03

people of anti-psychotics are

56:05

more, more common and more severe.

56:08

So absolutely, it's a real worry

56:10

with the developing brain.

56:12

And I think there's also, there's also a psychological

56:15

issue with giving antidepressants

56:17

to people who are still maturing

56:20

emotionally. You know, I've

56:22

talked about how they are emotionally blocking,

56:25

you know, and therefore maybe block

56:27

the emotions that we need to go through

56:29

in order to, you know,

56:30

to learn to manage

56:33

ourselves and manage our emotions.

56:35

And also, I think it just gives a really,

56:38

particularly when you're

56:38

giving them to, you know, to children, gives

56:41

a really dangerous message that,

56:44

you know, there's something wrong with you, you're flawed,

56:46

you're biologically flawed and you need to take

56:49

something. Yes.

56:52

So this has been

56:54

just incredibly illuminating. I'm so grateful

56:56

for you spending your time with us. And I

56:58

want to finish,

56:59

and I'm sure you would agree with me by just

57:02

mentioning that if you're listening to this, you're

57:04

taking antidepressant drugs and you're now

57:07

questioning whether that's a good idea,

57:09

please don't stop them immediately

57:11

on your own without consulting with

57:14

your physician or prescribing

57:16

clinician, whoever's doing that. There are some

57:19

risks to doing that cold turkey. And

57:21

as you know, Dr. Moncrief,

57:24

I'm going to have Dr. Mark Horowitz

57:27

as a guest in a few weeks, who

57:29

is an expert in how you safely

57:31

taper off of these drugs,

57:34

which is another thing instantly that

57:37

I found very low in awareness

57:39

about in the general medical community

57:42

and that patients are often not given

57:45

informed consent about how difficult it

57:47

might be to get off the drugs and how long

57:49

it might actually take to do that safely and

57:51

how to even get proper guidance for

57:54

how to do that. So I hope that

57:56

with the interview with Dr. Horowitz, we can,

57:58

you know, shed further light on that.

57:59

on that, but in the meantime, please don't

58:02

make any decisions without consulting your healthcare

58:05

provider. Is there anything you would like to add about

58:07

that?

58:08

Yes, just that. For

58:10

people who've been on antidepressants for

58:13

any length of time,

58:15

greater than a few months, really, you need to

58:17

be very careful about reducing them and make sure

58:19

you reduce them very slowly so

58:21

that you don't end up

58:24

with severe withdrawal symptoms.

58:27

Please. Are you working on

58:30

anything else right now on this? I imagine

58:32

you might need a little break after that paper

58:35

that you just published, but any

58:37

other lines of investigation

58:39

or areas that you're focusing on now?

58:42

I'm involved in various

58:44

projects looking at, looking

58:47

in more detail at withdrawal effects and

58:50

whether they're more severe in people who've been on medication

58:52

for longer and

58:54

that sort of thing, what might help people

58:57

get off them more easily. And

59:00

I'm also trying to write a book about the

59:02

whole experience of having published this paper because,

59:06

because, as I've said, I feel so

59:08

shocked and angry about the response to it.

59:11

Yeah. Well, for

59:13

what it's worth on a personal level, I want to thank

59:16

you because I personally benefited

59:18

from your work and helping

59:21

to debunk some of the

59:23

myths around what causes depression.

59:25

And then I can speak for the thousands

59:27

of patients that I've treated over the last 15 years

59:29

that have benefited from that. And

59:32

then I think also the hundreds of thousands, if

59:34

not millions of people who listen

59:36

to this podcast and read the blog

59:39

that have directly benefited from your work. So

59:42

if that's any consolation,

59:44

we are very grateful for you

59:47

persisting over so many years

59:49

against a lot of opposition. And

59:51

as you pointed out, not a welcoming

59:55

and solicitous reception

59:57

to this work. It's very important.

59:59

and invaluable. I genuinely

1:00:02

want to thank you for it. Thank

1:00:03

you, Chris, and thank you

1:00:05

for, you know, trying to get the message

1:00:07

out there to more people because I think that's

1:00:10

so important.

1:00:11

So yeah, thank you for helping me to do that.

1:00:14

And thanks everybody for listening to the show. Keep

1:00:16

sending your questions in to chriscruster.com

1:00:18

slash podcast question. We'll see you next time.

1:00:21

That's

1:00:22

the end of this episode of Revolution Health

1:00:24

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1:01:03

to stay abreast of the latest developments. Thanks

1:01:06

so much for listening. Talk to you next time.