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Drug Science Podcast: The 5-HT hypothesis of depression with Prof Philip Cowen and Dr Sameer Jauhar
In this episode of the Drug Science Podcast, David Nutt meets with psychopharmacologist Phil Cowen and Psychiatrist Sameer Jauhar to discuss the neuroscience behind and treatments for depression. Within the episode they touch on various neurotransmitters involved in depression as well as research studies into each of their impact, stigma around antidepressants and the role of psychedelics in treatment.
- Depression
- Serotonin
- Tryptophan
- Hamilton depression scale
- Antidepressants
- Geddes paper on preventing relapse
Prof David Nutt [General intro]:
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Hello, and welcome to the drug Science Podcast with me. David Nutt, here we’re bringing together experts and activists for a rational, honest and informed conversation about drugs.
Prof David Nutt [Introducing Podcast 125]:
Hello, everyone. Welcome to another Drug Science Podcast. So today I have a very old friend, and I can say that with confidence, because this is old me, Phil Cowan, we shared a bench together in the MRC Clinical Pharmacology unit in Oxford, working on various mechanisms of antidepressant action. And Phil is now professor of Psychopharmacology in Oxford, and a rising star, Sameer, Jauhar, who’s recently joined Imperial with a vision of ousting me and taking over the role leading the department there. So Sameer, he works at the much harder end of psychiatry. He works in first episode psychosis.
So the topic today is one which is slightly different. We’re going to talk about science and the brain and science and psychiatry now as an addiction psychiatrist, over the years, I’ve been assaulted verbally at least many occasions for arguing that there might be a biology to it’s not just a problem of free will. And I think historically, the world is at least accepting that there are some value in approaching addiction from a medical perspective as well as a social perspective. Last year, there’s been a similar attack on the idea that depression is a biological disorder, and that is interesting to me, because it’s part of a tradition that goes back. Certainly, as long as I’ve been a doctor, I remember Thomas Szasz writing his paper when I was an undergraduate, saying how there was a myth to mental illness, and over the years, we’ve had people like Kirsch and Gupta saying the same thing, that depression doesn’t really exist and the antidepressants don’t work.
But now we’re in a very unusual era, because we have a psychiatrist, Joanna Moncrieff, telling us that depression doesn’t exist, and she’s been making quite a lot of waves about this. So I thought it would be quite interesting to talk to some experts about the basis for that claim. And Phil Cowen has worked running depression treatment clinics for 40 years, and Sameer has done a lot of work in terms of biology of mental illness. I’ve invited those two along to help us make sense of this, this current challenge to our discipline. So thank you both.
So maybe I can start off with you, Sameer, because you have really led quite a powerful challenge to the analysis that Moncrieff and her team put out about 18 months ago, arguing that there was no evidence that serotonin was involved in depression, and maybe you could just introduce an oversight into that, what she what they did, and your, your critique of it, please.
Dr Sameer Jauhar:
Of course, my pleasure. Well, it just struck me. I woke up one morning and I heard, and there was a review saying that there was no serotonergic basis to depression. I thought, well, I like to think I keep up to date with things. Maybe I’ve missed something. And this was an umbrella review published in molecular psychiatry, which is a fairly eminent journal, and it looked at ways of measuring serotonin and examined it in terms of an umbrella review. So an umbrella review is when you take meta-analyses, you take the individual studies that make up the meta-analysis, and you analyse them yourself. So it’s supposed to be the highest standard of science. And what the authors propose to do was to measure serotonin in the blood, in the cerebrospinal flow, measurements of serotonin through molecular imaging. So that’s neuroreceptor imaging, where radioactivity is given tryptophan depletion studies, studies of pharmacological challenge and studies of gene interactions with serotonin. So it all sounds fairly sensible, and it’s a sensible thing to be looking.The only thing is the interpretation of the data and the way that it occurred just made no great scientific sense.
So I guess, I’ll start at the beginning an umbrella review. You’re supposed to go through all the studies yourself and analyse them. The authors didn’t do that. They basically picked reviews themselves and essentially cherry picked what they said. Reading through the review almost the antithesis of the scientific method. You pick your conclusion and you backwards, extrapolate. So essentially, what they did is they cited the world expert from reviews, and he came back and said, ‘Well, this is an umbrella review’, so that was the starter for 10. They said there’s no certainty to any of the measures. They set their own criteria for certainties. It’s a fairly arbitrary criteria. If you set your own criteria, well, odds are you’re going to find what you wish. And they did, and then they reported the reviews in a different fashion from the actual authors. I think it was sensible to be able to look at the gene interactions and say there’s nothing come out of that. But the biggest errors, I think, were in regard to tryptophan depletion. So pharmacological challenge of the serotonin system and the molecular imaging.
Prof David Nutt:
Well, let’s take that on. Let’s move to Phil. Because Phil, you know, you probably published more on serotonin in depression than anyone ever. So given that you’ve done Tryptophan depletion, you’ve done almost all the kinds of studies that emerged in the review. So tell us how you viewed it when it came out.
Prof Philip Cowen:
I suppose I was struck by another paper I’ve read that seemed to suggest that, in a way, that people who are most confident about stating an opinion tend to know least about it, and I suppose I spent a lot of time too long working on serotonin, so I have a level of uncertainty. I don’t quite know what its role is. And I think it’s all right to say that, if you’re a scientist, you know this is something which we’re working on, and we hope we can get a clearer picture.
I think the author’s paper wanted to argue that there’s nothing there at all. And as Sameer said, that’s not really correct. There are some abnormalities in serotonin in people with depression which are reliably elicited. And Sameer spoke about tryptophan depletion, and that’s important, because it’s the one where you can try and establish whether serotonin changes are causal. And because tryptophan depletion can cause depression in certain groups of people who are vulnerable to depression, that suggests that in some circumstances, serotonin can play a causal role.
I think it’s also worth mentioning that no professional nowadays would say that a complex condition like clinical depression is caused by deficiency of a single neurotransmitter, but I think Most of us would say serotonin is likely to be involved, but it’s one player in a large orchestra.
Prof David Nutt:
Yes, thank you. Maybe just remind people of your classic study with Katie Smith. So explain to people what tryptophan depletion is and how it reveals a vulnerability and depression.
Prof Philip Cowen:
So tryptophan depletion is a dietary manipulation, where you can lower brain levels of tryptophan as serotonin precursor over a few hours, and that lowers brain 5HT or serotonin levels. And so that’s a very good test of the hypothesis. Does low serotonin cause depression? And if you do this in people who are well and they have no risk factors to depression, try to find depletion does not cause depression. So in its simplest level, the serotonin hypothesis can be rejected. On the other hand, what my colleague Katie Smith showed was that if you carry out the same procedure in people who’ve been depressed but are well and off all treatment for many months they do become transiently depressed again at a clinical level after tryptophan depletion. So this finding suggests that low serotonin interacts with other vulnerability factors to cause depression in some groups of patients.
Prof David Nutt:
And I think you’ve also commented on the paper that they hadn’t properly evaluated the literature on low tryptophan in the population and vulnerability to depression. Do you want to explain that please.
Prof Philip Cowen:
Yes, that’s one of the simplest tests you can do. As I mentioned, tryptophan is a precursor of serotonin. It’s an amino acid which you can measure in the blood, and blood levels of tryptophan do have quite a strong bearing on levels of serotonin within the brain. And I think there have been three or four meta-analyses which have shown quite convincingly that low tryptophan in the blood is seen in patients with depression. I don’t think that literature was mentioned in the meta-analysis, which Sameer has referred to, but
Prof David Nutt:
Sameer, they did look at a lot of other pieces of evidence, some of which don’t seem immediately relevant to the same addressing the same question. I mean, and I think you, you wrote, you raised this issue of, you know, to what extent can you meta analyse a whole, right, everything’s anything, ranging from a gene polymorphism right through to a brain imaging study to try and try to make sense, to put them all into a single hole. I mean, do you want to just share with us some of the other flaws in that?
Dr Sameer Jauhar:
But essentially, if you’re doing an umbrella review, you have to look at homogenous entities and looking at gene environment interactions in the serotonin doesn’t really tally with molecular imaging or psychopharmacology. Now, molecular imaging and psychopharmacology do tally together. It makes sense to study them together, but I’d like to pick up Phil on one of the only occasions I think Phil’s made a mistake. He called it a meta-analysis. Phil, it’s not they didn’t analyse any of the data at all. They basically commented on other people’s reviews and selectively commented. So, for example, with the tryptophan depletion, they quoted a review and said there’s no decrease in healthy volunteers. We fully agree with that. Your study, the beautiful Lancet study, showed that they just neglected to mention the effect size of 1.96 in patients. So, you know, it’s selective with a capital S, and it’s just rather. There’s nothing else I can say. It’s just an embarrassment, to be honest.
Prof David Nutt:
Do you want to just comment a little bit on the imaging? Because I think they also got the direction of effect of some of one of the PET studies the wrong way around? Perhaps.
Dr Sameer Jauhar:
I think you know, you’ve conducted pet studies. Phil’s conducted pet studies. I’ve conducted them. And whenever we have a finding, interpretations are always difficult. There’s receptor density, there’s ligand binding. There’s so many different integers there, you’re always a bit uncertain about what it actually means. You know, it’s not the Wheel of Fortune. It’s not higher or lower if you find decreased receptor binding, and they seem to have made that conclusion when they’re commenting on someone else’s review, there are mistakes in terms of saying, you know, auto-receptors being predominantly pre synaptic, as opposed to post synaptic, just stuff that look. You wouldn’t expect people to know it. But if you’re going to talk as an authority, you do actually need to know your molecular neuroscience, and you need to be humble in how you report it.
Prof David Nutt:
I think you highlighted at the beginning same here, that the group didn’t seem to have any real expertise in many of these the areas they were they were analysing
Dr Sameer Jauhar:
I think that’s fine, but if you’re commenting on something, you do need to have understood what it’s like to analyse the data, to do the experiments. And I think for me, the biggest thing was when you’re quote, when you’re just commenting on someone else’s review, if the person who’s written that review disagrees with what you say, I would suggest you need to have the humility to say, well, you know, given that you wrote the review, you did the data analysis, maybe you know a little bit more about the science than I do.
Prof Philip Cowen:
I just want to make a point that this continues to be an ongoing research area, and I think shortly after the umbrella review was published, there was a very good PET study from the Copenhagen group showing, I think, in about 90 depressed patients a convincing reduction in serotonin type four receptors. And so, you know, that looks a strong finding, and I think this research needs to go on while we try and understand more about what the role of serotonin is in people with severe depression.
Prof David Nutt:
Well, the three of us were somewhat horrified by the quality of the analysis and bored by the conclusions, but we weren’t alone, were we? And Sameer, I think Sameer, you did two things. I mean, the first is that you orchestrated a group of experts to write a letter to the editor of the journal explaining why it had gone wrong and asking for corrections to be made. Do you want to share that with us, what we achieved or what we didn’t?
Dr Sameer Jauhar:
Well, I think we achieved a lot in that we got so many people and some original authors of those reviews to work together, to actually get scientists working together: difficult, we don’t agree on coffee, do we? So, you know, to get over 30 people to agree on just taking away anything emotional, because this needs to be focused on the science.
There were clear methodological errors. You had the world experts, every area covered in the review saying there are mistakes here. And I think that was the main collaborative thing for me. We wrote to the journal, and they published this along with a response by the authors. And I guess you have to allow the authors to make a response, but the response made even more mistakes than in the first paper, if that was possible, and we couldn’t keep on going with that, and I think we left it there with the journal. You know, I do feel for editors, because I think they’re, they’re dependent on the peer reviewers, but I haven’t seen an article engender so much agreement amongst experts as to the veracity of the science. And I think that was quite something.
Prof David Nutt:
If those so those of you who might want to go and dig a bit deeper into what we’re talking about, the original paper was published in a journal called Molecular Psychiatry and then you will find that there’s also, I think, Sameer, you’re the lead author of the critique of that, but the paper itself has already been cited many hundreds of times, and even by students seem to kind of it’s almost become, almost the sense in which people believe it, which I find really quite chilling. And it’s for us, it’s proved very rather difficult to try to get a balancing narrative out there, which is one of the reasons, of course, we’re, we’re having this podcast with you guys. But I also want to plug the fact that you two together wrote a much more cohesive and focused overview of this, of the reality, and that was published in J Psychopharm, I believe. And that’s why people should, should go if they really want to know exactly where the science is, is that correct? Everyone?
Prof Philip Cowen:
I think so. We produced a sort of scientific overview, and I suppose it shows the problem in the field in a way that is kind of less exciting and less dogmatic than the original review. So it might have excited less interest.
Dr Sameer Jauhar:
What I liked is, and it’s a thing you get from academics like yourselves. You go to the original citations and you read them. You don’t quote from an abstract. You don’t quote what you want, you know, you read the original, original Coppen paper, like, and we, we discussed it, didn’t we Phil and, you know, versus the American Schildkraut paper, and you discuss the voice that he had when he just, you know, when he talked about it.
And it’s other simple things. People talk about the chemical imbalance theory. And the citation given in the Moncrieff review is based on an Australian population. And when you read the actual paper, Australians are a very intelligent bunch. They’re saying that, you know, depression is much more likely to be life events related and problems. And, you know, with regard to social factors, chemical imbalance doesn’t come out tops there. And I think it’s a story in science, isn’t it? It’s very easy to see stuff you need to read the actual literature.
Prof David Nutt:
Well, that’s timely to move on to the in a way, what was the point of it all? I mean, I guess most people don’t realize that the NHS funded that body of research. It was funded by this research team, or research funds from I think, northeast London. And that would have cost many hundreds of thousands of pounds to put together all the meetings and the staff salaries and that to produce that. But what was the point of it? What you see is underpinning motivation for doing something, and even if you didn’t do it well, doing it at all.
Prof Philip Cowen:
I think it’s a political exercise, maybe. There are a group of psychiatrists and other people who think that the taking a medical scientific approach to psychiatric problems is fundamentally misguided, and that really we should be looking at social factors and trying to manipulate those if we want to help people with severe depression, for example. I think part of the attack is saying there’s no reliable evidence of any neurochemical changes in people with depression, therefore, we shouldn’t be using medications. So as I said, I think its part of that kind of understanding of that viewpoint that leads them to produce a paper like that. I mean, I think it’s basically been politics rather than science.
Dr Sameer Jauhar:
I think, you know, it’s someone and what I love about where we live is that people are allowed to express opinions. Of course they are, and that’s the way it should be. But this is, like I said before, it strikes me, that this is the opposite of the scientific method. You know, you have come to your conclusion. You’re backwards extrapolating everything from your conclusion. You mentioned Thomas Szasz. You know, if you believe depression doesn’t exist, well then everything else, backwards extrapolates from that. And all your reasoning, all your parent logic, comes from that. And so it’s such a fallacy. And it’s not controversial to say that’s a fallacy. Of course, it’s a fallacy.
Prof David Nutt:
But perhaps the most striking Knight’s move thinking in this whole theories of misunderstandings was the conclusion that, because they claimed that there was no role for serotonin in depressive illness, antidepressants didn’t work. And to my mind, that was that was rather, again, certainly very much an illogical and non-scientific statement. But let me turn to Phil is there any evidence to support the fact that antidepressants don’t work?
Prof Philip Cowen:
I mean, the evidence is that they do work. And I think the argument was that, if there’s no serotonin deficit in people with depression, there’s no plausible mechanism by which antidepressants might work, and clearly that’s a misunderstanding of how a treatment might work in a clinical condition. And so, for example, I have asthma, and I take an inhaler which activates beta-receptors in my bronchi, and that dilates the bronchi and relieves my asthma. But there’s nothing wrong with my beta receptors, per se. It’s just this is a treatment that helps by producing that particular physiological response. I think people have always been aware that an antidepressants quite likely work by producing other neuro-adaptive changes, not by simply reversing a biochemical deficit.
Prof David Nutt:
And if we look at the evidence for antidepressants working, it’s pretty hard to say that they don’t, given that so many of them have been approved by bodies like MHRA and NICE for a good 50 years. I think the best data is an extensive network meta-analysis by my colleague on Andrea Cipriani, which was published in The Lancet in 2018 and that shows unequivocally that all licensed antidepressants are superior to placebo in randomized trials. So, I mean, there’s no doubt that they work. You know, we’d like them to work rather better, but they do work.
Dr Sameer Jauhar:
And it’s amazing that they do work when you look at the degree of placebo response. And it’s amazing all the all the arguments that people make they’ve been dealt with over the decades. You know, people talk about effect size, and they say, well, oh, it’s only point three. But you know, that was Cohen’s measure for estimating the height of girls. It’s not clinically relevant. But if you look at the actual items in the Hamilton depression scale, mood improves. And what’s interesting is, mood improves with antidepressants, the scale improves despite the side effects that people get. Now people might say there’s un-blinding, and how do you un-blind that’s a problem throughout the whole of medicine, but our Scandinavian colleagues have shown people who get more side effects, actually, that doesn’t correlate with improvement in mood. And so to the best extent, there systematic reviews, which suggests that un-blinding isn’t happening in these trials. So, you know, those arguments are old, arguments badly made. And really the field, the field, moved on a long time ago from that, but it just seems to rear its head every single time, unfortunately. And, you know, I really can’t articulate it any better. It’s just very clear. Now, of course, there’s a proportion of people who don’t get a response. We all we know that with TNF-alpha, you know, medicines rheumatoid arthritis doesn’t mean that you don’t offer treatments. At the beginning
Prof David Nutt:
I’ll just share an anecdote with you, which neither of you probably know. So I worked in the States for two years, 1986-1988 and I came back in 88, and in 89 I was asked to review a paper with from Dr Moncrieff claiming that lithium didn’t work. And I thought that’s kind of slightly weird thing to claim, and it was based, as I now see on this series of miss-analyses of extremely compelling data on the effects of lithium in suicide. And worries me that there’s, there is this theme or stream running through some psychiatrists who don’t want drugs to work and again, I can sympathize with that. It would be nice if they didn’t. But what’s the evidence that the alternatives work at all, or certainly work as well? Either of you want to comment on that?
Dr Sameer Jauhar:
You know, I think it’s not rocket science. It’s not difficult. Its evidence based medicine. You just measure the quality of a trial, and you look at the comparators, and you look at the outcome measures. Let’s take psychotherapy. For example. There’s a nice paper called Apples and Oranges by Argyris Stringaris that’s just come out. They looked at antidepressants and psychotherapy in child and adolescents, and they’ve just found that the inclusion criteria are different in the trials and the outcome measures and quality of the trials different, and you have to take any intervention and subject it to the same degree of rigour.
You know, we had these exercise trials coming out showing efficacy and depression with self-report outcome measures versus treatment as usual. You know, any methodologist would say, do not pass go, do not collect. You know, a publication for this that ends up coming out in the BMJ and, you know, on the front page of newspapers, there’s a real need, I think, for the scientific media to take stock and not jump onto these things, because it’s basic.
Prof David Nutt:
Well, actually, that’s the question, isn’t it? Sameer, why the media so keen to dis psychiatric treatments? Do. I don’t apply the same kind of bias to other treatments. I worry that this is still a deep, maybe unconscious, maybe conscious stigma against psychiatric disorder, and the sorts of claims that are made by the mod creep team, they seem to be feeding into some of the current dialogue. Tony Blair saying, you know, well, just pull yourself together. Come on. You know, work for me, I’m not sure that’s going to help the people we see. As a psychiatrist, is it?
Dr Sameer Jauhar:
I think it’s saying severe mental illness doesn’t exist, and that is the fear. And we’re going to be biased by the patients we see, whether we like the fact that we do evidence based medicine or not. But when you’ve seen severe mental illness, you know you have to be honest and truthful with people about these things, I think. And we’re clear about depression, aren’t we? You know, the Baltimore study, the rate of recurrence is the recurrence of these disorders, and 50% of people might not have recurrence, and that’s fine, but of those who do, I think the treatments we have are reasonably effective. I think the frustration for people in the field is surely that we should be moving on.
Prof David Nutt:
Well, that’s true. We maybe we’ll touch on that, but I wanted to focus there was one other really important piece of evidence, which several studies have looked at and doesn’t get enough mention. And I guess the best paper is the Geddes paper from Oxford, Phil, showing that the real power of antidepressant medicines is to prevent relapse, is much more powerful in terms of producing a remission, but once people are well on them, they do seem to protect you. Want to comment on that Phil? The resilience from …
Prof Philip Cowen:
Yes, that’s right. And I think a later paper by Glenn Lewis’s group showed that even when people have been taking them for a number of years, when they’re randomized to either go on or to or to placebo, and they’re carefully stopped, there’s still a higher relapse rate in people who go on onto placebo. So this effect is maintained, and it’s still useful. People are just taking them long term because of habit.
Dr Sameer Jauhar:
And I think there’s a by a factor of about two. The sad thing is that some people relapse despite taking medicines. And what you’d wish for is for us to have time and resource to focus on those people, really, instead of sort of going back to the 80s or possibly the 70s, may I say David.
Prof David Nutt:
Yes [laughs to himself]
Now, as some of you will know, we’re exploring the possible utility of psychedelics or depression, and we find this quite commonly, people will say, well, I want a psychedelic, but I don’t want to go on a traditional antidepressant, because they’re dangerous and addictive. And you think that’s a slight, maybe they’re not. You’re rather exaggerating. You know, you’re believing an exaggerated hostility so many million people. I mean, I’ve been on for so many, so long, with such good outcomes and comparatively very, very low harms. Would you agree with my position on that?
Prof Philip Cowen:
I think so David. Though I think I’m also struck that when people talk about this, say on interviews or news programmes, though they might say, if they’re critical, I don’t believe these antidepressants work, but they must know that people listening to them in the audience, or even people working on the programme will know, either from themselves or their friends and colleagues that these medicines have been helpful for them, and there’s almost a stigma about saying that. It seems more socially acceptable to say you’ve been harmed by them, to say you’ve been helped by them
Dr Sameer Jauhar:
Yeah, well, I think you struck it when you said, believe, I believe. You know, I’m sorry, but you wouldn’t say I believe in insulin or I don’t believe in insulin, I don’t believe in antibiotics, I don’t believe in vaccines. Well, actually, some people might say that.
Well, I suppose one of just as I mentioned, Tony Blair and you pull yourself together, approach to mental distress. But I think I know, if you all know, but his spad Mark Campbell [Prof Nutt is referring to Alastair Campbell] he’s swears by his antidepressants. He had his serotonin in his pocket. Everything he does is the security that antidepressants have given to him for so long. He is a very good spokesperson.
Prof Philip Cowen:
I think he made a good programme about being depressed, and saw various people about it. And it was an interesting encounter with Joanna Moncrieff. They sort of met. And then she said something like, you know, I have to warn you, these drugs will change your mental state. And he said, but that’s what I want.
Dr Sameer Jauhar:
Well, intelligent people do know what they want, you know. Dave, is it all right to ask? Because the one thing you brought up before depression is more than just low mood, and that always strikes me when we have these sort of contretemps. You know, it’s not for someone else to dictate to us what they think depression is. This has been, you know, this has been since antiquity, hasn’t it? Hippocrates and the rest of them, depression, and Ken Kendler writes about it beautifully, doesn’t he? Depression? When you look at the textbooks from, you know, the 1900s there. Cognition, the movement, there’s so many different facets what it is to be human, and it’s not just that you’re, you know, that you’re feeling low. And I think it’s a bit embarrassing to be honest when people say that that’s their view of depression, and that we could all have it, because, you know, it just doesn’t do any justice to all the work that’s been done.
Prof David Nutt:
No. Quite. And the reason, I reason it’s so important we articulate this, is that 15 years ago, a certain person called David Cameron, when he became prime minister, decided that addiction wasn’t an illness, and moved addiction services out of the NHS and gave them to social services. Most addiction doctors were made redundant. Addicts, deaths from particularly opiates, went on a rampage. We’re still reaping every year, a new peak in terms of deaths because we stopped treatment. So these political statements, they have huge ramifications in NHS, resources and or worse. So it is important to make sure our politicians don’t get away with having those opinions turned into policies.
Can I just finish on that? We got a couple of minutes left. I just want to finish with this concept. Though I really struggle with the idea that anything that someone feels might not come from the brain. Is that or am I just old fashioned?
Prof Philip Cowen:
No, I think, I think that’s an old fashioned view, isn’t it? A kind of, kind of dualist view, that somehow depression is either going to be psychosocial or it’s going to be biochemical. And that’s the that’s the issue I have with this phrase chemical imbalance, which I think, as Sameer said, a lot of Australians endorsed, and the brain works by neurochemistry. You know, our drugs work because they act on those neurotransmitters. So when you have a profound change in your mental state, as you get in severe depression, to say there’s a chemical imbalance is rather stating the obvious. And I think as a clinician, the main task is to know whether you try to resolve the problem by acting at that level or by adopting psychological, social methods, or both. Because, of course, psychotherapy is going to change brain neurochemistry too. So I think trying to separate them out is misguided.
Dr Sameer Jauhar:
And it shows a complete lack of knowledge of neuroscience. You know, social determinants affect our brains and vice versa. It’s a bi-directional effect. You know, the biggest risk factor for cardiovascular heart disease is socioeconomic deprivation, but not everyone who is deprived as heart disease, and not everyone with heart disease is social deprivation. Social deprivation. It doesn’t take you sort that one out, does it?
Prof David Nutt:
No, quite and actually, as I say, when I’m asked about this by activists, why don’t you sort out social deprivation? I say, well, it’s tough enough sorting out depression. That’s a matter ….
Thank you so much. Gonna have to bring it to a close, but that’s been a really great discussion.
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