In the first instalment of this special two part episode, Rachel Handley talks to Professor Steve Hollon, international expert on the prevention and treatment of depression and co-author of the second edition of Cognitive Therapy of Depression about how we understand and treat depression.

Steve shares what first drew him to the field, his early encounters with Aaron T. Beck and the rise of cognitive therapy, and how insights from evolutionary biology, psychology and neurobiology can enrich our understanding of depression.

Next time: In Part 2, Professor Hollon discusses how CBT can be applied to a wide range of presentations, from more straightforward to highly complex and even tries his hand at devising a brief intervention for the President of the United States. Don’t miss it!

Resources and links

Cognitive Therapy of Depression (Second Edition)

Find out more about Steve and his research here

OXCADAT:

A wealth of useful videos and therapist resources for social anxiety, PTSD and panic disorder can be found here: https://oxcadatresources.com/

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This podcast was edited by Steph Curnow

Transcript:

Rachel Handley:  Welcome to Let's talk about CBT- Practice Matters, the BABCP podcast for therapists using cognitive behavioural therapy with me, Rachel Handley. Each episode we talk to an expert in CBT who will share insights that will help you understand and apply CBT better to help your patients.

My guest today is Professor Steve Hollon, who had so much fascinating information, theoretical and clinical insights and stories to share that we just had to produce a special two part episode. In this first part, Professor Hollon shares the reasons for his fascination with depression, the story of Beck's development of the cognitive therapy for depression model and insights from psychology, neurobiology and evolutionary biology that can help us understand the development and maintenance of depression.

Professor Hollon is an international expert on the prevention and treatment of depression and co-author of the long awaited second edition of Cognitive Therapy of Depression, the definitive and groundbreaking psychotherapy manual, first published by Aaron T Beck and colleagues in 1979. Professor Hollon is professor of Psychology at Vanderbilt University in the US but is no stranger to us in the UK and supporting the dissemination of evidence-based therapies here as he regularly provides training to services in the UK and teaches on the Talking Therapies Program at the IOPPN annually.

So welcome to the podcast, Professor Hollon.

Steven Hollon: Thank you very much. And Steve, please.

Rachel Handley: So Steve, you've been working in this field for quite some time now, you might not want to tell us how long, but can you recall for us who or what got you invested in the field of depression personally and professionally?

Steven Hollon: Yeah, I can't tell you exactly why I got interested in depression, but that goes way, way back. We have some family history that I got my own personal history of episodes of depression, but to make a long story short, I was in graduate school in Florida State which was good, strong program, but I was reading Aaron Beck and Marty Seligman and Jerry Claremont, the fellow that generated IPT and I was showing up, in those days we had libraries, we had stacks. And I was looking at some of the same journals that my then graduate student colleague Judy Garber, now 50 years now we've been together looking at the same kind of things and we just decided that we weren't getting the kinds of training that we absolutely wanted, as good as the program was in Tallahassee, we want to work with some of the leaders in the field.

So she wrote to Marty and cut a deal with him to run his research labs while he was off on sabbatical at the institute in London. And I was finishing up my dissertation collection data and I followed her up about six months later, with the notion that I would work for Beck. Of course, Tim Beck didn't know me from Adam and couldn’t get in to see him. And his cognitive therapy approach hadn't taken off yet, but we ended up seeing that his group was going to be presenting at a conference, Society for Psychotherapy Research in Boston. So we drove up the coast and went to the meeting there and I spent the next three days getting to know the other people in this research group and, talking with Maria Kovacs, really first rate psychologists who ended up becoming a leading figure in developmental psychopathology, Hungarian and wanted to go back to Hungary for an extended visit that summer and Tim was reluctant. They had a research grant going on. She was interviewing people that survived suicide attempts. I'm just hanging out on the fringe of the group, and I said, well, I'm a psychologist, I'll stand in for it. So I stood it on a volunteer basis and spent the next three weeks trying to make myself indispensable. We ended up negotiating my first year in Philadelphia as my clinical internship. Second year, with Tim's blessing, I went over to the psychiatry residency program, continued working with him, and then ended up going off to Minnesota for a job I was thoroughly unprepared for. Nonetheless, things went well, I got an offer and went out there. Judy graciously finished up her doctoral training at Minnesota and eight years later, we were left eight years and 16 winters later, we left for Nashville Vanderbilt and where we’ve both been on faculty for close to 50 years.

Rachel Handley: Wow, that's quite a trajectory. I'm old enough to remember what it's like to go down into a basement of a library and roll the stacks along and actually have to find a physical journal paper, not just type it in on the internet. Right. But from there to working at the heart of the revolution, really, of cognitive therapy with Beck and his team must have been quite something.

Steven Hollon: It was something, but it was not a thing yet. Tim Beck, Philadelphia Penn was heavily psychodynamic, he was heavily ostracized. He'd been dropped by the Philadelphia Psychoanalytic Society. Every year they'd have the various psychiatry faculty meet with the residents, and when he met with the residents, virtually nobody showed up. It became a thing with the publication of the first outcome trial, the Rush et al study that suggested that cognitive therapy not only held its own with medications, it was actually better than turns out. It only looked better than because we did a terrible job with the medication comparison, but everything since that's done a good job with cognitive therapy, done a good job with medication treatment suggested they're about comparably effective and cognitive therapy has an enduring effect that cuts subsequent risk by about half something medications can't do.

Rachel Handley: And as you hinted there, that was the journey for Tim Beck as well. He came from this psychodynamic background training team, anyone with a passing interest in cognitive therapy now knows about or has started by training in the principles and practice of cognitive therapy for depression. But can you tell us a little bit about his story and the development of the approach?

Steven Hollon: Yeah, he was, although he was marvellous fellow, a marvellous human being, but originally wanted to be a pathologist because you could get definitive answers, but he ended up getting diverted into psychiatry. And in those days, the late 40s, early 50s, everybody was trained dynamically. He was trained by some of the best. And of course, the dynamic explanation for depression was it was anger turned inward. These were unconscious motivations laid down in early infancy, to be angry with your parents about something, some kind lack of sexual gratification and the notion was you had to, the patient himself or herself couldn't be aware of what their true motives were because there were defence mechanisms that got in the way. So you had to sneak up on them. You had to rely on free association. People would take the couch and just say, first thing that popped into their head, or you would interpret dream content, and you might spend two or three years exploring the underlying motivations without ever approaching them directly. The therapist might go, certainly better part of a session without saying anything. So it was a very long term, expensive therapy form of therapy. Tim was interested with his interest being a pathologist was interested in doing some research as well. And he was struck by the fact that the things his clients to him and their free associates in their dreams, which is like what they told him when they were walking into the office. I'm an addict. I'm unlovable. I'm a loser. I never do anything right. As, and they weren't screens for underlying, sexual and aggressive drives, They were just what they believed. He did some research where he investigated dream content, investigated free associations, and as hard as he looked, he could not find evidence of anger turned inward. It just wasn't there.

He did an experimental study with colleagues across the street in psychology at Penn where they manipulated outcomes on a performance task. And it turns out if you want to get somebody who's not depressed really activated and motivated to try harder the next time, give them a failure experience. Rig it so they don't win. If you want to get somebody who's depressed activated the next time, give them a success experience, contrary to what they expect that then gets them mobilized. And on the basis of that, he started, I think, in ‘63. he was writing those things up in the late 50s, but a ‘63 article in what was then the Archives of General Psychiatry, laid out the basic notions of the theory. And in ‘64, he came back and described some of the things he was doing therapeutically, which were really almost common commonsensical, if you take your client's beliefs at face value, you have them exactly the accuracy of their beliefs, and it got him dropped by the Philadelphia Psychoanalytic Society, ostracized by his colleagues, but the last laugh, he wrote his ‘67 book on depressions now considered a modern classic an things took off from there.

Rachel Handley: Well, that's the kind of failure we can all live with, right?

Steven Hollon: Exactly. The one thing Tim would always say is it much like, working with people who are depressed is you always want to turn adversity to advantage. Something goes wrong, find out a way to get something out of that.

Rachel Handley: That's what he did. And it sounds like, very much took that, that, that pathology approach. He was dissecting the presentation, what was in front of him and understanding it rather than the bringing theory a priori to the presentation.

Steven Hollon: Yeah, absolutely. He was always driven by data, which is again given a psychiatric background, you wouldn't necessarily have expected that, but he did and he was. He also spent at least a year at Oxford in the early 80s. Michael Gelder picked up on this growing phenomenon fairly early on and invited Tim over for a year sabbatical and he did, and that's where he had contact with people like David Clark and Paul Salkovskis. And, just, in some respects, England moves a little closer to Beckian Cognitive Therapy than we do in the States. We have a lot of folks that came to cognitive behavioural approaches from a more behavioural background, and they still have a little trouble thinking about the meaning behind the belief, for them, but a cognition is just another behaviour. You reinforce that in you replace negative thoughts with positive ones, as opposed to getting people to examine the accuracy of their beliefs. So there's a bit of a contrast. And I would think nowadays, David Clark, Paul Salkovskis and Anke Ehlers are closer to Beck in spirit than the states and depression. But, most of the rest of the folks over here, particularly anxiety, stress, et cetera, are more nearly behavioural with cognitive over than are you guys are in England.

Rachel Handley: So there's that difference of emphasis and approach, but depression is a worldwide problem where we're used to thinking about and hearing about the statistics and figures like one in five, often quoted in terms of what lifetime prevalence is a big burden on the health of the world population. But it's been suggested that even those high figures might be an underestimate. How significant, Steve, is depression as a problem?

Steven Hollon: Yeah, I do a undergraduate class. I'll go and do another meeting later on this afternoon where the whole focus of the class is everything we were wrong about a decade ago, and one of the things we were most wrong about is, we've always thought of depression as the single most problem with psychiatric disorders, and it is, but it turns out it's about 4 to 5 times more prevalent than we realised. And our estimates were based on good retrospective epidemiological surveys, the kind of thing we did in the States with the National Comorbidity Study. Ron Kessler, superb epidemiologist, did that but the methodology is to interview a large number of people over the course of a year, and they range in age from their late teens up to the 80s. And when you do that, about once a year, you'll start getting calls from journalists that say, I noticed that people in their 80s have fewer episodes than people in their 20s. Is there an epidemic? No, there's no epidemic. Just people in their 20s remember an episode of their 20s. People in their 80s don't. So it's a memory problem.

If you look at the birth cohort studies that follow people from birth on, like the marvellous Dunedin sample that Terrie Moffit and Avshalom Caspi have inherited and followed, where the sample is now in the mid-forties, you get estimates of depression which are at least 3 to 5 times higher than what we get from the retrospective surveys. And the biggest proportion of extra cases that we hadn't realised are single episode patients. We've always assumed that depression was quite common, about, as you say, about one person in five but highly recurrent. Turns out it's much more common than that. The Dunedin sample, over half of those folks have now had at least one episode of depression, but the bulk of them don't go on to have a second. And what it turns out is that, what it looks like is what an evolutionary biologist would call a species typical behaviour. Any one of us could get depressed if something bad enough happens.

Now, there's a subset of folks that go on to have multiple episodes. We don't have a good explanation as for why that is. Scott Monroe and Kate Harkness did a terrific pair of articles, 2019, in Psych Review, and then 2022, I think, in Annual Review where they suggested a dual pathway model that some folks hit adolescence at elevated risk which sounded very compelling. I thought they're really onto something. I remember writing very positively about that. But when you check in the distribution of episodes, in the Dunedin sample it's purely linear. Most folks that have an episode only have one, the next largest group of people have two, next larger group of three, et cetera. But there's no bimodality and that were something like intelligence where there are a large number of factors, no one of which counts for much of the variance. You got a nice normal distribution with a small number of people, genetic anomalies, birth, trauma, et cetera, at the low end, get a little bump. We don't get anything like that. Or if you think of gender or height is normally distributed within women, normally distributed in men, but the two together make a bimodal distribution. If there were really some kind of diathesis that accounted for a large number of cases of recurrent depression, you would expect bimodality, and we just don't see that in the data.

Rachel Handley: And so when we look at current reports of increasing incidents of depression since COVID, for example, would your perspective be that's more likely to be measurement area error? Or is that just something so bad has happened that we can get depressed from that.

Steven Hollon: yeah, I mean, things happen. We had increases during the depression and increases in suicide, usually suicides, a hard index, and more people jumped out of windows in the 1930s than before or after. I do think when bad things happen, more people are going to get depressed, so it wouldn't surprise me if we have an excess, I would be surprised if they go on to become recurrent.

Rachel Handley: Okay. So it doesn't necessarily mean in the longer term, we're going to see an increase in of people presenting for therapy, but we don't know.

Steven Hollon: We don't know. I'll be curious. My wife's a developmental psychopathologist. And what she would say is that the thing you don't want to do to 12, 13-year-olds is not let them be in classrooms with other 12 and 13 year olds and make them go through social media, feel criticised, et cetera, that's a recipe for generating angst in young adolescents.

Rachel Handley: Absolutely. And given this huge prevalence that you're talking about of single episode depression and then these other presentations where people have recurrent depression, when you see a presentation like that, so pervasive across the species, it might lead you to speculate about is something adaptive about this? And when we look at anxiety, for example, it can seem obvious that being alert to threat would have some adaptive functions, perhaps even things like anger, the function around seeking justice or restoring kind of normal social norms. What might be the value of a depressed mood?

Steven Hollon: We thank God for first responders, they keep the rest of us alive. But in our ancestral past, if you didn't walk up to the edge of a cliff, you're more likely to live and have offspring than if you did. So anxiety does serve a function. We've never had a problem with that. Pain serves a function, and pain keeps you from doing additional damage to injured tissues. We've never thought about depression as having a functional advantage. Paul Andrews, the evolutionary biologist at McMaster in Canada, has I think really come close to nailing this. The number of good evolutionary biological theories of depression, any one or all of them might be true to greater or lesser extent. The thing I like particularly about, Andrews and Andy Thompson, his colleague, in a paper they published back in 2009 in Psych Review. When I first read it, I thought, hey, these guys, lovely, but they have no idea what they're talking about, they just got it wrong. And over the last decade of arguing with the two of them, I'm now convinced they were more right than I was. The thing I like about that, what they say is that depression evolved because it gets us thinking very hard and long about social, complex social problems. And in our ancestral past, the one thing young primates couldn't afford to do was be thrown out of the troop. If you were, you're going to get picked off by predators. And if you're a young adolescent female, who's probably already been impregnated, it's going to be a double whammy evolutionarily because you and the offspring are going to be lost to posterity. Now the problem with, you can avoid falling off a cliff if you don't walk near the cliff. but if you've offended the elders in the troop, you got to sort out how you're going to deal with that.

Now we know, and by the way, let me just say there's a major difference between unipolar depression and depression as it occurs as part of a disorder, the depressions are virtually identical. However, unipolar depression is not only our single most prevalent single psychiatric disorder, and a lot more prevalent than we used to recognise, but it is so high prevalence, modest heritability. It's heritability is about 0. 3 to 0.4, which makes it less heritable than political preference and huge gender distribution from early adolescence on, women about twice as likely to get depressed as men. I suspect it's because they tend to get involved with men, but what do I know?

The bipolar disorder, you don't necessarily have to have a depression to get diagnosed with bipolar disorder, although most folks will have depressive episodes as well, but the defining feature is one or more episodes of hypomania or mania. And of course, mania, hypomania are the mirror opposites of clinical depression, virtually all the same symptoms are involved, they just go the opposite direction. But it's highly heritable. 0. 7 to 0. 8. along with the schizophrenias, it's the next most heritable disorders to autism. The gender distribution, there's no split, every bit as common in women as in men. And even though the depressions are virtually identical, you just don't see the swing to hypomania/mania.

Now, there's some reason to think that we are sometimes diagnosing people that truly belong in the bipolar spectrum as unipolar if they hadn't had a major manic episode, the individuals who tend to be hypomanic don't regard that as abnormal. I mean, I wouldn't have realised- I've mentioned earlier, I have my own personal history of depression, three bona fide episodes. I always thought of myself as somebody that had a history of unipolar depression. I'm out to dinner one time with colleagues in Amsterdam and they'd invited in Jules Angst, the great Swiss psychiatrist of marvellous longitudinal studies. And I didn't know the guy before, but they were kind enough to invite me to join and we're talking over dinner and I just gotten in that morning and, he mentioned in polite conversation was I concerned about jet lag? I said, well, I don't get jet lag. I just, I get a little speedy. But the rate of speech picks up a little bit, and he asked me a few other questions. He said, you've had depression? I said, yes. He said, well, are you unipolar? I said, yes. He said, no, you're bipolar. You're in the spectrum.

Rachel Handley: Wow. It's not necessarily what you expect when you accept a dinner invite.

Steven Hollon: Yeah, well, you do when you meet with a Swiss psychiatrist who devote their career to longitudinal research, open for anything. But it's probably true. And I wouldn't want to lose that. I mean, some people take drugs so they can get the sense of great energy, a little bit of grandiosity. And except for occasionally making an inappropriate comment, it's never gotten my way. And I suspect, half of my publications come from getting a buzz on something and 3 days later coming up for air.

So we know that Bipolar II is one of the hardest diagnoses to get right. And it turns out if you, as we often do with clinic interviews, you ask the individual himself or herself, they don't see it, to them it’s just normal coincidence. If you ask their significant others, the people that live with them, coworkers, they all recognise it. So it's not hard to diagnose if you ask the people that live with the person, but it's hard to ask the person himself or herself.

At any rate, psychotic depression is a problem, but we also are learning now, and a lot of that's coming out of research, people doing at the Social Genetics Institute at the Institute of Psychiatry, one of the things we're learning with these large GWAS studies is that the serious mental illnesses, the schizophrenias and the psychotic affective disorders, particularly, psychotic mania are more closely related genetically than bipolar disorder is to unipolar, or at least as closely as bipolar disorder is to unipolar disorder, and non-psychotic unipolar disorder is at least as closely related to the anxiety disorders. So, the evolutionary biologists are calling for reorganising our nosologic system, so that we're separating out the serious mental illnesses, all of which are highly heritable, low in prevalence, and show no gender disparity, and almost always need to be treated with medications or somatic treatments from the non-psychotic disorders; anxiety, stress, depression, unipolar depression which are modestly heritable, usually have a big gender disparity an, tend to respond at least respond to neuropsychological intervention often with an enduring effect.

Rachel Handley: And it sounds like you were saying this might have a difference for how we view the adaptive properties of these different types of presentations. So you were talking about unipolar depression, and I'm on tenterhooks to hear what is it? So, so I've offended the elders, and I've got to solve a social problem. How do I get there?

Steven Hollon: Of the several various good evolutionary biological theories of depression, something like conservation withdrawal, which is when things go wrong, you don't want to expend a lot of energy. So you hunker down. it's probably the case because that's older. You find that in organisms that don't have cortexes. So, molluscs show a conservation withdrawal when the environment is not supportive, and it looks for all the world like a depression. One of the things Paul Andrews and colleagues would point out is we have at least three symptoms that revolve around negative affect stress and they are, sickness, starvation and then clinical depression. And in sickness, quotes, depression, energy gets routed away from the cortex, it gets routed away from growth, reproduction. It gets routed away from hedonic pursuits like sex and food and towards the immune system. If you've got an infection, what you got to do is survive the infection so a lot of the energy goes there. If you're starving the energy gets routed to the maintenance of our organs, the brain, the heart, the liver, et cetera, the extremities waste away. If you're thinking about anything, it's only food and if your behaviour changes at all, it's only spend more time foraging, looking for food, it turns down the nucleus accumbens. So again, you lose interest in sex, you don't want to go out on dates, you lose interest in other kinds of things.

In clinical depression, the energy goes to the cortex. And it doesn't go to the immune system, it doesn't go to maintenance of vital organs, and it goes to the cortex. And when it goes to the cortex, it does a couple of things. The Raphe nucleus deep in the brain stem is where all of the neurons in the brain that use serotonin as a neurotransmitter have the cell bodies. It's very ancient, probably came in with the mitochondria- God knows how long ago when we had separate organism organallia, and it was probably mitochondria, probably separate or just the blast pharmacist in all organisms. Now they're what convert sugars into energy, that's how we get energy to do things. But serotonin was very closely associated with that. And it looks like serotonin's primary role in the brain, in the body and in the brain, is not so much to be the target for antidepressant medications, which it is. It was to shift energy back and forth between positive hedonic pursuits and negative pursuits, avoiding danger. And any organism has to do two things over the course of the day, it has to get lunch without becoming something else's lunch and our positive affective responses push the former; sex, food, et cetera, things good for the individual, good for the species. And our negative hedonic pursuits push the latter. Jeffrey Gray, who started Oxford and was for years the head of psychology down at the Institute of Psychiatry, really lay out the neurobiology that, probably two decades ago now. And, with dopamine seems to be the primary neurotransmitter driving it. Dopamine is not the “I like it” neurotransmitter, it’s the “I want it” neurotransmitter. And when you pursue things, the dopamine neurons are lighting up. Norepinephrine is the primary neurotransmitter involved in regulating negative affect. If you're going to have a panic attack, it's when the locus coeruleus fires, which is where all the norepinephrine neurons in the brain have their cell bodies. At any rate, when the raphe nucleus fires, it projects to the amygdala, which gets you paying great attention to whatever it is that's distressing to you at the moment. It projects to the hippocampus which activates short term memory, which is energetically expensive, it burns up a lot of energy to think hard about something. It projects to the prefrontal cortex, which makes you resistant to distraction. It projects to the nucleus accumbens, which turns down hedonic pursuits, sex, food, et cetera, and it projects to the hypothalamus, it cuts down activities like growth and reproduction. Basically, when the Raphe Nucleus fires, it makes the brain ruminate. And then it asks itself the question, why in God's name would evolution set something up which makes you ruminate about things?

Rachel Handley: Because we hear rumination in therapy and we think that's a bad thing. We don't want to be there.

Steven Hollon: We all got it wrong. I spent the last 40 years trying to help patients not ruminate and an evolutionary biologist like Paul Andrews comes up and says no, that's what depression was designed to do. And it's a basic principle of evolutionary biology that any intervention which facilitates a function that an adaptation evolved to serve is preferred over one that doesn't. And it works in the following way, what I think we do with cognitive therapy is we structure people's rumination, so they don't get stuck and any client I've ever worked with gets stuck blaming themselves for their misfortunes. Now, sometimes they've engaged in behaviours which can be trip into the misfortune, sometimes they haven’t, it’s just the piano fell out of the second floor and hit them on the head. But, mostly everybody I've ever worked with is convinced when they come in that either they're unlovable if they're interested in affiliative concerns, or they're incompetent if they're pursuing achievement kinds of concerns or both. And when I first read the dual pathway model by Monroe and Harkness. I thought that seems weird that that's the diathesis. And we have good data that people go into, for example, college with the propensity to blame themselves when things happen or more likely get depressed during their college years. However, with the absence of bimodality, you got to think maybe that's one of the things that gets triggered when you get depressed and not necessarily something that predates the depression. That's one of those mysteries we still have to sort out. But I'm with all of this is Andrews and Thompson's approach, accounts for what goes on in the brain and where the energy goes in a way that no other existing, evolutionary theory does. And on, on that basis, I got to think there, there are too many little factoids that it accounts for it. You just couldn't account for any other way.

Rachel Handley: So let me check. I've understood what you've said. So it. We started thinking about what might be adaptive about low mood and that might lead to this kind of prevalence of depression. And you said that the changes that go on in the brain are really well positioning us to focus our attention very closely on the problems, the threats that we're dealing with in the here and now and to resist distraction, to be absolutely able and ready to, in effect not eaten-we want to solve the problem, the threat that's out there, that we're dealing with and you still.

Steven Hollon: Exactly, although the threat here isn't getting eaten, it's being ostracised.

Rachel Handley: So it's a social problem. It's there. I've offended my elders. I've offended those around me. I don't want to get, become an outcast from the social group. So low mood is really setting us up well to problem solve our social problems, but it gets stuck. It gets hijacked when you think I'm unlovable or unworthy.

Steven Hollon: Thats that's what I think. Now, again, I'm still arguing with Paul Andrews about this, but my hunch is in two to three years he will have convinced me. He would say, if you make people sad, just an experimental task, like having them do expressive writing risk happen, they'll start switching into this type two thinking. And there's nothing exotic about the type two thinking. Daniel Kahneman talks about thinking fast versus thinking slow. If you don't want to step on a poisonous snake in the woods (unless you're in Ireland and we don't have to worry about it) there's something squiggling on the ground, you put your foot back before even aware of what you think the dangerous, that's thinking fast, heavily heuristic driven. And there it's having a fire alarm that rings when there's no fire. It's okay to have some false alarms. You don't want to miss a true fire. Depression seems to activate when you get sad, it activates type two thinking, which is slower, requires short term memory.You have to store the stuff in memory, sort out. Could it be this? Could it be that? What can I do about it? And it's energetically expensive. So you don't want to spend your time doing other things that are going to distract you. You don't want to be pursuing other kind of hedonic values. Get your complex social problem solved and then you go on with your life.

And if you track the longitudinal work, what Andrews would say is that the first thing that's going to happen when you get sad, it's going to take you into what he calls root causal analysis. What went wrong? What went wrong? What went wrong? Which then feeds relatively logically on to problem solving. What can I do about it? And if you track people across time, across the course of an episode, they go from sadness to root cause analysis, heavy focus on where have I screwed up or what screwed up to the problem solving? What can I do about it? And the problem solving is negatively correlated with subsequent depression. The problem solving brings it down. It looks like evolution built a mechanism which helps you identify and resolve a complex social problem which would have led to ostracism from the truth. The fact that depression, highest incidents, highest levels of onsets of more than half the folks ever get depressed, unipolar depression kicks off in early adolescence and twice as common in women as in men.

Rachel Handley: And some folk get stuck there. So it doesn't solve their problem. They get stuck there.

Steven Hollon: Some folks, I mean, I'm so used to working only with the people that get stuck, that, I've been really been looking for what the diatheses are. And that doesn't mean there aren't diatheses, certainly, some people have more genetic predispositions than others. Some people have childhood trauma, et cetera, a number of things we know increase the odds for getting depressed down the line but how much of that played into our evolutionary past, ancestral past, who knows.

Rachel Handley: So, you've said a lot about where depression may come from, what role it might play in us as a species. We've talked about a bit about vulnerability, what we know about that, you said bad things happen, people get depressed, gender can play a role, and there may be other factors that we as yet don't know that play a role. Once depression is set in motion (we love a great formulation on this podcast) we love to know what keeps it going, what maintains depression. But we don't have boxes or arrows, we love those in CBT, but on the podcast, we have to do this without any boxes or arrows or diagrams. That’s your challenge.

Steven Hollon: Yeah, I mean, that's why God made napkins. You got to drop your calls in the office. The, the, how

Rachel Handley: I'm getting it. I'm getting a good picture of your dinner parties, drawing diagrams on napkins.

Steven Hollon: Well, I show up at family gatherings with slides, really annoys them. But, gee, I think it works almost in the following way, almost nobody in a first episode comes in for treatment unless it's become chronic. So we don't see the bulk of the people that get depressed. And by the way, I don't know what they're doing in ICD now, but in the States, we have an ongoing debate about what do you do with grief reaction. Somebody loses a spouse, losing a child is most depressogenic, it could happen to anybody. And we know what grief is like, Freud in his classic article back in what, ‘17 we published in ’21, to differentiate between mourning and melancholia. He said in mourning, your life is diminished and in melancholia, you see yourself as diminished. And, increasingly, we're not sure that there's a difference between the two, that a loss that you would get in mourning triggers the same underlying mechanisms. But you're still going to have to think your way through that.

I remember watching a family member, lose a husband young, with a couple of young kids and watching the grief reaction set in. She had to do a lot of sorting things out. Had to decide how is she going to provide for her children, how is she going to cover their college expenses? Because they were, going to be going from early teen on. She had to navigate once again, the dating role. All kinds of things, problems she didn't have three months earlier. And she had to think about things. So if Andrews and Thompson are right, evolution built a mechanism which almost always is going to help a depression resolve, almost always going to lead you to have to think your way out of whatever the situation is that you're in, that you probably weren't in before something bad happened to you.

Now, that's not to say necessarily that they're right, but there's a grief reaction neurobiologically it’s a depression, so why would you separate out. For some reason, the field has always assumed that if you know what the reason is that somebody is depressed, then it's not a depression. And that's just silly. And, what's the saying? If it looks like a duck, if it walks like a duck, if it quacks like a duck, it's a duck. So, once you start bringing that in, then any one of us could have the propensity to get depressed if something bad enough happens. Mercifully, most of us don't have that many bad things happen, but if they do we're going to have multiple episodes. Now, it could well be that people learn the wrong things in the midst of a depressive episode. And I think that's where the treatments come in. Again, I've never worked with anybody that didn't have a propensity to do what, Paul Salkovskis would say, their theory A is something wrong with me. And an alternative theory B is usually, well, maybe you're using the wrong strategies. So what we try to do in cognitive therapy is to pit one against the other. We'll start with what their theory is walking in the door, I'm unlovable. I'm inadequate, whatever that may be. Get them to do self-monitoring, where they monitor their experience over a couple of days or weeks, getting them to start paying careful attention to what's going through their head when the affect is triggered. And by the way, it’s the lovely book that you held up, thank you, in the very beginning, is Cognitive Therapy for Depression, but you treat the person, patient that walks through the door. And, when we do one of our trials with people who meet criterion for major depression, two thirds of them meet criterion for other things, anxiety disorders, stress disorders, about a third of them would meet criterion for substance use disorders, so whatever you're going to do, you have to be a generalist, you have to meet where they are.

And one of the other things that comes out of evolutionary biology, they would say that Jerome Wakefield, the, social worker who has been a major critic of existing diagnostic categories, Wakefield would say for something to be a disease must meet two criteria. It has to represent a dysfunction in an evolved adaptation, something has to have broken down and it has to cause functional impairment. And an example he would give of the latter is a very small percentage of people are born with the hearts on the right side of their body. But they don't do anything to them. They go to their lives, same kind of life expectancy, et cetera. So there is a breakdown of the mechanisms wherever the in utero, the various organs are shown where to go and where to develop. For them it develops on the wrong side but doesn't affect their lives at all. So it, meets the first criteria and it's a breakdown and evolved adaptation, but it doesn't cause dysfunction.

On the other hand, something like a brief reaction, may not be a breakdown and evolved adaptation be exactly what the brain evolved to do, which is to think long and hard about a problem. If you've got a problem, you have to deal with that you didn't have to deal with before. The reason I go there is the other thing that for years as a psychologist, I'd say, well my colleagues up in psychiatry want to talk about diseases and most folks get depressed, they don't have a disease. What they have is a disorder. From an evolutionary biological perspective, it's also not a disorder. It's very orderly. And anytime, there, what a evolution biologist would say is that, our adaptations evolved to generate a whole body response given the different threats that we're exposed to. If there is something dangerous rustling in the bushes, you want to experience anxiety. You want your physiology to get turned up, sympathetic nervous system to fire up so you can run away fast, and your behavioural impulse is going to be to flee. The cognitions are, I'm in danger. I'm in danger. I'm in danger. All orderly. It's not disorder. It's orderly and it's an orderly adaptation.

If you are challenged, particularly interspecies challenged, the affect's probably going to be anger. They shouldn't do this, et cetera, et cetera. The physiology again is going to get elevated. You've got sympathetic arousal so you can fight, if that's your natural inclination, the behavioural impulse is going to be to attack and the cognition is going to be they have no right doing that to me. How dare they. It's orderly.

In depression, the affect is sadness, physiology gets turned down, it's more parasympathetic than sympathetic. You get this whole dropping feeling in the pit of your stomach, and the behavioural impulse is to do nothing except sit and think. And the cognition is going to be, what did I do wrong? What did I do wrong? What did I do wrong? Or at least what went wrong? Again, orderly. And the thing that evolutionary biology is going on is all of our negative affects are unpleasant to experience, but they all organise a whole body response that in our evolutionary past was probably the optimal response for whatever it was, wherever the different threat was that we had to deal with at the moment.

Now, individuals differ in the way they interpret different situations, which means they're going to generate different whole-body responses, often to the same situation. My wife, absolutely lovely, but East Coast ethnic and her whole family has to and does spend a lot of time worrying about things, which is good because I never do it. It balances off the relationship nicely. But if we get bad news, she'll go oh, that's awful. And I’ll go, that's inconvenient. Just different. Her autonomic nervous system gets triggered faster than mine does, which is beneficial in some respects. And, God knows, I certainly have done stupid things like said, gunfire, let's go see what it is. It just, some folks can live longer given that kind of thing. But if different individuals interpret the same situation differently, then we're going to trigger different whole-body responses. But it's our evolutionary process that gave us the different whole-body responses and virtually nobody can't feel anxiety, anger, grief, depression, et cetera, they just sometimes do it in response to different kinds of things.

One of the first things I'll try to do with any client in the first session is go to that marvellous circle diagram, that Chris Padesky and Kathleen Mooney came up with. They call it the five-factor model, which has five factors. It's the original ABC model, antecedent, events, beliefs, and that the consequences of the behaviour are affected. They expanded it they put the environment out and then they have a circle which is the organism, it’s classic without really realising its the classic SOR behavioural, learning model. And you've got the environment, things happen. And then within the organism, you're going to feel, you're going to have physiological reaction, have behavioural impulses, and you're going to have cognitions. And what I would say as a cognitive theorist is the cognition drives the others at what's determined, what you're going to get and what cognition you have may be determined by your prior life experience, maybe somewhat by temperament, et cetera, but it all was laid down by evolution. They're adaptive processes that left to run their course in the millennials before we had therapists or medications, we had nothing else. And one thing we know about depression is they almost always go away, we have spontaneous remission, even if you don't get treated depression is going to resolve.

I don't know what they're doing in England now but I know in the States, 90 percent of the people who are clinically depressed get medicated and they get medicated by the primary care physician, and primary care physicians are marvellous. They have to worry about 80 different things, 40 of which will kill you. Depression isn’t one of them, but if you mentioned being depressed or anxious they’ll put you on an SSRI because they're relatively safe. The problem with the antidepressant medications is they anesthetise the distress so the facilitate the function that depression or anxiety or anger revolved to facilitate.

Rachel Handley: So just stepping back slightly, we started with a thinking about a maintenance model of depression. And it sounds like what you were saying is loss can happen to all of us. Sadness happens to all of us, but if someone has a particular set of beliefs, thoughts, ways of interpreting the world habitually, like that's awful rather than that's inconvenient, or that's personally this sense that there's something wrong with me, what's happened means there's something wrong with me. This will trigger this kind of evolutionary, instilled physiological whole-body response. It leads to kind of natural behavioural responses, of withdrawal and down regulating our kind of impulses for behaviour

Steven Hollon: Well, it does all that until you sort it out. And once you decide what you're going to do, then it, and again, it's, it, follows a sequence, which ends up generating an action plan, which then if you carry out, it resolves the depression.

Rachel Handley: So, if all works well, it resolves, and we move on. But we know that when we do see people for psychological therapy, when we are treating them that actually we tend to see them when they're stuck, when they're in that kind of disordered place that you've spoken about when its functionally not helpful for them anymore.

Steven Hollon: We tend to see them when they're stuck. And the stuck is almost always is something deeply wrong with me. And, again, back to Paul Salkovskis and that brilliant observation about Theory A, Theory B, which I never had heard about until I started working with folks in IoP, they taught it to me. Theory A is almost always defective in some way, usually unlovable or incompetent, depending on what you most want in your life or both. And Theory B is almost, well, maybe you're going about it the wrong way. And to give an example. I had a client I worked for way, way back when in Minnesota. I talk about him in the, in the revision of the manual. He was a sculptor by training, he was teaching at a small community arts college. Their entire art department, I think three people, got retrenched during the first Gulf crisis. And now three years later, he's working as a handyman on a condominium complex. Hates it. Hates it. Hates it. Think what he has is a reality-based depression. How could he not be depressed? A sculptor by training, he's doing a blue collar job. He's getting paid more than he was as a low grade academic but as far as he's concerned, that's a terrible, awful thing that's happened to him. The one thing he hasn't done in three years is apply for another job in academia. And you ask him, how come? He said, well, I start to think about it and then I get overwhelmed. So, he'll start to take the steps, what he has to do if he wants that kind of job, is to apply. They're not going to come find him at his home, but he has to apply. So, what we did is laid out the notion, his notion is he's not doing that because he is inadequate, he's incompetent. And the alternative, coming off of Paul Salkovskis is just you choosing the wrong strategies, which is, when you go out in the garage and try to do everything all at once in one evening, you get overwhelmed, and you don't start. So, how about we take the large task and break down it into steps for me, which he did. He knew I didn't know. He broke it into a half dozen steps each night to go out and do one. And if you don't finish first time to come back and finish the next night. Within three weeks, he had a portfolio together. That's how sculptors get their jobs. And he was mailing it out to places. So, I mean, it's not rocket science. It's just taking a big task, break it down into smaller steps. That's the behavioural component, but in the process, we would differ from a more pure behavioural therapist is we don't only do that, we get him testing his beliefs. His belief was it's my confidence; it’s gotten in the way, the alternative hypothesis is you’re choosing the wrong strategies. Not repeating his theory A, something deeply wrong with me, is theory B which is I'm going about it all wrong so let me try something different. And it worked out better for him.

Rachel Handley: So the principle underpinning the theory is that the cognitions, the thoughts, the referential beliefs are the main obstacle to him being able to effectively problem solve, break that down.

Steven Hollon: That's right. Yep. The main obstacle, I think, and that's why Tim Beck called it cognitive therapy and not cognitive behaviour therapy, as far as he was concerned, that was the primary mechanism that was going on there. And I think, somebody like David Clark would talk about panic disorder, the main issue is you have these catastrophic cognitions. You interpret benign physical sensations or psychological sensations catastrophically. And that's the real issue. There are things you can do about that behaviour that help move the process along. I think Anke with stress disorders would talk about the failure to recognise that that was then, this ain't then, this is different-and getting past that focus that, that belief right at the moment is the kind of thing. So always we would see the cognition at the core but often use behavioural strategies to go after the accuracy of those beliefs. David and Anke don't bother with thought records at all. And they get people moving very rapidly into behavioural experiments, going into stores on the, on you guys have what high streets or something where you have shopping districts, with a rouge on their face or obvious stains in their underarms, that kind of thing. Or I'll go have people going back to the park where the rape occurred that to regain their lives.

We'll make a lot more use of thought records with somebody who's clinically depressed because so much, well, I think so much of what revolves in the depression is the self-referential, the blaming of the self. And for that, you want to get people out testing things, testing their beliefs, et cetera, in real world experiences. But a lot of that stuff, you got to go back and trace down what it meant to them that it did work.

Rachel Handley: So you have to take some time identifying, seeing the patterns, the habits, the…

Steven Hollon: I could be wrong. Somebody's come, come along from Oxford that's going to blow that out of the water and show you, you can do all this stuff, wrap it up in two, in 20 minutes. But, so far I've done this for 50 years, I'm probably not going to be the one to do that.

Rachel Handley: But it sounds like an important part about the point about the terminology. So it's not that cognitive therapy isn't incorporating behavioural techniques at all. It's just that where behavioural techniques are incorporated as they frequently are, it's in service of changing the cognitions

Steven Hollon: Yeah to test the accuracy of the cognition. And this goes way back to Tim Beck, and he picked up on this back in the early sixties. Even if the primary problem is, what you believe the best way to test it out in the real world is to put it against an alternative and let the data decide.

Rachel Handley: So this seems like a good point to take a break to allow you to ruminate, hopefully in a healthy way, on part one. Those of you with extra stamina may wish to dive straight into part two where we get to work discussing the application of cognitive therapy of depression to the problems people present with, both more straightforward and much more complex. And Steve even has a go at planning a brief hypothetical invention for the president of the United States.

Thanks so much for listening, and as always, till next time, look after yourselves and look after each other.

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