Clinical Psychology is a young profession little more than a hundred years old. Its origins are said to date back to the founding of the first psychology clinic in 1896 by Lightner Witmer (1867-1956) at the University of Pennsylvania (Routh 1996). Witmer was a student of Wundt and is credited with coining the term ‘clinical psychology’ in 1907 when he used that term after launching the first journal in this new field called The Psychological Clinic. In the first half of the twentieth century, clinical psychology was focused primarily on psychological assessment, but over the last fifty years clinical psychology has expanded its scope to delivering treatment and psychotherapy, conducting research into aetiology and the development of new interventions, and is centrally involved in the provision of care and support for children and adults with mental health problems and learning difficulties. Many of the advances in assessment and treatment over the past fifty years have resulted from a unique combination of clinical practice and evidence-based research, and the future potential of clinical psychology lies in its capacity to maintain a strong clinical focus in research and to progress emerging lines of research developed by pioneers in various domains of clinical psychology (Overholser, 2014). As such, clinical psychology has a history that has significantly defined the current state of the discipline, and describing the link between that history and contemporary clinical psychology practice is the purpose of the chapters in this book.
                Choosing the “classic” studies to critique in a book like this is difficult, so before I drew up a final list of influential studies I used Twitter to ask the clinical psychology community their views on what they considered should be in a list of classic studies. Those views have significantly influenced the final list, and chapters cover studies that have shaped modern day conceptions of diagnosis and assessment, contributed to our current understanding of aetiology across a range of different mental health problems, and led to developments in contemporary therapeutic practice. In this book, we’re privileged to have contributors who are international experts providing their detailed critiques of these classic studies and giving their informed opinions on the ways in which each study has influenced modern day clinical psychology and clinical practice.
              A number of these classic studies were controversial at the time they were published, and are still controversial today. For example, Chapter 1 - written by Richard Bentall - covers one such study, namely David Rosenhan’s 1973 study entitled “On Being Sane in Insane Places”. This imaginative and provocative study claimed to show that psychiatrists at the time were unable to distinguish between symptoms of severe mental illness and ‘normal behaviour’. While many aspects of this study and its conclusions have been criticized over subsequent years, it undoubtedly influenced the following four decades of discussion about what exactly constitutes a “mental illness”, and has certainly contributed to ongoing debates between psychiatry and clinical psychology on the role of diagnosis in mental health provision (e.g. Bentall, 2017).
            Almost every undergraduate psychology student will have come across the “Little Albert” study published by behaviourist John B Watson and colleague Rosalie Rayner in 1920. This was Watson’s attempt to demonstrate that basic conditioning processes could generate simple emotional reactions such as fear and anxiety, and in Chapter 2 we explore this textbook classic and its contribution to clinical psychology. The chapter authors Dirk Hermans, Yannick Boddez and Bram Vervilet ask “What would a parallel universe look like in which the romantically linked Watson and Rayner had never met?” Well, it’s very plausible that modern day treatments for anxiety would not be exposure-based and behaviour focused. We might all be practicing psychoanalysis today were it not for Watson’s inspired desire to show that a clinical application of empirically-validated principles of conditioning was possible.
            Undoubtedly, one of the most significant influences on modern day clinical psychology practice has been Aaron Beck, arguably one of the founding fathers of modern day cognitive behaviour therapy (CBT). So for that reason, we’ve included two articles authored by Beck, one on the origins of cognitive therapy (Beck, 1964), and one discussing his influential cognitive model of depression (Beck, 1987). In Chapter 3 Adrian Whittington discusses Beck’s 1964 paper, a paper that was arguably a first step that has eventually led to millions of people having access to short-term, effective psychotherapy for common mental health problems such as anxiety and depression – psychotherapy provided through initiatives such as the improving access to psychological therapies (IAPT) programme pioneered in the UK by David Clark and colleagues (Clark, 2011). In Chapter 5 Clara Strauss covers Beck’s influential 1987 paper outlining in detail his cognitive model of depression. Beck developed his theory of depression from the observation of clients in his clinical practice. It was a theory that had cognitive psychological processes at its core in the shape of cognitive biases that could not easily be explained either by the biomedical psychiatric theories of the time or the psychoanalytic theory in which Beck had originally trained. In this sense, Beck was truly groundbreaking, creating an approach to mental health problems that was arguably defining a new paradigm incorporating explanation and treatment – an observational, pragmatic and evidence-based approach embracing empirically testable psychological processes and called cognitive therapy.
            One of the challenges in the development of a science of mental health is the isolation and identification of individual conditions. Discovering commonalities in symptoms and disabilities across different individuals suffering mental health problems suggests that there may be a single set of underlying causes for these clusters of features. At a time when child psychology and child psychiatry were only just emerging as coherent disciplines, an Austrian named Leo Kanner published the first English language textbook on child psychiatry in 1935, and in 1943 went on to publish a landmark paper that has helped to identify and define the developmental disability now known as autism spectrum disorder (ASD). In Chapter 4, David Mason, Victoria Grahame and Jacqui Rodgers describe how Kanner was ahead of his time in rather accurately defining a collection of behaviours that have since become the foundation of our understanding of autism. He insightfully described autism as an ‘innate’ disorder, and even today our diagnostic criteria for ASD still reflect many of Kanner’s original observations about difficulties with social communication and the presence of restricted and repetitive patterns of behaviour.
            Some classic studies gain their ‘classic’ status because they spark controversy and debate that remain unresolved to the present day. Such is the topic of “repressed memories” - the view that experiences of trauma can be ‘repressed’ or ‘forgotten’ and may be recalled later in life. Repression is a psychological process originally proposed by Freud in which negative feelings of shame, embarrassment or the like could lead to the loss of memory for an event – especially traumatic events occurring in childhood, such as childhood sexual assault, physical assault or even childhood neglect. It was in the 1990s that some individuals were coming forward claiming that they had been sexually abused in childhood but then had forgotten about it for many years. It was almost by coincidence that a study by sociologist Linda Meyer Williams was published around the same time. In her study she investigated whether adults known to have experienced childhood sexual assault remembered the incident or had forgotten it (Williams, 1994) – many it seems had forgotten it, even though hospital forensic records suggested they had been subjected to sexual assault. In the following decades, an intense debate known as “The Memory Wars” ensued (e.g. Goodman et al., 2003), with clinicians taking sides that either supported the view of repressed memories or in other cases claiming that recovered memories were in fact merely “false memories” implanted by various authorities, including therapists. In Chapter 6, Gail Goodman, Samara Wolpe and Lauren Gonzalves examine Williams’ study, discuss the so-called “Memory Wars” that followed, and trace the evidence on this topic to the modern day. While the controversy raised by Linda Meyer Williams study is still alive (Lynn, Evans, Laurence, and Lilienfeld, 2015), it was a study that led to further empirical research on adult memory and its role in childhood trauma.
            The study of cognitive processes has shown us that unwanted negative thoughts play a significant role in the development and maintenance of many mental health problems – especially the common mental health problems defined by anxiety and depression. Unwanted thoughts facilitate negative or dysphoric mood and act as triggers for symptomatic behaviours. A typical response to the distress caused by these unwanted thoughts is to try and suppress them, but as Daniel Wegner and colleagues demonstrated nearly 30 years ago, suppressing such thoughts is not a simple nor easy process. In Chapter 7 Maree Abbott & Alice Norton review the history of the role of thought suppression in psychopathology, and describe the classic study by Wenzlaff, Wegner & Klein that elegantly demonstrated the relationships between thought suppression, the rebounding of thoughts, and the role of mood in this process (Wenzlaff, Wegner & Klein, 1991). The relevance of this work is transdiagnostic and informs a wide range of clinical presentations. It also teaches us that our intuitive responses to our internal experiences are not always the most helpful, and can have an effect that maintains rather than alleviates distress. As a consequence, the findings of Wegner et al., have influenced a broad range of modern-day therapeutic interventions that help us to challenge unwanted thoughts, and our beliefs about these thoughts.
            By training and by research clinical psychology is a profession whose interest lies primarily in psychological processes and their relationship to mental health problems. Traditionally it has been the medical model championed by psychiatrists and other medically trained practitioners that has dominated both the research into the mechanisms of so-called “mental illnesses” and their treatment. But psychiatry is still searching for biomarkers for common mental health problems such as anxiety and depression (Kupfer, Kuhl & Regier, 2013) even though such biomarkers remain elusive after many years of biomedical research. Then along come some theoretical views that we can rightly say are game-changers and are at the forefront of confirming the fact that empirically established psychological processes are as good, if not better, explanations of some mental health symptoms than biological or neurological processes. One such paper was published in 1986 by David Clark, and another by Paul Salkovskis in 1985. Both identified psychological processes that contributed to the development and maintenance of symptoms in panic disorder and obsessive-compulsive disorder respectively, and gave rise to highly effective psychological-based treatments for these conditions.
In Chapter 8 Louise Waddington describes the model of panic proposed by David Clark in 1986 and how it superseded the existing biological models at the time. It became one of the first genuine modern psychological models of a major mental health condition, has generated highly successful cognitive-based therapies for panic disorder, and has become a model for how we should relate theory to therapy in clinical psychology.
            In Chapter 9 Christine Purdon describes how Paul Salkovskis presented one of the first integrated cognitive and behavioural models of obsessive-compulsive disorder in his 1985 paper. Salkovskis took his lead from the earlier work of Beck on depression (Beck, 1976), arguing that Beck’s work had demonstrated that cognitive-behavioural conceptions of OCD were as legitimate and important as any other. The model proposed by Salkovskis has become a cornerstone of cognitive-behavioural approaches to obsessive-compulsive disorder and has helped to shape psychological treatment for the disorder for the past three decades.
            In Chapter 10 Ed Watkins explains how, until the 1970s, the predominant treatment approaches for depression were psychoanalysis and the use of antidepressant medication. Along with the use of medication, attempts to explain depression at this time were mainly grounded in biological models alluding to deficits in brain neurotransmitters. However, the classic study published in 1978 by Abramson, Seligman & Teasdale has an important place in the history of clinical psychology because it was at the forefront of a movement towards specific testable psychological accounts of depression, and away from biological explanations to cognitive ones. As Watkins points out, the attributional account of depression proposed by Abramson et al. in 1978 provides a perfect illustration of the iterative nature of theoretical advances in science, proposing incremental changes to an existing theory (learned helplessness), and, in turn, it was itself subsequently modified to form another theoretical model in the 1980s (the Hopelessness Theory of Depression, Abramson, Alloy & Metalsky, 1989). The impacts of this paper have been multiple. The idea of negative attributional style is now fundamental to conceptualizations of depression; the theory forms an important component of many modern-day cognitive therapies for depression, and has acted as a spur for subsequent cognitive-behavioural research into depression.
            Even today, psychosis is often seen by many as an “inherited disease” – a view reinforced by the fact that since the 1950s the main medical treatment for people with a diagnosis of schizophrenia has been antipsychotic medications. But what we also know today is that life adversities, trauma and an individual’s social environment are key factors in the development and maintenance of psychotic symptoms, and the overarching conceptualization of psychosis is a diathesis-stress model (Zubin & Spring, 1977). The diathesis-stress model views psychosis as a predisposition to experiencing symptoms of psychosis, but symptoms may only be triggered as a result of exposure to life stressors. In Chapter 11 Filippo Varese and Gillian Haddock describe the seminal study by Brown & Birley conducted in 1968. The study found that people who had recently experienced an acute psychotic episode reported an increased rate of “crises and life changes” in the weeks immediately preceding the onset of their psychotic symptoms – research that pointed to the significance of life events in the course of conditions such as schizophrenia, and subsequently gave rise to diathesis-stress models of that particular mental health problem. This classic study was the starting point that triggered an awareness of psychotic experiences as complex reactions to stressful life events and social circumstances, and debate still rages today on the relative significance of inherited predispositions to psychotic symptoms versus life stressors and social conditions as causes of psychosis (e.g. Bentall, 2017).
            The psychopathic personality first came to public attention in the 1940s with the publication of Hervey Cleckley’s book The Mask of Sanity. But although psychopaths lacked moral and ethical principles and their behaviour was often destructive and violent, clinicians had difficulties addressing psychopathy because the cluster of characteristics associated with psychopathy was broad and difficult to quantify. Indeed, in 1952, the DSM defined the “sociopathic personality” very loosely as “ill primarily in terms of society and conformity within the prevailing cultural milieu” (American Psychiatric Association, 1952). It was American psycho-physiologist David Lykken who set out to seek a clearer framework for diagnosing what we now call antisocial personality disorder by investigating whether psychopaths had a distinctive level of physiological reactivity different to non-psychopaths in traditional Pavlovian fear conditioning procedures. He discovered that psychopaths were less easily conditioned to produce an anxious response in fear conditioning procedures, and they were less capable of avoidance learning where anxiety is necessary for such learning. In Chapter 12 Scott Koenig and Yu Gao explore the background to Lykken’s classic 1957 study and assess it’s impact on our understanding of psychopathy and antisocial personality disorder. By utilizing physiological measures and fear conditioning paradigms, Lykken brought a greater sense of objectivity to the study of psychopathy and provided some objective criteria that could be used to identify and diagnose sociopaths.
            In the final chapter, Rudi Dallos discusses the highly influential work of Salvador Minuchin, and in particular the clinical research he conducted in his 1975 paper with co-authors Bernice Rosman and Ronald Liebman. Minuchin’s original training was in psychoanalysis but from observations of juveniles in reform school and clinical settings he began to develop views on how personal development and ‘internal’ mental states were critically interlinked with family dynamics. Minuchin’s major contribution was to the field of family therapy, and eventually to the role of family systems in the development and maintenance of eating disorders. Apart from being centrally involved in the development of systemic approaches to therapy, Minuchin’s approach has come to form the basis of the Maudsley Anorexia Nervosa Treatment model that today is recommended in the UK National Institute for Health & Care Excellence (NICE) guidelines as an intervention of choice for anorexia nervosa in under-16s (NICE guideline, Eating Disorders: Recognition & Treatment, 2017).
            Finally, we are all aware of modern-day clinical psychology as a coherent and dynamic profession – using empirically-based research to seek out the causes of mental health problems, and developing and delivering ever more effective interventions for the broadest range of mental health conditions. But let’s not forget the stepping-stones that brought us here, stepping stones provided by pioneers in empirical research and psychological theory. For each of those whose studies and theories are highlighted in this book, their contributions are still brightly reflected in modern-day clinical psychology research and practice. In some cases those contributions have been to scientific and clinical practice, in other cases to the radical reconceptualization of mental health problems and their treatment, and in still other cases, some of those pioneers identified matters of controversy – fundamental controversies about mental health that remain unresolved even today. But one thing is sure, clinical psychology still needs radical-thinking pioneers. Those new pioneers will shape the future of the profession and provide new insights into the psychology of mental health problems and develop ever-more effective therapies to aid recovery. That is how clinical psychology progresses.
 
References
 
Abramson, L. Y., Alloy, L. B., & Metalsky, G. I. (1989) Hopelessness depression – a theory-based subtype of depression. Psychological Review, 96(2), 358-372. doi:10.1037//0033-295x.96.2.358
 
Abramson, L. Y., Seligman, M. E. P., & Teasdale, J. D. (1978) Learned helplessness in humans – Critique and reformulation. Journal of Abnormal Psychology, 87(1), 49-74. doi:10.1037//0021-843x.87.1.49
 
American Psychiatric Association (1952) Diagnostic and statistical manual of mental disorders (1st ed.). Arlington, VA: American Psychiatric Publishing.
 
Beck, A.T. (1964) Thinking and depression: 2. Theory and therapy. Archives of General Psychiatry, 10, 561-571
 
Beck, A.T. (1976) Cognitive therapy and the emotional disorders.  New York: International Universities Press.
 
Beck, A. T. (1987) Cognitive Models of Depression. Journal of Cognitive Psychotherapy, 1, 5–37.
 
Bentall, R. P. (2017). Six myths about schizophrenia: A paradigm well beyond its use-by date. In J. Poland & S. Tekin (Eds.), Extraordinary science: Responding to the current crisis in psychiatry. Boston: MIT Press.
 
Brown G W & Birley J L T (1968) Crises and life changes and onset of schizophrenia. Journal of Health and Social Behavior, 9(3), 203–214. 
 
Clark D M (1986) A Cognitive Approach to Panic.  Behaviour Research & Therapy, 24, 461-470.
 
Clark, D.M. (2011). Implementing NICE guidelines for the psychological treatment of depression and anxiety disorders: The IAPT experience. International Review of Psychiatry, 23, 375-384.
 
Cleckley, H (1982) The Mask of Sanity. Revised Edition. Mosby Medical Library.
 
Goodman, G. S., Ghetti, S., Quas, J. A., Edelstein, R. S., Alexander, K. W., Redlich, A. D. & Jones, D. P. H. (2003) A prospective study of memory for child sexual abuse: New findings relevant to the repressed-memory controversy. Psychological Science, 14, 113-118.
.
Kanner, L. (1943) Autistic disturbances of affective contact. Nervous child, 2(3), 217-250.

Kupfer D J, Kuhl E A & Regier D A (2013) DSM-5 – The Future Arrived. http://jamanetwork.com/journals/jama/fullarticle/1656312 

Lykken, DT (1957) A study of anxiety in the sociopathic personality. Journal of Abnormal and Social Psychology, 55 (1), 6-10.
 
Lynn, S. J., Evans, J., Laurence, J-R., & Lilienfeld, S. O. (2015) What do people believe about      memory? Implications for the science and pseudoscience of clinical practice. Canadian Journal of Psychiatry, 60, 541-547.
 
NICE guideline, Eating Disorders: Recognition & Treatment (2017) https://www.nice.org.uk/guidance/ng69/resources/eating-disorders-recognition-and-treatment-pdf-1837582159813

Overholser JC. (2014) Protesting the decline while predicting the demise of clinical psychology: can we avoid a total collapse? J Contemp Psychother 44: 273-81. 

Rosenhan DL (1973) On being sane in insane places. Science, 179, 250-258
 
Rosman, B.L.,  Minuchin, S., Liebman, M.D.  M.D. (1975) Family Lunch Session: An Introduction to Family Therapy in Anorexia Nervosa, Amer. J. Orthopsychiat. 45(5):846 – 853

Routh D K (1996) Lightner Witmer and the first 100 years of clinical psychology. American Psychologist, 51, 244-247.
​
Salkovskis, P. M. (1985) Obsessional-compulsive problems:  a cognitive-behavioural analysis.  Behaviour Research and Therapy, 23, 571-584.
 
Watson J.B. & Rayner R. (1920) Conditioned emotional reactions. Journal of Experimental Psychology, 3, 1-14.
 
Wenzlaff, R.M., Wegner, D.M., & Klein, S.B. (1991). The Role of Thought Suppression in the Bonding of Thought and Mood. Journal of Personality and Social Psychology, 80 (4), 500-508.
 
Williams, L. M. (1994) Recall of childhood trauma: A prospective study of women's memories of child sexual abuse. Journal of Consulting and Clinical Psychology, 62, 1167-1176.
 
Zubin, J., & Spring, B. (1977) Vulnerability: a new view of schizophrenia. Journal of Abnormal Psychology, 86(2), 103.
​

​Worrying is something we all indulge in – many of us on a regular daily basis. Some of us find it helpful, but for others it's a distressing monster that seems uncontrollable and feeds rather than calms our anxieties. Generalized Anxiety Disorder (GAD for short) is the diagnostic category that defines the worry monster. It’s one of the most common of the anxiety disorders, and is a pervasive condition in which sufferers feel continual apprehension and anxiety about future events and experience intense, uncontrollable worry.
 
I’ve been a “worry” researcher for much of the past 25 years, so have had a keen interest in what turns “normal” worrying in to the pathological worrying that people find so distressing. And I’ve been particularly interested in whether anxiety symptoms such as worrying are on the increase or not – interested enough to write a whole book on the topic (1).
 
What was perplexing during the writing of  “The Anxiety Epidemic” was that almost everyone – in almost all spheres of life – were claiming that anxiety symptoms were on the increase in a modern world that not only exacerbated traditional anxieties but also created new forms of stress that generated brand-new sources of anxiety (2,3) - yet, it was difficult to find any reliable evidence over time that anxiety symptoms were increasing in frequency. Was this ‘Anxiety Epidemic’ a result of more people being mental health aware and seeking treatment when they may not have done in previous times, or was it a genuine increase in the severity and frequency of anxiety symptoms?
 
Just a few months ago, an informal survey by the BBC suggested that the number of students seeking mental health support while studying at university had increased by more than 50% in five years (4). So, was this an example of greater mental health awareness leading students to seek help, or was it a genuine increase in the frequency and severity of mental health problems in this population?
 
Much of the research on worrying we’ve carried out at the University of Sussex has been conducted on undergraduate students, so we have 20-25 years worth of data on worrying from this group. Just last week, we’d finished an on-line questionnaire designed to validate a new worry scale specifically for university students. Interestingly, in this study we also included a traditional and reliable measure of pathological worrying called the Penn State Worry Questionnaire (PSWQ). This scale has been around for 30 years and is considered the gold standard measure of pathological worrying.
 
What caught my attention was the mean PSWQ score for this study (N=217). The mean score was 57.39 (SD 9.87). This seemed rather high – and most of the data in the survey was collected outside of exam and assessment periods that might have inflated the scores.
 
Looking at the available norms for the PSWQ, the average score given for college student samples was 47.42 (5)– 10 points lower than the mean for our current group. But this norm was based on college student data from almost 20 years ago. Was this an indication that worry had indeed increased in frequency and severity in this population over the past two decades?
 
I decided to look back at the PSWQ data we’d collected from student populations at the University of Sussex over the past twenty years. I found 18 studies spanning the years 2001 to our present survey conducted in 2019 providing data from a total of 1369 respondents. Some of these data were collected during lab-based experiments others during questionnaires and surveys, but even in the case of lab-based studies, the PSWQ was completed at the outset of the study and scores would not have been influenced by any experimental manipulations. I must admit, I wasn’t expecting such a clear pattern of results.

​Over the years from 2001 to 2019 there is a steady increase in mean PSWQ scores from the norm quoted in 2003 (47.42) to the mean in our current study (57.39) – an increase of over 20% in mean scores over 18 years. The increase is not sudden at any one point in time - it’s a gradual increase seemingly occurring year by year during this period.
 
So what do we make of this? First, this seems to demonstrate a real increase in reported anxiety-related symptoms over time. This is consistent with student populations not just becoming more mental health aware and being increasingly likely to seek help, it signals a genuine increase in the frequency and severity of these symptoms as indicated by reliable measures of student worry. Second, the mean score for the PSWQ in 2019 is alarmingly close to the PSWQ scores normally considered to be a reliable indicator of Generalized Anxiety Disorder (a minimum PSWQ score of between 62-68(5)). Indeed, in our most recent survey, 26.4% of student respondents scored 62 or higher on the PSWQ and 11.6% scored higher than 68. That’s equivalent to 1 in 4 of all students on a campus suffering diagnosable GAD or sub-clinical GAD symptoms – enough to overwhelm any university counselling and medical services.
 
What’s causing this unrelenting increase in anxiety-related worrying in students? At this point, who knows? There are lots of suspects – and I cover these in more detail in my book “The Anxiety Epidemic”. Some of these suspects include increasing student debt since the introduction of university fees in the UK in 1998, increasing student numbers resulting in less support from academic staff, increased systematic educational testing introducing youngsters to the possibility of failure from an early age, and the rise of social media since the mid-1990s which has been identified as a cause of social anxieties and disconnectedness as we view daily what seem like the rich lives and social successes of others(6). But whatever the cause, there is certainly an anxiety epidemic on the university campus.

(1) Davey GCL (2018) The Anxiety Epidemic. Little Brown Books.
(2) https://www.nytimes.com/2017/06/10/style/anxiety-is-the-new-depression-xanax.html
(3) http://www.telegraph.co.uk/health-fitness/mind/how-anxiety-became-a-modern-epidemic-greater-than-depression/
(4) https://www.bbc.co.uk/news/uk-england-45824598
(5) Startup HM & Erickson TM (2003) The Penn State Worry Questionnaire (PSWQ). In GCL Davey & A Wells (Eds) Worry & Its Psychological Disorders. Wiley.
(6) Davey GCL (2018) The Anxiety Epidemic. Chapter 3. Little Brown Books.

Here are 10 things to do that will successfully enable you to miss out on most of the exciting opportunities that being an academic has to offer.
 
1.         Stay narrowly focused for your whole career on the one specific area you researched in your PhD. As a tenured academic you have a license to research almost anything you like. Always have at least two or three entirely different strings to your research bow. Stick a poster on your office wall that simply says ‘Serendipity’! (But refer to point 10)

2.         Tell publishers that you can’t write books because your HoD has told you to only engage in activities that are highly REF-able in research assessment exercises. What’s wrong with writing books? Writing books allows you that bit more freedom to express your ideas than a competitive, highly judgmental and often arbitrary journal publication process (and you get royalties for it!).

3.         Complain that you haven’t been able to publish any research because your teaching load is too high. Is your teaching load the same as everyone else in your department? Be honest with yourself - are your time management skills good enough?

4.         Fail to appreciate that everything you write needs to be engaging and accessible. So you’re happy to spend a lifetime churning out stodgy, turgid papers that don’t even raise a smile of appreciation in your most devoted research fans?

5.         Fail to appreciate that there's a whole world of lay people out there who would love to appreciate your knowledge in terms that they can understand. Who’s going to take knowledge to the people if you don’t?

6.         Treat dealing with final year dissertation students as a chore. So you give them all slightly different topics on your one main research project, even get them to work in pairs on the same data rather than spend time exploring new ideas with them each individually - new ideas that might expand and invigorate your own research horizons and introduce your students to the exciting contributions they can make personally to research and knowledge. 

7.         Consider yourself to be a struggling small cog in an impersonal monolithic research machine. If so, you’ll miss out on being someone who is creative, makes discoveries and furthers knowledge.

8.         Be defensive about your research and teaching. This will allow everyone - faculty and students - to see that you’re neither passionate about nor excited by what you’re doing. 

9.         Avoid going to Departmental meetings and Boards of Study because you find them boring. If you want the working and research environment that suits you and your colleagues you need to contribute actively and vociferously to the organisational and management processes that create your working environment as an academic. You don’t necessarily have to shout and make a fuss - but you need to participate.

10.     Spend your time solely chasing funding. Nowadays Universities are businesses chasing financially advantageous partnerships, income streams, and business deals - and you’re told without reservation that you personally need to throw yourself heart and soul into this desperate scramble for money. Tell your HoD and your university’s senior management team that as an academic you’re the ideas person, the knowledge generator, the creative hub, the teacher, the mentor, their reason d’être. Don’t be treated like an office worker who’s been asked to put their hand into their own pocket to pay for everything in their office they might need to do their job! Go to your HoD or your VC and ask the generous and increasingly wealthy organization that employs you to fund you properly to do the job your contract requires of you! .... and let me know how you get on!

In the past 12 months I’ve been lucky enough to travel to a number of Psychology Departments in the UK and Europe to give talks on Experimental Psychopathology. This is not as simple as it sounds. Travelling and meeting researchers who are doing translational research has been a genuinely uplifting experience. However, writing a talk on what Experimental Psychopathology is has not been so easy.

There are three reasons for this:

First, while everyone understands very broadly what is meant by the term ‘experimental psychopathology’, it doesn’t seem to have a ‘manifesto’ as such (it is indeed the study of psychopathology using experimental and empirical methodologies – but, students, don’t quote that, it’s a tautology!). What I mean by this is that there is no manual that you can consult that tells you exactly how to do this kind of research and what the guiding principles are. As a result we get a lot of mixed quality research masquerading under the label experimental psychopathology, and this is something I’ve alluded to in other blog posts (e.g. “does a menu explain a restaurant?”).

Second, one important feature of experimental psychopathology is the creation of psychological models of mental health problems, and the development of such psychological models seems to have been significantly overshadowed in recent years by the bugeoning influence of neuroscience and genetics. One reason for this is that mental health research is still viewed primarily as a domain of medicine. The advent of DSM-5 has continued to fuel the misguided need to seek neurobiological markers for psychological disorders, and – most unfortunately – medics rarely, if ever, get training in how to develop or understand psychological models, and so inevitably undervalue them. The challenge here is to project Experimental Psychopathology as an empirical approach to knowledge that is equivalent to neuroscience and genetics, but is explaining psychopathology at a different level to the latter two. This, of course, means that neuroscience, genetics and psychological models are not mutually exclusive forms of explanation, but each complement each other to provide a rich understanding of mental health problems.

Third, much Experimental Psychopathology research is conducted on healthy individuals – often university undergraduates - and there are many ways in which this fact is used to project experimental psychopathology as a ‘second class’ contributor to mental health research. For example, many journals will now only publish psychopathology research conducted on individuals with a clinical diagnosis (e.g. “The Evils of Journal Scope Shrinkage”), and – perhaps quite reasonably – experimental psychopathologists are regularly urged to justify how their findings from nonclinical populations have relevance to clinical populations. It is this latter issue that needs both clarification, and a well-articulated set of validation rules. These validation rules are needed to describe quite clearly the pathway from basic psychological models developed with healthy individuals to models that have obvious relevance to the distinctive characteristics of clinical populations.

So what are the advantages of developing psychological models of mental health symptoms using an experimental psychopathology approach? Here are just a few:

• It permits the use of experimental models to mimic psychopathology processes in healthy individuals.
  
• It allows the study of clinically-relevant processes under highly controlled conditions.
  
• Controlled experiments provide evidence of causal relations between events that are a critical component of theory building.
  
• Experimental Psychopathology regularly borrows models and procedures from other areas of core psychological knowledge in order to understand mechanisms of psychopathology.
  
• Through controlled experimentation Experimental Psychopathology can help to identify the active ingredients in interventions developed directly from clinical practice.
  
• It allows the testing of psychopathology models in circumstances where doing so with clinical populations may be problematic.
  

These benefits can provide clinical psychology with a rigorous set of scientific principles for developing psychological models of psychopathology, and – perhaps more importantly – can help to prevent clinical psychology from re-inventing the wheel. What do I mean by this latter statement? Well, unfortunately many clinical psychology researchers tend to research psychopathology directly from their clinical experience, and without exploring the existing core knowledge available in the literatures on cognitive, social and biological psychology that may already provide many of the answers to the theoretical questions they are asking.

Finally, the $64,000 question – how do we convincingly argue that our psychological models developed on healthy individuals have relevance to clinical populations? Well, start by reading this excellent paper by Bram Vervliet & Filip Raes published in Psychological Medicine in 2013. They define a number of different levels of external validity that can be used as criteria to bridge the translational gap between healthy individuals and clinical populations – and these range from weak criteria to relatively strong criteria. What also occurred to me is that you can use these various levels of external validity to construct a research pathway that begins with the development of simple psychological models or proof of concept studies and then moves with each step closer to the strict criteria that will determine whether those models have genuine relevance for clinical populations.


The pathway goes like this (from weak to strong criteria):

 Step 1 – Face Validity: This is the degree of formalistic or phenomenological similarity between the behaviour in the laboratory model and the symptoms of the disorder. This is a relatively weak criterion for validity, and might simply represent the fact that the behaviour in the model simply “looks like” the behaviour in the disorder. Examples might include the induction of anxious or depressed moods in healthy participants and observing the effect of this on cognitive processes relevant to the psychopathology (e.g. Davey, Bickerstaffe & MacDonald, 2006; Hawksley & Davey, 2010)

Step 2 – Predictive Validity: This is the degree to which performance in the laboratory model predicts performance in the disorder. Basically, can you use the laboratory model to predict the performance or outcomes in your clinical population? This may require the collection of case histories to demonstrate that the processes specified by your model can be identified in the etiology of clinical cases (e.g. Davey, de Jong & Tallis, 1993), or the application of the model to clinical patients in experimental procedures to show that the same processes operate in the disorder as in the laboratory model (e.g. Chan, Davey & Brewin, 2013)

Step 3 – Construct Validity: This criterion seeks to show that the model developed in the laboratory can be compared favourably with existing clinical models of the disorder. It needs to be shown that the processes described in the laboratory model parallel the clinical process of interest, and that theories of the psychopathology and processes specified by the laboratory model allude to the same theoretical processes. For this criterion to be useful, there needs to be a well-elaborated laboratory model of the disorder as well as a valid clinical model of the disorder. In this case, elaborating and developing the laboratory model should be a valid means of extending and developing the clinical model. For example, in the 1980s and 1990s, there were many clinical models of anxiety disorders based on conditioning theory, and because we had an extensive knowledge of conditioning theory from animal learning we could use this knowledge to extend and test the clinical models (e.g. Davey, 1989; White & Davey, 1989).

 Step 4 – Diagnostic Validity: Finally, it may be necessary to demonstrate that your laboratory model taps into processes that are unique to patients or are genuinely representative of clinical populations. I was slightly skeptical of this criterion to begin with because there is good reason to believe that many common psychopathologies are on a continuum of severity rather than being qualitatively different to sub-clinical forms of the disorders, so we wouldn’t necessarily expect processes to be ‘unique’ to individuals with a diagnosis. However, if your model has been developed on healthy individuals, this does raise the question of why everyone doesn’t exhibit symptoms of psychopathology? Perhaps everyone does – but in all probability clinical populations may possess characteristics or have had experiences that make them significantly more vulnerable to the important causal variables in your model. I now believe this is probably the final link required to validate your laboratory model, and is a criterion that would help to explain the jump in severity in symptoms between your healthy laboratory volunteers and individuals with a clinical diagnosis. We’ve begun to explore this possibility in our own mood-as-input model of perseverative psychopathologies, and examples of this can be found in Meeten & Davey, 2011, p1266-1269).

My preferred pathway for taking experimental psychopathology research from a simple laboratory model to a genuinely clinical-relevant theory is to plan your research to sequentially explore Steps 1, 2 and 4 in that order. In Step 1 you can use existing core psychological knowledge (together with clinical experience) to develop your model on healthy individuals in the laboratory, in Step 2 you can test out whether the relevant processes in your model predict symptoms in clinical populations, and Step 4 allows you to clinically validate your model by identifying features in your model that might be representative of clinical populations and make them specifically vulnerable to more severe symptoms.

Perhaps principles such as these might form the beginnings of a ‘manual’ for Experimental Psychopathology. It would be a manual that would allow researchers to plan research programmes for psychological models of mental health that would be the intellectual and scientific equals of neuroscience and genetic approaches.

I've just spent a very stimulating and enlightening couple of weeks, first at the Rome Workshop in Experimental Psychopathology, and then at the University of Exeter - both times talking about experimental psychopathology. But these talks were not just about how to do experimental psychopathology, they were also about how many other researchers were simply not equipped to do experimental psychopathology, or simply had no idea about what this scientific paradigm was. And that has some very dramatic consequences for mental health funding, as well as our broader understanding of the mechanisms that contribute to mental health funding.

Let’s be quite clear about the main issue here. Most funding for mental health research goes to high profile, expensive, medically oriented research on the biological substrates of mental health problems. Why is that? Well, while psychologists learn about both biological mechanisms and psychological mechanisms, medics simply don’t learn about psychological mechanisms - in fact they tend to have no knowledge whatsoever of the inferential methodologies that allow psychologists to develop models of psychological processes - but rather sadly, there is a majority of those medics on the panels of most funding bodies for mental health research.

Is this important? Yes it is, because, I'm quite happy to assert that most common mental health problems are acquired through perfectly normal psychological mechanisms that involve attention, decision-making, learning, memory and other general cognitive processes - so the mechanisms are not in any way abnormal - only the outcomes of the process are abnormal - so why do we waste research time and taxpayers money trying to look for abnormal neurological mechanisms or medically aberrant signatures of psychopathology when they probably do not exist?

As an experimental psychologist studying learning in nonhuman animals I learnt a lot about inferential experimental methodologies that allowed us to infer cognitive processes in any organism – human or nonhuman. These are the same types of methodologies that are used to understand most human cognitive processes - such as memory, attention, decision-making and learning. What many researchers from a medical background do not grasp is that scientific method allows us to infer the nature and structure of psychological mechanisms without having to know anything about the biological underpinnings of these mechanisms. In fact, whatever medical or biological research does subsequently to psychologists elaborating these mechanisms will merely be to substantiate the infrastructure of these mechanisms – and indeed, as radical as it may seem, it will be very little more than that.

Experimental psychopathologists should have the lead on all research questions to do with the aetiology of mental health problems. Their research is cognitive, experimental, inferential, provides evidence for the causal relationships that underlie the acquisition of mental health problems, and allows the development of testable models of mental health problems – and it’s a hell of a lot cheaper than most other medically driven approaches!

I have recently been heard to say that experimental psychopathology needs a manifesto to enable it to compete with other explanatory approaches to mental health problems such as neuroscience and genetics – well, it does. We need this manifesto to prevent other disciplinary lobbies from monopolizing funding and – most importantly – from hijacking the way we explain mental health problems. Most mental health problems develop out of perfectly natural psychological processes – not medical problems. Understanding those processes in the normal, inferential way that psychologists do research will provide the basis for good mental health research.

This blog post is about the negative effect that journal impact factors can have on the progress and development of scientific research. But I need to begin with a specific example.

About three years ago Andy Field and I decided there was a gap in the scientific journals market for a journal specifically publishing experimental psychopathology research – a journal willing to publish a range of good quality, empirically-based studies that contributed to our understanding of psychopathology and its treatment – including relevant studies conducted on non-clinical populations (especially since many clinical psychology journals had recently purposefully restricted their scope to clinical populations – and that’s an issue that I’ve posted about before)

We decided that we wanted to have complete control over the journal, including its format, the nature of the material we published, how often we published, to offer the journal to researchers and institutions as cheaply as we could, to directly reach out to the relevant research community to ask what kind of journal and content they would like (rather than be driven by a business model that sought only to sell the journal to librarians and institutions – a model that seems to be the norm for most large international scientific publishers), and to provide a range of open access options.

That journal, the Journal of Experimental Psychopathology (http://jep.textrum.com) is now about to go into its fifth volume in 2014, and has already grown from four issues a year to five.

Now here comes the dilemma. We are at a point where we can now apply for ISI registration. If successful that would mean the journal would be listed in the Thomson-Reuters Web of Knowledge index – arguably the most widely used scientific indexing database in the world. That would, of course, make the articles published by our authors more widely available to researchers than they would previously have been.

But the downside of this (some, sadly, might call it an upside!) is that in being accepted into the Web of Knowledge means your journal will now be given an impact factor and be listed in a league table of journals publishing in the same area as you. We all know that the impact factor of a journal is “highly valued” – the higher that score, the higher the supposed scientific quality of your journal and the greater the kudos to those researchers who publish in those journals. This has the effect of placing immense pressure on researchers – especially young, up-and-coming researchers – to publish primarily in high impact journals, for the sake of their “academic integrity”, and more importantly the sake of their careers (and, of course, ultimately their salary, their ability to pay their mortgages and support their families).

Who holds impact factors in highest esteem is a moot point. It is probably not researchers – but publishing in high impact journals is probably a secondary gain imposed on researchers by others. Publishing in “high impact” journals is sold to us as the gold standard for good research by university administrators, research funding bodies, research assessment exercises, librarians, and even the journal publishers themselves (there is hardly a journal website these days that doesn’t prominently display its impact factor on its home page).

But here lies the dilemma. Once the Journal of Experimental Psychopathology has an impact factor, it will judged by its position in the impact league table, this will immediately impose a pressure on us to take steps to move the journal up that table. Because we are an e-journal and are not subject to the same space and print-run limitations of paper journals, we can effectively publish all articles that our reviewers and associate editors believe are well conducted, well analyzed, relevant, and provide a contribution to knowledge – however small. And this is what we currently do. Once we have ISI registration, there is immediately the temptation to begin to set targets that will “weed out” those articles that are likely to be cited only rarely – even though they are well conducted and have been accepted through peer review. How many times have all of us, as researchers, received that decision letter from a journal editor saying something to the effect that “your submission was well received, but as you know we receive a great number of submissions and we can only accept a minority…” Most journals pride themselves on the size of their rejection rates! That is quite strange when you think they ought to be trying to encourage researchers to submit articles to them – so are they really just trying to impress the librarians who buy their subscriptions?

What I have described will be just one immediate consequence for us of acquiring an impact factor – do we make the decision not to publish perfectly acceptable pieces of research that we judge may not be well cited (with the emphasis there on the word “judge”). This in itself will make life more difficult for many researchers who find it hard to find outlets for their perfectly acceptable research.

Judgmental processes like this also distort the scientific process. As Nobel prize winner Randy Schekman has said recently, pressure to publish in high impact “elite” journals encourages researchers to cut corners and pursue trendy fields of science instead of doing the more important groundwork that science requires – a problem exacerbated by editors who are often not active scientists. It is arguably the less well-cited research that provides this groundwork for science and is important in developing consensus views of accepted knowledge through converging evidence. But this is exactly the kind of research that is most likely to be rejected from journals desperate to protect their impact factor.

Around three years ago Andy Field and I, with the help of a number of very valued friends, created a new Experimental Psychopathology journal. Our reasons for doing this were that we thought that experimental psychopathology was being unnecessarily squeezed out of clinical psychology journals, was undervalued as a research approach to understanding mental health problems, and – perhaps rather sadly – was being eclipsed by large-scale biologically-oriented approaches to mental health – particularly many crassly descriptive neuroscience approaches, large-scale, multi-authored psychiatric RCTs based around a small number of privileged clinical research centres, and piece-meal genetic research utilizing a small number of extensive, but probably valuable, databases.

Doing the latter kinds of research is surely important, and allows researchers to publish in a range of primarily psychiatric journals with high impact factors. But experimental psychopathology was getting unnecessarily marginalized – especially because many Psychology Departments were being seduced by the hype of psychiatry, medically-relevant research, genetics, and the high impact value of research that could be published in medically-related journals.

Interestingly, last week I was a discussant in a symposium about perseverative psychopathologies (pathological worrying and depressive rumination) at the Annual Conference of the British Association of Behavioural & Cognitive Psychotherapies (BABCP). I ended up making two particular points:

(1) That it was so nice to see four papers that were looking specifically at the mechanisms of perseverative thought – what were the processes that led someone to begin a worry bout, perseverate that bout, feel increased distress through that bout, and then end it without feeling better? My point was that if you could understand the mechanisms that underlay a single bout of worrying, you would probably understand everything you needed to know in order to begin helping someone who was a pathological worrier. This is not something that I could easily believe that either genetic or neuropsychological approaches would have much to say about in the first instance.

(2) Sadly, those approaches to mental health research that have stayed outside the medical approach have over the last 15-20 years themselves become insular. Not that they don’t have journals to publish in – they have many of them. What is so depressing is that they have ended up creating their own incestuous and confused approach to mental health research. I have to admit that I am not a clinical psychologist – I am an experimental psychologist who for many years now has enjoyed using the various research skills I was trained with to study psychopathology. But I am always dismayed by the fact that clinical researchers continually attempt to re-invent wheels very badly. Much of the information we need to understand how mental health problems develop, are maintained, and can be treated is already there in the core psychological literature – and is entirely ignored by clinical psychology researchers who are happy to create idiosyncratic clinically-experienced based models of psychopathology that would take your average psychologist many decades to comprehend. This incestuous approach is compounded by the fact that clinical psychology journals continue to restrict their scope in ways that mean that clinical psychology researchers will only ever get exposure to the imperfect and insular research perpetuated by these journals.

And as a consequence, experimental psychopathology gets squeezed. But one of the uplifting aspects of our experience of creating and publishing an Experimental Psychopathology journal is that experimental psychopathology is clearly appreciated as an approach to researching mental health problems in a number of countries, especially European countries such as The Netherlands, Belgium, and Germany, and also countries like Australia and Canada. I would hope that we can push forward and convince researchers that experimental psychopathology is a highly valuable methodology for understanding mental health problems in a way which elaborates underlying psychological and cognitive mechanisms, which utilizes core psychological knowledge and which has direct relevance to treatment.

But sadly, we have to create the journals in which to publish this research, we have to make it clear that clinical psychology research is not just about medicine, we have to explain that understanding mental health problems will require us to understand the moment-to-moment processes that operate during psychopathology (and not just the genetics or neuroscience of psychopathology), and we have to convince universities that good mental health research is not simply stuff that is medical, generated by large research consortiums with privileged access to databases or client groups, or is restricted to expensive neuroscience procedures that simply light up bits of brain. We also have to convince a rather large group of clinical psychology researchers that their discipline will neither progress academically nor make inroads into the tight grip that psychiatry has over mental health without them making good use of an existing and well researched core psychology literature.