Thursday, May 13, 2021

Zenobia Morrill

Zenobia Morrill
MIA Research News Team: Zenobia Morrill is a graduate of the dual master’s counseling psychology program at Columbia University. As a doctoral student and researcher at the University of Massachusetts in Boston, she seeks to understand the context informing psychology research and the underlying social factors that influence individual psychology. She is currently involved in projects examining the impact of structural violence.

Experiences of Depression Connected to Declining Sense of Purpose

Research has suggested that there is a divergence between scientific understandings of depression and the way that depression is experienced by those diagnosed. A new study, conducted by a team of researchers led by Miraj Desai at the Yale University School of Medicine, explored these discrepancies further. In-depth interviews with individuals who had screened positive for depression indicated that their experiences were connected intimately to a declining sense of purpose.

People who screened positive for depression were “dealing with profound ruptures to what they were living for—their dreams for work, relationships, and a meaningful life,” Desai and his co-researchers write. Rather than describing their experience in terms of a “depressive illness,” participants in this study traced their declining sense of purpose to the ways their goals and values in life had been threatened. In turn, they experienced accompanying constrictions in their energy, action, and body.

“The present study found that the experiences underlying a positive depression screen were best characterized as a context-dependent, life-historical phenomenon,” Desai and team write, adding:

“The problem for participants was a world in which they now faced a declining sense of purpose and incapacity to reach goals. During moments when various individuals did reflect on their situation, the experiences in question were viewed more in terms of their biographical import (e.g., a “noble struggle” for social justice), rather than as a biomedical illness or disorder.”

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Incongruencies that exist between patient perspectives and scientific conceptualizations raise various problems. Patients’ viewpoints affect how they go about seeking help, their preferences for treatment, treatment engagement, the patient-provider collaboration process, and finally, the outcomes of treatment. In other words, how individuals understand their experiences of depression matters, and if this perspective is overlooked, it can impinge healing and resolution.

Notably, wider discrepancies between biomedical explanations of depression (e.g., depression is a medical illness) and beliefs about depression that exist in communities of color have been observed. African Americans and Hispanic Americans are more likely to view depressive experiences as related to social difficulties, including financial problems, caretaking burdens, and inadequate housing. One study found that Chinese Americans who had screened positive for depression often did not perceive themselves as having a psychiatric condition.

Desai and colleagues conducted their study “to narrow the gap between community perspectives and scientific knowledge.” Using a qualitative approach designed to explore the meanings participants initially make of their experiences, phenomenological inquiry, the researchers endeavored to remain as close as possible to participants’ understandings of depression and abstain from applying external interpretations.

Participants included patients who were seeking help for medical conditions at a primary care clinic in New York City. While waiting for their regular physician’s appointment, participants were recruited who were not currently utilizing behavioral health services, had screened positive for depression, as measured by the Patient Health Questionnaire-9 (PHQ-9) instrument. To focus on the study’s aim to explore possible divergent perspectives, patients who were currently receiving mental health treatment were not included.

Overall findings of this study revealed that those who screened positive for “depression” characterized the experience as the destruction of what they were living for, of “what they centrally valued in their lives,” write Desai and team. They did not describe it as a clear, distinct depressive illness or disorder. In this way, the nature of their suffering as rooted in threatened life goals and values was only partially captured by screenings that focused on individuals’ thoughts and bodily experiences.

Rather than being central to their experience, constrictions of participants’ bodies, actions, and energy were described as paralleling and accompanying the overarching decomposition of their life’s purpose. Desai and team write:

“The ensuing experiential process, in the face of decaying life purpose, involved enjoyment of their situations turning to sadness about them, their active body becoming passive, time becoming stuck in a hollow present as the future collapsed, and space contracting.”

Participants expressed this experience in different ways. Many discussed a moment in their lives when they were grappling with an unclear future—the sense that they were heading in an unsteady or uncontrollable direction. Desai and colleagues write that he participants “understood important, even cherished life goals and pursuits—in the course of their quest for love, work, and meaningful participation in the world—as under threat, facing the possibility of destruction, or having been actually destroyed.”

Moreover, individuals focused primarily on the challenges they faced regarding important life commitments as a core feature of the experience. They did not understand their situation as a formal health condition. Unlike how depression has been framed in the scientific community, participants did not describe a clear constellation of symptoms. Desai and team write:

“Many did not use the word ‘depression,’ and for those who did. . . the word typically carried life historical meanings, often implying great sadness at losing the good or frustration in relation to thwarted life pursuits, rather than a medical condition.”

One participant described different types of depression that she experienced. Each type was related to a loss. She shared: “Sometimes I feel depression coming when I think back to times. When I think back to better times.” She later added, “That’s another depression, when you can’t do what you want.”

Sadness, passivity, and stuckness characterized participants’ experiences. “In the midst of failing efforts toward goals,” write Desai and team, “individuals’ lives and bodies, now without a central unifying purpose, started to erode.” Furthermore, participants experienced a sense of being devalued, experiencing low social worth, and a sense of failure.

They felt blameworthy, incapable, and worthless. This demonstrated a complex, interdependent relationship between self and other. For instance, feeling a greater sense of self-worth is connected to experiences of being valued and chosen by others (e.g., obtaining a job, maintaining a relationship).

Desai and colleagues describe this experience by those diagnosed and demonstrating a teleological structure. Individuals’ sense of direction and purpose was at the heart of participants’ wellbeing. The collapse of these life goals and values “underpinned a positive depression screen.” Is the loss of this direction and purpose then, that in turn manifests as problems in “body, behavior, emotion, and thought.”

They summarize the meaning of this finding:

“We contend that this structure has not been adequately accounted for in the mental health literature, nor given an equal footing in the wider world of theory and research design, which remain mostly focused on illness, intrapsychic, cognitive, and context-independent conceptualizations and explanations.”

Implications offered for how treatment approaches can change based upon this data are plentiful, including the need for providers to respond directly to patients’ goals and commitments. Adherence must be reframed such that it is not only referring to patients adhered to decontextualized treatment requirements. Desai and colleagues discuss this further in a concurrent paper.

In addition, these data may be used to draw connections and bridge the gap between science and community life. Desai and team conclude:

“We are essentially seeing a type of experience that is understood in relation to its purpose or future-directedness, from which it receives its organization and meaningfulness. Thwarted goals at work, in relationships, and in fostering social change signified the loss of direction in life; without direction, one’s energy, body, actions, and even self lost value and purpose.”

They continue:

“This directedness to something beyond themselves, or transcendent quality of experience—for which everything including so-called ‘symptoms’ carried meaning—has typically not entered the frameworks of mental health causality, which tend to remain on the level of physical cause (e.g., biological substrate, physical disease, or even mental disorder) or internal-mental cause (e.g., intrapsychic factors, a cognitive model of illness, etc.).”

More careful consideration of the “sufferer’s perspective” and multiple sources of discontent in the world are needed to better inform how we understand and approach such distress.



Desai, M. U., Wertz, F. J., Davidson, L., & Karasz, A. (2019). An investigation of experiences diagnosed as depression in primary care—From the perspective of the diagnosed. Qualitative Psychology. (Link)

Adding Fluoxetine to Therapy Not Superior to Therapy Alone in Depressed Teens

A new study found no evidence that the addition of the antidepressant fluoxetine to Cognitive Behavioral Therapy (CBT) treatment improves depressive symptoms for youth diagnosed with moderate-to-severe Major Depressive Disorder (MDD). These findings, published in The Lancet Psychiatry, contradict guidelines recommending fluoxetine as the first-choice antidepressant for this age group.

The researchers, led by Christopher Davey, Michael Berk, and Patrick McGorry, write:

“The results have important implications for treatment. The study did not find evidence to support adding antidepressant medication to psychotherapy for the treatment of young people with moderate-to-severe depression.”

Photo Credit: Flickr

Given that antidepressants are commonly used to treat young people, the researchers set out to determine if adding fluoxetine to CBT improves depressive symptoms in this cohort. The effectiveness of combining CBT with antidepressants has been contested. One Cochrane Review concluded that there is insufficient evidence to recommend a combined treatment approach.

In addition, concerns about the safety of antidepressants in youth have mounted following the U.S. Food and Drug Administration’s (FDA) black box warning that antidepressants increase suicidal thoughts and behaviors. However, some studies have suggested that fluoxetine is the only antidepressant more effective than placebo in treating child and adolescent depression and may not carry the same safety risks.

In this multi-center study, Berk, McGorry, and team examined whether combined treatment of fluoxetine and CBT was more effective than treatment with placebo pills and CBT. Participants included 153 adolescents (aged 15-25 years) who were randomly assigned to take either fluoxetine (50%) or placebo (50%) in addition to weekly, 50-minute CBT sessions. Participants fit criteria for MDD, as defined by the DSM-IV.

This was a double-blind study meaning that neither participants, clinicians, nor research assistants were aware of which participants were assigned to placebo versus fluoxetine. Depression symptoms were primarily rated by interviewers using the Montgomery Asberg Depression Rating Scale (MADRS) at the 12-week mark.

Based on the results of this study, combined treatment with fluoxetine and CBT was no more effective for reducing depressive symptoms than placebo and CBT. Similarly, participant self-reports of depressive symptoms, measured by the Quick Inventory of Depression Symptomatology (QIDS) scale, also exhibited no evidence that the addition of fluoxetine was more helpful than placebo in reducing depressive symptoms. There were no significant differences in suicidal attempts and non-suicidal self-injury between groups.

However, the researchers share that, based on subgroup analyses, findings indicate that combined treatment “might be more effective for anxiety symptoms and for self-reported depressive symptoms in youth aged 18 years and older.” These findings were indicated by this age group’s comparative reductions in QIDS scores and some comparative reduction in MADRS scores.

They conclude:

“Our results did not provide evidence to support the addition of fluoxetine to CBT for further reducing depressive symptoms in young people with moderate-to-severe MDD. This finding is particularly so for patients younger than 18 years.”




The researchers included the following declaration of interest:

“Declaration of interests OMD has received grant support from the Brain and Behavior Foundation, National Health and Medical Research Council, Simons Autism Foundation, Stanley Medical Research Institute, Lilly, and ASBDD/Servier, and in-kind support from BioMedica Nutracuticals, NutritionCare and Bioceuticals. NK receives royalties from Guilford Publications, Inc, Springer Publishing, and Routledge Press (which includes royalties from books on the topics aligned with this research). MB has received research support from the Simons Autism Foundation, Stanley Medical Research Foundation, MBF, beyondblue, Rotary Health, Meat and Livestock Board, AstraZeneca, Woolworths, Avant and the Harry Windsor Foundation, and book royalties from Oxford University Press, Cambridge University Press, Springer Nature, and Allen and Unwin. He has been a speaker for AstraZeneca, Lundbeck, Merck, and Servier, and has served as a consultant to Allergan, AstraZeneca, Bioadvantex, Bionomics, Collaborative Medicinal Development, Grunbiotics, Janssen Cilag, LivaNova, Lundbeck, Merck, Mylan, Otsuka, and Servier. The other authors have no competing interests to declare.”

They also disclosed within the manuscript that “The funder of the study had no role in study design, data collection, data analysis, data interpretation, or writing of the report.”



Davey, C. G., Chanen, A. M., Hetrick, S. E., Cotton, S. M., Ratheesh, A., Amminger, G. P., … & Rice, S. (2019). The addition of fluoxetine to cognitive behavioural therapy for youth depression (YoDA-C): a randomized, double-blind, placebo-controlled, multicentre clinical trial. The Lancet Psychiatry. S2215-0366(19)30215-9 (Link)

The Creation of a Conceptual Alternative to the DSM: An Interview with Dr. Lucy Johnstone

Last year, Lucy Johnstone, Mary Boyle and their colleagues in the UK launched the Power Threat Meaning Framework (PTMF), a set of ideas that represented a sharp departure from the biomedical conceptions that animate the American Psychiatric Association’s Diagnostic and Statistical Manual (DSM). This framework shifts the notion of “What is wrong with you?” in the DSM to “What has happened to you?” and by doing so rejects medical process of diagnosing “disorders” in favor of a narrative response that tells of contexts, power dynamics, and systems.

At a time when the Global Mental Health Movement is exporting the Western biomedical model around the world, Johnstone, Boyle and the PTMF project team, which includes those who identify as service users/survivors, are seeking to promote a radically different way of understanding distress. Responses to the PTMF have ranged the gamut from criticism to gratitude.

Johnstone, a consultant clinical psychologist who has experience working in adult mental health settings for many years, believes that the current mental health system has failed, and we are now in the process of witnessing the crumbling of the medical paradigm of emotional distress. She believes we need an approach based on fundamentally different principles. The PTMF, which draws on a wide range of evidence and examples of existing alternatives, is an attempt to outline what that might look like. The PTMF project team hopes that it can be a contribution to the much needed revolution.

Johnstone described the PTMF in an earlier MIA interview. In this interview, 18 months after the launch, she reflects on the reaction to the PTMF, and the impact it has had so far. How are the ideas being used? Does it stand a chance of becoming more widely adopted? She also describes how her own life experiences have influenced her work.

The transcript below has been edited for length and clarity. Listen to the audio of the interview here.

Zenobia Morrill: To begin, why do you believe we need an alternative diagnostic framework? In other words, what’s the problem with the DSM?

Lucy Johnstone: We don’t think we need a new diagnostic framework, we think we need a new framework that is nondiagnostic. So that’s what we attempted to provide. But you and anyone who visits Mad in America will be well aware, as many other people are, that the current diagnostic framework is facing a lot of problems.

Of course, experiences of distress are very real. People really do feel suicidal and desperate and anxious and hopeless and hear hostile voices and have mood swings and so on, but it’s never been demonstrated that these very real experiences are best understood as medical illnesses that need diagnosing. There is also a great deal of evidence that people are ultimately responding to events in their lives when they go through these very difficult experiences.

We clearly need something different (from the DSM). Now, of course, people have varying ideas about what that different system should look like; whether it should be in some sense a better, more effective diagnostic framework, or whether it should be something completely different. But it’s obvious I think to everybody on every side of the debate that the current diagnostic system is not working. We do need at least something different and it’s our view that the big difference needs to be a fundamental shift away from the assumption that these difficulties and these forms of distress are best understood as medical illnesses.

Morrill: How would you respond to people who say that the DSM or ICD are helpful in that they group together people with like symptoms for research purposes, provide a common language for practitioners, or even helpful for reimbursement purposes and categorizing different treatments for people with similar symptoms?

Johnstone: Legitimate diagnosis, medical diagnosis, does do those things. That’s why we have it, so we can group symptoms together and suggest the best treatments or interventions. I would actually challenge that language, first of all. The language of “symptoms” and “illnesses” and “treatments” all implies the same unproven model. Actually, I think it’d be very hard to maintain that psychiatric diagnoses perform any of the functions that diagnosis does in what I would call legitimate branches of medicine.

We do need ways of grouping different kinds of experiences together so that we can think about the best way forward and all the rest of it, but the diagnostic system doesn’t do that. We are claiming that we’ve come up with something that does that better. Equally, it’s true that in the current system, diagnosis is needed for some practical purposes, like access to welfare and benefits, and for the foreseeable future, probably will be. We want to claim that we found that there are more effective ways of doing that that don’t require you to subscribe to a label, which is actually not valid and is experienced by many people as very damaging.

Do you feel that the DSM has helped form societal and professional thinking about psychiatric difficulties in a way that has been harmful?

Johnstone: The DSM and its European equivalent, the ICD, have certainly had a profound effect on forming societal and professional thinking, and it’s chicken and egg isn’t it? It’s arisen out of a certain way of thinking about things. It’s had a profound effect. I would certainly argue, as would many other people, that the overall effect has been very damaging.

I think it’s almost impossible to overestimate its influence and to grasp how deeply it’s infiltrated in all sorts of areas of our lives. It’s not just services, but the legal system, the welfare system, and it’s to the extent that people are actually coming along having diagnosed  themselves. This language is everywhere–it’s in campaigns, like anti-stigma campaigns, it’s on Google, it’s in the media, it’s in people’s training programs. It’s become something that Mary Boyle, in her useful phrase, calls “the DSM mindset.”

There’s an awful lot of evidence, and you will know this of course, but people like Robert Whitaker have shown, I think quite conclusively, that this kind of approach coupled with the psychiatric drugs that it invites, does not, over the long term, on average, help people or make them better. In fact, levels of disability across countries rise in tandem. The fundamental model clearly isn’t working, and we clearly need something different.

Morrill: You’re noting that this system has done harm, it lacks validity, and it’s not working. And, that the Power Threat Meaning framework (PTMF) offers something else. What are the core aims of the PTMF?

Johnstone: The Power Threat Meaning Framework is a ridiculously, ludicrously ambitious attempt—an ongoing attempt, not a complete answer—that we hope will start to outline a conceptual alternative to the diagnostic model of distress.

We already have a number of different ways of approaching distress, that aren’t diagnostically based, and we’ve drawn from a lot of those. An awful lot of what is in the framework isn’t new. We chose the word “framework” deliberately. It’s kind of an umbrella that supports, centers, and gives some more evidence and credibility and support for the many nondiagnostic ways of working that already exist, as well as suggesting new ways forward.

We’re intending it as a major step away from not just a particular use of language, a particular use of labels, but a whole way of thinking—getting away from the whole DSM mindset. That’s partly why it had to be so long, dense, and detailed because we didn’t really want just to tweak the existing system. We didn’t just want to say, “Well, here’s an extra way of doing things that might be helpful.” We wanted to go beyond that, which required us to really dig quite deeply into the philosophical and conceptual principles of the DSM approach and do a massive overview of all the relevant research.

The aim is to move, in simple terms, away from the “What is wrong with you?” towards the “What has happened to you?” question. To put it at its briefest, we’re evidencing, we hope, the idea that peoples’ distress is understandable in context, but we wanted to think about context in its broadest form. One of the things we wanted to do was to really make very clear the link between personal distress and social context, social inequality, and social injustices. In other words, to put power on the map. Power is not only missing from psychiatric thinking, but it’s also missing from a lot of psychological thinking, and it’s missing from much psychotherapeutic thinking.

Along with that, we wanted to have a framework that supports people to help tell their stories, narratives of all sorts. So the simplest answer to “What do you do instead of diagnosis?” is “you listen to people’s stories.” This is a framework, we hope, that both validates the idea that narratives are an alternative to diagnosis and supports the construction or co-construction of particular narratives and looks at patterns in those narratives.

Finally, the third important thing to say is that the framework applies to all of us. We really wanted to get away from this whole idea that there’s a group of people who are somehow mentally ill or different in some fundamental way. We’re all subject to the negative influence of power. We all suffer distress at times. The framework is actually about all of us.

One of the key things about the framework is actually giving people the knowledge, the information, to make up their own minds about how they want to describe their own experience. That’s a really important form of restoring people’s power: the ability to make their own meanings. Ultimately, to create new narratives that make more sense.

Biomedical model psychiatry is a prime example of the use of ideological power because it is a worldview that does not have any evidence to support it, that never has had evidence to support it, that clearly operates in the interests of people who are already quite powerful—professionals, drug companies, and so on—clearly operates to the disadvantage of people who are already less powerful, or else they probably wouldn’t be in services in the first place. It clearly operates by imposing a form of meaning on people, which goes along the lines of: you have a mental illness of X, Y, or Z sort. If you start to challenge that, you will quickly find out that the power lies elsewhere. You’re not allowed to challenge it. All sorts of consequences may follow from challenging it.

Morrill: How has your personal and professional background influenced your participation in and construction of the PTMF?

Johnstone: I’ve always believed that madness has meaning, but also I think probably all of us in the project group would say the same thing. In a way, the framework is the culmination of our life experience both personally and professionally. We, all of us, brought a range of experience to that task which covered research, clinical practice, training, and personal experience. Together, I think it made a rich mix whereby all of us, those aspects of our experiences, were able to feed it into the production of the document.

If I think about myself, I would certainly say it’s not an accident I went into mental health work and developed the views that I do have. I’m an unremarkable person. I come from an ordinary UK middle class background, my parents are both school teachers, I have a brother and a sister, I went to a decent school. . . I mean, in one sense nothing awful happened to me. In another sense, there were a number of ways that I was always very unhappy as a child, as a teenager, as a young woman, and I spent a lot of time thinking about that. It’s clear to me that there were reasons for that.

I come from a generation that was still quite influenced by the so-called antipsychiatry movement. When I started training as a psychologist, there were still people around, some of whom were very inspiring to me, who had worked with Laing, for example. Those ideas were still around. It all fitted for me. The personal thread of experiences, that distress or madness has meaning, very much chimed with some of the currents that are still around in the culture. I’ve always believed that, I’ve always followed that thread through.

Morrill: What was the intellectual process like of constructing the PTMF?

Johnstone: In one sense, the starting point is the position statement that the Division of Clinical Psychology issued in May 2013 at exactly the same time as DSM-5 was published, and I was  part of that position statement, as were a couple of other people who were in the group. In essence, it was a whole professional body calling for the end of the disease model of distress, which is quite a brave and challenging thing to do.

One of the recommendations was that if we’re going to call for this, then we need to be able to work out what an alternative would look like and join with survivors and other stakeholders to see what that might look like.

It kind of evolved from that, without any plan. Mary and I were the project leads. I’ve never been involved in anything as ambitious as that before. I think it helps that the core group, we’ve all known each other for years, if not decades. We all knew where we were coming from and I don’t think any other group would have been able to take on such a task nearly so easily. There was a large degree of shared trust and friendship and shared ideas and understandings.

We started to meet regularly. We started to firm up some of our ideas. We started to assign different aspects of the document to different people to take a lead on it. We started to draw in other members and people to give advice and consultation. We had set up an advisory group of service users and carers. About three years down the line, Mary and I realized that unless we devoted some really solid time for this, it’s never going to happen. We essentially spent two years unpaid in front of our computers, each of us, putting it together, and then it came out.

It was very stressful at times. I think it’s fair to say that for about two years I think I felt, and I know Mary felt, and I think probably the others felt, that we’re kind of thinking, “What the hell have we done here? It feels like we’re wandering in an intellectual wilderness.” Firmly as we believed that the existing model is not fit for this purpose, it’s actually a much bigger task to put together something that is going to hold together and something different to put your money where your mouth is, as we say in the UK. So it was very stressful and difficult at times, but we’ve emerged at the other end with an imperfect, evolving document, but one I think that we overall feel very proud of.

Morrill: What do you believe the PTMF has accomplished? How do you wish it to be used, and how would it change societal and professional thinking if it were to be adopted?

Johnstone: We had no idea how it was going to develop and it’s still an evolving thing. I don’t know how far it’s going to go or what it’s going to look like. If it is really fully implemented, then the landscape would look so different. I think it is actually quite hard to conceptualize because you’re bringing up some really fundamental questions, like, “Do we need a mental health system?” Not all cultures and countries have had, or do have, a mental health system. Do we even need one? That’s a very big question.

At a more immediate level, we deliberately haven’t set out specific answers about, “How might I work differently with this person?” or “How might services look differently?” because we wanted this to be a conceptual resource, a set of ideas. It’s really up to people themselves to think about how they might put it into practice. We want to be collaborating, letting it go so other people can do what seems helpful because they will be the experts in their setting and their position. The second stage of the project is for that to happen as much as it happens. We hope to get feedback on that.

We hope to learn from how people are using it, what’s worked, what hasn’t worked, and so on. I guess what we mainly wanted to accomplish is some sense of support for people who do want to think and do things differently or see their lives differently–some ideas for them to put into practice to take them further down that road. That is how it seems to be working out. That’s great. It’s an ongoing journey, so we’ll see.

Morrill: How do the core aims of the PTMF fit in or clash with the movement to globalize mental health?

Johnstone:  One of the biggest scandals of our age, I think, is not only that the diagnostic model is comprehensively failing in the largely Western industrialized countries within which it was developed, but it is that at the same time— and this may not be a coincidence—it is being exported across the world.

This is generally seen to be a good thing and I’m sure people are well motivated, well, most of them, in doing it—not quite so sure about the drug companies—but I think we’re too close to see what a scandal this is. It reminds me quite a lot of how a hundred years ago, 80 years ago, this would have been missionaries exporting Christianity, dutifully and well-motivated, but actually this is in some sense similar, but I would say more damaging. It’s a form of colonization and it’s an insidious one because it’s about taking over people’s minds and actually persuading people that this is what they want, these wonderful, new Western scientific ways of treating so-called illnesses. One of the strong messages of the framework, we hope, is a message of respect for the many, many different culturally specific and culturally appropriate ways of understanding, expressing, and treating distress across the globe.

This is very different from the DSM perspective because the DSM perspective has a great deal of trouble in trying to accommodate culturally specific expressions of distress. Because if these are medical illnesses, they would look roughly the same, wouldn’t they? Diabetes, a broken leg, malaria, or whatever looks roughly the same wherever it happens. Expressions of distress could look extremely different. They can look extremely different across time as well as cross culturally. In the Power Threat Meaning Framework terms, that absolutely makes sense because one of our core arguments is that instead of understanding distress through biological patterns, patterns that are borrowed from the kinds of patterns that we see when things go wrong in our bodies, we need to understand distress through patterns that are organized by meaning. They’re organized by meaning, not by biology, which is a big conceptual leap, one of the fundamental conceptual leaps I think we made.We need to be thinking about how those patterns are based on or organized by social and cultural meanings, not by biology and something that’s gone wrong with our bodies.

As soon as you get your head around that, you realize, from a framework point of view, of course, expressions and experiences of distress are going to look very different cross-culturally because they’re different cultures with different meanings, norms, and assumptions. That sets the scene for saying, well fantastic. If that works, that’s great. Actually, to go further than that and say there may be things we can learn from non-Western non industrialized cultures rather than the reverse “We’re going to impose our ‘modern’ views.”

Morrill: What criticisms have you received and how has psychiatry responded to the PTMF?

Johnstone: Well, psychiatrists vary. It’s been kind of interesting because there is a group of psychiatrists in the UK called the Critical Psychiatry Network who are very outspoken critics of the way psychiatry works. I was invited to speak at their annual conference this year. They were very supportive, very interested, very welcoming. Other psychiatrists, of course, have viewed it rather differently and, as expected, have, well, I like to think that the usual line of defense goes ignore, attack, assimilate.

Any approach that challenges the status quo you tend to see: ignore, let’s pretend no one has said this, attack, let’s tear this apart, assimilate—in some ways, the most dangerous stage, because it’s like “We’ll take some bits and pieces of this, but we’ll ignore the fundamental message” and the whole road show continues much as before. We’ll have psychiatry as before, but we’ll have a hearing voices group for half an hour once a week on the ward, where we give people a few coping strategies and otherwise, everything will go on as before. Although, interestingly, we seem to have gone straight to the attack phase with the framework. I don’t know what that means, but I do want to say that it’s really much bigger than, as it’s sometimes unhelpfully phrased, psychiatry versus psychology. This is about a way of thinking that is deeply embedded in all of our minds, in every professional of any background.

I think it’s important to listen to everything that comes back at you—but some of it strikes me as quite odd. For example, one of the big criticisms we’ve got is that “Your framework isn’t evidenced.” Well, the diagnostic model isn’t evidenced, that’s for sure. We have actually got 70 pages of references and a massive overview of the evidence. Some of the less constructive criticisms are saying “You’re antipsychiatry,” which, in the UK, is a kind of all-purpose way of dismissing you.

The system isn’t going to change easily, and by the system, I mean all the professionals who are involved in it. But, as I said, that’s not mainly where we’re aiming. I think the time has come to, as much as we can, step aside from all that stuff and promote good practice and different practice where we can and where there are people willing to listen and try out new things.

Morrill: There has been a critique of service user and survivor involvement in the PTMF project. Can you discuss those critiques as well as your responses to them?

Johnstone: We’ve had some really, really heartwarming feedback from particular people who said, “I see my difficulties in a very different way, I don’t have to feel so different or guilty or ashamed,” and so on. And we’ve had some very fair criticism, particularly that it’s not very easy to read it in most of its current form. I think that’s fair. I think we want to think about more accessible forms and we are doing that.

There are people who say, “It doesn’t really seem to fit or describe me.” That’s absolutely fine. And people who are happy with the diagnostic model that does fit and suit them, and that’s absolutely fine too because it is really not our aim, nor is it within our power, to go imposing this framework on people. It’s for people to pick up if they want.

We’ve had some quite angry criticisms that I think are based on misunderstandings and I can’t blame anyone for not reading through the whole document—it is long—but the risk is you pick up ideas that aren’t actually what we said. One of the regular comments we get is, “I need my diagnosis for welfare and service access, so you’re going to take away my diagnosis.” Also, “The system is going to leap on this and say ‘oh these people aren’t ill, we don’t need to give them support,’” and so on. Actually, we’ve very clearly said, at a number of points in the document, the first priority must be to protect people’s access to benefits and services. Of course, it must be. This is a discussion document. It’s not a plan for services or benefits offices, it’s a way of discussing ideas.

I would still maintain that the current benefits system is not working now and the same people who are, understandably, anxious about “Will this make life even more difficult?” I think would be the first to admit that the system is appalling in the UK, not just in the UK. Diagnosis is very often used to exclude as well as include people, and most people are really struggling and they have to go through a humiliating process of describing themselves on their worst day and accepting a label that they may not be happy with in order to have the bare minimum to live. This system really does need changing. It needs changing in a way that doesn’t put people more at risk. But I think we have to have these discussions.

There are other people who I think have understood it or misunderstood it as saying, “We’re going to go around the country tearing people’s diagnoses off people and saying, ‘you’re not allowed to use this language.’” Again, we’ve clearly said people have to have the right to describe their experiences in a way that makes the most sense to them, but people are very rarely offered that choice. They are very rarely offered that choice.

Morrill: Where do we go from here? The world of psychiatry still seems to be mostly governed by the DSM. Does the PTMF feel like a lost cause if that’s the case?

Johnstone: It doesn’t feel like a lost cause because my view is that we are actually witnessing the crumbling of an entire paradigm. With or without the framework, the days of the diagnostic paradigm are numbered. If you read that stuff, the Thomas Kuhn stuff, the “Structure of Scientific Revolutions,” we’re seeing all the signs of the crumbling of a paradigm. We’re seeing massive contradictions within the paradigm, desperate attempts to shore it up, a mountain of evidence that is not correct, or that other ways are a better way forward.

One of the things that Thomas Kuhn says is that all these things can happen and yet, the paradigm won’t fundamentally shift unless or until there’s somewhere else to jump. Well, I think there are actually a number of places to jump, and I think the trauma-informed perspective, which we’ve drawn on to quite a large extent in the framework, is one of them, but I think the framework itself, I hope, can also be seen as additional support for that kind of approach, and as a place to jump to in itself. If it becomes a small part of that inevitable process, and I do think it’s inevitable, then we will be pleased and proud.

Morrill: That’s heartening to hear.

Johnstone: You can see I’m a total optimist.

Morrill: Anything you’d like to add?

Johnstone: I don’t think so. I’d encourage people to read the links you’re going to put at the bottom to find out more. Make of it what you will.


More about the PTMF

The British Psychological Society: Introducing the Power Threat Meaning Framework

Lucy Johnstone discussing the primary features of PTMF

Presenting the PTMF in Australia

Presenting the PTMF in New Zealand


MIA Reports are supported, in part, by a grant from the Open Society Foundations

The Effects of Antidepressant Exposure Across Generations: An Interview with Dr. Vance Trudeau

On MIA Radio this week, MIA’s Zenobia Morrill interviewed Dr. Vance Trudeau, a professor at the University of Ottawa in Canada. Dr. Trudeau describes a recent study he conducted, alongside a team of researchers, led by Dr. Marilyn Vera-Chang, that has implications for understanding of the long-term impact of antidepressant drug exposure (see MIA report).

The study, titled “Transgenerational hypocortisolism and behavioral disruption are induced by the antidepressant fluoxetine in male zebrafish Danio rerio,linked antidepressant exposure to decreased coping behaviors in zebrafish that lasted several generations.

Dr. Trudeau is the research chair in neuroendocrinology at the University of Ottawa, where he studies how the brain regulates hormonal activity in fish and frogs. Such analyses offer important insights into the effects of environmental exposures on human health because these hormonal systems are shared across species.

What follows is a transcript of the interview, edited for clarity.


ZM:  Welcome, Doctor Trudeau, thanks for joining us.

VT:  It’s nice to be here.

ZM: We really appreciate having you here to tell us more about this interesting study. Could you start by giving us a brief overview of the study, what you did and what you found?

VT:  We’ve been interested in how pollutants get into the environment, especially pollutants that we generate through our use of pharmaceuticals. So when you take any pill, aspirin or Prozac or what have you, it goes into the sewage treatment plant, it degrades a little bit, but not all, and then, it’s released to the environment, to lakes or streams or rivers. So we started looking at fluoxetine, the active ingredient of the drug Prozac, quite a few years ago.

Our angle was much more on the impacts on the environment. But then, of course, you realize that these are bioactive substances that we’re taking quite a lot, depending on the statistics, it can be quite high in the human population. So we started from there and then we had questions about, uh, you know, how long would an effect last? And that’s where we started getting into this first generation, second generation, third generational studies. So that’s kind of where we came from to begin this study.

Right. And so you ended up looking specifically at fluoxetine and zebrafish for this study?

VT:  Yes. fluoxetine has gone generic, so it’s in quite a few different antidepressant medications now, and it’s considered an environmental pollutant along with quite a few other of these types of chemicals. And we chose the zebrafish because it’s a very powerful biomedical and environmental model.

The study system was, of course, the stress hormone system, which is identical in fish, frogs, cats, dogs, and humans. The hormone cortisol is the same in fish as it is in humans, and the brain control and the pituitary control of that hormone production in the adrenal gland are very similar between all of these different animal groups. And you can do transgenerational studies in a small fish in a few years. It would take a few lifetimes if you wanted to do it in humans. So, we can get an answer, at least hints, of what might be happening across generations relatively quickly.

ZM: And so what did you observe and how did you go about exposing the zebrafish to fluoxetine?

VT: We started with an early exposure: three hours after fertilization. And that lasted for six days. In the zebrafish embryo, this is very early. This is when you’re getting the formation of organs, and formation of the brain and the actual brain circuits that would be affected by something like fluoxetine, and also, within a day or so as well, the stress hormone system is also being formed. We targeted this first six days of life because those two systems are forming.

Fluoxetine affects a brain system called the serotonin system, and it affects the uptake and the amount of serotonin that might be in the brain. So that’s why we started very early. And then we let them grow into adults, so six months later, in freshwater, so they were only exposed for six days. And then we found that their stress hormone levels, in sort of normal daily life, and under different stresses, were much reduced.

This was a first big surprise. So, we looked at that and tried to figure out what was going on. At six months, they’re adults so we can breed them. We said, “What about the next generation?”

Their reproduction was normal, but the next generation had the same effects: reduced cortisol in daily life and under stressful conditions. And then we did it again in the third generation, and we saw virtually the same thing. So this was obviously quite surprising to us that it would last three generations. That’s a long time, in human terms. That means your great grandparents are affecting your stress, ability to deal with stress now. You don’t even know your great grandparents, probably.

ZM: Yeah, I think that’s part of what readers are wondering is how much can we take a six-day fluoxetine exposure in zebrafish and understand how that might affect humans?

VT: There’s a couple of things. We also observed that these animals had altered behavior. We use a test that’s kind of a test of exploratory behavior; it’s called the “novel tank” test. You put an animal in a tank, and they swim around, and they swim a lot, looking for hiding places. In animals that were treated six months before with fluoxetine, they don’t explore very much.

We have some videos available too that could be very interesting for people to look at. But this is exploratory behavior. What was remarkable is that lasted for two generations. So also a very long time. And we could link the two observations.

One of the more basic discoveries was that the hormone cortisol actually controls this behavior. Cortisol is allowing the animal to explore its environment. And if you lower it by Prozac or by other treatments, they explore less.

The equivalent is in a child, you know, if they go into a room and there are new people, and they look around, and they say “hello,” that’s normal behavior. If you don’t explore the room, it’s called kind of like an internalization of behaviors. And that’s an odd thing. And that’s what Prozac does to kids too. If the mom is taking Prozac, her children have more internalized behaviors. That is kind of a similar thing.

So we have the behavior change lasting for two generations and the stress hormone changes for three generations. How does that translate into potential effects in other animals, including our own species, including humans? Well, cortisol is cortisol. It’s the same hormone, and the same brain hormones control the same hormones in the pituitary and the identical steroid hormones in the adrenal gland. It’s clearly related to other species and the way we think this inheritance is happening, how it gets transferred from one generation to the next, even when the fluoxetine is no longer around for generations, is that it is an epigenetic mechanism. Not a DNA mutation, but something that alters the structure of the DNA. So not the sequence change, something on top of the DNA or DNA methylation or some other mechanisms.

Epigenetics is all the rage at the moment, of course, in the scientific literature. And we haven’t proven that. That’s some of our next studies, but it’s clearly the next thing we should do. And this mechanism, of epigenetic inheritance, is conserved. The mechanism is the same in every single vertebrate.

There’s no reason to think that humans would be different. I mean we study mice and worms and fish and human cells in a dish to get ideas, and it’s shown that these epigenetic mechanisms are really the same. This raises the question of whether it might happen in other species for sure, including humans. So that’s the next big question for medical researchers. Is it happening in humans?

ZM: I know that you mentioned having cited some studies in the actual article that you published about human studies and what happens when that fluoxetine can pass the placental barrier.

VT: This is very interesting work. It was a couple of different labs around the world, looking at what happens when you have a prepartum– during pregnancy–treatment of antidepressants to help moms in trouble, and also postpartum as well. But prepartum, what professor Tim Oberlander at the University of British Columbia has found is that there are effects on the children.

He’s done a few studies in early life, uh, three months, a few years, I forget exactly, but he sees low cortisol levels, and in these people, whose moms took antidepressants, he also sees an increase in internalization behaviors. The lack of exploration of novel environments, for example. So he sees what we were able to see over several generations, and I believe his studies are ongoing. Those patients are, I don’t know how old they are, but it’s a very longterm study to try to see what’s happening to those now young adults.

ZM: Sure. And that’s the advantage, right, of looking at Zebrafish?

VT: Well, any fast-growing, fast-breeding animal would be a great model. Mice, zebrafish, other models have been used for these types of studies. We chose fish because we can ask two questions. What if you control the embryonic environment with human-relevant doses, or if you give them a much lower concentration of fluoxetine than would be found in the environment, would it affect the fish? And we found it did. Low environmental levels that might be in a sewage pipe, in a contaminated river, affected the cortisol levels for several generations. It wasn’t so effective at changing the behavior over generations, but it definitely affected the cortisol.

A fish living in the wild, they need cortisol for many things. They need it for aggression; they need it for growth; they need it for exploratory behavior. Cortisol is super important for survival in changing environments. I mean it is the adaptive hormone. Stress is an adaptive response.  The work of Hans Selye in the 40s and 50s shows that what stress hormones are important for is helping us cope. Coping behaviors and the coping response, in terms of hormones, is altered over generations. There is less of an ability to cope with the daily challenges–kind of the opposite to what you’d expect for an antidepressant.

ZM: That’s what I was about to say. It sounds like the suppression of the ability to cope or the ability to have exploratory behaviors would almost read as a depressed sort of state for someone.

VT: It’s the opposite of what you might expect. There, we have to explore that a little bit, but we’re treating very early in life, the first six days of life, and that’s setting up those hormone systems that I was talking about before, and it looks like it’s changing their path of function and development for several generations.

ZM: I think these findings are are major and have a lot of implications that we ought to be considering. I know that, l to quote one of our Mad in America commenters, Sylvain Rousselot,  why is it that such an important study is not on the front page of scientific journals?

VT: I read that too. And it wouldn’t be on the front page of other scientific journals; it was published in one, the Proceedings of the National Academy of Sciences. They made press releases that many, many, journals, took up, popular articles, radio shows, et cetera, et cetera. And also your own show as well. So I’ve been very happy with the press coverage. Many people are asking detailed and important questions. SoI believe that people are becoming aware. And, you know, there’s the big media splash in the first weeks, but you know, people have to think and read about these types of studies and really get into it before you start worrying about it. Some of the questions you’re asking are really important.

We have to face these facts now that pharmaceuticals can have long impacts, not only Prozac. There are other chemicals that have been shown to have transgenerational effects.

One is a fungicide; this is the most famous study. And another one is, is bisphenol a (BPA), the estrogenic chemical that’s found in plastics. And this can alter offspring behavior and reproductive outcomes.

So we should be asking ourselves as a society, are we ready to face up to this challenge, which is that some of the things we do last generations. Is that a good thing or a bad thing?  We have to ask that question. I think it’s going to depend on which treatment and which chemical. In the case of this example, an inability to cope across generations is not a good thing, no matter what you do, what you say, it’s clearly not a good thing for the fish.

ZM: Y I think there are people who hear this and read these findings and wonder what they should be considering, and should they be worried on their antidepressants, or should prescribers be thinking about prescribing these differently?

VT: This is a really loaded question that many people have. I’m not a medical doctor, and I’ve been asked this question a few times, and for me, it is very clear. If you have concerns, you must discuss it with your physician or psychiatrist or psychologist, to whoever you’re talking with, and do not change treatment until you get professional, expert advice. I think it’s important to ask questions of your physician, about what is going on. Ask them to read this article, and other articles, because I should imagine many people are not yet aware. So, certainly, do not change what you’re doing. You really must seek professional advice on that, and I can’t emphasize that any more. It’s really important to discuss it with people who are helping you.

ZM: It seems that there is that important piece of integration: discussing this with your physician, but also making sure physicians get the information in a study like this, that maybe they’re not necessarily looking.

VT:  I mean we have to ask ourselves now, does it have implications for our own species? And that’s what I think the next wave of research, for example, Oberlander’s work, will help to answer.

ZM: Do you know about cortisol and humans? We were talking a bit about a child who maybe wouldn’t demonstrate exploratory behaviors or ways to cope, but what might that look like in people?

VT: Well, suppressed cortisol, in the human condition, is called hypocortisolism. So most people think of the bad aspects of stress as too much stress and too much cortisol. So that’s hypercortisolism, and there are all kinds of studies on that. It can affect memory, it can immunosuppress you, when you get more susceptible to colds and viral infections and what have you, and that’s been studied quite a lot.

But in the last decade, it’s becoming apparent that low cortisol is also not very good. There’s kind of an appropriate level of cortisol to have for you to be able to adapt. Too low cortisol means you won’t be able to adapt to the daily challenges as efficiently as if you had regular cortisol levels.

The kinds of human conditions that have been associated with low cortisol are PTSD. These unfortunate people have trouble dealing with challenges in life, in PTSD situations. Some disruptive behaviors in children, both boys and girls, are often associated with having low cortisol levels.

So there are certain behavioral problems like that that are associated with low cortisol. There seems to be a good amount of cortisol, if I can say it like that, and too little or too much seems to get us in trouble. This is relatively new, but hypocortisolism is also going to be something to look for in the future as researchers dig through the data and try to understand what low cortisol means as well. There are a few important examples.

ZM: In doing your research and looking at examining pollutants in the environment, did you expect that you would get these studies or that you would be here having this discussion about antidepressant medication?

VT: That’s a good question. I mean, our earlier studies, where we’re treating adult fish on the short term and looking at reproductive outcomes, you can alter reproductive hormones on the short term in various treatment regimes. So, we set out thinking that we were going to give an early life exposure and affect reproduction, but we didn’t. There’s no change in reproduction over three generations. The big surprise was an effect on stress.

In the past 20 years, I have not worked very much on stress hormones. In fact, I avoided it because there are so many other good researchers working on stress hormones. But here we are, this is a major effect, and we are trying to figure out what’s going on.

The tissue that produces cortisol is the adrenal gland in mammals, and in fish, it’s a got a slightly different structure, but the cells are virtually the same, they’re just embedded in the kidney instead of on top of the kidney, like our own adrenal gland is, and those cells are altered. We did something called RNA sequencing to look at all the different genes that would be up and down regulated in the animals treated three generations before. And we found that the enzyme pathways, important for cortisol synthesis, were altered in these animals three generations later.

That tells us that the adrenal gland is functioning differently in these animals. We also think that the brain will be functioning a little bit differently. So, in the next wave of studies, we’re trying to examine where cortisol is acting in the brain, and where fluoxetine is acting in the brain, and finding where they transect. Which cells in the brain are actually affected in these animals? The next study is really trying to understand a little bit more on the brain side of things.

ZM: That is what you are going to pursue?

VT: We’re doing it right now. Yes.

ZM:  I guess you couldn’t avoid studying stress then?

VT: Nope, I have to go for it.

ZM: I think for most people, at first glance, if you don’t and aren’t familiar with cortisol and what that means, it can be hard to understand why that feels important. But as you talk about the effects of fluoxetine exposure, it feels like cortisol and low cortisol, or too high cortisol levels, potentially, can be implicated in presentations where people receive diagnoses, like you were saying, PTSD or disruptive behavior. So, I see how you’ve ended up there when you didn’t expect to, and I see how it’s something that we ought to be, as you said, rethinking in terms of what that means for our species.

VT: Well, cortisol is such an interesting hormone because it has many, many functions. It’s considered a metabolic hormone because it helps you generate energy and metabolize things. It’s the coping hormone. It’s a super important for many, many processes, memory, behavior, all kinds of things. It’s a multifunctional hormone. That’s why I became very, very interested because it has implications for many processes in the body, not just coping behaviors.

We have to dig a little deeper in there. Cortisol can affect many, many tissues in the body as well, both in a good way, for metabolism and daily life, and in a bad way, in super stress situations. For example, suppressed immune system, you know? How many times have you studied like crazy and you’re stressed and you take the exams and you feel great, but three days later you get a cold? This is immunosuppression because of stress. So there are lots of angles to this?

ZM: So it’s really far-reaching that cortisol would be implicated and that we see this across two, three generations. And correct me if I’m wrong, but that was without a diminished effect, right?

VT: Yes. It was especially evident in the males, and we also saw it in the females, but we focused most of the study on the males because it was a little bit more obvious. And we’re now pursuing this sex differences as well. We’re just writing the next paper in the series to look at early exposure and then following males and females a little more closely. So there is a difference in the response.

The other thing is we just published a paper a week or so ago that’s showing that at least part of this reduced cortisol is inherited from the mother. The mom seems to be putting things in the egg before fertilization to set up her children to be having lower cortisol levels. This is something that’s very fascinating, and we have to dig a little deeper. It’s kind of just getting going, and we don’t completely understand our own observations yet. But it’s something to look for in the future, how the parents are actually telling the offspring what’s going to happen.

So the drug treatment is being passed on to the next generation through, in this case, the mother. In other situations, it can be through the father. So the parents are actually passing on this epigenetic information and kind of instructing the embryo what to expect in a way. It’s so fascinating. I mean, it has many, many implications for many types of studies. And there’s a lot of great labs working on it.

ZM: Absolutely. And I’m so fortunate to have you here explaining, talking us through what this means. Are there any other significant aspects of these findings that you’d want to bring up?

VT: I think we’ve covered most of it. There are still lots of questions of course. And, and we’ve covered a bit of that and some of the future studies we will do. Hopefully, other researchers also get some ideas, and we can expand and get to the answer.

ZM: What are some of the other questions that maybe we haven’t gotten to, but that are on your mind?

VT: Well, what are, what are the implications for other bodily functions? So we just looked at the exploratory behavior as a coping response, but what are some of the other cortisol-depend things?

The immune system. For a fish, cortisol helps the animal deal with the aquatic environment. It regulates functions in the gill. In our own species, it helps the formation of the surfactant in the lungs at birth. So it’s important for respiration as well.

There are many other things that one could look at in terms of what would low cortisol do to the animal. I suspect that some functions will be just fine because you can adapt to lower hormone levels over time. And we saw that with the behavior, they eventually adjusted their exploratory behavior even though cortisol was low, but there may be some functions that are permanently changed so we could get into that as well.

ZM: Right. I was curious, how did that eventual adaptation look?

VT: Well, if we look at the exploratory behavior in the third generation, it kind of looks normal, but they still had low cortisol levels. It’s almost like an adaptation to a lower level. That’s all we could conclude.

We don’t really have a good idea of how it would happen. But you know, your body, it’s called homeostasis, your body tries to adjust to changes, right? Short term and long term. And eventually, some other parts of the hormonal system may help to deal with that low cortisol. We really don’t know how, but they did return sort of to normal in their behavior at the third generation. But in the second generation, they were still having very, very low exploratory behavior. That’s like your grandparents affecting your behavior. It’s still a very long time in human terms.

ZM: Yes it is. And I think that point, of what we do know is that cortisol is implicated in a lot of different mechanisms and functions, paired with, and there are a lot of things we still have yet to understand about that, brings up—does bring up a lot of questions about, so what does that mean for interrupting that process or changing the structure of genes through fluoxetine?

VT: I mean that’s where we’re going to go in the next couple of years, for sure.

ZM: Any other questions coming up for you?
VT: That’s about it. That’s going to keep me really busy, and hopefully, I can get some help from some other labs.

ZM: Who is funding this research and are you able to get collaboration from other people?

VT: Who is funding? That’s a good question. It was myself and professor Tom Moon, co-supervisors of Dr. Chang, and we used our research funding, but we did not have a specific grant for this study. It would be hard to convince an agency to fund for three years when you don’t know what’s going to happen. I think maybe now we would have better luck getting funding because we’ve published the paper, but this is NSERC in Canada that’s provided the money.

ZM: In a way, some of these findings are presenting a warning for antidepressant medication, or a cautionary sort of thing to consider. Have you gotten any reactions that weren’t positive to this study?

VT: Not really. There was a couple of people commenting on “It’s always bad, antidepressants are always bad,” saying, you know, that it adjusts, and all that. But this was one or two people.

Most people are being very analytical–they are less public members, other scientists–and asking deep questions about what it means rather than being hyped up about it. I mean, people are being extremely careful. I was contacted by a patient from another country. They were asking about things, and I could not give them advice, of course, but the news is getting out there. I recommended to that person that they discuss in detail with their own physician. Most people are being very, very thoughtful and insightful, actually.

That’s heartening to hear because I think there are a lot of steps that need to be taken next based on what you’ve found. Thank you for your work and thank you for being here with us.

VT: Well, thanks for a great interview. Very interesting questions to get me thinking about other things to do.

Photo credit: Isabelle Mailloux Pulkinghorn, University of Ottawa


MIA Reports are supported, in part, by a grant from the Open Society Foundations