The impact of framing depression as a functional signal
As we move towards a framing of depression that incorporates functionality and adaptivity, we should not lose sight of important conceptual and scientific nuances
Hans Schroder and colleagues have published the results of a randomized controlled trial in which they investigated the impact of framing depression as a functional signal and not a disease. This trial comes in the context of existing research that suggests that biogenetic explanations of mental disorders can worsen forms of stigma, such as pessimism about recovery, increased perception of dangerousness, and the desire to keep individuals with mental illness at a social distance, even though they reduce stigma in the form of decreased self-blame. This new RCT is therefore an important contribution to this literature and offers some guidance on how we begin to remedy some of these negative consequences.
Schroder et al. summarize the findings as follows in the abstract:
“Depression is often framed as a disease or dysfunctional syndrome, yet this framing has unintended negative consequences including increased stigma. Here, we consider an alternative messaging framework – that depression serves an adaptive function. We describe the historical development of popular messages about depression and draw from the fields of evolutionary psychiatry and social cognition to describe the alternative framework that depression is a “signal” that serves a purpose. We then present data from a pre-registered, online randomized-controlled study in which participants with self-reported depression histories viewed a series of videos that explained depression as a “disease like any other” with known biopsychosocial risk factors (BPS condition), or as a signal that serves an adaptive function (Signal condition). We then present data from a pre-registered, online randomized-controlled study in which participants with self-reported depression histories viewed a series of videos that explained depression as a “disease like any other” with known biopsychosocial risk factors (BPS condition), or as a signal that serves an adaptive function (Signal condition). In the entire sample (N = 877), three of the six hypotheses were supported: The Signal condition led to less self-stigma, greater offset efficacy, and more adaptive beliefs about depression. Exploratory analyses revealed these Signal effects were stronger among females (N = 553), who also showed a greater growth mindset of depression after the Signal explanation. Results suggest that framing depression as an adaptive signal can benefit patients and avoid harmful consequences of popular etiological presentations.”
Let’s take a look at some important details.
This study was conducted in participants with a history of depression but no extensive treatment (that is, there was no history of being treated with prescribed medication from a psychiatry specialist and no history of psychotherapy; individuals with such histories were excluded). Furthermore, this history was self-reported based on a response of either 3 or 4 on a 4-point Likert scale that asked, “Have you ever in your life considered yourself to be depressed?” (1 = Definitely not, 2 = Probably not, 3 = Probably yes, 4 = Definitely yes). Participants were recruited from the general community using an online market research firm.
In other words, this was not a clinical sample of individuals with depression requiring specialized psychiatric or psychological treatment. This was a sample of people in the general community who considered themselves to have experienced depression at some point in their lives. They were asked to imagine that they were currently depressed, and that they were seeing a clinical psychologist for an initial telehealth appointment.
This is important to appreciate because the responses of individuals who are crippled by clinical depression, whose depression has driven them to the point of contemplating suicide, whose lives and careers have suffered irreparably, individuals who have benefitted from antidepressants and/or psychotherapy, and individuals who have encountered moralistic attitudes may very well be substantially different in real-world clinical settings.
Additional details about the two framings:
“Participants were then presented with a video introducing the psychologist who talked about the symptoms of depression and then randomized to watch a series of three videos from this psychologist. The videos explained that depression was a disease like cancer or diabetes, with behavioral, environmental, and biological risk factors (Biopsychosocial Risk Factor condition) or a functional signal that alerts the individual that something in life needs more attention (Signal condition).”
The use of the “biopsychosocial” explanation for comparison purposes is a relative strength here as previous studies have relied on “biogenetic explanations” which is problematic in many ways.
There were 6 pre-registered hypotheses. Researchers hypothesized that participants in the depression-is-a-signal arm would
Report greater “depression offset efficacy” (how much agency they have in reducing their depressive symptoms)
Report a greater growth mindset of depression (increased belief that depression is malleable).
Report less stigmatizing attitudes. Self-Stigma was assessed using the 2 items: “I fear that others would know that I am a person with mental illness” and “I avoid interacting with others because I am a person with mental illness”.
Report feeling more responsible for their depression.
Endorse more positive treatment-seeking attitudes.
Endorse more adaptive beliefs about depression. Authors note, “In retrospect, this hypothesis served more as a manipulation check.” It is to be expected that depression-is-a-functional-signal would, if accepted by the individuals, lead to more adaptive beliefs about depression. This doesn’t tell us much other than the fact that participants didn’t actively reject or disregard the information being provided to them. Differences in adaptive beliefs are the most robust finding of this study, but they also mean the least.
Among these 6 pre-registered hypotheses, a statistically significant result was found for two hypotheses: self-stigma and adaptive beliefs. Since the adaptive belief hypothesis, as noted, should be considered more of a manipulation check, the main finding is that of decreased self-stigma. The effect size was small (d=0.15), however, authors accurately note, “small effects are increasingly recognized as realistic in psychological science, which focuses on phenomena that are multifaceted and complex.”
There wasn’t a statistically significant result for offset efficacy overall, but there was a difference in the positive-worded subscale. There were no statistically significant differences with regards to growth mindset, responsibility, and treatment attitudes. In exploratory analysis, a significant difference on growth mindset was noted for women only. In males, none of the differences were statistically significant except for adaptive beliefs.
Authors summarize: “This study suggests that a functional framing of depression may be preferable to a disease-based biopsychosocial framing of depression, and is associated with positive impacts on offset efficacy, self-stigma, and beliefs about the adaptive nature of depression. Among females, the Signal condition also led to greater endorsement of the growth mindset of depression – the belief that depression is changeable. Compared to a conservative biopsychosocial framing, the Signal message had no statistically significant impact on treatment-seeking attitudes or onset responsibility.”
And discuss in conclusion: “Our hope with this paper is to promote messaging that optimizes motivation to attend to the sources of depression and to do something about it. We do not aim to downplay the biological, chemical, or genetic factors that may play a role in depression, but simply to advocate for a more nuanced and understandable discussion between patients, providers, and the public. Sometimes it is helpful to acknowledge the chemical and genetic components to depression. However, it is likely that ending the discussion at that point does not promote curiosity and further introspection about the underlying social and psychological causes of depression. From a clinical perspective, this signal messaging may encourage deeper exploration and promote helpful self-examination among patients with depression, speculations that will need to be rigorously evaluated.”
My major grievance with this study is that there is inadequate recognition of the heterogeneity of depression as a clinical problem. Some depressions are adaptive, many are not. The sort of chronic depression that has been classically recognized as the target of psychiatric intervention is usually not adaptive. The expansion of diagnostic boundaries has allowed for a lot more adaptive states to come to clinical attention, so considering depression as adaptive remains important, but we should not resort of binaries in the face of this heterogeneity.
Depressed mood can be the symptom of a legitimate disorder with dysfunctional mood regulation, despite having functional value. We have numerous analogies from medicine that illuminate this point (pain, cough, fever, etc.). Rather than comparing depression to diabetes, it may be more appropriate to compare depression to a condition such as chronic pain. Saying that depression is a functional signal leaves unexplained, on its own, the impairment and disability that often accompany severe and chronic depression in the clinic.
Depressed mood can be the symptom of a legitimate disorder with dysfunctional mood regulation, despite having functional value. We have numerous analogies from medicine that illuminate this point (pain, cough, fever, etc.). Rather than comparing depression to diabetes, it may be more appropriate to compare depression to a condition such as chronic pain. Saying that depression is a functional signal leaves unexplained, on its own, the impairment and disability that often accompany severe and chronic depression in the clinic.
It is interesting to note that there were no differences in treatment attitudes in the two groups, which means that despite considering depression to be a functional signal, individuals nonetheless saw it as a condition meriting clinical treatment. This is reassuring because it goes against the critical view that if depression has adaptive/functional value, it should not be considered a medical condition.
The gender differences are also salient and should be taken into account, particularly the fact that this framing had little to no impact on males.
Most importantly, perhaps, the authors do not make any clear distinction between “low mood” as symptom that is often experienced in ordinary life and “depression” as a clinical and diagnostic syndrome. This problem is further compounded by the likelihood that most study participants had a history of subclinical or mild form of depression. The significance of this distinction is evident in the evolutionary psychiatry literature. For example, Randolph Nesse (2022) writes in his chapter on evolutionary psychiatry:
“Mood disorders that reduce fitness are not adaptations, they are harmful products of dysfunctions in evolved mechanisms. They do not have evolutionary explanations in terms of their functions. However, the capacity for having and regulating mood is an adaptation…
It will be essential to distinguish evolutionary explanations for the mood system from explanations for why it is vulnerable to dysfunction. Are cases of depression seen in psychiatric clinics mostly normal, useful low mood or mostly pathological depression? My impression after experience with thousands of depressed patients is about the same as that reported a century ago by Aubrey Lewis, the inaugural chair of the London Institute of Psychiatry: about a third of patients have low mood somewhat appropriate to their situation, about a third have grossly excessive responses to a life situation and about a third have fundamentally abnormal mood-regulation mechanisms (Lewis, 1934). However, studies using modern methods have yet to address the question systematically.
Why did natural selection leave mood regulation mechanisms vulnerable to dysfunction? That question is fundamentally different from the question of why the capacity for normal low mood exists at all.”
I’ll refer back to some points I brought up in an early post on this newsletter, Diagnosis as Self-Understanding & Self-Alienation, about aspects of psychiatric disorders and mental health problems that are important for us to highlight in communication to the public. We should not lose sight of these details and nuances even as we move towards a framing of depression that incorporates functionality and adaptivity:
Scientific research so far suggests that most psychiatric symptoms are continuous and dimensional in nature. There is no natural point at which everyday misery ends and clinical symptoms begin. The boundaries we draw are pragmatic, based on considerations of distress, impairment, maladaptivity, and harm.
Mental health problems are heterogeneous: people differ in how they present, in what factors are involved in their symptoms and impairments, what they need from professionals, and how they respond to treatment.
The “medical” is not at odds with the “psychological.” Psychiatric disorders involve bodily changes and have a detrimental impact on overall health, but they are not meaningless quirks of brain chemistry. It is not enough to say that psychotherapy is an effective treatment. It has to be emphasized that psychiatric symptoms are meaningful and subject to psychological understanding in a way that symptoms in general medicine typically are not.
Low mood and anxiety — like pain and cough — are inherently adaptive. They exist to signal the existence of and respond to a variety of problems and threats that we encounter in our day to day life. Low mood, for instance, may be adaptive in fostering disengagement from commitments to unreachable goals. Depressive and anxiety disorders represent instances when low mood and anxiety have become maladaptive, disabling, or arise in a manner that has is disconnected from their adaptive functions (See Good Reasons for Bad Feelings by Randolph M. Nesse). Given the dimensional nature of psychiatric symptoms and the broad nature of diagnostic categories, the adaptive functions and maladaptive roles can be difficult to distinguish, especially at the milder end of the spectrum. Examining the adaptive and maladaptive nature of psychiatric symptoms offers another way of challenging the perception of mental health problems as meaningless quirks of brain chemistry.
I think your analysis of this study is spot-on, Awais. I think the first thing to say about it is (as you indicate) that the population studied is quite unlike the patients seen by most psychiatrists in clinical settings; i.e., the authors studied "...participants with a history of depression but no extensive treatment history (no prescribed medication from a psychiatry specialist and no history of psychotherapy)...."
Accordingly, it is impossible to tell how many--if any--of the study subjects met criteria for Major Depressive Disorder (MDD). So far as I can tell, the term "depression" as used in the study is clinically ambiguous, if not meaningless.
As you note, having a "low mood" is a useful alerting signal that "something is wrong" and needs correction. But that is a far cry from what some have argued (notably Andrews and colleagues); i.e., that clinically significant depression is in any evolutionary sense "adaptive". (I think the quotes from Nesse make this clear). I looked at the "adaptive rumination hypothesis" (ARH) in detail some years ago and found little empirical support for it. See:
https://www.psychiatrictimes.com/view/major-depression-adaptive-clinical-data-say-no
At the same time, it is not unreasonable--as a didactic strategy--to teach patients that low mood ("depression" in a very superficial, colloquial sense) represents a "...functional signal that alerts the individual that something in life needs more attention (Signal condition)." I think this is almost trivially obvious to most clinicians.
But again--when we are seeing patients with the full panoply of MDD symptoms and signs, who are clearly incapacitated and suffering, it is far from clear that the "signal condition" explanation is either empirically justifiable or clinically useful. In any case, such an "explanation" is clearly not a fact regarding the ultimate nature (ontology) of major depressive disorder.
Regards,
Ron
Ronald W. Pies, MD
I love this one. I see the appeal of seeing depression as functional -- it really does shift the meaning for me. As someone with bipolar, however, it’s been most helpful to me in recent depressions to use more of the disease model. Or, to be more honest, this mild depression. As in: I’m down now, I was up before, but there’s nothing wrong with my life, it’s full of meaningful work and connection, and I’m just going to keep doing those things that are meaningful to me, and I know it’ll shift. I might sleep more during this time and be less social, and maybe I’ll eat too much candy for comfort, or conversely maybe I’ll try to live really well knowing that might bring solace faster, but I know it’s temporary and is just part of how my chemistry works.
If I asked myself, what is this depression telling me, I (and maybe many depressed people) might see it like: something is WRONG with my life, I better fix it, which in a depressed state isn’t an especially effective thought, as we might get stuck on “something is wrong” and be too depressed to try to fix it.