Stories help us heal when our thinking deepens over time

Shekhar Kapur gestures while telling a story, illustrating when it is that stories help us heal

[1]

Stories help us heal when they add understanding

One of the exciting aspects of the Linguistic Inquiry and Word Count program was that we were able to identify word categories that reflected the degree to which people were actively thinking. Two of the cognitive dimensions included insight or self-reflection words (such as think, realize, believe) and another made up of causal words (such as because, effect, rationale).

The people whose health improved the most started out using fairly low rates of cognitive words but increased in their use over the four days of writing. It wasn’t the level of cognitive words that was important but the increase from the first to last day.

In some ways, use of insight and causal words was necessary for people to construct a coherent story of their trauma. On the first writing session, people would often spill out their experience in a disorganized way. However, as they wrote about it day after day, they began to make sense of it. This greater understanding was partially reflected in the ways they used cognitive words. These findings suggested that having a coherent story to explain a painful experience was not necessarily as useful as constructing a coherent story.

We can get stuck, and while we’re stuck it’s no longer true that stories help us heal

This helped to explain a personal observation that had bothered me for years. When the first writing studies were published, my work was often featured in the media. At cocktail parties or informal gatherings, I sometimes found myself to be a trauma magnet. People who knew about my research would gravitate to me in order to tell me all about their horrific life experiences. Many of them also were in very poor physical health. At first, I thought that their talking about their stories would be good for them. However, I’d see the same people at another gathering months later and they would often tell me exactly the same stories and their health would be unchanged.

The word count research revealed the problem. The people telling their traumatic stories were essentially telling the same stories over and over. There was no change to the stories, no growth, no increase in understanding. Repeating the same story in the same way is not unlike ruminative thinking—a classic symptom of depression.

Stories help us heal when they add perspective

There is an important lesson here. If haunted by an emotional upheaval in your life, try writing about it or sharing the experience with others.

However, if you catch yourself telling exactly the same story over and over in order to get past your distress, rethink your strategy. Try writing or talking about your trauma in a completely different way. How would a more detached narrator describe what happened? What other ways of explaining the event might exist?

If you’re successful, research studies suggest that you will sleep better, experience better physical health, and notice yourself feeling happier and less overcome by your upheaval.

Thanks to the Linguistic Inquiry and Word Count program, we found that three aspects of emotional writing predicted improvements in people’s physical and mental health: accentuating the positive parts of an upheaval, acknowledging the negative parts, and constructing a story over the days of writing.

Stories help us heal when we switch between perspectives, and we include first-person

The more people changed in the ways they used function words from writing to writing, the more their health later improved. As we started to focus on different classes of function words, one particular group of culprits stood out as more important than the others: personal pronouns. More specifically, the more people changed in their use of first-person singular pronouns (e.g., I, me, my) compared with other pro- nouns (e.g., we, you, she, they), the better their health later became. The effects were large and held up for study after study.

The writings of those whose health improved showed a high rate of the use of I-words on one occasion and then high rates of the use of other pronouns on the next occasion, and then switching back and forth in subsequent writings.

In other words, healthy people say something about their own thoughts and feelings in one instance and then explore what is happening with other people before writing about themselves again.

The multiple perspectives in stories help us heal, in a way, like therapy helps us heal

This perspective switching is actually quite common in psychotherapy.

If a man visits his therapist and begins repeatedly complaining about his wife’s behavior, what she says, how aloof she is, and so forth, the therapist will likely stop the client after several minutes and say, “You’ve been talking about your wife at length but you haven’t said anything about yourself. How do you feel when this happens?”

Similarly, if another client—a woman in this case—with marital problems sees her therapist and spends most of her time talking about her own thoughts, feelings, and behaviors without ever talking about her spouse, the therapist will probably redirect the conversation in a similar way by asking, “You’ve told me a lot about your own feelings when this happens—how do you think your husband feels about this?”

Perhaps like good therapy, healthy writing may involve looking at a problem from multiple perspectives.[2]


  1. Kapur, Shekhar. “We are the stories we tell ourselves.” com, Mar. 2010, www.ted.com/talks/shekhar_kapur_we_are_the_stories_we_tell_ourselves/transcript. Accessed 14 June 2017.
  2. Pennebaker, James W. The secret life of pronouns. What our words say about us. Bloomsbury Press, 2011, Scribd pp. 23-27.

Cognitive therapy neural networks are increasingly well known

Cognitive therapy neural networks are changed bottom-up in antidepressant therapy and top-down in cognitive therapy

Hypothetical time course of the changes to amygdala and prefrontal function that are associated with antidepressant medication and cognitive therapy, illustrating major cognitive therapy neural networks

Hypothetical time course of the changes to amygdala and prefrontal function that are associated with antidepressant medication and cognitive therapy.

a | During acute depression, amygdala activity is increased (red) and prefrontal activity is decreased (blue) relative to activity in these regions in healthy individuals.

b | Cognitive therapy (CT) effectively exercises the prefrontal cortex (PFC), yielding increased inhibitory function of this region.

c | Antidepressant medication (ADM) targets amygdala function more directly, decreasing its activity.

d | After ADM or CT, amygdala function is decreased and prefrontal function is increased. The double-headed arrow between the amygdala and the PFC represents the bidirectional homeostatic influences that are believed to operate healthy individuals.[1]

Cognitive therapy neural networks –
– work together (along the black lines) to produce depressed symptoms
– feed back the results (along the gray line) to generate depressed symptoms in the future

Information processing in the cognitive model of depression illustrates cognitive therapy neural networks, showing feedback loops

Information processing in the cognitive model of depression.

  • Activation of depressive self-referential schemas by environmental triggers in a vulnerable individual is both the initial and penultimate element of the cognitive model.
  • The initial activation of a schema triggers biased attention, biased processing and biased memory for emotional internal or external stimuli.
  • As a result, incoming information is filtered so that schema-consistent elements in the environment are over-represented.
  • The resulting presence of depressive symptoms then reinforces the self-referential schema (shown by a grey arrow), which further strengthens the individual’s belief in its depressive elements.
  • This sequence triggers the onset and then maintenance of depressive symptoms.[2]

Untreated cognitive therapy neural networks take negative schema information and fan it out, and add in overgeneral negative information

Cognitive functioning in a healthy individual vs. in a depressed individual illustrates functionality in major cognitive therapy neural networks

Cognitive functioning in a healthy (a) or depressed (b) individual.

  • In a depressed individual, a negative self-schema and an over-general mode of processing concur to automatically prime and activate information that is congruent with the negative self-schema, via a cognitive interlock (resulting in rumination), biased memory and attention.
  • In a healthy individual, a concrete mode of processing counteracts these automatic activations.

Cognitive therapy neural networks information flow (in the diagrams above) maps directly to neural regions (in the pictures below)

Brain networks involved in various cognitive functions of cognitive therapy neural networks

Brain networks involved in
(a) self-referential processes and rumination,
(b) cognitive interlock and mood congruent processing,
(c) episodic buffer,
(d) attention bias,
(e) memory bias,
(f) overgeneral processing.

dmPC: dorsomedial prefrontal cortex,
vmPFC: ventromedial prefrontal cortex,
mPFC: medial prefrontal cortex,
iPFC: inferior prefrontal cortex,
mOFC: medial orbitofrontal cortex,
aOFC: anterior orbitofrontal cortex,
dlPFC: dorsolateral prefrontal cortex,
aITC: anterior inferotemporal cortex,
STG: superior temporal gyrus,
AnG: angular gyrus,
Ins: insula,
ACC: anterior cingulate cortex,
PCC: posterior cingulate cortex,
PCun: precuneus,
Rsp: retrosplenial cortex,
dmTh: dorsomedial thalamus,
HPC: hippocampus,
Amy: amygdala,
Hab: habenula,
Acc: nucleus accumbens,
Cd: caudate,
Pu: putamen,
Re: nucleus reuniens,
DG dentate gyrus of the hippocampus.[3]


  1. DeRubeis, Robert J., Greg J. Siegle, and Steven D. Hollon. “Cognitive therapy versus medication for depression: treatment outcomes and neural mechanisms.” Nature Reviews Neuroscience 9.10 (2008): 788-796.
  2. Disner, Seth G., et al. “Neural mechanisms of the cognitive model of depression.” Nature Reviews Neuroscience 12.8 (2011): 467-477.
  3. Belzung, Catherine, Paul Willner, and Pierre Philippot. “Depression: from psychopathology to pathophysiology.” Current opinion in neurobiology 30 (2015): 24-30.

Early psychiatric diagnosis is rare, but possible, and kind

Early psychiatric diagnosis is all too rare, but it’s possible, and it’s kind

Many disorders begin early in life, and early psychiatric diagnosis is possible [1]

Early psychiatric diagnosis is all too rare

Median delays among cases eventually making contact ranged from 3.0 to 30.0 years for anxiety disorders, from 1.0 to 14.0 years for mood disorders, and from 6.0 to 18.0 years for substance use disorders.

…early-onset disorders were associated with lower probabilities of initial treatment contact in most countries. One explanation for this finding may be that minors need the help of parents or other adults to seek treatment, and recognition is often low among these adults unless symptoms are severe… In addition, child and adolescent- onset mental disorders may be associated with normalization of symptoms or development of coping strategies (e.g., social withdrawal in social phobias) that interfere with help-seeking later in life.

…our earlier analyses of the U.S. data revealed that even those with severe and impairing disorders have substantial delays in initial treatment contact…[2]

Young people are less likely to seek help if they:

  • are experiencing suicidal thoughts and depressive symptoms;
  • hold negative attitudes toward seeking help or have had negative past experiences with sources of help; or
  • hold beliefs that they should be able to sort out their own mental health problems on their own.[3]

Early psychiatric diagnosis is possible

Initial treatment contacts appear to be fastest for mood disorders, perhaps because these disorders have been targeted in some countries by educational campaigns, primary care quality improvement programs, and treatment advances… On the other hand, the longer delays for anxiety disorders may be due to the earlier age of onset of some conditions (e.g., phobias), fewer associated impairments, and even fear of providers or treatments involving social interactions (e.g., talking therapies, group settings, waiting rooms)…

Women have been shown in prior research to be faster than men at translating nonspecific feelings of distress into conscious recognition that they have emotional problems, perhaps explaining the significantly higher rates of initial treatment contact by women in some countries…

More recent cohorts were also significantly more likely to make eventual treatment contact, perhaps suggesting a positive outcome of programs recently attempted in some countries to destigmatize and increase awareness of mental illness, of screening and outreach initiatives, of the introduction and direct-to-consumer promotion of new treatments, and of expansion of insurance programs…[2]

Young people are more inclined to seek help for mental health problems if they:

  • have some knowledge about mental health issues and sources of help;
  • feel emotionally competent to express their feelings; and
  • have established and trusted relationships with potential help providers.[3]

Early psychiatric diagnosis is kind

Lifetime Prevalence of Disorders

Any anxiety disorder
Any mood disorder
Any impulse-control disorder
Any substance use disorder
Any disorder
28.8%
20.8%
24.8%
14.6%
46.4%

[4]

Depression is a major human blight. Globally, it is responsible for more ‘years lost’ to disability than any other condition. This is largely because so many people suffer from it — some 350 million, according to the World Health Organization — and the fact that it lasts for many years. (When ranked by disability and death combined, depression comes ninth behind prolific killers such as heart disease, stroke and HIV.) [5]

…preclinical, epidemiologic, and trial data… suggest that even milder disorders, if left untreated, lead to greater severity, additional psychiatric comorbidity, and negative social and occupational functioning…[2]


  1. Merikangas, Kathleen Ries, et al. “Lifetime prevalence of mental disorders in US adolescents: results from the National Comorbidity Survey Replication–Adolescent Supplement (NCS-A).” Journal of the American Academy of Child & Adolescent Psychiatry 49.10 (2010): 980-989.
  2. Wang, P. S., et al. “Delay and failure in treatment seeking after first onset of mental disorders in the World Health Organization’s World Mental Health Survey Initiative.” World psychiatry: official journal of the World Psychiatric Association (WPA) 6.3 (2007): 177-185.
  3. Rickwood, Debra J., Frank P. Deane, and Coralie J. Wilson. “When and how do young people seek professional help for mental health problems.” Med J Aust 187.7 Suppl (2007): S35-S39.
  4. Kessler, Ronald C., et al. “Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication.” Archives of general psychiatry 62.6 (2005): 593-602.
  5. Smith, Kerri. “Mental health: a world of depression.” Nature 515.7526 (2014): 181.

Cognitive therapy gains can be sudden and large

Cognitive therapy gains can be sudden and can be early in therapy.

Cognitive therapy gains can be sudden, and can spiral upward

Psychotherapy does not always follow a linear path.

Most… research is based on the assumption that treatment progress in psychotherapy is linear, or log-linear, and follows some form of regular dose-response relationship… However, this assumption regarding the macro, or average level of change, does not necessarily hold for a finer grained analysis of individual progress…

The prevalence of sudden gains found in several studies from different research groups varies between 17% and 50%…

…sudden gains are a phenomenon of cognitive behavioral therapies (CBT) and result from CBT-specific techniques. …substantial cognitive changes could be observed in the therapy session preceding the sudden gains. Sudden gains were followed by a better therapeutic alliance and more cognitive changes in the session after the sudden gain. Thus, the authors postulated an upward spiral, i.e., cognitive changes during the pregain sessions foster the therapeutic alliance and eventually result in additional cognitive changes…

In this paper the frequency of sudden gains as well as sudden losses will be investigated in a large naturalistic outpatient sample (n=1500) with repeated measurements of session progress.

Sudden losses are less frequent, and are more-or-less random

…23.4%… of the patients in the sample experienced at least one sudden gain…

…4.5%… of those experienced a sudden gain and a sudden loss…

…18.9%… had only sudden gains…

…5.47%… experienced only sudden losses.

In contrast to sudden gains, sudden losses occur over the course of treatment without a typical peak of occurrence.

Cognitive therapy gains are greater for people who are hurting more

…those patients who experienced no sudden shifts at all and followed a more linear trajectory had the shortest therapies. At intake patients with no sudden shifts tended to be significantly less disturbed on average… than the three groups with sudden shifts… … post-hoc tests revealed that patients with no sudden shifts were less impaired… compared to sudden gain patients…

…patients with both sudden gains and sudden losses stayed in treatment longer than those in the other groups.

Patients with sudden gains… did not rate the therapeutic relationship significantly higher on average than patients with sudden losses… Results further confirm previous findings that a large amount (about 42%) of sudden gains tend to take place early in therapy and they are part of the phenomenon of early change… But the phenomena also occur later in treatment (about 58%). …we found shorter treatments for patients experiencing sudden gains early in treatment. Patients with early sudden gains showed the highest effect sizes… at the end of treatment.[1]


  1. Lutz, Wolfgang, et al. “The ups and downs of psychotherapy: Sudden gains and sudden losses identified with session reports.” Psychotherapy Research 23.1 (2013): 14-24.

Psychiatric medication development restrained by insurance regulation and FDA

Restraint of patient in stretcher illustrates restraint of psychiatric medication development by insurance regulation and FDA
[1]

Psychiatric medication development declined steeply after the 1950s and 1960s

…there has been a steep decline in the development of new medication classes. Instead of new molecular entities, slight molecular modifications producing ‘‘me-too’’ drugs attempted to garner market share.

The current deficit in novel agents contrasts sharply with the 1950s. Then, there was a sudden efflorescence of potent psychiatric therapeutic agents. The pace of discovery of entirely new classes of psychotropic drugs was dizzying. These included lithium, lysergic acid diethylamide (LSD), chlorpromazine, iproniazid, reserpine, imipramine, chlordiazepoxide, haloperidol, and clozapine.

These discoveries resulted from chance observations of unexpected clinical benefits rather than being derived from basic neuroscience. All major classes were serendipitously discovered by 1969. For instance, chlorpromazine was a pre-surgical antihistamine sedative whose antipsychotic properties were completely unsuspected. Imipramine was developed as a chlorpromazine ‘‘me-too,’’ but turned out to be an antidepressant. Conversely, clozapine was a potential antidepressant, but turned out to be an antipsychotic with remarkably low extrapyramidal toxicity and superior efficacy.

What stymied generative serendipity over the next 40 years? A number of elements came together.

  • The most important factor may have been the drastic change in medical practice economics. Hospital-based academic research was supported from clinical income. That freed up clinicians for therapeutic explorations. However, ‘‘managed care’’ declared this irrelevant to patient care and markedly shortened hospital stays.
  • Second, often patients were discharged before the effects of a new therapeutic regimen became clear.
  • Third, industry became concerned with immediate return on their investments, which were limited by extensive regulations, liability concerns, and exhaustive preclinical animal model testing.
  • Fourth, the growth of clinical research organizations (CROs) diverted industrial support from investigator-initiated academic research to relatively inexpensive, pre-set industrial protocols.

Psychiatric medication development trials could be much better for patients both in trials and in treatment

The standard randomized parallel-group design leaves a crucial causal ambiguity. If 60% of those treated with medication have substantial improvements, while only 30% of those on placebo improve (assuming statistical significance), then in about half of those who seemed to have a direct drug benefit, the drug was actually not required. Identifying individuals who actually require medication to improve and maintain their gains remains obscure. Therefore, attempts to determine how a drug brought about its benefits by studying those who improved during drug treatment are handicapped by study of a causally heterogeneous mixture.

…an alternative design would be to initially and openly treat all patients with the putative medication, titrating for the individual’s optimal dose, until it is clear if the patient was not a treatment responder. These subjects would leave the trial. Apparent responders would be maintained on medication for a period, but then randomly, and in double-blind fashion, switched to placebo or remain on medication. All patients would be followed independently and closely, blind to treatment status, for defined signs of worsening. At a predetermined level of modest worsening, double-blind medication retreatment would start. A worsening rate higher in the placebo-substituted group than in the medication-maintained group would provide clear evidence of medication efficacy. Those individuals who worsened on slow placebo substitution and then improved on medication re-treatment are very likely specific drug responders. Those who switched to placebo and nevertheless continued to do well would be far less likely to be specific medication responders.

To summarize, this design would determine individuals very likely to be medication-specific responders, very likely non-specific responders, and non-responders.

Other practical benefits are that all patients initially receive active treatment. This fosters recruitment, since many patients will not risk being initially assigned to placebo. In addition, patients will learn if medication is necessary for them to remit or that they have sufficient resources.

In fact, academic investigators have successfully used this design.


  1. Weingart, Scott. “Podcast 060 – On Human Bondage and the Art of the Chemical Takedown.” org, 13 Nov. 2011, emcrit.org/podcasts/human-bondage-chemical-takedown/. Accessed 25 Feb. 2017.
  2. Klein, Donald F., and Ira D. Glick. “Industry withdrawal from psychiatric medication development.” Revista Brasileira de Psiquiatria 36.3 (2014): 259-261.

Thoughts determine perceptions, feelings, and actions

Thoughts bias memories and attention, and are crucial to psychological disorders.

A 19-year-old college junior, Louis, learned that his girlfriend had committed suicide…

One year after… Louis… feels “on-edge” and “down” most of the time… stopped playing sports… no longer spends much time with his friends who knew his deceased girlfriend… feels tired all the time… sleeps 10 to 12 hours a day… has trouble focusing in school… “constantly snaps” when he’s around people… frequently has upsetting dreams… drinks six to eight alcoholic drinks each night to fall asleep.

… when Louis was 7… his younger sister was killed… he was supposed to be in the same car… it took him a long time to deal with her death.

Louis… feels the worst in the evening… alone… “I’m never going to be happy again,” “There is no point getting close to people,” and “I should have known she was going to kill herself. ”

The clinician noted… biased expectancies…. (… “I’m never going to be happy again”), overgeneralization (… “There is no point getting close to people”), and emotional reasoning (… “I should have known she was going to kill herself”)…

Louis and the clinician collaboratively identified three main goals:
(a) identify, examine, and modify inaccurate or unhelpful thoughts Louis has about his future and others;
(b) examine his thoughts about his perceived role in his girlfriend’s suicide; and
(c) increase his level of social interaction.

With practice, Louis was able to independently modify his thoughts so that they were more accurate and helpful.

The clinician dedicated a significant amount of time to helping Louis examine the evidence for his thoughts… that he should have known his girlfriend was suicidal… and adopt a… thought that his girlfriend’s desire to commit suicide was something he could not have predicted.

Louis agreed to slowly increase his social activity… evaluate his belief that it would be too unbearable to see his friends who had known his girlfriend… Louis reported feeling grateful that he had reconnected with some of his old friends.

Louis… independently designed a behavioral experiment to test his thought that it will take him “forever to fall asleep without drinking.”[1]


  1. Beck, Aaron T., and Emily AP Haigh. “Advances in cognitive theory and therapy: The generic cognitive model.Annual review of clinical psychology 10 (2014): 1-24.

Psychiatry on East Coast and West Coast lagged behind Midwest

Lying on psychiatry couch, patient reads that doctor's diploma is from Institute of Professional Help.
[1]

…by 1960 psychoanalytically oriented psychiatry had become the prevailing model for understanding all mental and some physical illnesses.

…the whole thrust of psychoanalytic psychiatry at the Massachusetts Mental Health Center, and perhaps at Harvard Medical School in general, was not simply to develop better psychiatrists but to develop better therapists—therapists prepared to understand and empathize with the patients’ existential problems.

…a lack of critical questioning seemed to be widespread in Boston and at many other institutions on the east and west coasts of the country.  There were… no grand rounds at the Massachusetts Mental Health Center. No outside speakers were invited to address the house officers on a regular basis to discuss current clinical or scientific issues.

…in 1965… several of us tried to recruit a psychiatrist in the Boston area to speak about the genetic basis of mental illness. We could find no one; not a single psychiatrist in all of Boston was concerned with or even had thought seriously about that issue…

…new and effective treatments, in the form of psychopharmacological drugs, began to be available. Initially, a number of supervisors discouraged us from using them, believing that they were designed more to aid our anxiety than that of the patients.

…scholarly concerns were not lacking at Washington University under Eli Robins, at a number of other centers in the Midwest, or at Johns Hopkins University under Seymour Kety…

By the mid-1970s… psychiatry… had effective treatments for the major mental illnesses and something that began to approach a practical cure for two of the three most devastating diseases: depression and manic-depressive illness.

…led first by Eli Robins at Washington University and then by Robert Spitzer at Columbia University’s New York State Psychiatric Institute, new clinically validated and objective criteria were established for diagnosing mental illness.

…Seymour Kety used his leadership position at NIH to spark a renewed interest in the biology of mental illness and specifically in the genetics of schizophrenia and depression.[2]


  1. Stevens, Mick. “man lying on psychiatrist’s couch looks up at diploma on wall: ‘Institute… – Cartoon.” CondeNastStore, www.condenaststore.com/-sp/man-lying-on-psychiatrist-s-couch-looks-up-at-diploma-on-wall-Institute-Cartoon-Prints_i8640495_.htm. Accessed on 12 Nov. 2016.
  2. Kandel, Eric R. “Biology and the future of psychoanalysis: a new intellectual framework for psychiatry revisited.” American journal of Psychiatry 156.4 (1999): 505-524.