Tag Archives: depression

When the Yellow Grows into Gold and Happy Breaks Out

Lower Grove Creek 7 14 17This morning the clock said 3:51am. My lungs felt refreshed. Then a memory from last night bubbled up. You know how they do.

Rita and I discovered mold in our garden. It was yellow and green and it shared its spores with my lungs before we recognized or best option: retreat inside to formulate our battle plan in response  to the attack of the multicolored mold.

Google was waiting. All the postings were about White mold or Black mold, or even yellow dog-vomit mold. Nothing fit our mold. I read with great and trepidiacal interest of a U.K. man who died from inhaling compost mold; my lungs were burning. Not good.

But sleep came.

Then 3:51am came.

And then the thoughts came.

At 3:52am it seemed odd that I could hear my pulse in my ear on the pillow. It seemed fast. That U.K. man had a rapid pulse. I could either choose to lift my head and take my pulse and while waiting for the digital clock to move to the next minute, or I could look at my fit bit. But my fit bit is charging. But I decide, anyway, to roll over and grab it and attach it to my wrist and look at the pulse rate. It flashes, 113. Not good. I check again, 112. Not good. Not normal. I compulsively check again, 111. The fit bit is probably still adjusting, now it’s 109. Stop checking, the voice in my head says. Let it be. Let it settle. Thirty seconds later, it’s 55. I am normal again.

At 3:54am, I find another troubling thought. Today is July 14, 2017. My Theories text revision is due in 31 days. I have five more chapters to revise. That’s six days per chapter. Plus references. Plus table of contents and preface and . . . . Not good. I’m a bad author.

At 4:12am, I’m up, turning on the computer. I’m a bad author and a bad husband and a bad father and a bad friend. All I do is write meaningless drivel that maybe 12 people a year will read and then immediately forget. Forgettable, I am. Even my own students can’t answer my pop theories quiz questions when they drop by my office. I wonder why they don’t stop in so much anymore.

Good thing I’m revising CBT today. God and Albert Ellis know, I sure as Hell need it.

One of today’s content areas is called, Thinking in Shades of Gray. It’s a description of a cognitive technique to help people get out of destructive, irrational, and maladaptive black-white (aka polarized) thinking. It’s boring. Of course it’s boring. Shades of gray? It’s a technique to help with depressive thoughts. I can hear the Albert Ellis voice in my head. WTF? You work with depressed people and you teach them how to think in shades of gray. What the Holy Hell are YOU thinking?

Later this morning, as I ride through Lower Grove Creek with yellow flowers and the Beartooth Mountains looming, I stop for a photo. There are no cars, no deer, and not even a trace of fungal spores. Just me and my breath and my bike and the yellow flowers and shades of gray, black, and white rising above. Why are there no colors in the shades of gray activity? There’s more to our thinking (and our client’s) thinking than black, white, and gray. Today, with the wind in my face and Tippet Rise to my starboard, I want to be an art therapist. “Let’s put a little yellow there,” I say. And the yellow grows into gold and happy breaks out.

But sooner or later, you and I know. We. Know. The yellow will catch dust and lose its sparkle and turn to mold, until a future morning at 3:51am, when a red seed of awareness gets planted among the anxiety bushes and purple flowers bloom, replacing the moldy browned-up yellow, and then we will remember. We have been here before. And it was wondrous and terrible and everything in between.

At that point, it’s not a bad idea to find your fit bit, take your pulse, and embrace the ever disintegrating now that is morning. You have your next 31 days and I have mine. Let’s meet somewhere in the middle and celebrate the next disintegrating now with all the passion and monotony we can muster. You know we can. We’ve done it before.

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Teenagers and Depression

Every year, every month, and every day, many teenagers complain of feeling down, depressed, or sad and some of them just act with immense irritability. You probably knew that. But, how many teens are experiencing symptoms of depression?

Estimates are wide ranging. The National Institute of Mental Health reported that approximately 12.5% of U.S. youth from 12-17 years-old experienced at least one episode of major depressive disorder. That’s a huge number of American teenagers (about 3 million).

Add to that the many more teenagers who complain of feeling depressed or down, but who don’t officially meet the diagnostic criteria for clinical depression. By some estimates, that brings the number to close to 50% of teens who are consistently bothered by sad, bad, and irritable feelings.

If you’re a parent of a teen, it’s easy to feel concerned about your teenager’s emotional health.

You may have questions like the following

  • Is my teenager clinically depressed or just going through the normal emotional ups and downs of adolescence?
  • Should I take my son or daughter to a mental health professional?
  • What about medications? Are any of the antidepressants safe and effective for teenagers?

The answers to these questions are complex. It’s hard to tell whether a teenager is in a normal emotional angst or experiencing something more insidious and chronic. And, the answer to the question about whether antidepressant medications are safe and effective with teens is a solid: “Maybe, but maybe not.”

In the latest Practically Perfect Parenting Podcast, Dr. Sara and I take on the serious topic of teenage depression. There are no laughs or giggles, but you’ll get to hear Sara ask me many questions about teen depression, and you’ll get to hear me try to answer them, which is sort of funny. You’ll hear the answer to my favorite trivia question: “What percent of children “recovered” from their depressive symptoms in the first-ever double-blind, placebo-controlled study of antidepressant medications?” And yes, once again, you’ll hear Sara find a way to mention sex during our podcast.

If you have teenagers yourself, or you know someone who has teenagers, or you’re a helping professional who works with teenagers, this podcast may be of interest or helpful to you. Check it out here on iTunes: https://itunes.apple.com/us/podcast/practically-perfect-parenting-podcast/id1170841304?mt=2

If you listen and like it, please share it, and then do us one little favor—rate the podcast on iTunes. That way Sara and I can keep climbing up the charts in reality—rather than just in our imaginations.

JSF Dance Party

Post-Partum (now Peripartum) Depression: What you should know . . . and some resources to help you know it

Note: This post is provided for individuals interested in learning more about post-partum or peripartum depression. It’s also a supplement for the recent Practically Perfect Parenting Podcast on “Post-Partum Depression.” You can listen to the podcast on iTunes: https://itunes.apple.com/us/podcast/practically-perfect-parenting/id1170841304?mt=2

stillwater-winter-view

For the first time ever on planet Earth, the latest version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) includes the diagnosis of Peripartum Depression. Although I’m not usually a fan of labeling or big psychiatry, this is generally good news.

So, why is Peripartum Depression good news?

The truth is that many pregnant women and new moms experience depressive symptoms related to pregnancy and childbirth. These symptoms are beyond the normal and transient “baby blues.” Depressive symptoms can be anywhere from mild to severe and, combined with the rigors of pregnancy, childbirth, and parenting a newborn, these symptoms become very difficult to shake.

But the most important point is that Peripartum Depression is a problem that has been flying under the RADAR for a very long time.

Approximately 20% of pregnant women struggle with depressive symptoms. The official 12-15% estimates of post-partum (after birth) depression in women are thought to be an underestimate. What makes these numbers even worse is the fact that society views childbirth as a dramatically positive life event. This makes it all-the-more difficult for most pregnant women and new moms to speak openly about their emotional pain and misery. And, as you probably know, when people feel they shouldn’t talk about their emotional pain, it makes getting the help they deserve and recovering from depression even more difficult.

Jane Honikman, a post-partum depression survivor and founder of Postpartum Support International has three universal messages for all couples and families. She says:

  • You’re not alone
  • It’s not your fault
  • You will be well

Keep in mind that although peripartum depression is thought to have strong biological roots, the first-line treatment of choice is psychotherapy. This is because many new moms are reluctant to take antidepressant medications, but also because psychotherapy is effective in directly addressing the social and contextual factors, as well as the physiological symptoms. Additionally, as Ms. Honikman emphasizes, support groups for post-partum depression can be transformative.

Below, I’m including links and resources related to peripartum or post-partum depression.

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A very helpful informational post by Dr. Nicola Gray: http://cognitive-psychiatry.com/peripartum-depression/

Books by Jane Honikman can be found at this Amazon link. Her books include: I’m Listening: A Guide to Supporting Postpartum Families.  https://www.amazon.com/s/ref=dp_byline_sr_book_1?ie=UTF8&text=Jane+I.+Honikman&search-alias=books&field-author=Jane+I.+Honikman&sort=relevancerank

Although it’s true that peripartum depression can be debilitating, it’s also true that it can be a source of personal growth. Dr. Walker Karraa shares optimistic stories of post-partum related trauma and growth in her book:

https://www.amazon.com/Walker-Karraa/e/B00QTWH9PW/ref=dp_byline_cont_book_1

 

A Brief History and Analysis of Antidepressant Medication Treatment for Youth with Depression Diagnoses

The popular press intermittently acts surprised that antidepressant medications actually have little scientific evidence supporting their efficacy. It’s old news, but it’s still important news and I’m glad for the recent reports. See: http://www.everydayhealth.com/news/did-studies-lack-key-data-on-link-between-antidepressants-youth-suicides/

Rita and I published an article about this in 1996. Below, I’ve pasted a pre-print excerpt from an article I published with Duncan Campbell in 2009 in the Journal of Contemporary Psychotherapy. It includes a brief summary of antidepressant medication research through 2008 or so. Check it out:

A Brief History and Analysis of Antidepressant Medication Treatment for Youth

Medication treatment for depressed youth has evolved over three relatively distinct periods. First, prior to 1987, small exploratory studies examined tricyclic antidepressant (TCAs) efficacy with young patients diagnosed with major depressive disorder (MDD). Second, from 1987-1994 there were a number of randomized, controlled trials (RCTs) of TCA efficacy; these efforts often employed double-blind procedures and inactive placebo controls. Third, since 1997, research efforts have primarily focused on evaluating selective serotonin reuptake inhibitor (SSRI) efficacy with RCTs.

Early Research: Pre-1987

In the early 1980s, psychiatric and pharmaceutical researchers began testing TCAs with youth. Early conclusions about the safety and efficacy of TCAs were generally optimistic (Klein, Jacobs, & Reinecke, 2007). This is a tendency that has been identified in the literature and it may be due to methodological limitations, confirmation bias or an allegiance to the medical model, or financial incentives associated with the pharmaceutical industry (Klein et al., 2007; Luborsky et al., 1999). For example, on the basis of existing studies and their very small double-blind trial with nine prepubertal children, Kashani and colleagues (1984) concluded that amitrityline was possibly efficacious for treating depression in children. Interestingly, the authors’ tentative claim was made despite the fact that no statistically significant effect was observed for amitriptyline and even though 11% of their sample “developed a hypomanic reaction while on the protocol” (p. 350).

RCTs with TCAs

From 1965 to 1994 there were 13 published RCTs evaluating TCA efficacy. Most of these studies were conducted from 1987 to 1994 (Fisher & Fisher, 1996; Sommers-Flanagan & Sommers-Flanagan, 1996). These RCTs confirmed the premature hopefulness of Kashani and colleagues’ early claims. Indeed, no study ever published showed that TCAs outperformed placebo in the treatment of youth depression (Hazell, 2000). More importantly, it is currently recognized that TCAs possess dangerous side effect profiles, while offering no demonstrable advantage over placebo in the treatment of youth depression (Hazell, 2000; Pellegrino, 1996).

In the mid-1990s there was considerable speculation about why TCAs were ineffective for treating youth. The primary hypothesis for involved the fact that children appear to have immature adrenergic synaptic systems. This possibility precipitated a more systematic inquiry of serotonergic medications.

RCTs with SSRIs

Using PsychInfo and PubMed searches combined with cross-referencing, we identified 12 published RCTs evaluating SSRI efficacy with 11 of these studies from 1997 to 2007. In total, these studies compared 1,223 SSRI treated patients to a similar number of placebo controls. On the basis of the researchers’ own efficacy criteria, six RCTs observed outcomes favoring medication over placebo, and six observed nonsignificant differences. Researchers described efficacious outcomes for fluoxetine (3 of 4 studies; G. J. Emslie et al., 2002; G. J. Emslie et al., 1997; Simeon, Dinicola, Ferguson, & Copping, 1990; Treatment for Adolescents With Depression Study (TADS) Team, US, 2004), paroxetine (1 of 3; Berard, Fong, Carpenter, Thomason, & Wilkinson, 2006; G. Emslie et al., 2006; M. B. Keller, 2001), sertraline (1 of 1; K. D. Wagner et al., 2003), and citalopram (1 of 1; K. D. Wagner et al., 2004). Neither of two studies observed efficacy for venlafaxine (G. J. Emslie, Findling, Yeung, Kunz, & Li, 2007; Mandoki, Tapia, Tapia, & Sumner, 1997), and the single escitalopram study returned negative results (K. D. Wagner, Jonas, Findling, Ventura, & Saikali, 2006).

Methodological Issues

Assessing a medication’s efficacy is a complex process with challenges that are difficult to address. We believe, however, that the six aforementioned RCTs favoring SSRIs suffered from methodological problems and issues that temper their positive conclusions. For example, (a) two of the three fluoxetine studies were characterized by unusually high and disproportionate discontinuation rates in the placebo conditions; (b) 11 of the 12 studies based their conclusions exclusively on a structured psychiatric interview; (c) despite simultaneous examination of several outcomes, no study used statistical adjustments for multiple comparisons; (d) placebo washouts and statistical approaches that advantage medications were nearly always employed (R. P. Greenberg, 2001); (e) no procedures were used to evaluate double-blind integrity (R. P. Greenberg & Fisher, 1997); and (f) despite documented inter-racial differences in medication metabolism and responsiveness, conclusions were generalized to all youth and inappropriately failed to account for racial/cultural specificity (Lin, Poland, & Nakasaki, 1993).

Side Effects and Adverse Events

In RCTs and other studies, patients treated with SSRIs experienced substantially more disturbing side effects and adverse events than those not treated with SSRIs. For example, in one of the most rigorous studies to date, the Treatment of Adolescents with Depression Study (TADS), 11.9% of the fluoxetine group evidenced harm-related adverse events (compared to 4.5% in the Cognitive Behavioral Therapy [CBT] group) and 21% experienced psychiatric adverse events (1% in the CBT group). Further, as the authors noted, “…suicidal crises and nonsuicidal self-harming behaviors were not uncommon and, with the caveat that the numbers were so small as to make statistical comparisons suspect, seemed possibly to be associated with fluoxetine treatment” (March et al., 2006; The TADS Team, 2007 p. 818; Treatment for Adolescents With Depression Study (TADS) Team, US, 2004).

Findings like these necessitate critical inspection of study results and should attenuate positive conclusions about medication safety. For example, Emslie et al.’s (1997) study of youth depression was the first ever to demonstrate superior outcome for an SSRI. In addition to the study’s numerous methodological problems, the authors noted that 6.3% of the fluoxetine patients (n = 3) developed manic symptoms. Although this percentage may sound small, extrapolation suggests that 6,250 of every 100,000 fluoxetine-treated youth might develop manic symptoms. Ultimately, despite data based solely on psychiatrist ratings and a placebo condition discontinuation rate approaching 46%, the authors concluded that fluoxetine “…is safe and effective in children and adolescents with MDD” (p. 1037). Moreover, the authors’ intent-to-treat analysis possibly conferred an advantage for the active drug group. In our opinion, this methodological problem and the mania data make it premature to conclude that fluoxetine is safe and effective in children.

Similarly, despite striking data that appear to demonstrate otherwise, authors of the single positive paroxetine study concluded that paroxetine is “safe and effective” for young patients (M. B. Keller et al., 2001). However, in their results section, the research team reported serious adverse effects, “…in 11 patients in the paroxetine group, 5 in the imipramine group, and 2 in the placebo group” (p. 769). More specifically, five adverse effects in the paroxetine group involved suicidal ideation or gestures. Despite these data, the researchers presented their results as evidence for the efficacy and safety of paroxetine treatment for adolescent depression. Because 12% of the paroxetine-treated adolescents experienced at least one adverse event and because 6% of these patients manifested increased suicidality or suicidal gestures (compared with zero in the imipramine and placebo groups), we believe the authors’ conclusion departs from the data in a significant and concerning way.
Shortly after publication of the Keller et al. (2001) study, regulatory agencies in France, Canada, and Great Britain restricted SSRI use among youth. In September of 2004, an expert panel of the U.S. Food and Drug Administration (FDA) followed suit and voted 25-0 in support of an SSRI-suicide link. Later, the panel voted 15-8 in favor of a ‘black box warning’ on SSRI medication labels. The warning states:

“Antidepressants increased the risk compared to placebo of suicidal thinking and behavior (suicidality) in children, adolescents, and young adults in short-term studies of Major Depressive Disorder (MDD) and other psychiatric disorders. Patients of all ages who are started on antidepressant therapy should be monitored appropriately and observed closely for clinical worsening, suicidality, or unusual changes in behavior. Families and caregivers should be advised of the need for close observation and communication with the prescriber.”

In 2006, the FDA extended its SSRI suicidality warning to adult patients aged 18-24 years (United States Food and Drug Administration, 2007).

Combination Medication and Psychotherapy Treatments

Many view the 2004 TADs study as a ‘state of the science’ comparison of SSRI medication (fluoxetine; FLU) with CBT and their combination (FLU + CBT). To date, it represents the largest placebo-controlled study comparing mono-therapy (FLU or CBT alone) with combination therapy. Not surprisingly, the TADs study has generated numerous publications and much controversy (Antonuccio & Burns, 2004; Diller, 2005; Weisz, McCarty, & Valeri, 2006).

To summarize, initial 12-week outcomes showed that 71% of FLU + CBT patients evidenced “much” or “very much” improvement on the on the CGI-Improvement item, a clinician-based assessment. FLU alone produced a similar outcome (60.6%), whereas the CBT alone (43.2) outcome did not differ significantly from placebo (34.8%). Based on these outcomes, several CBT researchers and practitioners criticized the specific CBT delivered to TADs participants. Brent (2006), for example, described TADS psychotherapy as a relatively “dense treatment, with multiple CBT strategies, each delivered at a relatively low dose” (p. 1463). In comparing the initial TADs CBT outcomes with previous and subsequent CBT studies, Weisz et al. (2006) suggested that the TADs CBT was weaker than most CBT interventions, for various reasons:

“the CBT ES (effect size) generated in TADS is not characteristic of most CBT or psychotherapy effects on youth depression; 20 of the 23 other CBT programs. . . showed larger ES than the TADS version of CBT, and the mean ES value across the non-TADS CBT programs. . . was 0.48, markedly higher than the -0.07 ES associated with the TADS CBT intervention” (p. 147).

To complicate issues further, follow-up data suggest that the TADs CBT evidenced delayed effectiveness, as it eventually “caught up” with FLU and CBT+FLU (The TADS Team, 2007). At week 18, for example, there were no statistically significant differences between CBT and FLU, and by week 36 there were no statistical differences among the three groups (CBT, FLU, and CBT + FLU) on primary outcome measures. Although the interventions including FLU might evidence a speedier antidepressant effect, these results suggest that CBT is equally effective over time.

The depression treatment literature frequently includes recommendations for combined interventions in order to maximize outcomes (Watanabe, Hunot, Omori, Churchill, & Furukawa, 2007). Unfortunately, however, little data exists to support these recommendations. In addition to TADs, the only other published RCT comparison of mono- and combination treatments for depressed adolescents reported partial remission rates of 71% for CBT, 33% for sertraline, and 47% for combination (Melvin et al., 2006). Medication group patients also evidenced significantly more adverse events and side effects. Although the researchers attributed the delayed response in the combination group to sertraline, they concluded with the puzzling statement that “CBT and sertraline are equally recommended for the treatment for adolescents with depression, each demonstrating an equivalent response” (Melvin et al., 2006 p. 1160).

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Reformulating Clinical Depression: The Social-Psycho-Bio Model

At a 2007 Mind and Life Conference at Emory University, I had the privilege of watching and listening as Charles Nemeroff, M.D., presented a professional paper to His Holiness the Dalai Lama. [As my older daughter would likely say, Dr. Nemeroff is a very fancy biological psychiatrist.] Nemeroff noted, with some authority, that we now know that one-third of all depressive disorders are genetically-based and two-thirds are environmentally-based. Following this statement, Nemeroff continued to discuss the trajectory of “depressive illness,” focusing, in particular, on findings linked to mice with early maternal deprivation and related findings regarding trauma and depression. His conclusion was that, for some individuals (and mice), the brain is changed by early childhood trauma, while for others, the brain seems unaffected. Interestingly, at that point in the conference the Dalai Lama interrupted and there were animated interactions between him and his interpreter. Finally, the interpreter directed a question to Nemeroff, stating something like, “His Holiness is wondering, if two-thirds of depression is caused by human experience and one-third is caused by genetics, but that humans who are genetically predisposed to depression have to have a trauma for the depression to be manifest, then wouldn’t it be true to say that all depression is caused by human experience?” After a brief silence, Nemeroff responded, “Yes. That would be true.”

Most of us have heard about the biopsychosocial model in contemporary medicine. Below I’ve included some information about its origin (this info is adapted from a 2009 Journal of Contemporary Psychotherapy Article; you can find the whole article here: http://www.coping.us/images/Sommers_Campbell_2009_EBP_for_Kids.pdf).

In his 1980 call to medicine, Engel (1980; 1997) encouraged adoption of a biopsychosocial model of health and illness. Despite this recommendation and the increased use of ‘biopsychosocial’ language among non-medical practitioners, medicine has demonstrated little movement toward embracing a biopsychosocial perspective (Alonso, 2004). To some extent, the Nemeroff-Dalai Lama interaction illustrates medical professionals’ tendencies to formulate mental health problems as disease states even when their own data are contradictory. At the Mind and Life Conference, Nemeroff continued to present his illness-based depression formulation even after conceding environmental causality of depression (Nemeroff, 2007).

Although we (Sommers-Flanagan & Campbell) generally advocate medicine’s biopsychosocial model, we see utility in a slightly more radical reconceptualization of depression–especially among youth. This belief rests upon knowledge about the etiology, course, and treatment of depression, equivocal data regarding antidepressant medication effectiveness, potential developmental and medical dangers associated with short- and long-term SSRI use, research on child development and trauma, and our own clinical experience (Sommers-Flanagan & Sommers-Flanagan, 1995a; Sommers-Flanagan & Sommers-Flanagan, 2007). In short, instead of a biopsychosocial model for understanding and treating youth depression, we believe a social-psychological-biological approach is more consistent with current scientific and clinical knowledge.

A Social-Psycho-Bio Model of Clinical Depression

All humans are born into pre-determined social and cultural settings, which directly influence emotional, psychological, social, and biological functioning and development (Christopher, 1996; Sue & Sue, 2013). Although space precludes complete articulation of the social-psycho-bio model, we describe the major components below.

Social-cultural components. Many cultural factors contribute to children’s emotional and psychological development. For example, in the United States, babies are often born to socially isolated mothers living in poverty. These mothers may also be depressed themselves and have little community and governmental support (Goosby, 2007; Knitzer, 2007). In contrast, more communal and supportive cultural settings place less of a parenting burden on individual mothers, thus possibly decreasing depression. It’s likely that different degrees of cultural support to families and children translate into different degrees of relative risk for depressive experiences in children.

Recent research affirms diverging cultural assumptions about depression etiology. Whereas South Asian immigrants viewed depressive symptoms as stemming from social and moral influences (Karasz, 2005), European Americans attributed depression to biological influences. These cultural formulations or expectations likely influence medication or psychotherapeutic efficacy. Although biomedical researchers emphasize genetic contributions to depression, an individual’s depressive predisposition may be strongly influenced by overarching cultural factors. Given Nemeroff’s admission that depression is rooted in human experience, it seems appropriate to us that depression formulations lead with social and cultural, rather than biological factors.

Early caretaker-child interactions. Early caretaker-baby interactions appear to stimulate depression development in very young children. The best example of this comes from studies of maternal depression, which demonstrate that mothers’ depressive behaviors influence their children’s own emotional suffering and other neurological changes (Ashman & Dawson, 2002). This evidence for a direct effect of caregiver behavior on children’s neural activity and possible brain development supports the social-psycho-bio model.

Child trauma. Garbarino’s (2001) statement, “Risk accumulates; opportunity ameliorates” (p. 362) suggests that repeated trauma in the absence of support or opportunity can deeply damage children. Trauma typically occurs within a social and cultural context, and without requisite support and opportunity, it can initiate cognitive, emotional, and social pathology. Sufficiently intense trauma may also produce lasting “psychic scars” (Terr, 1990). Additionally, early childhood trauma drains children and adults of meaningfulness (Garbarino, 2001). There is little doubt about the powerful contribution of trauma to the development of clinical depression and other mental disorders.

Psychological/cognitive development of depressive symptoms. Considerable evidence supports a cognitive model of depression in adults, and to some extent, in adolescents and children (Kazdin & Weisz, 2003). The pioneering work of Aaron Beck (1970) emphasizes that personal experiences lead individuals to acquire specific negative beliefs about themselves, the world, and the future (i.e., the cognitive triad). Although empirical support for the cognitive triad’s contributory and maintenance roles in depression is strong, these belief systems do not rise autonomously within the psyche. Instead, as Beck notes, these deeply ingrained beliefs are learned vis-à-vis interpersonal experiences.

The development of schemata or internal working models. Theorists spanning analytic, neoanalytic, cognitive, and attachment perspectives have proposed concepts that can be described as schemata or internal working models (Ainsworth, 1989; Glasser, 1998; Morehead, 2002; Young, Klosko, & Weishaar, 2003). Although each theoretical perspective articulates the concept somewhat differently, all involve development of a psychological pattern of repetitive automatic beliefs and expectations. These beliefs and expectations, which implicate the self, the world, and others (or objects), generate repetitive behaviors and affect. A cognitive schema or internal working model arises from early social interactions and may contribute to depression and other emotional and behavioral maladies. From a behavioral perspective, depressogenic working models involve early maladaptive reinforcement contingencies, which must be unlearned before one can acquire more adaptive behavior patterns.

Regardless of theoretical orientation, the internal working model concept forms the foundation of many psychological interventions. For example, it clearly underlies CBT and interpersonal therapy (IPT), two evidence-based practices for treating depression in youth (Kazdin & Weisz, 2003). Essentially, internal working models or schemata include internalized early experiences, and they constitute the “psycho” component of the social-psycho-bio model. When positive, adaptive, and healthy early experiences predominate, internalized working models buffer or immunize the individual against stress and trauma. When critical, negative, and maladaptive experiences predominate, schemata can predispose an individual to acute, chronic, or recurrent depressive episodes.

Neurological (brain-based) manifestations of depression. In addition to social, cognitive, emotional, and motivational experiences, current and recent research has identified cortical functioning correlates of depression. These correlates include neurochemical changes and neural activity, which can be observed via Positron Emission Tomography or functional Magnetic Resonance Imaging. Typically, brain imaging studies in animals, youth, and adults are presented as evidence of biomedical or biogenetic causal factors of depression. In the social-psycho-bio model described here, we suggest that neural changes are natural and inevitable correlates of internalized depressive life experiences. Because we are all biological organisms, observable neural changes associated with clinical depression should come as no surprise. It is important to note, however, that brain changes represent a physical phenomenon correlated with depression; these changes may or may not be causative.

Individuals with more extreme, recurrent, or chronic depressive experiences are perhaps more likely to evidence neurochemical states that add to or maintain depression. Again, we view this as a natural biological process. In some circumstances, this state might require a biological agent (or medication) to be used in combination with psychotherapy to facilitate depression recovery.

Our social-psycho-bio model advocacy does not exclude biomedical contributors to depression. Instead, it identifies biological manifestations as correlates of social and psychological dimensions of depression. This argument has been articulated before, but without much success. We attribute the failure of this view to the din of medication marketing and a cultural orientation toward quick fixes. In fact, we are all biological creatures with intricately interconnected brains characterized by dazzlingly complex electrochemical communication. The search for fMRI and PET scan differences between depressed and non-depressed individuals represents a logical and natural development in our understanding of depression as it exists within the whole person. Although neurochemical changes might maintain depression, it is not necessarily the case that neurochemical factors (or the vernacular ‘chemical imbalances’) initiate depressive processes. Indeed, these neurochemical changes are just as likely to be consequences of depressive conditions. Based on this depression re-formulation, we believe that it would be appropriate to initiate antidepressant medication treatment as an adjunctive approach if previously attempted experiential interventions, including exercise, dietary adjustments, and psychotherapy failed to achieve desired effectiveness. Further, conceptualizing neurochemical changes as depressive correlates rather than causes, lead us to agree with others who maintain that medication treatment should be considered a palliative and not curative treatment (Overholser, 2006).

[Again, please note that much of the preceding is adapted from a previously published article in the Journal of Contemporary Psychotherapy. The article was titled, “Psychotherapy and (or) Medications for Depression in Youth? An Evidence-Based Review with Recommendations for Treatment.” Citations are available in the original article.]

 

The Return of Mother’s Little Helper . . .

This week Allen E. Ivey (the creator of the microcounseling approach) sent me a link to an article claiming that exercise is better for long-term brain functioning than medications. He was “venting” because he thinks this is not “new” information and instead constitutes basic common sense that everyone should embrace. The fact that exercise is good for neurological development and functioning is obvious and it can be frustrating to see the media acting surprised over and over again that life experiences—including counseling and psychotherapy—improves health, life satisfaction, and brain functioning.

Dr. Ivey’s comments and the article he sent reminded me of an unpublished piece I wrote a few years ago. It was a sarcastic commentary on a recent (at the time) publication touting the efficacy of antidepressants in treating depressive symptoms in mothers.

Here’s the piece. Sarcasm included.

The Return of Mother’s Little Helper

            Mother’s little helper is back.

            In a recent landmark study published in the Journal of the American Medical Association, a prestigious group of researchers reported that children with depression improved or recovered when their depressed mothers became less depressed. The researchers were surprised and optimistic that an environmental change—mothers becoming less depressed—could directly help children whom they thought had biological depression. This is an important finding, especially given concerns about prescribing psychotropic medicines directly to children.

            Having closely followed pharmaceutical research in child psychiatry, I’m always skeptical about landmark studies and promising new drugs, but try to stay balanced and hopeful. When I mentioned the research results to my graduate students in counseling and social work, all of whom happened to be women, they felt no need for balance or hope. They responded in unison.

            “No duh. Obviously children will do better if their mothers aren’t depressed. Who needs a study to tell you that?”

            I felt instantly defensive for pharmaceutical researchers everywhere. Okay, maybe the study demonstrated the obvious, but helping children be less depressed is clearly a good thing.

            My students weren’t convinced. They asked, “What treatment did the mothers’ get?”

            “Mostly they got Celexa.” Celexa is very similar to Prozac. They’re both classified as ‘SSRIs,’ meaning they selectively focus on making serotonin more plentiful in crucial brain regions.

            My cynical students pressed on: “Did the makers of Celexa fund the study?”

            “No,” I responded. “Forest Laboratories makes Celexa, but the study was funded by the National Institute of Mental Health.” I felt redeemed; the study was objective.

            “How many of the authors were paid by Forest Laboratories?”

            I happened to have the article with me, so I looked at the back page where financial disclosures are conveniently listed—in very small print. I squinted my way through: “Only 3 authors name Forest Laboratories as giving them money. And Forest Laboratories is thanked in the fine print for supplying all the medication for free.”

            Actually, that wasn’t too bad. There were 15 coauthors on the study; only 20% were linked to Forest Laboratories.

            But my picky students wanted to know about the numbers, so I explained that 151 mothers started the study, but 37 (24.5%) dropped out before three months. Overall, 38 of the 114 remaining mothers recovered from their depressive condition and another 16 improved somewhat. The authors report an overall response rate of 47%.

            A student pecked at her calculator and declared. “No way! Fifty-four of 151 isn’t 47%, it’s 36%; they’re either lying, cheating, or very bad at arithmetic.”

            “How about the kids,” another asked.  “How many of them got better?”

            “Well, it’s complex and hard to say, but overall the researchers report that, of 105 kids, 9 were significantly affected during the study, 4 in a positive direction and 5 in a negative direction.”

            The students mumbled and grumbled. “Are you kidding? That’s not much improvement.” They went on to rant a bit about never knowing a depressed, sleep-deprived mother—including themselves—who looked forward to 18 hours of screeching children and smelly diapers? One student, now a grandmother, noted that Valium (the original mother’s little helper) was the most prescribed drug in the U.S. from 1969-1982 and such a big pharmaceutical success that it inspired a Rolling Stones song. Unfortunately, Valium turned out to be terribly addictive, but now apparently, there’s Celexa, Prozac, and other options for overwhelmed mothers.

            After a few more stories, my students asked, “What were the study’s conclusions?”

            I read aloud: “. . . these findings suggest that it is important to provide vigorous treatment to mothers if they are depressed.”

            Throughout the room, eyes began to roll.

            “That’s a big surprise. They want depressed moms to feel guilty if they don’t take antidepressants. That’s what they mean by ‘vigorous treatment.’ As if a hard life is made better by serotonin? How much did they spend on that study anyway?”

            “I really don’t know,” I answered.  “Maybe half a million?”

            The student with the calculator pecked away again: “They should use that money to do a study on something that might really help depressed mothers.”

            “Like what?” I asked.

            “Like maybe a study on the effectiveness of splitting half a million among 114 moms—that’s over $4,300 each. They could just give them the money, or pay for some counseling and parenting consultations, or health club memberships, or childcare, or massages, or vocational training. Better yet, the researchers could use the money to train fathers to hang around the house and be helpful, rather than lying around watching sports and reading Penthouse.”

            At that point I decided class was over. I’d learned about as much as I could handle for one day.