Tag Archives: dalai lama

Neuroscience New Year’s Resolutions for 2016

In case you forgot or never knew, 1990 to 2000 was championed as the decade of the brain. You would think one decade would be enough, but judging by how much of a darling neuroscience is in the media, it looks like the brain will be hogging the whole 21st century too. And so in celebration of our perpetually “New Brain Science,” I’m offering six neuroscience-based New Year’s resolutions for 2016

1. For years, the Dali Lama has been advising everyone to develop a “Loving Kindness” meditation practice. Even if his advice doesn’t change the world, having a consistent loving kindness meditation practice can change your brain. Mindfulness meditation strengthens a region in the brain called the insular cortex, an area broadly linked to self-control and good judgment. This makes 2016 a good time to start meditating. We could all use a little more self-control and good judgment.

2. You should sit down for this one. Or stand up. And then sit down again. This is because scientific research supports brain-body connections. Exercise facilitates everything from sleep to sex. If you want a sharper brain for 2016, then stand-up and get walking or stretching or running or lifting or dancing your way to clearer thinking.

3. Last year might have been the year of the gut. There’s been plenty of talk about the “gut” being our second brain. Of course, this isn’t about growing your gut or striving for a dad-bod. It’s all about digestive health. The best way to get your second brain to support your mental health is to feed it whole, fresh foods, probiotics, and fermented foods (like kombucha, sauerkraut, and kimchee), while avoiding the evils of eating highly processed white sugar/white flour.

4. Exercise is great and good sex may be better, but loving and gentle touch is the bomb. Make 2016 the year—not only for consensual hugs and kisses—but also for shoulder and neck and foot massages. You can even put brushing each other’s hair on your “this-just-might-improve-my-mental-health” to-do list.

5. In 2015 sleep research was hot. It’s more obvious than ever that sleep deprivation is generally bad for your brain; it contributes to clinical depression, suicide, accidents, and illness. Finding a way to sleep well in 2016 means turning off your screens at least 30 minutes before bedtime, cutting out the caffeine after 2pm, and establishing a steady personal and family sleep routine. Sleep is the new black.

6. For those of us in the helping professions, the biggest neuroscience news is all about what psychotherapists call empathic listening. Turns out, listening in an effort to understand others grows the brain in ways similar to mindfulness meditation. That means the more you practice listening with empathy, the more you’ll grow that all-important insular cortex . . . and the more you grow your insular cortex, the less likely you are to engage in violent behaviors that threaten the planet. So if you want a more peaceful planet, put empathic listening on your New Year’s resolution list.

There’s one big principle that underlies all of the new brain science: Whatever behaviors you rehearse, practice, or repeat, are likely to strengthen your skills and grow your brain in those particular regions. What this means is that if your goal is to be a couch potato for 2016, you should spend lots of time couch potatoing so you can develop mad skills in that area, with a neurological net to match. On the other hand, if you want a healthy brain and body and awesome friendships and romance in your life, you should engage in the activities listed above—especially the mindfulness meditation and empathic listening—and you’ll grow a brain and skills that just might bring health, love, and peace in 2016.

Note: I submitted this awesome resolution list to a couple newspapers just before the New Year, but only got rejections. And so I decided to submit it to myself and, voila!, it got published right here on my very own blog (smiley face). Please share and pass it on so that all the newspaper editors who keep rejecting my work start feeling the deep regret they deserve.

Outstanding in Field


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.]