The Wandering Mind: A Friend or Foe? The Supervisory Role of Metacognitive Awareness in Overseeing the “Default Network”

(And in the spirit of posting term papers related to my burgeoning interest in all things metacognitive...)

In-progress revision of term paper submitted for Jamie Morris' "Graduate Social Neuroscience" seminar, Psyc 7559, UVA, Fall 2011

Though it was only with the advent of recent methodological advances in cognitive psychology and neuroscience that we could take our first strides toward measuring this elusive phenomenon in the laboratory, the actual fact that our minds wander is not exactly a trade secret. Indeed, as will be no great surprise to many of us, neuroimaging findings have suggested that mind-wandering - alternatively referred to as “stimulus-independent thought” (e.g. Gilbert, Simons, Frith, & Burgess, 2006) - may be our “default” mode of operation, in that it corresponds to the network of brain areas that consistently show heightened activation when individuals are mentally “at rest” and not being instructed to focus on any task in particular (e.g. Buckner et al, 2008; Raichle et al, 2001). Areas associated with the default network include the ventral and dorsal medial prefrontal cortex (MPFC), the posterior cingulate cortex (PCC)/precuneus, portions of the lateral parietal cortex, and the temporoparietal junction (e.g. Mason et al, 2007). Not only do these areas show activation when individuals are told to relax and indulge in their own unconstrained stream of thought, but they also show increased activation during the performance of tasks that have become practiced and familiar (Mason et al) as well as on low-demand reaction time tasks (Gilbert et al, 2006). Furthermore, the self-reported tendency to daydream is positively correlated with the extent to which an individual shows increased default network activation during a “practiced” task relative to a novel one (Mason et al). 

The tendency, for better or worse, appears to be quite a common one: according to a recent iPhone-based experience-sampling study of about 5000 people from 83 different countries, most people spend nearly half their waking hours mind-wandering, regardless of the activity they are engaged in—despite reporting less happiness to the extent that they are doing so (Killingsworth & Gilbert, 2010).

Such findings raise the question: do we mind-wander because it is somehow good for us? Or just because we can't help it?

The question is worth asking, because in fact there is research suggesting that we can help it: for instance, converging behavioral and neural findings from a number of recent studies of sustained attention in individuals who have undergone intensive meditation training suggest that self-reported mind-wandering, as well as the associated neural activation patterns, are significantly reduced in these individuals, not only while they practice meditation (e.g. Hasenkamp, Wilson-Mendenhall, Duncan, & Barsalou, 2012) or engage in other focused tasks (e.g. a dichotic listening task; Lutz et al, 2009) but even when simply at rest (Brewer et al, 2011).  Such preliminary findings suggest that the tendency to mind-wander is malleable and can be reduced with training, at least in some people. 

Nonetheless, the role of the “default network” in human cognition and social-emotional functioning is a source of much contention among scientists, especially given the heterogeneity of findings and theoretical approaches that have all shined different lights on the complex patterns of neural connectivity to, from, and within the regions of this “network.” However, certain general patterns have begun to emerge, and given the apparent ubiquity of the “default mode” throughout so much our waking lives, it is worth exploring the question of what we stand to gain or lose from “spinning our wheels” through the apparently well-worn pathways of our default network.  By briefly reviewing some of the adaptive, maladaptive, and downright pathological forms of “mind-wandering” and underlying neural activation that have been reported in a range of healthy as well as clinical populations, I aim to sketch a preliminary theoretical account of the default network’s proper and improper function—by identifying the role that metacognitive awareness should ideally play in tuning and channeling it. 

At a glance, many of the recent neural and behavioral findings on the consequences of “stimulus-independent thought” and corresponding default network activation paint a rather dismal picture of the havoc that our mind-wandering can wreak on our task performance, as well as our mood and overall well-being.  In addition to the above-mentioned correlation between self-reported mind-wandering and unhappiness across a wide range of activities (Killingsworth & Gilbert, 2010), several laboratory studies employing “thought probes” to sample participants’ real-time subjective experiences of mind-wandering have reported that participants make more response inhibition errors, and do a poorer job of encoding episodic information (based on later retrieval scores), on trials completed during a “mind-wandering” episode than during a mentally on-task episode (e.g. Christoff et al, 2009; Smallwood, McSpadden, & Schooler, 2007). Not surprisingly, the interference from spontaneous, internally generated thought drew participants’ attention away from the task at hand and impaired their ability to monitor and control their responses to the stimuli being presented.

Moreover, while the consequences of these occasional attentional lapses in healthy individuals may be relatively benign, the costs associated with what one might term “unbridled default network activation” unfortunately do not seem to stop there: in fact, hyper-activation of the default network has been implicated in a range of clinically impairing psychological and neurological disorders, including ADHD, depression, and schizophrenia (e.g. Whitfield-Gabrieli et al, 2009). In depressed individuals, excess activation of the default network usually indexes rumination, which is conceptualized as the reflexive, perseverative internal processing of negative self-related information that exacerbates depressed mood (e.g. Nolen-Hoeksema et al, 2008). Like other forms of mind-wandering, rumination is often passively initiated in the absence of any external environmental cues, and in this sense is a form of “stimulus-independent thought.” However, when further imbued with the motivational salience of affectively loaded, personally relevant negative thought content, the otherwise transient and occasionally distracting tendency to mind-wander gets amplified in intensity, accessibility, and attentional costliness, thus coming to resemble depressive rumination (Smallwood et al, 2007).  In this light, it is perhaps no great wonder that depression is associated with a range of executive functioning impairments that, in turn, are mediated by rumination (e.g. Watkins & Brown, 2002). Indeed, by experimentally inducing either rumination or distraction immediately prior to an executive functioning task, Watkins and Brown showed that depressed individuals equaled healthy controls in executive functioning performance following the “distraction” induction, whereas depressed individuals induced to ruminate showed the expected impairment in executive functioning relative to healthy controls. This finding intriguingly suggests that the deficit in executive functioning observed in depressed individuals does not reflect any underlying impairment in the capacity for cognitive control, but rather is a secondary consequence of the attention-depleting effects of rumination. Berman et al (2010) further demonstrated a direct relationship between rumination and abnormal, excessive default network connectivity in depressed individuals, and found a deactivation of the default network to a level comparable to healthy controls when depressed individuals were instructed to complete an engaging distractor task. Consistent with these findings, longitudinal studies examining changes in executive functioning before and after recovery from depression have shown promising findings that these deficits are state-like rather than trait-like in nature, and that most aspects of executive functioning had been restored to normal, healthy levels following recovery (e.g. Biringer et al, 2005). These findings again suggest that maladaptive mind-wandering and rumination can be reduced and their negative effects reversed, as further corroborated by the effectiveness of “attentional control” and “mindfulness” training interventions (e.g. Teasdale, Segal, & Williams, 1995) as well as a rumination-focused therapeutic intervention (Watkins, 2011) for depression.

As further evidence for the apparently pernicious role of a hyperactive default network in predicting executive dysfunction, individuals with traumatic brain injury (TBI) have been shown to exhibit increased default network activation (particularly in the PCC/precuneus) during cognitively demanding tasks, which in turn was associated with the degree of attentional impairment they exhibited (Bonnelle et al, 2011).

Similarly, overactivity in the default network during active task performance has been correlated with both performance impairment (Harrison et al, 2007) and clinical symptom severity (Garrity et al, 2007) in individuals with schizophrenia. Moreover, greater activation in the default network during passive resting-state periods was directly associated with the positive symptoms of schizophrenia, including hallucinations and delusions (Garrity et al).

Finally, a similar pattern of default network hyper-activation during cognitively demanding tasks has also been implicated in ADHD (e.g. Fassbender et al, 2009), which, unsurprisingly, is characterized by impaired attentional control and reduced ability to inhibit task-irrelevant distractions. Specifically, children with ADHD show less deactivation of ventromedial PFC with increasing task difficulty than do healthy controls, and this lack of deactivation is positively correlated with increased distractibility on the task (as indexed by greater variability in reaction times) (Fassbender et al).

In view of this rather disheartening “hit list” of cognitive, emotional, and behavioral impairments associated with "too much" default network activation, one might begin to wonder whether all this unprompted neural activity is just a waste (at best) of precious cognitive and attentional resources. We must be careful, however, not to throw out the proverbial baby with the bath water: in fact, for every finding that suggests a maladaptive function for the default network, there are at least as many that implicate increased default network activation in human creativity and moments of insight (e.g. Kounlos et al, 2006; Kounlos et al, 2008), in self-awareness, social competence, and theory-of-mind (e.g. Moriguchi et al, 2007; van der Meer et al, 2010), and even in overall intelligence (e.g. van der Heuvel et al, 2009).  By the same token, decreases in resting-state activation and in overall functional connectivity within the default network are associated with a range of clinical disorders, including Alzheimer’s Disease (e.g. Greicius et al, 2004), Autism Spectrum Disorder (ASD; e.g. Kennedy and colleagues, 2006), and, paradoxically enough, schizophrenia (e.g. van der Meer et al; Lynall et al, 2010). Clearly, then, activation in the default network is neither inherently the “work of the devil” in our brains, but nor is it a "gift from God" to be cherished unconditionally; its value or disvalue appears to be entirely relative to the function it is serving in a given context. What, then, is the context in which the default network becomes our friend rather than our foe, and how might we go about cultivating it?

Some clues can be gleaned from the contextual factors that were at play in a number of the studies discussed above: for instance, in the mind-wandering study by Smallwood et al (2007), participants’ performance was impaired only on trials during which mind-wandering without prior awareness of doing so (referred to as “zone-out”) was reported, whereas performance during mind-wandering with awareness (referred to as “tune-out”) was on par with performance during on-task, no-mind-wandering periods.  Providing further neuroimaging support for this finding, Christoff et al (2009) found greater activation in default network regions (including the medial PFC, PCC, and temperoparietal cortices) during periods when participants reported having mind-wandered without awareness than with awareness. Thus, it appears that our default mental mode is most active when we are least aware of having, in effect, defaulted to it—and yet this is also when we are at greatest risk of being impaired and distracted by it.  

Analogously, a closer and more context-sensitive examination of the nature of default network dysfunction in ADHD, ASD, and schizophrenia reveals that the problem is rarely one of “over-activation” or “under-activation” per se, but more often of decreased connectivity with areas of the brain that are likely involved in regulating its activity in context. For instance, in healthy individuals, a negative or “antiphasic” relationship is usually observed between activation in the default network and in those brain areas most commonly associated with top-down, goal-directed executive control (particularly the dorsal anterior cingulate cortex, or dACC, and the dorsolateral prefrontal cortex, or DLPFC)—suggesting that the executive control centers are recruited in suppressing or down-regulating the default network when needed (e.g. Castellanos et al, 2008). Indeed, a temporal analysis of on-line changes in neural activation during task performance revealed that decreased activity in top-down attentional control regions (including the dACC, right inferior frontal gyrus, and right middle frontal gyrus) consistently preceded healthy individuals’ “momentary attentional lapses,” as indexed by slower response times (Weissman et al, 2006). Correspondingly, these periods of lapsed attention were also positively associated with activity in default network regions (especially the PCC and precuneus). Thus, it appears that the temporary lapse or relaxation of cognitive control over one’s task-relevant focus is at least one mechanism, at least in healthy individuals, through which default network activity can “pipe up” at unwanted times and interfere with goal-directed performance. Correspondingly, a decrease in this inverse or “anticorrelated” relationship between top-down executive control centers and default network regions could signify a deficit in functional connectivity and efficient communication between these regions, which in turn would make the goal-driven suppression of default network activity more difficult. Sure enough, this decreased connectivity between default network regions and executive control regions (particularly the dACC) has indeed been found in individuals with ADHD (e.g. Castellanos, 2008; Liddle et al, 2011). Similarly, the dysfunctional patterns of default network activation observed in Schizophrenia likely have more to do with a weakening of functional connectivity both within the default network and with top-down regions normally involved in controlling and regulating it (e.g. Lynall et al, 2010), than with either “too much” or “too little” activation per se. In other words, in clinical samples as well as in the population at large, the default network can be activated for good or for ill, depending on both the situational and neural context.

On one hand, this news sounds heartening, in that it implies that we have some measure of control over the wayward wanderings of our default network. It still does not explain, however, why we “know” to exercise that control in some cases but not in others, or why there is so much individual variation in even healthy, neurologically unimpaired people’s ability and willingness to exercise it (even despite most people’s general recognition that they tend to be less happy when they mind-wander; Killingsworth & Gilbert, 2010). Is mind-wandering like a drug or a Facebook addiction or some other bad habit, in that we technically know it is bad for us (at least when indulged in excess) but somehow we just cannot stay away? 

In some respects, it may well be analogous, in that mind-wandering and the underlying hyper-activation of default network regions occur largely through automatic, unintentional force of habit (e.g. Smallwood & Schooler, 2006) and are sometimes conceptualized as failures of cognitive self-control (e.g. McVane & Kane, 2010). Extending this analogy to addictive behaviors still further, off-task forms of mind-wandering must have some motivational salience to us if they are to draw our attention away from the task at hand—which means that, like drugs and other substances, they must provide us with some form of real or anticipated reward. Indeed, in his control-theory account of the factors that distinguish between “constructive” and “unconstructive” repetitive thought (a construct closely tied to mind-wandering), Watkins (2008) proposes that these often unbidden, automatically generated thoughts arise and continue to play on “repeat” in response to discrepancies between desired end-goals and their perceived current state. For instance, if we are currently trying to compose a work e-mail but are meanwhile waiting to hear back about the outcome of an important job interview, it is easy to imagine our mind wandering from the comparatively mundane e-mail to thoughts of what we said or wished we had said in our interview, projections of how our rival candidates might have performed, recollections of what the interviewers’ faces looked like and what kinds of comments they made, worried ruminations about what we might do if we do not get the job, etc. 

In other words, it is not as if our thoughts actually bring us any closer to achieving our desired goal (of getting the coveted job, in this case), but the temptation to mentally “work” on this goal is nonetheless potent—sometimes in disregard of current contextual constraints on our ability to do anything about it (Watkins, 2008). Even for realistic goals that do require further action and attention from us before they can be achieved, the situational context sometimes prevents us from working on them right now; for instance, we may be knee-deep in the process of submitting job applications, and even have a long unfinished “to-do” list associated with it (or worse, the dreaded sense that we had better make a “to-do” list, and the fear that it will be too long to complete before deadlines are past), and yet our current focus has to be on the meeting we are in or the groceries we need to buy.  Unfortunately, however, our automatic brains are not always especially sensitive to such ever-changing contextual factors, and are liable to want to think about what is globally “most important” to us at all times (Watkins). Thus it may well be necessary for us to use effortful control resources to inhibit or temporarily suppress those highly salient internally generated thoughts, redirecting our attention instead to external cues or demands that are currently more pressing. For this reason, Watkins identifies executive control as one of the individual difference variables that might moderate the extent to which someone is able to regulate his/her repetitive thought processes, encouraging the productive ones (e.g. creative brain-storming or assimilating of new ideas with relevant knowledge from one’s biographical memory when at rest) while inhibiting or re-directing the unproductive ones (e.g. rumination or compulsive worry about currently or permanently unattainable goals).

This account of what gives salience to certain repetitive thoughts, and thus keeps them “looping” and consuming attentional resources when not overridden by conscious control, might also shed light on the fact that the same regions implicated in the default network (particularly the ventral and dorsal MPFC) are also frequently associated with “self-referential processing” (see van der Meer et al, 2010, for a review).  If the default network is prone to the processing of whatever unattained goals are currently most readily accessible to consciousness, then it is no surprise that self-relevant content receives the greatest attention, since the most self-relevant concerns tend to be the most salient ones. Indeed, in reviewing a range of empirical findings that have sought to distinguish the neural correlates of self-relevant versus other-relevant processing, van der Meer describes a number of findings suggesting that affective salience may be a better predictor of ventral MPFC activation (which has been most consistently implicated in self-relevant processing) than self-relevance as such (e.g. Gusnard et al, 2001). In light of such findings, it is not so surprising that the default network reflects our habitual mode of operation, and that it “kicks in” whenever our attention is not consumed by specific external task demands: it is where we, in effect, mentally chew on (which, curiously, is one of the literal meanings of “ruminate”) and work to digest all that which feels somehow important to us.  

            However, as is the case with most physical and psychological addictions, what feels important and right to be indulging in (whether in thought or in action) is not always what is actually best for us—and yet it can be extremely hard to shake.  Moreover, whereas the surest cure for most addictions is a sustained period of abstinence, during which the oft-reinforced stimulus-response and reward-seeking pathways associated with the addiction are starved of further reinforcement and gradually weakened, the temporary cessation of all internally generated thought is hardly a viable treatment option. So the question remains: how do we ever know whether we're doing the "good" or the "bad" kind of thinking? Wouldn't we need to be able to somehow "meta"-think our way out?
           Well, yes - but in fact, some intriguing experimental and neuropsychological findings suggest that we might be able to do just that. In fact, it may be that one or more of the very same regions commonly associated with the "default network" are actually involved - or, at least, can be involved - in the task of metacognitively presiding over our own thoughts.   In particular, a recently growing literature of neuroanatomical and imaging findings has identified the anterior prefrontal cortex (aPFC), which anatomically overlaps with both the MPFC and the more traditionally cited “top-down” control centers in the lateral frontal cortex, with some of the very cognitive control functions that may be crucial for monitoring and facilitating communication between the task-focused, externally oriented executive and the non-task-focused, internally oriented "default" mode (e.g. Burgess et al, 2007; Gilbert et al, 2008). For example, in a study that compared the neural patterns observed when individuals were engaged in a basic response time task, requiring very little effortful processing, versus two more cognitively demanding tasks, the expected increase in activation was observed in the MPFC, including the medial aPFC, during the easy relative to the more difficult tasks; contrary to the predictions of the standard “default network” hypothesis, however, it was found that the degree of activation in the aPFC was positively correlated with the speed of individuals’ response times on the easy task—suggesting that, contrary to the distraction-induced slower performance that would be expected in the presence of off-task mind-wandering, the aPFC actually enhanced participants’ ability to sustain attention on the task. This finding is consistent with the “gateway hypothesis” of aPFC function (Burgess et al, 2005), which posits a metacognitive role of the aFC in monitoring both the internal and external environment for goal-related attentional cues and maintaining a “readiness” to direct attention outward or inward as needed. In contexts where there is potential for competition between internal and external inputs, as when task-demands are low enough for potentially distracting internally generated thoughts to arise, proponents of the gateway hypothesis suggest that the aPFC responds by “biasing” attention toward either external or internal inputs, thus tuning our automatic attentional processes to the demands of the task (e.g. Gilbert et al, 2008). Interestingly, the study by Gilbert et al further demonstrated that individuals with ASD show dysfunctional patterns of aPFC activation during this task, which is consistent with other findings which have isolated the aPFC as a locus of cognitive and social impairment in ASD (e.g. Schmitz et al, 2006). Thus, the “hypo-activation” of the default network in patients with ASD may actually indicate an impairment in this specific form of cognitive control, which consists in the goal-based allocation of attentional resources in situations where conflicting or mutually compatible options present themselves. This possibility is supported by a wealth of neuropsychological and behavioral findings that point to this distinct pattern of executive functioning impairment in patients with ASD (Gilbert et al, 2008).

Bringing these alternative accounts of the default network full-circle, a survey of the neurobiology of depression literature reveals that, in fact, lesions of the anterior PFC have produced depressive symptoms in some individuals (Davidson, 2002), and that clinically depressed patients show decreased regional Cerebral Blood Flow (rCBF) in the anterior PFC (e.g. Drevets et al, 1992; Ishizaki et al, 2008).

Thus, while still highly preliminary, these supposed metacognitive functions attributed to the aPFC may serve to relieve some of the strain that many experience in managing their ambivalent relationship with their wandering minds. If there is indeed a functionally distinct “gateway” that allows us to continuously monitor and purposefully integrate the internal and external processing inputs that impinge on us throughout our waking hours, then the default network need not be a feared foe; instead it can be a friendly and valuable resource that we utilize as and when the opportunity or need arises. In fact, recent neural findings confirm that even trained meditators periodically mind-wander (Hasenkamp et al, 2012); the apparent difference, however, is that they are able to redirect themselves more quickly and less effortfully (Lutz et al, 2009) to the task at hand, and that, as the “gateway hypothesis” might predict, they show greater aPFC activation throughout (Yu et al, 2011). In other words, it is some possibility that the metacognitive monitoring ability associated with the aPFC can be trained and strengthened, much like a muscle.  Moreover, this increased aPFC activation during focused attention meditation may mediate reductions in negative mood following meditation practice (Yu et al)—which is particularly good news for the depressive ruminators among us.

In sum, although much future research is needed to further explore the role of metacognitive monitoring, as possibly indexed by the aPFC, in the regulation of internally generated thought and associated default network activation, this much at least seems to be clear: the default network is neither intrinsically "for" us or "against" us. Rather it offers us an arsenal of cognitive/neuronal resources that can be used for good or for ill, and that serve us best when wielded responsibly.   

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Addendum to "'An Unsettling Sombriety'; The Humbling 'Wow' Factor of This Week's Articles"

Do please to take note, gentle reader, that I have meticulously steered clear of making any reference, in the commentary below, to the Coan papers on our reading list for the week, owing, of course, entirely to the fact that I've meticulously steered clear (as yet) of reading the Coan papers on said reading list, owing, in turn, entirely to the fact that I wished to steer meticulously clear of any possible accusation of merely reading and commenting on them in the petty interest of pleasing the professor (who, as a matter of happenstance, is none other than the very selfsame Coan). This carefully considered policy of mine is of course entirely a function of such ennobled considerations and by no means a function of my having run out of time to read any articles that were marked with little "optional" crosses in the syllabus. Needless to say, therefore, I will duly endeavor to have read the Coan articles in question by the time we commence our class discussion tomorrow, so that I can contribute meaningfully to said discussion, having now satisfactorily laid to rest all possible aspersions of doubt on the untainted scholarliness of my motives.

Thank you very much,
Gena the Gentle Scholar

"An Unsettling Sombriety"; The Humbling "Wow" Factor of This Week's Articles

My head has been spinning at a faster and more disorienting rate since I embarked on this week's "Controversy"-themed readings than it has for any week prior. For all the furiously scribbled "Wow's," "What the's," and "Seriously??"s that pepper the margins of my copies of both the Lilienfeld and the Dawes et al papers, and the general sense of stunned disillusionment I felt with the vast majority of practitioners - and researchers! - within this field I'm venturing into (I mean, "rebirthing" as a "therapeutic treatment" eligible for continuing education credit from APA, at least as of 2002? Seriously??), the main themes that emerged from all my margin notes and scribblings were two-fold: 1) wow, more power to statistical analyses and rigorous empirical tests of existing theories for calling out the clinicians and self-assured "professional psychologists" on their dogmatic, obstinately fact-resistant, and often harmful B.S.! and 2) wow, so many exciting openings for good, fresh, explicitly articulated and empirically testable new theory to walk on the scene and finish off what the statistical expose started!

Before attempting to explain what I mean by either of these "themes," I should throw in the disclaimer that I'm still tangled up in massive conclusions regarding some of the claims made in each of these articles, and I don't claim to be at all certain that my interpretations and criticisms of what I took to be various conclusions that the authors seem to be arguing for aren't just the direct result of my own faulty understanding. I can't wait to address some of my confusions in class on Wednesday and get a better handle on what exactly was found in some of the clinical vs. actuarial judgment studies that Dawes cites, for example, and how it was that "accuracy" of prediction was measured in cases of psychiatric diagnoses and the like, and many other such questions. But meanwhile, I figure I might as well attempt to articulate my own current interpretation and the source of my at-least-partial dissatisfaction with the authors' conclusions in, which at least might shed some light on what exactly it is that I'm confused about.

So, with all that said, here goes: tackling first the Lilienfeld "Psychological Treatments That Cause Harm" article, with all its bone-chilling exposes of therapeutic "treatments" that continue to be done despite multiple research findings showing that they do more harm than good, I was completely on board and even cheering for Lilienfeld's explanation of what can be gained from studying potentially harmful treatments - such as a greater degree of caution and humility on clinicians' part, on account of realizing that not all therapies are equal and that there can be unknown and unintended consequences to even the most seemingly sound and uncontroversial treatments (such as relaxation therapy for Panic Disorder), and also a greater understanding of the specific mechanisms of change that underlie various therapeutic treatments and when, and with whom those mechanisms can most effectively be applied. But I parted ways with Lilienfeld when he made the claim that the identification of potentially harmful treatments should be accorded "higher priority" than the identification and testing of effective, evidence-based treatments, because I don't see that this solution would go deep enough to address the underlying problem. The article cites multiple examples of clinicians continuing to implement certain treatments, and the APA continuing to sanction them, despite the availability of ample data suggesting that those treatments do more harm than good. What reason have we to expect that gathering more such data - by focusing on the sorts of non-empirically-supported "fringe" treatments Lilienfeld describes and proving through further comparisons and statistical analyses that those treatments make at least some patients worse instead of better - would motivate those clinicians to change course and admit that they've been doing a fruitless or even harmful treatment all this time? Lilienfeld also observes in the article that most of the clinicians out there who are conducting these treatments are perfectly well-meaning and sincerely convinced, more and more so after years of selective information processing, self-fulfilling prophecies, and confirmation bias, that their treatment of choice is the most effective way to help reduce the suffering of the people who come through their door. What, then, would serve as a more compelling argument for them - a few more replications of treatment outcome trials whose results say that some patients got worse instead of better (which the clinicians who read this report can just dismiss on the grounds that "well, the therapists in the study were obviously poorly chosen and didn't do the treatment right" or "well, they didn't give the therapy enough time to work before testing the outcome - everyone knows 3 years isn't long enough to bring out all 13 of the repressed 'alters' in a DID patient's psyche and get them all to be friends again!")? Or a re-conceptualization of the basic causal mechanisms involved in the disorder and in the corresponding therapeutic change process, which in turn sheds direct light on the connection between what the clinician has been doing (e.g. Critical Incident Stress Debriefing) and the harm that results (e.g. recall of traumatic event get more firmly and elaborately encoded in long-term memory)? To my mind, at least, this is far more inescapable and compelling an argument - especially if paired with an alternative proposed treatment approach whose effectiveness is similarly explained in terms of known, basic causal relationships. As a case-in-point, I don't think anyone did extensive randomized controlled trials or meta-analyses to determine the possibly deleterious effects of bloodletting or phrenology or faith healing; rather, the advent of new empirical and theoretical breakthroughs in medicine and neurology led to radical re-conceptualizations of what causes certain illnesses, what sort of relationship exists between the structure and function of the human brain, etc. gradually replaced the once-universally-accepted treatments of old, rendering them implausible and obsolete.

And I had a strikingly similar reaction to Dawes et al's "Clinical vs. Actuarial Judgment" article, though it'll be even harder for me to articulate given my confusion about some of the main statistical results they cite; in a nut-shell, though, my fundamental question is: sure a mathematically derived formula does better at consistently extrapolating from a theory to a predicted outcome than any number of clinicians can do with their "bare hands," so to speak (actually their bare brains, in this case - which, as the article astutely observes, are really bad at doing multi-variable computations); but doesn't any actuarial measure ultimately hang or fall on the validity of the theory on which it was based (e.g. which variables and hypothesized predictors the creators of the measure saw fit to analyze in the first place)? And doesn't the theory itself depend crucially on "clinical judgment" - though hopefully of a more explicit, systematic, theoretically supported kind than the sort described in most of the studies the article reports on? When the authors cite the finding that an actuarial measure derived from a bunch of expert clinicians' ratings of various symptom categories outperformed the clinicians themselves in the "accuracy" or consistency of its predictions, that only tells me (importantly and non-trivially, I realize) that clinicians are very unreliable at applying their theoretical knowledge to the computation of diagnoses and predictions "by hand," whereas a calculator programmed with the variables and predictors postulated by their theory (which is essentially what an actuarial measure boils down to, if I understand correctly) does it better. Well, ok; but unless the actuarial measure is getting near-100% accuracy (which, in the studies reported here, it never seems to come anywhere close), we still don't know whether the theoretical assumptions behind the actuarial measure are sound. I can think of numerous examples of this problem, such as the various algorithms I've seen for computing diagnoses based on the DSM - or the problem of getting IQ scores with the WAIS and other cognitive tests that appear to reflect a lack of intelligence, based on the "actuarial" prediction, but are in fact much more likely to reflect an attentional or motivational or auditory processing deficit or the fact that the examinee didn't speak English as a native language. But my broader point is that, while I agree with these authors' admonitions that we strive to minimize the effects of human error and subjective bias in our science and as well as our practice, I'd also want to be quite wary of the complacent reliance on "actuarial tests" as substitutes for theoretically-based judgment and continued monitoring/revision - just as I'd be wary of the reliance on further replications of RCT findings without the corresponding conceptual/theoretical advances to bolster our claims.

Interactions, Pt. 3 (we're on a roll here!): Borderline *What*?

This week's papers caught me by the most pleasant surprise of any we're read so far. I admittedly embarked on these readings with dread and apprehension, colored by my general ambivalence and uncertainty about the elusive Axis II diagnoses (which I've thus far regarded as far more slippery and confusing and unconvincing in their claims to "category" status than even the Axis I's). Granted, I've liked what I've read of the theoretical framework for DBT thus far, but usually these were bits and snatches from articles that identified certain radical behavioral principles at large or therapeutic principles at large and didn't go into any rigorous detail about the specific nature of "Borderline" Personality Disorder (other than some vague reference to emotion dysregulation, which, let's face it - what psychological disorder doesn't involve *some* degree of emotion dysregulation?), which led me to tacitly conclude that the principles of DBT were simply very effective at treating patients who had major psychological problems and were generally regarded by therapists as very hard to treat.  In fact, it's funny, but according to the Linehan paper, one of the features that psychoanalysts proposed at one time as a defining characteristic of Borderline PD was "intense anger and helplessness on the part of the treatment personnel dealing with them" - which is consistent with the impression I've always gotten to date that "Borderline" is just a keyword for "oh no, red flag, it's another one of those patients!" I think it's sadly telling that in all the time I've heard the term "Borderline" being flung about, I never thought for a second to wonder what it was that those patients were thought to be on the "borderline" of; in my mind I think it implicitly stood as "borderline-crazy" or something of that sort (which, apparently, is also not too far off from some of the older definitions, with the "border" between "neurosis" and "psychosis" as one of the early conceptions).

But alas, I was happily disabused of my expectations as I read Linehan's paper - which presented an actually theoretical, not to mention compassionate rather than dismissively pejorative, account of what basic interactive processes underlie and are common across the myriad cases of at least one common subtype of Borderline Personality (namely the type that includes parasuicidal self-injury) but that very likely generalizes to BPD more broadly. My favorite part, perhaps unsurprisingly given what my favorite parts of all the other papers we've read by the founders of various theory-based therapeutic treatments, was the part in which Linehan recounts the process of clinical observation and logic that led her to formulate her theory (which, in turn, she proceeded to test empirically): for instance, the whole section debunking the commonly held view that Borderline patients are "manipulative" in their self-injury and suicidal behavior, meaning they are motivated by some conniving, underhanded intention to pressure you into protecting or saving or attending to them (her argument, in a nut-shell: 1. just because a given behavior - in this case, self-injury and crying out for help - tends to solicit a certain response, such as increased attention or help from the therapist, doesn't mean it was originally motivated by the desire to get that response; 2. her clinical observations belie the "manipulation" hypothesis and lead her to alternate explanations, such as that patients are attempting to reduce their anxiety or otherwise escape the very real (and often largely externally imposed) misery in their lives. I also loved the section in which she identifies the seeming opposites of extreme, intense outbursts of anger in some and "overcontrolled," rarely expressed anger in other patients; tracing them both to a common cause - an underlying difficulty at regulating and perceiving themselves as in control of their anger - that explains each "extreme" once you add certain interacting factors.

And above all, of course, I loved Linehan's account of the actual nature of the "dialectic" in "dialectic behavior therapy": the striking of a fine balance between “acceptance” and “change." Even more so than the last time we ran across this account (in much less thorough, summary form, as part of a larger article on third-wave behavioral therapies), I realized how much this idea of the "dialectic" is aligned with and clarifies my intuitions about “unconditional positive regard” as being “conditional” in a sense and also “unconditional” in a deeper sense--in that you never dismiss a person on the basis of individual patterns of behavior or particular unlikeable traits or habits, but rather you respect them fundamentally for their humanity and act as their advocate when you collaborately work with them toward certain changes. It is out of genuine caring for them, the living, emoting human being underneath all the particular behaviors, who is both capable and worthy of growth and progress toward a happier life and who is worthy of our empathy and compassion in the meantime, that you engage in efforts to change particular maladaptive behaviors with them and to help them improve their lives.

And now I'm out of time to comment on the similar features of the Moffitt article that demystified and lent a conceptual, theoretical framework to Antisocial Personality Disorder, which had previously stood in my mind as a mishmash of symptoms that could only be collectively described as the "bad person syndrome"; but suffice it to say (for now) that the article's quest for underlying etiological differences and interactive relationships between biology, environment, and stress had a great deal to do with it. And so we once again come around to the same theme: Interactions, interactions, interactions!

Interactions, Pt. 2: The Paradox of "Opposites"

A thought that often occurs to me when I come across the accounts of various "opposites," such as "inhibition" vs. "disinhibition," "positive affect" vs. "negative affect," parental "overinvolvement" vs. "underinvolvement," etc., in papers on the nature and etiology of psychological disorders, is: how "opposite" are these, really? My former P.I. at Mass General, who conducts longitudinal studies examining the role of temperamental inhibition and disinhibition in predicting future psychopathology, was somewhat surprised to find that extreme disinhibition as well as extreme inhibition in 2-5-year-old children predicted the development of social anxiety by the the time those kids hit adolescence. What was so surprising about this result? According to the BIS/BAS model my P.I. was working from, behavioral inhibition is supposed to predispose individuals to fearful responding and avoidance of unfamiliar or novel stimuli, which in turn leads to shyness and difficulty initiating and sustaining social interaction; disinhibition, on the other hand, is thought to manifest in impulsive, risk-taking behavior and a low threshold for approaching and initiating interactions. Now, as someone intimately acquainted with the toxic cocktail that can be mixed from the combination of disinhibited, extraverted temperamental traits with a neurotic personality style with a school full of mean kids who have very little patience for an oversensitive chatterbox, I found nothing remotely unexpected in my P.I.'s finding. Again, as I think the articles we read this week shed a great deal of light on, it is not "inhibition" or "disinhibition" or "negative affect" or "positive affect" or any other single variable that causes anxiety; it is the interaction of these characteristics in a way that produces a common phenomenon of anxiety. 

Wait - "common phenomenon"? Am I talking about a single underlying characteristic that all anxious people have in common after all? Well, let's say the phenomenon of pathological "anxiety" always reduces to something like what Barlow suggests in the article we read this week: a chronically low perceived control over those aspects of one's environment and experience which one cares about. But this can already broken down into a million different parts that can be arrived at in a million different ways: for instance, does a person's "perceived" lack of control arise from an actually erratic, capricious environment (e.g. from authoritarian parents who arbitrarily punish and overcriticize them, or "helicopter parents" who exert excessive control over every nook and cranny of their lives)? Or from a temperamental tendency to act impulsively and a deficiency in self-regulation? Or from a learned selective attention bias for negative, threatening stimuli? Or (what seems likeliest) from some combination and reciprocal interaction of many or all of these? And the same kinds of questions can be asked about the other part of the sentence, "those aspects... which one cares about": what determines which aspects of one's environment and experience one "cares about" and finds positively or negatively reinforcing? Perhaps the intensity of one's emotional experiences - positive or negative - in reaction to certain kinds of stimuli has more to do with it than the particular valence (if either) that tends to be more common and prominent for a particular individual; and perhaps intensity is positively reinforcing for some and negatively reinforcing for others, depending on their temperament or their biological wiring or their current cortisol level or their level of social connectedness or some other characteristic (or interaction of characteristics) altogether.

Long story short, I'm struck by the degree to which etiological explanations are interactive - so much so that seemingly opposite extremes of a given variable (such as temperamental inhibition) can produce potentially identical results, depending on the way they interact with other variables (such as neuroticism, locus of control, or a class full of cruel and intolerant middle schoolers). 

Interactions

Last week I was charmed by the connectedness of everything; this week I've discovered a new and fascinating application of this principle: the, for lack of a better word (or non-word), interactiness of everything! Seriously though, amid my growing frustration with the refusal of all of our various readings this semester to satiate my desperate need for instant gratification by laying out, in one fell swoop, the causal mechanisms underlying all things, I feel as though I've been offered a glimpse at the gratifying light at the end of this very long scholarly tunnel: as both the Coyne article and the Kendler et al article seem to suggest, whether through explicit intention or just incidentally, a key to identifying the latent causal factor(s) that produce depression (and, presumably, other psychological phenomena too) is not necessarily to look at any one variable in isolation (as the members of each respective "camp" - the "cognitive" camp, the "attachment" camp, etc. - seem prone to doing, with all the ensuing methodological problems of third variables and unseen mediators that Coyne cites compelling examples of them running into), but rather to look for the critical interactions between multiple variables. So, for instance, the role of invalidating or abusive interpersonal relationships in precipitating depressive episodes and triggering relapses is substantial, though it apparently gets ignored wholesale by many of the depression researchers and theorists who are presumably too wedded to their pet hypothesis (be it "learned helplessness" or "ruminative thinking style" or "negative attributions," etc.) to ask what the other people in a depressed person's life might be contributing to the equation; on the other hand, as Coyne himself points out, interpersonal patterns repeat themselves and "play themselves out" in an eminently non-random fashion, and such internal characteristics as neuroticism, implicit expectancies of failure and personal inadequacy in one's relationships, deeply conditioned responses to external distress, and, perhaps most prominently, a history of past depression no doubt contribute to the seemingly inexorable cycle of depression-triggering interpersonal contexts in which a person with depression often repeatedly finds him/herself. If one wants to move toward a better understanding of what causes depression, then, it seems ill-advised to select a single variable a priori and then cling to it, while tacitly dismissing any other possible contributing factors by simply neglecting to measure them (a la the studies Coyne described in which college students completed a self-report measure of attachment style, for example, which classified them according to which of four one-sentence descriptions they chose as most reflective of them - without any data collected on the actual characteristics of their past or current attachment figures or the quality of their relationships).

In light of all this, the approach taken by Kendler et al in their study of the interactions between neuroticism, sex, and stressful life events uniquely appealed to me, and even inspired a renewed hope that maybe I won't have to wait too long for the gratification of my causal-mechanism-lust after all. Why? Because, instead of formulating their hypothesis in terms of a specific variable they were particularly attached to (as it were), they posed a theoretical question that could turn out in at least 2 different ways depending on the nature of the interaction between several different variables previously shown to be implicated in depression. There is something about this approach that makes profound intuitive sense to me as a means of getting at causality; perhaps this is actually utterly irrelevant and just seems associated due to some superficial similarity that will eventually turn out to be moot, but - it seems to me like causality, by its very nature, is interactive. ("No duh," you say. "So what's your point?" But, hear me out here.) One thing causes another thing to behave in a certain way given the specific nature and characteristics of both "parties," not just the one doing the causing. It makes no sense to say, for example, that "fire causes boiling"; if that were the case, then I should be able to apply fire to shirts and shoes and cabbages and lines and tigers and bears (why not) and make them all "boil" alike. But in fact, fire causes water to boil - because of certain properties of water that interact in a specific way with certain properties of fire. Fire causes a very different phenomenon when applied to, say, paper, and a different one still when applied to gasoline, etc.  Similarly, I don't think it makes much sense to say "Stressful life events cause depression," any more than it makes sense to say "Cognitive distortions cause depression" or anything else in that form. This seems analogous to the nonsensical "Fire causes boiling" type of claim. Rather it makes a lot more sense to me that, for instance, "Stressful life events of a certain kind (say, rejection by a loved one) cause individuals with vulnerabilities to certain kinds of stressful life events (say, interpersonal events that reinforce their feelings of inadequacy) to get depressed." This is just a vague and overly wordy template, of course, and I'm not about to claim that it epitomizes the kind of causal explanation that might someday be reached for the characterization of depression; nor can I claim, for that matter, that depression can necessarily be boiled down to any single causal explanation. But by way of contrast, I have a hunch that this type of statement gets closer to approximating the form of an effective causal explanation than any of the "univariate" explanations do.

Connections

My favorite aspect of being a grad student, so far, is the daily-growing sense that everything is connected - our courses to each other, our courses to our research interests (and vice versa), our courses to our clinical training (and vice versa), our Friday clinical lunch talks to our courses and clinical training and all the rest of it, and, last but not least, our courses and research interests and clinical training and all the rest of it to our lives. This week's readings made this growing network of connections especially palpable for me - and not just because we had a clinical lunch speaker just this past Friday whose presentation focused on the implementation of a web-based Stimulus Control treatment for insomnia, which complements and applies the principles presented in the Bootzin & Epstein paper perfectly. I also noticed "vertical" connections in addition to the "horizontal" ones - for instance, the connection between the broad relationship we've been studying between environmental context and conditioned behavior (as well as thought and mood), on the one hand, and the particular manifestation of this relationship in domains of life that I'm so intimately well-acquainted with (as are most of us, I imagine) - such as sleep and food, for example.

It was striking and actually somewhat inspiring to me to learn from our speaker last week, Frances Thorndike, that simply improving people's sleep patterns by strengthening the association between their bed (the stimulus) and sleep (the conditioned response), and meanwhile cutting the associations between the bed and other, non-sleep-related responses (such as eating, working, worrying, etc.) actually helps to reduce depressive symptoms in individuals with comorbid depression and insomnia. This not only made certain things "click" into place even more in my brain in connection with our class discussion of behavioral conditioning and environmental contexts last week (and how did this "clicking" in my brain actually occur? Perhaps via interactions between that region in the prefrontal cortex whose name I already forgot - the one we designated with green sharpie - and those automatic circuits coursing through the amygdala and hippocampus and all those other structures which we designated with red sharpie?), but it also reinforced for me certain observations I've made - or half-made, or started to make but lacked the motivation (and self-efficacy, for that matter!) to follow through on - about the automated stimulus-response associations that cause frequent problems and disruptions in my own sleeping and eating patterns (particularly, surprise surprise, when things get stressful!).

But the most important connection, at least the most important for me at this current stage of my connection-making, was the account of the reciprocal "feedback loop" that exists between all these various connected parts: e.g., submitting to cravings in response to high-risk contexts and triggers deals a blow to a recovering addict's self-efficacy (don't I know it, at least as far as my chronic food addiction is concerned!), whereas lack of self-efficacy in turn makes it harder to effectively handle such "lapses" and avoid a relapse into addiction; similarly, stress lights up the brain circuits that propel us to self-medicate with alcohol and other addictive substances (like food!), which then further lead the charge of "remodeling the brain" (what a scary and apt description!) by increasing its dependence on what are essentially "dopamine shots" and ultimately strengthening the circuitry that underlies stress, depression, and, for that matter, insomnia. Everything is connected, I tell you!

Speaking for myself, this realization is itself, in turn, a kind of positive reinforcement, in that it promises that everything I learn, everything I observe and attempt to change in myself, every article or book I read and every report write-up I toil over in Assessment class - all will make a non-trivial impact on my brain and thought and mood and, ultimately, on the quality of my life. So not only am I more motivated (at least for now!) to do all that stuff in light of this realization, but I'm also more motivated to make sure I'm doing it right. And what's more, I've got a clearer guidepost now for determining what's "right" for me: namely, what kinds of behaviors and thoughts and emotions does it condition in me, and are they ones I want conditioned?