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Book Review: Co-Dependence: Healing the Human Condition

2012-01-22T23:01:00.000-08:00

4.0 out of 5 starsExhaustive for It's Time... with Major Pointers for the Future, January 22, 2012

Exhaustive for It's Time... with Major Pointers for the Future

Rodger Garrett "SighKoBlahGrr" (Loma Linda, CA USA) - See all my reviews
(REAL NAME)

Co-Dependence - Healing the Human Condition (Paperback), by Charles Whitfield, Deerfield Beach, FL: Health Communications, 1991.

Frankly, I'm surprised there are so few reviews of what is still the single most theory-grounded, comprehensive and predictive of all the many books on the topic during the '80s and '90s. Whitfield had done his homework, and it shows. He's pretty solidly grounded in psychodynamic object relations (though, oddly, Harry Stack Sullivan is missing; go figure), as well as state-of-the-art addiction theory c. 1990. His reference list makes that clear, and serves present day readers as a pretty complete rundown of the major published material in the rubric's first heyday.

Which is useful, as it looks like Co-Dependence as a means of understanding why our interpersonal relationships aren't working is making a comeback, as well as beginning to be the "next thing you do" if you're a female in AA or Alanon.

Whitfield ties it all together for adult children of alcoholics and dysfunctional families as co-dependents far better than either of CoDA's or ACA's 12 Step "big books" (as good as both of them are).

That said, Co-Dependence... is a product of it's times, which almost means "ancient history" in the current era of the evidence-based and brain-scan-informed neuropsychological therapies like CBT, DBT, ACT, MBCT and SIQR. Whitfield was definitely headed in the right direction in suggesting a "spiritual solution," but in his mind, that was something closer to A Course in Miracles than to the research-grounded, Buddhist-based "experiential" therapies that are so popular with most HMOs these days. (Because they teach skills one can use by themselves and produce results in a hurry.)

(ACIM came and went in the '80s and '90s, even with Marianne Williamson's considerable help in the later stage of its popularity. Essentially Judeo-Christian in flavor, a) it ran into the wall of resistance typical of those who suffered from cult-ist or fundamentalist religious crazy-making, and b) it's a very long, arduous and demanding system.)

Even in the new age (but not "New Age") of the mindfulness-based cognitive therapies, however, Co-Dependence... joins Pia Mellody's simpler and more easily-grasped, but no less effective, Facing Codependence as one of the two very best "grist mills" for modern therapy. Most readers seem to get the picture sufficiently that they acquire enough realization, identification and sense of history, as well sense of current dysfunctional behavior, to move them through Prochaska & DiClemente's first three stages of recovery into "commitment" and "action."

Whitfield's book does not supply the "actions" in anything close to sufficient operational detail, but authors like New Harbinger's Steven Hayes, Matthew McKay, Victoria Follette, Thomas Marra, John Forsyth, and others do. And with the guidance of a DBT, ACT, MBCT or SIQR therapist, what the reader learns in either Co-Dependence..., Facing Codependence, CoDA's Co-Dependence Anonymous or ACA's Adult Children of Alcoholics / Dysfunctional Families will serve him well.

Compassionate Boundary Setting for ACA’s & Co-Dependents

2012-01-21T19:16:00.000-08:00

Overcoming Fear of Abandonment & Fear of Abuse at the Bottom of “The Bottom.”

"In all our relationships each one of us builds an image of the other, and these two images have a relationship, not the human beings themselves." - Jiddu Krishmurti

I have seen the phenomenon so many times now in the world of co-dependent adult children (see Anonymous, Anonymous, and Whitfield), that my sense is that it must be more than merely “widespread.” My sense is that it is a stage that many – perhaps most – in their recovery from “common cult-ural child abuse” must work through.

My not-okay inner child (see above plus Berne, and Harris) had become so normalized (see Henry) to the expectation of being abused again as a child that my sense of trust (as Erikson used the word) was largely compromised and twisted into an expectation of harm.

No surprise, then, that in a 12 Step world full of recovering abusers, as well as abusees, that not-okay inner child saw potential abusers, as well as abusees, in many of his fellow recoverees. Shortly after entering “advanced” 12 Step recovery two decades ago, I began to feel very ill-at-ease around many of the others in the meetings. Through Karpman’s eyes, I could see the “rescuers,” the “covert controllers,” and the “persecutors,” as well as the “victims” in the Drama Triangle (see Garrett, and Karpman) right before me in the meeting rooms. Without realizing it, my abuse-fearing, not-okay inner child began to set overly dense boundaries (see Anonymous, Anonymous, Beattie, Evans, Mellody, Schaef, Weinhold & Weinhold, and Whitfield) between itself and the others there.

It didn’t take long for the overly thick boundaries to morph into unrecognized, perfectionistic, judgmental disgust. Unaware of what was going on, my not-okay inner child led me right out of those meetings and back into its world of borderline-organized over-neediness here and suspicious distrust there (see Garrett, Kernberg, Masterson, and Meissner).

Recognizing a return to increasingly uncomfortable co-dependence some years later, I trotted my self back into CoDA and ACA, only to re-discover that same, distrust-driven judgmentalism and increasing disgust with the Karpman Drama Triangle dynamics I saw in the meetings. By then, however, I’d had the benefit of much further education and experience, which set me on a path towards un-covering and being able to define and describe the phenomenon I was not only seeing in myself, but in so many others.

As was my experience in other, more “basic” 12 Step meetings, I began to see that there tends to be a common path of progress in CoDA and ACA (as well as Alanon). And it is this: Having gone so long without functional boundaries and having played “doormat” for so many others, many recovering co-dependents parrot the new concept of boundary-setting... and start flipping back and forth from extremes of the overly thin, diffuse and porous boundaries to overly thick, solid and dense boundaries.

We pull others towards us, suddenly experience them as threatening (or at least, “disgusting”), and push them away. Then, of course, we get anxious and pull them back. And, and, and.

And no one points it out. The mass market and “conference-approved” literature, mostly from the 1980s and ‘90s, barely discusses the issue at all, and if it does, does not dig into it in any depth. Worse, however, I have seen that without illumination, discussion and regular reminders, the socially normalized polarities of all-good or all-bad, all-right or all-wrong, all-or-nothing flip-flopping become set in concrete.

My observation over 20 years is that it is so perverse, widespread, mutually reinforced and socially normal among recoverees of all types that it hardens into a unconscious pattern of flip-flopping between absolute boundaries here and total abandonment of boundaries there. (It looks to me like it’s a “way of life” in the large AA club or NA group.)

The men and women who cannot see, acknowledge, “radically accept” (see Brach, Hayes et al, and Linehan) their continuing sex and romance addiction (see Mellody) provide very obvious examples. They “talk the talk” but cannot “walk the walk.” They can parrot the homilies from the literature... and they should; it’s very often how we “get it.” Many may even share in depth and detail how they have “broken through” and “set firm boundaries” against a narcissistic or dependent – or abusive – mate, only to allow their boundaries to collapse again when the anxieties built on their other fear of abandonment begins to resurface.

Black and white, all or nothing absolutism works poorly in politics, in religion, and in personal relationships (see Beck et al, Dyer, Ellis et al, Knaus, Meichenbaum, Rokeach, Ruggiero, and Wessler et al). But it is very deeply ingrained in the unidentified, unexplored, unexamined, unaccepted and unowned belief systems (see all above) of those whose minds were so damaged by ACA childhoods and conditioned by over-exposure to the black and white, all or nothing thinking of the common cult-ure at large.

It is not their fault. But as many in Narcotics Anonymous wisely point, “We are not responsible for our disease, but we are responsible for our recovery.” To clear the hurdle of our deeply conditioned fears of both abandonment and abuse – the conflicting fears that keep us stuck in co-dependence – we will have to identify, acknowledge, radically accept, own and consciously experience them as regular events in our emotional experience (see Dimeff & Koerner, Hayes et al, and Linehan).

The essential conflict between those fears of abandonment and abuse is barely touched upon in the mass market literature, although Whitfield mentions them briefly here and there in his 1991 book, Co-Dependence: Healing the Human Condition. He does not, however, see them quite as Mellody did in her 1992 book, Facing Love Addiction, even if she did not dig into as deeply as others have. Complex classroom texts like Kernberg’s Severe Personality Disorders and Meissner’s The Borderline Spectrum gave the two conflicting fears sufficient description that I could run with it and develop the concepts further in my own work on “borderline organization” (see Garrett).

I now understand the conflict to stand at the very foundation of most forms of behaviorally conditioned (as opposed to genetically caused) mental illness, regardless of the “official diagnosis.” The not-okay inner child is actually two inner children. It is actually two, separate and distinct, systems of core beliefs, values, ideals, principles, codes and rules.

One is frightened of being neglected, isolated and alone, and will do anything it can to avoid the emotional experience of anxiety (or even terror) that results from appraising itself as “intolerably alone.” The other is equally scared of being humiliated, embarrassed, invalidated, invaded, molested, incested, battered or otherwise abused… and will do anything it can to avoid the emotional experience of anxiety (or terror) of being subjected once again to “intolerable harm.”

Precisely as Mellody explained it for the first time in simple language in 1992, the ACA / co-dependent’s not-okay inner child is caught in a battle between the abuse- and abandonment-fearing, “split off parts” of itself (see Bion in Symington, Fairbairn, Kernberg, Klein in Mitchell, Masterson, Meissner, Scharff & Scharff, Whitfield, and other “object relations” theorists). The abuse-fearing inner child is easily angered by the abandonment-fearing inner child’s need to be “loved,” placing the abuse-fearer in the line of fire of some new seducer who’ll knock him or her around again. The abandonment-fearer is equally enraged by the abuse-fearer’s reluctance to engage in what the abandonment-fearer insists are “loving” relationships.

And they fight relentlessly over control of the body to do their respective will.

In borderline organization, these two, split apart, not-okay inner children never see, know or understand the other. This is because most people are quite understandably totally unaware of their inner children, their fear of each other gaining control of the body, and their projections of “awful things” when the other one takes control.

I understand that I have taken the “long way around Robin Hood’s barn” here. But without an understanding of the “psychodynamics” of co-dependence and ACA behavior, one cannot see the other conflict described 20 odd paragraphs ago: the one between the needy seeker of approval from others in the recovery group vs. the increasingly disgusted judge of the others in that same room. The conflict between the needy approval seeker and the needless disgusted judge is the conflict between the abandonment- and abuse-fearing, not-okay inner children.

And the recovering ACA / co-dependent will have to come to look for, recognize, acknowledge, “radically accept” and own this conflict in him- or herself before he or she can send it to the mental digestive system. The needy-here / needless-there (see Mellody, and Whitfield), love-addicted here / love-avoidant there (see Mellody), obsessed with connection here / obsessed with protection there, borderline-organized ACA / co-dependent will have to discover empathy and compassion toward his or her split-off, not-okay inner children.

And that discovery will have to be nurtured, developed and carefully tended to so that it can grow to become strong and sturdy enough to overcome the fears of those two, warring inner children. To “get there,” the recovering ACA / co-dependent will have to come to be able to experience and accept him- or herself as the separate, living, bodily container or “residence” for those two inner children and identify them as separate and distinct, not only from each other, but from the very, evolving consciousness that can now see and accept them (see Linehan, truly the expert on this).

You will not read about this war anywhere in the ACA or CoDA literature. It is not there. The bits and pieces of scientific research on human nature that has made the descriptions in this article possible had, for the most part, occurred by the time those books were written. But until the advent and widespread use of the Internet in the later 1990s and early 2000s, very few people knew of the fragments I have described here.

And no one, to my knowledge, anyway, had put them together in this fashion.

So. Acquiring such grasp as I have had to acquire for my own recovery from child abuse and resulting borderline organization, I have been able to come to see how far in the “right directions” Pia Mellody and Charlie Whitfield had come 20 years ago. Mellody’s incredible simplification of borderline organization into the push-pull dynamic of “love addiction” and “love avoidance,” and Whitfield’s equally astonishing distillation of object relations theory into the notion of the “split apart inner child,” were seminal works. Sadly, however, they both became so caught up in bright lights that shown upon them for so doing that they seemed to have lost the thread.

I am trying here to regain it. And in so doing, point squarely at Tara Brach’s Radical Acceptance and the discourse therein on compassion as seen through the eyes of a practicing Buddhist, as well as way back to Carl Rogers and the descriptions of “empathy,” “emotional congruence” and “unconditional positive regard” in his On Becoming a Person. For it is in those descriptions that I see the light at the end of the tunnel of the combined fears of abuse and abandonment.

And I will call that light “compassionate boundary setting.”

In the simplest words I can come up with: “Neither too much, nor too little.” For too much of any good thing is not necessarily a “good” thing. (The law of too much and too little applies all over the place, of course.) With mindfulness skills developed from direct, meditative experience of one’s feelings and appropriate distancing from one’s beliefs, values, ideals, principles, codes and rules (see Hayes et al, and Linehan), anyone can learn to set compassionate boundaries that ere neither too thick nor too thin.

In my own experience of discovering, acquiring and utilizing “CBS,” I have come to see that the idea provides me with an instant grasp of my emotional and behavioral steering wheel. Regardless of how afraid my inner children may be of either abuse or abandonment in any present moment, my practice of being aware of their thoughts (be they approval seeking or judgmental) and emotions (be they fearful or disgusted) reveals them to me. When I can see and feel them, I can acknowledge them, own them, comfort them, and calm them down. And as a result, experience that my inner children can let go of the need to overly attach or detach from others whose inner children are just as wrapped up in their fears of abuse and abandonment as mine are.

Working from Table 2 in Chapter 13 of Paul Gilbert's Compassion Focused Therapy, I developed the following schematic to differentiate "compassionate self-correction" (CSC) from "shame-based criticism and attacking" (SBC) of myself and others:

1) CSC focuses on the desire to have a better realtionship with myself and others; SBC focuses on the desire to condemn and punish myself and others.

2) CSC focuses on growth, maturity, expansion and enhancement; SBC focuses on punishing past errors.

3) CSC is forward-looking and aimed at a better future; SBC is backward-looking and stuck in "shameful" past.

4) CSC is given (to myself and others) with encouragement, support and kindness; SBC is given with frustration, contempt, anger, disappointment and discouragement.

5) CSC is self- and other-empowering; SBC is self- and other-disempowering.

6) CSC is about responsibility; SBC is about blame.

7) CSC rewards (and reinforces); SBC punishes (and reinforces).

8) CSC focuses on specific attributes and qualities in oneself or another; SBC globalizes the self or another as "all good" or, if not all good, then "all bad."

9) CSC focuses in hope of a better future; SBC focuses on expecting the worst.

10) CSC embraces a confidence in success; SBC is rooted in fear of failure.

11) CSC embraces "healthy guilt," personal responsibility and engagement in the recovery process; SBC wallows in shame, fear of reprisals and avoidance.

12) CSC is a display of courage; SBC is a display of caving in to learned helplessness.

13) CSC accepts sorrow and remorse for the results of one's conditioning by others; SBC rejects the truth of our social programming.

14) CSC supports amends and reparations; SBC compels avoidance or aggression.

Are we stuck forever in the multiple, repeated conditionings of a cult-ure of shame-based criticism and attacking? Or can we learn a new intra- and inter-personal paradigm and compassionate self-correction, as well as compassionate, but appropriately boundary-setting, tolerance of others who are only acting as they do because of psychic aches and pains that very closely resemble our own?

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Woititz, J. G.: Adult Children of Alcoholics, Pompano Beach. FL: Health Communications, 1983.

Woititz, J. G.; Garner, A.: Life Skills for Adult Children of Alcoholics, Pompano Beach, FL: Health Communications, 1990.

Young, J.: Cognitive Therapy for the Personality Disorders: A Schema-Focused Approach, 3rd Ed., Sarasota, FL: Professional Resource Press, 1999.

© 2012 by Rodger Garrett; all rights reserved. Links are okay. Please inquire or comment to not_moses@fastmail.fm. Thank you.

Book Review: The Cognitive Behavioral Workbook for Anxiety

2012-01-20T23:27:00.000-08:00

3.0 out of 5 stars Good REBT + Exposure, but not DBT, ACT, SIQR or MBCT

Rodger Garrett "SighKoBlahGrr" (Loma Linda, CA USA) - See all my reviews

(REAL NAME)

This review is from: The Cognitive Behavioral Workbook for Anxiety: A Step-by-Step Program (Paperback), by William Knaus, Oakland: New Harbinger, 2008.

Professionals:

Coming as it does from the New Harbinger stable, one might expect Knaus's book to include an in-depth review of mindfulness-based, experiential techniques along with CBT. One would be wrong.

Knaus is solidly rooted in Albert Ellis's rational emotive behavioral therapy, as well as the old-school exposure therapies of the '70s and '80s (think "Edna Foa"). But in this book (published well into the MBCT era in 2008), the "radical acceptance" and progressive self-awareness techniques that mark the MBCT's like acceptance and commitment therapy, dialectical behavior therapy, and self-talk identification, questioning and revision, are not discussed.

Those whose anxiety and panic are fundamentally the products of left hemisphere dominance and irrationality may derive a lot of useful information and method here. But those whose anxiety and panic are essentially the products of right hemispheric hyper-emotionality (e.g.: hysteric borderlinism) should not expect much help... or, at least, not the "complete package."

Put in terms of personality theory, this might be a good book for people with DSM Axis II Cluster A traits, but probably not for those with traits from Cluster B. And in terms of neuropsychology: Those with over-myelinated downlinks from an over-thinky neocortex seem likely to do better with this than those with little neurological governance of their limbic systems.

Moreover, if the patient's anxiety is a function of dissociated terrorizing and complex PTSD, New Harbinger offers other workbooks more likely to help the patient acquire the skills base he or she will need to get some affective comfort. Among them: the Blocks' Mind Body Workbook for PTSD, Marra's Depressed & Anxious, Follette & Pistorello's Finding Life Beyond Trauma, and Hayes & Smith's Get Out of Your Mind & Into Your Life.

That said, the two pages on "A Case of Managing Panic" distills some of the most useful and artful translation of Selye and Wolpe I have thus far run into in a mass market volume. I wish I had understood overrunning the General Adaptation Syndrome and shipwrecking the autonomic nervous system as well as those notions are portrayed in those two pages a decade and a half ago.

Book Review: Mind and Emotions

2012-01-09T21:37:00.000-08:00

4.0 out of 5 staAll the Science, But Not the Art, of the MBCTs... Maybe =Too= Generic

4.0 out of 5 stars All the Science, But Not the Art, of the MBCTs... Maybe Too Generic

Rodger Garrett "SighKoBlahGrr" (Loma Linda, CA USA) - See all my reviews

This review is from: Mind and Emotions: A Universal Treatment for Emotional Disorders by Matthew McKay, Patrick Fanning and Patricia Zurita Ona (New Harbinger Self-Help Workbook) 2011

My expectations may have been too great. Having waded through several of the other New Harbinger work books (all of them at least four-star), it may be that I thought a "best of" compilation would somehow be a genuine step further.

While the procedures / methods / techniques are all here, and it's hard to fault the nuts and bolts of M&E, I came away a little (though not "greatly") disappointed. McKay and a different group of co-authors did a wonderful job capturing and operationalizing Marsha Linehan's DBT in 2007.

But I recall thinking after I was a ways into that book that it was bit less "artful" than Marsha herself (at least on stage; her 1993 masterwork reads like a Chilton auto repair manual). The DBT Skills Workbook just lacked the metaphorical and other "tonal" quality of Steven Hayes's stunning Get Out of Your Mind and Into Your Life and Thomas Marra's Depressed & Anxious.

Maybe it's that I'm personally very attracted to Miller & Rolnick's Motivational Enhancement Therapy. Because, after all, the real challenge is in the denial / pre-contemplation and contemplation / consideration phases of the specific withholds any "seeker" may still have... despite his or her willingness to dig into meaningful ACTion in the already recognized and "radically accepted" areas of affective or behavioral difficulty.

The "art" of psychotherapy is most often required in those first two phases, after all.

Of course, it really comes down to how and when the book is used. For the "seeker" who's already been down the road a ways, and/or is already familiar with the methods and techniques of the mindfulness-based cognitive therapies, M&E strikes me as fine source of rehearsal and skills acquisition. It's just that my experience tells me that the very shame-based, anxiety-soaked patient may have more difficulty gaining traction with M&E than he or she would with Follette & Pistorello's Finding Life Beyond Trauma, or the two workbooks mentioned above.

I suppose what I'm suggesting is that it might be useful for NH and the authors to look at expanding what's already a very solid rundown of the most empirically proven of the DBT / ACT / MBCT skills with a little more metaphorical and other MET-style "sauce" to make them more appealing.

Book Review: The Mind at Night

2012-01-08T00:40:00.000-08:00

Actually Explains Why Mindfulness Meditation Works

Rodger Garrett "SighKoBlahGrr" (Loma Linda, CA USA) - See all my reviews
(REAL NAME)

This review is from: The Mind at Night: The New Science of How and Why We Dream, by Andrea Rock; New York: Basic Books, 2004 at http://www.amazon.com/Mind-Night-New-Science-Dream/dp/0465070698/ref=sr_1_1?s=books&ie=UTF8&qid=1326005667&sr=1-1.

The mere fact that someone has written a book in which Bill Domhoff up at UC Santa Cruz is liberally quoted will probably send the authoritarian, wealth-sucking, one-percenters up the wall. Bill, you see, may be one of our major dream researchers, but he's also the author of Who Rules America? Challenges to Corporate and Class Dominance, now in no less than its sixth edition since Noah's dog was a pup. That he showed up in a book about dreams struck me dumb (at first).

Listen: If you're the average guy or gal, stop reading right now; this is not going to shake your tree. This is not a book about dream interpretation and dramatic deciphering. (Look for Calvin Hall or Carl Jung or the grand old man from Vienna, himself.)

Because this is a book about the evolution of mid-20th century and millennial era neuropsychology as it relates to how important dreams appear to be to the maintenance of a healthy brain, not to mention growth towards greater effectiveness and creativity. There's no method here, but there's a lot of explanation of why the emerging rubric of mindfulness is changing the humna potential, as well as psychotherapeutic, map.

Figure this: If you do the mindfulness meditation / Power of Now / Radical Acceptance / Get Out of Your Mind and Into Your Life do, you can pretty much expect after reading The Mind at Night that the mindfulness meditations package our emotional and cognitive experiences in a way that works really well to make sense of it all during sleepytime.

Frankly, we used to think that MM did the job all by itself in some mysterious way we hadn't figured out yet. But this book went a long way toward blowing that theory out of the water. Research since the publication of the book has pretty conclusively demonstrated that MM wraps the dis-integrated bits and pieces of our sensory and emotional experience and evaluative efforts to make sense of them in neat little, pre-digested biscuits that are almost ideally organized for REM sleep processing.

I've been doing the do for some time now. Utterly life-changing. Wouldn't give it up if you put a gun to my head.

So for those of you who haven't gotten on the bandwagon yet, Rock's very sophisticated journalistic endeavor may be edifying. And it may even increase your motivation to start meditating Vipassana-style. (Everybody loves a good "explanation" now and again.)

Motivational Interview Questions for Cult Members

2012-01-07T21:51:00.000-08:00

The following is a first-blush run-through of suggested, awareness-raising questions in a motivational interview schematic for members of cults subjected to family or individual intervention at the denial / pre-contemplation or contemplation / consideration stages. It is essentially grounded in Shaffer et al’s notion of a universal syndrome model of addiction, much as I treated it in a pair of earlier papers cited in the References.

The questions are set up for “yes” (this is the case) or “no” (this is not the case) answers.

It may be that a first tier for cult members in denial / pre-contemplation and a second tier for members in contemplation / consideration (see Prochaska & DiClemente) will be more positively result-productive.

Bear in mind that many committed members at denial / pre-con may refuse to answer the questions. When that is the case, the questions should be read to them without requiring that they answer or respond in any way. Most con / cons will answer all or most of the questions, but may refuse here and there.

Vis Miller & Rolnick’s Motivational Interview Technique (from their Motivational Enhancement Therapy; see also Rolnick & Miller), the object is not so much to provide an immediately convincing list of “yes” answers under the “test” taker’s nose as it is to introduce concepts into conscious awareness in such a way that the test taker is moved toward a state of cognitive dissonance vs. the beliefs indoctrinated by the cult.

I am not proposing an ordering of the questions here. One can argue for linear “chaining” of three or more questions in a row to move a respondent up a ladder of abstraction (see Korsybski, and Hyakawa) or for disconnecting the links of the “chain” to make them less evident to the test taker. One might also argue for re-phrasing the questions so that “no,” as well as “yes” answers are aligned to reality.

The psychodynamic underpinning for the specific, suggested questions is as follows:

1) Deconstruct existing support and/or dependency systems and replace them with new support and dependency systems (See Lifton, Singer, Schein, Galanter, and Taylor relative to cults; and Carver, Rotter, Shaffer & LaPlante, and Evans relative to similar dynamics in family systems and other interpersonal relationships; I will insert a semicolon to demarcate the citations throughout this list).

2) Develop, reinforce, and then appeal to an un-admitted and denied sense of powerlessness, then helplessness, then hopelessness (see Lifton, Schein, Hoffer, Singer, and Taylor; Bandura, Seligman, Bowen, Golomb, Jackson, Branden, Carver, Rotter, Skinner, Watson, Lidz, Henry, and Laing).

3) Use love-bombing in the early stages followed by withdrawal thereof followed by increasing pressure to conform to get “love,” followed by threat of abandonment over non-conformance (see Singer, and Taylor; Beattie, Cermak, Schaef, Rapson & English, and Mellody).

4) Manipulate and trigger already established – and then enhanced – introjections of guilt, shame, worry, remorse, regret and anxiety (see Lifton, Schein, Singer, Hoffer, and Taylor; Tangney & Dearing, Jackson, Lidz, Bowen, Branden, Golomb, Henry, and Laing).

5) Employ stimulus deprivation and/or amplification, rapid deep breathing (to induce hyperventilation), repetitive motion exercises, chanting, meditation, guided imagery and/or trance induction to create dissociation, de-realization, depersonalization and/or excitotoxic (nerve-damaging) anxiety (see Singer; and DeBellis, Cozolino, Gazzaniga, Heim & Nemeroff, Kaszniak, and Panksepp relative to neurobiology).

6) Use sleep deprivation, diet control, restriction of urination and/or defecation (i.e.: “re-potty training”) to stress, break down the ego and infantilize (see Lifton, Singer, and Taylor).

7) Compel personal history examination, revision and group sharing to induce painful affects and peer-influenced appraisals thereof (e.g.: “I am bad for having done…”) (see Lifton, Schein, Singer, Hoffer, and Taylor; and Ross).

8) Use ever increasing group jargon to enhance in-group identification and out-group rejection, as well as to make it increasingly difficult for members to communicate effectively with outsiders (see Schein, Singer, Hoffer, and Taylor; and Griffin & Moorhead and Kets de Vries relative to organizational dynamics).

9) Manipulate peer pressure to conform to group norms, including group think and group jargon (see Lifton, Schein, Singer, Galanter, Hoffer, and Taylore; and Griffin & Moorhead, and Kets de Vries; and Rokeach, and Henry).

10) Employ Karpman Drama Triangle dynamics: covert control as both rescue and subtle – or not so subtle – persecution to victimize the lower-level recruits and induce compliance via the discomfort of subtle threat (see Karpman, Beattie, Weinhold & Weinhold, Whitfield, and Garrett).

11) Use deception, debilitization, dependency and dread to weaken member’s egos and increase compliance (see Schein, and Singer; and Schore relative to affect regulation).

12) Use authoritarian dominance and submission ploys, games and exercises to identify “proper” and accepted, sadomasochistic roles for leaders vs. followers (see Lifton, Singer, Galanter, and Taylor; and Altemeyer, Baumrind, Benjamin, Sullivan, Rotter, Berne, Byrne, Bernstein, Carver, Golomb, Lidz, Henry, Laing & Esterson, Lifton, and Peterson & Zurbriggen relative to non-cult interpersonal dynamics).

13) Establish ambiguities and conflicts to destabilize existing core beliefs, utilizing paradoxical injunctions, threat of harm or abandonment and other means to induce double binds (see Bateson, Laing, and Watzlawick et al).

14) Induce identity-diffused, ego-dis-integrated, borderline organization (see Kernberg, Meissner, Masterson et al, and Garrett) via compartmentalization of unconsciously opposing, compelled beliefs (“shoulds,” “musts,” “oughts,” “have-to’s”) to support the mutually opposing fears of abuse and abandonment that make it impossible to resolve group-induced conflicts.

15) Induce anxious attachment (as per Bowlby, Shaver & Mikulincer, and Cassidy & Shaver) to place the member in a state of learned helplessness (see Seligman, Schore, Mellody, Whitfield, and Rapson & English).

16) Employ increasing and finally, absolute, control of information and communication among members (see Lifton, Schein, Singer, Hoffer, Galanter, and Taylor).

17) Compel regression on both the Piagetian and Eriksonian scales, from formal operational (hypothesis and test, dialectical) processing, autonomous identity and elective generativity… to concrete operational (black & white, all or nothing, dichotomous /absolutistic) processing, infantile trust and lack of autonomy, respectively (see Piaget, Erikson, Beck, Ellis, Meichenbaum, Schore, and Rokeach).

18) Compel relentless loading of the sympathetic branch of the autonomic nervous system to set up the leader(s)’s ability to trigger the fight, flight, freak or freeze response to support learned helplessness whenever desired (see Selye, Wolpe, and Seligman).

A list of suggested MIT questions:

Were you invited to a lecture or a dinner to introduce you to your group?

Are you allowed to question your group’s leaders in public?

Are you required to live with others in the group?

Do the group’s leaders suggest that you chant or meditate when not working or otherwise occupied?

Are you pretty busy most of the time with group activities?

Are you required to recruit new members to the group?

Are you required to solicit donation or raise funds for the group?

Have you been told to stay away from or not talk to members of your family?

Do you live with other members of your group in a remote location?

Have the group leader(s) asked you to quit school or work?

Have you been asked or required to work for the group or its leaders without compensation?

Do you often experience being tired, fatigued or “worn out?”

Did you feel truly and/or greatly loved and accepted at first… then criticized and belittled later on?

Did you have to give up your automobile to the group or use it often to provide transportation for group members?

Have you been told that the ideas, beliefs and/or values you had when you joined the group are wrong, inaccurate or bad?

Have you been told by the leader(s) to have or not have a sexual or romantic relationship with another member of the group?

Have you been told by the leader(s) of the group to have or not have a sexual or romantic relationship with someone outside the group?

Are you required to keep an eye on and report on the behavior of other members to the group leader(s)?

Have others in the group told you that your thoughts or beliefs are “evil?”

Do you sometimes feel like you’re “caught between a rock and a hard place?”

Do you depend upon the group for your meals?

Are you required to eat certain foods and/or not eat certain foods?

Are you required to confess your bad behavior, past or present mistakes or sins to the leader(s) or other members of the group?

Have you ever been put on the “hot seat” and subjected to questioning and/or criticism by the leader(s) or other members of the group?

Have you ever felt as though you should talk and/or act a certain way in the group?

Do you ever act as if you understand things the group members or leader(s) are saying that you actually do not understand?

Have you ever been told or made to feel by the members or leader(s) that you are “defective,” “resistant,” “incompetent,” or “troublesome?”

Have you been threatened with expulsion from the group for failing to meet standards that sometimes seem very difficult or even impossible to meet?

Have you ever been “made wrong” in front of the group?

Are you often so tired that you’ve no energy for anything other than the group?

Do you sometimes feel like a hero or a rescuer of others, and sometimes like a persecuted victim?

Are you sometimes uncomfortable with being required to be dominant and then submissive?

Do you sometimes feel like a “fool” in front of the other members?

Save for reporting to the leader(s), are you required not to gossip about others in the group?

Do you sometimes feel isolated from other members of the group?

Do you sometimes feel isolated from the rest of the world?

Are group members required to learn and talk in words and phrases that are different from those outside the group?

Do you find it difficult to talk with people who do not speak as the group does?

Is it easier to confine your conversation to other members of the group now?

Does the group or its leader(s) have special names or terms for people outside the group?

Do the special names or terms for those outside the group make you feel better about yourself?

Does the leader discourage friends and family members from outside the group from visiting you at the group residence?

Has it been suggested that most significant friends and family members not know where you live or attend group events?

Do you feel strongly that the beliefs, ideas, views, opinions and attitudes that you have learned from the group and/or its leader(s) are right even though they disagree with most beliefs, ideas, views, opinions and attitudes of outsiders?

Do you agree with and support the group’s and/or leader’s “absolute truth?”

Do you see the world outside the group as being absolutely or totally wrong about matters important to the group and/or its leaders?

Does it feel to you like you are “wrong,” “mistaken,” “stupid,” “incompetent” or “dumb” much of the time?

Are you required to keep a truth-telling diary and present it to the leader(s) upon demand?

Do you experience annoyance, irritation, resentment, defensiveness or hostility when asked if you felt coerced, manipulated or intimidated to join the group and remain committed to it?

Are you “on board” with the group’s and/or leader’s sense of “higher purpose?”

Do you often feel disturbed, anxious, fearful or frustrated with the leader(s) or other members even though you agree with the group’s and/or leader’s vision of reality and purpose?

Have you gained or lost more than 25 pounds since you joined the group?

Does it seem to you sometimes that your group’s or leader’s ideas are not quite square with your own sense of reality?

Does you group or leader(s) present proof of the group’s or leader’s ideas in the form of a single book you view as special?

Do you see yourself and other members of the group as more informed, more competent and more capable than most (or all) of the people outside the group?

Have you ever been accused of being “resistant?”

After some period of being “on the fence,” did you finally come to completely accept without question the views of the group and its leader(s)?

Have you ever felt pressured to follow what other members or leaders define as “the proper path to purity?”

Have you sometimes wondered if everything you were being told by the members or leader(s) was the truth?

Are you required to witness to, preach, carry the message or otherwise communicate the group’s and/or leader’s views to others outside the group?

Have you been subjected to harsh criticism, group disapproval, ostracism or loss of rank, status, rights or freedoms for your thoughts or behavior?

Have you ever been accused of being “strong-willed” or “rebellious?”

Have you ever been told that the devil was beside or within you?

Do you believe strongly in the concept of sin?

Do you often feel guilt, remorse, regret, shame or worried?

Do you ever have anxiety attacks or long periods of thinking “I’m no good?”

Do you often lose track of time?

Do you sometimes feel like you’re in “a separate reality?”

Are you sometimes told to breathe at a very rapid rate during group meetings?

Does it feel safer to turn your will and your life over to the will of the group leader?

Do you often feel condemned by others in the group or the group leader?

Do you sometimes sense that you are being unduly dependent, submissive or suggestible?

Do you often feel embarrassed, shamed or humiliated during group meetings?

Are you required to meditate precisely as the leader instructs you to?

Are you prevented from seeking medical or dental care outside the group?

Are you restricted from shopping, going to the movies or the activities by yourself?

Do you sometimes experience being outside your own body looking at yourself?

Do you sometimes feel as though your surroundings are unreal or “fantastic?”

Do you sometimes feel numb, tingling or very hot or very cold?

Do you sometimes feel like you are “going crazy” or “losing your mind?”

Do you ever feel like a “ticking bomb about to explode?”

Are you ever afraid of trying to live outside the group?

Do you fear reprisal or retribution from the group or leader(s) if you decide to leave the group?

Has the leader or leaders ever asked you to turn over your money, jewelry or bank account to them?

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Business, Politics & Mindfulness

2012-01-05T23:14:00.000-08:00

A preliminary entry on the ramifications of functional brain scan research in power-seeking modalities... and the correlations of business concerns with those of clinical treatment.

Ask often – or even just keep the channels open long – enough, and the answers one has been seeking will often turn up. I wanted to know if the mindfulness rubric that has so considerably changed the nature of clinical psychology and psychotherapy in the past decade or so, has found its way to those with wealth accumulation and power imperatives.

Indeed, if Powell’s article and the various citations therein are sufficient evidence, the power elite is not only paying attention but dropping its discoveries right into the lap of “applied psychology.” The implications are probably “good” for those who have to compete with the labor advantages of offshore competitors who may not “get hip” real soon, but if not “bad,” then at least “of concern” relative to potential for even more sophisticated manipulation of billions of vastly less sophisticated consumers.

Beyond that, there’s the issue of “creeping corporate cultism” that has been fostered by the neural linguistic programming (“NLP”) and large group awareness training (“LGAT”) programs that are being increasingly normalized in the business consulting world. The top echelons of the NLP and LGAT consultancies built their programs on scientific research of mass manipulation by the likes of Lifton, Schein, Singer, Galanter, Taylor and others, and would apper to be playing close attention to the brain function mappers for what they can glean that is of use to them.

But there is also plenty in Powell’s article with obvious applications for the clinician who doesn’t yet fully understand the very new neuroscience of personal values directly resulting from millennia of evolutionary natural selection. Few articles – or books – I have encountered cover the topic of the neuroscience and conditioning of affect regulation in the work-a-day world so thoroughly.

Significant callouts relative to brain function include:

“…loss aversion is neurally encoded in the striatum and ventrolateral prefrontal cortex…”

“…implicating the ventromedial PFC in the neural encoding of willingness to pay across a wide spectrum of products, activities, and experimental conditions…”

“…escalations of commitment correlated with brain activity in areas of medial PFC and anterior cingulate cortex consistent with a genuine expectancy of positive rewards…”

“…anticipatory functions of the nucleus accumbens, as well as well-established reward functions of the ventral tegmentum.”

“…ultimatum game. In the fMRI analysis, subjects who received low offers showed increased activity in three areas of the brain: dorsolateral PFC, anterior cingulate cortex (ACC), and the anterior insula. The magnitude of insula activations increased with the perceived unfairness of the offers and was greater for unfair offers from humans than from computers. It is known that dlPFC encodes uncertainty and updates experience with new facts and that the insula registers negative emotions associated with taste and odor, particularly disgust. Together, the findings suggested that low offers in the ultimatum game induce neural conflict between executive cognition in PFC and visceral disgust in the insula, mediated by information processing in the ACC.”

“…affect labeling reduced activity in the amygdala… writing negative emotions on paper activated an area of PFC (right ventrolateral PFC) which, in turn, led to a dampening of negative response in the amygdala…”

“…talking about negative emotions can make the situation worse by heightening arousal in the amygdala, insula, and cingulate cortex…”

“reappraisal engages more areas of PFC, while down-regulating amygdala arousal using right ventrolateral PFC…”

“…trained mindfulness practitioners engage regions such as dorsolateral PFC and somatosensory cortex, which support emotional regulation and external sense perception…”

“…amygdala is associated not only with fear, but also with bodily movements and the perception of sharp corners and musical tones; and the insula is associated not only with disgust, but also with empathy, pain, spatial learning, pitch perception, and speech production…”

“an area of the brain stem (the nucleus locus coeruleus) controls neurotransmitters that regulate the balance of exploration and exploitation…”

The original text, courtesy Wiley-Blackwell’s free service, appears in black; my comments are in dark red, as usual.

Neurostrategy

Thomas C. Powell

Article first published online: 27 OCT 2011
Strategic Management Journal, Volume 32, Issue 13, pages 1484–1499, December 2011

http://onlinelibrary.wiley.com/doi/10.1002/smj.969/full

Abstract

Brain research has contributed to economics, marketing, law, and other fields. Does strategic management need neuroscience? This paper examines the potential contributions of brain research to strategic management research and practice. The paper discusses the aims and methods of neuroscience, its strengths and limitations in social and economic research, and its potential contributions to strategy. The paper identifies specific research questions at the intersection of strategy and neuroscience and appraises the prospects for substantive collaborations between neuroscientists and scholars in strategic management. Copyright © 2011 John Wiley & Sons, Ltd.

Introduction

Without a doubt, brain research has arrived in the social sciences. Brain research has taken hold in economics (Camerer, Loewenstein, and Prelec, 2005), political science (Amodio et al., 2007), social psychology (Willingham and Dunn, 2003), law (Chorvat and McCabe, 2004), anthropology (Adenzato and Garbarini, 2006), archaeology (Ben-Ari, 2008), and sociology (Franks, 2003). Output in neuroeconomics has risen exponentially for nearly a decade, with no signs of slowing (Glimcher et al., 2009). Business schools are close behind, with researchers applying brain research to marketing (McClure et al., 2004), leadership (Rock and Schwartz, 2007), finance (Kuhnen and Knutson, 2005), and human resource management (Lane and Scott, 2007).

This paper examines the potential fit between neuroscience and strategic management. Does strategic management need neuroscience? In at least one sense, the answer is clearly yes. Strategic management has long-standing interests in executive judgment and decision making and in the psychological foundations of strategy practice (Hodgkinson, 2008). If executive decision making and behavior matter, then the brain is already in the game; and the more we can learn about it, the better.

At the same time, strategy researchers need to understand what neuroscience can and cannot do and to maintain a healthy skepticism toward its more extravagant claims. In strategic management, some scholars may wonder whether processes within the individual brain can really inform research that takes the firm and industry as its primary units of analysis (Rumelt, Schendel, and Teece, 1994). In fields where brain research is further along, as in economics and social psychology, scholars have raised serious objections to brain research, some of which are relevant to strategic management.

The following section discusses new opportunities and potential contributions of neuroscience to strategy, and the next section discusses weaknesses and limitations. The paper then proposes specific research agendas in neurostrategy, and appraises the prospects of brain science for advancing research and practice in strategic management.

The Case for Neurostrategy

Brain localization is an ancient science, traceable at least to Hippocrates and the Roman physician Galen, whose localization theory came from inspecting the brains of sheep. In the modern era, Marie-Jean-Pierre Flourens (1794–1867) localized brain function by damaging a part of the brain and observing behavioral deficits, a method known as experimental ablation; Jean Baptiste Bouillaud (1796–1881) located speech in the frontal lobes and pioneered the theory of lateral asymmetry (differences in the left and right hemispheres); and Paul Broca (1824–1880) located speech in the part of the left frontal lobe now known as Broca's area.

In the present day, neuroscientists study brain localization at several levels of analysis—molecular, cellular, systemic, and behavioral. Behavioral neuroscience includes disciplines such as neuroeconomics and neuromarketing, which link activity in the brain to reputation, status, cooperation, trust, and altruism (social neuroscience); learning, perception, memory, and decision making (cognitive neuroscience); and feelings, passions, sentiments, and motivational states (affective neuroscience). Clearly, some of these areas address research problems in strategic management and suggest the possibility of linking strategy and neuroscience.

The case for neurostrategy relies on strategy's long-standing emphasis on general managers. The Academy of Management defines business policy and strategy as ‘the field concerned with the roles and problems of general managers and those who manage multibusiness firms or multifunctional business units.’ Nag, Hambrick, and Chen (2007: 944) defined strategy as ‘the major intended and emergent initiatives taken by general managers on behalf of owners, involving utilization of resources, to enhance the performance of firms in their external environments.’

Strategic management rests on the assumption that the thoughts, feelings, and social relations of general managers influence the activities and performance of firms. This is evident, for example, in strategy research on upper echelons (Hambrick and Mason, 1984), executive perceptions (Sutcliffe, 1994; Starbuck and Milliken, 1988), risk preferences (March and Shapira, 1992), beliefs (Denrell, 2008), cognitive schema (Prahalad and Bettis, 1986), attention (Ocasio, 1997), causal attributions (Powell, Lovallo, and Caringal, 2006), competitor perception (Zajac and Bazerman, 1991) and aspirations (Mezias, Chen, and Murphy, 2002). To the extent that cognition, affect, and social perception are seated in the central nervous system and brain, strategy researchers should welcome opportunities to explore the contributions of behavioral neuroscience.

But what are those contributions, exactly? The remainder of this section draws examples from neuroeconomics and other fields to explore the potential upside of neurostrategy. Three potential contributions are discussed: construct validation, theory testing, and informing strategy practice.

Construct validation

Strategy theories often use unobserved psychological constructs to explain observed behavior. For example, Fiegenbaum and Thomas (1988) inferred the existence of loss aversion in a sample of U.S. executives based on COMPUSTAT data. One of the ways neuroscience contributes to social research is by linking unobserved mental constructs such as loss aversion with physiological events in the brain. For example, it is conceivable that the psychologist's concept of loss aversion would give no clear pattern of brain activity or would give different patterns of brain activity under conditions regarded as theoretically similar. Tom et al. (2007) investigated this question and found evidence that loss aversion is neurally encoded in the striatum and ventrolateral prefrontal cortex (PFC). Such evidence does not prove the existence of a mental state called ‘loss aversion;’ however, in combination with behavioral findings, it provides prima facie support for the construct validity of loss aversion and facilitates further hypothesis development in prospect theory (Fox and Poldrack, 2009; Hsu et al., 2009; DeMartino, Camerer, and Adolphs,2010).

Another important mental construct in behavioral strategy is willingness to pay. A consumer's willingness to pay derives from perceptions of subjective value or of differentiation in the firm's products and services. In strategic management, willingness to pay is essential to theories of competitive advantage, such as the resource-based view, which explain the excess of willingness to pay over the firm's opportunity costs. Is willingness to pay a valid psychological construct? Research in neuroeconomics has linked willingness to pay with specific regions of the brain, implicating the ventromedial PFC in the neural encoding of willingness to pay across a wide spectrum of products, activities, and experimental conditions, including the valuation of junk food, cash, and charitable contributions (Padoa-Schioppa and Assad, 2006, 2008; Chib et al., 2009; Plassmann, O'Doherty, and Rangel, 2007; Hare et al., 2010). The findings show that subjective valuation uses a common neural currency, providing prima facie evidence of the construct validity of willingness to pay.

In social psychology, Willingham and Dunn (2003) argued that neural evidence can help establish the separability of mental constructs. For example, many psychologists regarded aggression and passivity as extremes on one spectrum of behavior, but others regarded them as separate constructs. The debate could not easily be resolved by traditional means, but fMRI evidence showed that decisions to approach and withdraw engaged different parts of the brain, providing support for the latter view. Similarly, Amodio and Devine (2006) showed that prejudice and stereotyping, although conceptually related, involved different neural activations; Ersner-Hershfield, Wimmer, and Knutson (2009) showed that temporal discounting increased as people differentiated between present and future selves; and neural evidence showed that racism and sexism activate different parts of the brain, suggesting different psychological foundations (Dovidio, Pearson, and Orr, 2008). Given the prevalence of bipolar constructs in strategic management—exploration-exploitation, cost-differentiation, cooperation-competition—strategy researchers may find that neuroscience offers new ways of establishing construct validity and separability.

Theory testing

In some circumstances, neural evidence may help adjudicate theoretical debates. For example, in social psychology, theorists debated for many years whether people's mental images are mainly pictorial or language based. The debate could not be resolved using traditional methods, but researchers using fMRI and brain lesioning showed that mental images are formed in the visual cortex, supporting the pictorial theory (Willingham and Dunn, 2003). In economics, Camerer (2008) argued that neural evidence may offer the best means of reconciling theories of ambiguity aversion—that is, the reluctance to choose when payoffs or probabilities are ambiguous.

RG: The Western mind wants dichotomous, either/or, all good or all bad clarity, which, it appears, cannot be achieved at the level of verbal representations of ambiguous events. In the Eastern view, such clarification can (only?) be achieved to a relative extent via Vipassana-style, meditation-based, ACT-method, values clarification (see Hayes et al). The person who has conscious experiential grasp of his essential values appears to have a better shot at resolving value conflicts and clearing the hurdles of ambiguity aversion. This looks to be the result of having transcended the verbal representations (including arguments for and against) in favor of direct affective experience of the “either” and the “or” based upon more basic, direct, affective experience of his core values.

EG1: The mindfully experienced, recovering sex and romance addict is believed to have direct, conscious experience of the major affects (emotional states and sensations) he has associated with the costs and benefits of his sex and romance addiction; a circumstance known since Buddha’s time to provide clarity for decision-making relative to choosing or avoiding potential partners.

EG2: The mindfully experienced, recovering substance abuser is believed to have direct, conscious experience of the major affects (emotional states and sensations) he has associated with the costs and benefits of his substance abuse; a circumstance known since Wilson’s and Kannon’s time to provide clarity for decision-making relative to choosing to either re-engage in or avoid re-engagement in substance use.

EG3: The mindfully experienced, recovering obsessive-compulsive is believed to have direct, conscious experience of the major affects he has associated with the costs and benefits of specific circumstances of control of his environment (e.g.: his automobiles) in such a way that conflicts about what to do with them when they need expensive repairs can be resolved according to input from his detached observation of his affective experience about the issue, as well as “hard data” from external sources about the relative value of repairing or discarding the automobile.

EG4: The mindfully experienced, recovering workaholic is believed to have direct, conscious experience of the major affects he has associated with the costs and benefits of specific circumstances of control of his career occupation in such a way that conflicts about what to do to either “advance” or “stay put” (or even “fall back”) when challenged with high levels of job-related stress can be resolved according to input from his detached observation of his affective experience about the issue(s).

According to Camerer (2008: 372), ‘the point of such tests is not to establish the neuroscience of ambiguity-aversion per se (although that may interest neuroscientists). The point is to use brain evidence to adjudicate empirically among theories which are particularly difficult to distinguish using the market-prediction test (for ordinary types of data).’

A key research topic in behavioral strategy is causal attribution, and many research questions remain open (Staw, 1975; Bettman and Weitz,1983; Salancik and Meindl, 1984). For example, it is unclear whether self-serving attributions stem from errors in information processing, the need for self-esteem, or deliberate impression management (Powell et al., 2006). Brain research on attribution is still in its infancy, but an fMRI study by Harris, Todorov, and Fiske (2005) found that dispositional attribution [RG: a form of emotion-loaded logic] (the fundamental attribution error) recruits brain regions similar to those of mentalization, suggesting that people explain causation by mentalizing the views of human actors. Neural evidence also shows that differences in American and Asian attributions (Americans tend to make more dispositional attributions) are linked to cultural differences in automatic and controlled processing (Mason and Morris, 2010). Neural research on attribution needs further attention and offers a promising method for explaining the psychological foundations of attributional errors.

RG: Such research has been underway for more than two decades among the so-called mindfulness-based cognitive therapy adherents like Hayes et al, Linehan, Forsyth et al, Marra, Siegel, and others. In line with their research, as well as my own secondary research into institutional and media manipulation of the masses, I have a point of view:

RG: My hypothesis is that Americans tend to have been socialized and normalized to make more dispositional attributions by the constant onslaught of emotion-triggering messages delivered by organized religion, political pundits and candidates, and the commercial mass media. It is also my guess that Asians will become increasingly socialized and normalized to make more dispositional attributions by the constant onslaught of emotion-triggering messages delivered by organized political authority and the commercial mass media being employed to motivate them to work harder to produce and consume more of the gross national product.

Many researchers have examined the escalation of commitment to failing strategies (Staw, 1981; Zajac and Bazerman, 1991), but its psychological motivations remain unclear—for example, escalation could stem from attribution errors, justifying past commitments, the need for decision consistency, or a genuine expectation of future payoffs (Schwenk and Tang, 1989). Using neural evidence, Campbell-Meiklejohn et al.(2008) found that escalations of commitment correlated with brain activity in areas of medial PFC and anterior cingulate cortex consistent with a genuine expectancy of positive rewards. They also found that loss chasing had a strong appetitive component, not unlike the cravings of cocaine dependency.

RG: Thus, loss-chasing may involve the recently discovered anticipatory functions of the nucleus accumbens, as well as well-established reward functions of the ventral tegmentum (see Knutson et al, and Bozarth, respectively).

Decisions not to escalate involved cortical areas associated with uncertainty avoidance and disgust, suggesting that escalation involves at least two separate neural systems. The debate is not yet resolved, but neural evidence will play a key role in testing alternative explanations.

In some cases, neuroscience has assisted both in construct validation and theory testing. For example, behavioral economists have used games such as prisoner's dilemma and the ultimatum game to study the role of trust and social norms in competitive interactions. In the ultimatum game (Güth, Schmittberger, and Schwarze, 1982), player A is given $ 10 to divide in some proportion between player A and player B, and player B can then accept or refuse the proposal. For example, player A may propose to keep $ 8 and give $ 2 to B. If B accepts, A gets $ 8 and B gets $ 2; if B refuses, both players get nothing.1

A review of experimental results for the ultimatum game found that, on average, player A offered more than $ 4 to player B and if the offer was less than $ 2, B refused about half the time (Camerer, 2003). These results support the behavioral view that people do not act out of pure economic self-interest, but also take account of social norms and fairness. However, behavioral experiments could not establish the psychological validity of motivations like punishment and fairness or establish clear links between these motivations and observed behavior. For example, it was unclear whether subjects refused low offers out of revenge, disgust, or perceived injustice.

In a widely cited study, Sanfey et al. (2003) used fMRI scans to observe brain activity in 19 participants in 30 rounds of an ultimatum game. In the fMRI analysis, subjects who received low offers showed increased activity in three areas of the brain: dorsolateral PFC, anterior cingulate cortex (ACC), and the anterior insula. The magnitude of insula activations increased with the perceived unfairness of the offers and was greater for unfair offers from humans than from computers. It is known that dlPFC encodes uncertainty and updates experience with new facts and that the insula registers negative emotions associated with taste and odor, particularly disgust. Together, the findings suggested that low offers in the ultimatum game induce neural conflict between executive cognition in PFC and visceral disgust in the insula, mediated by information processing in the ACC.

Informing strategy practice

Practitioners in applied fields like law, marketing, and politics have begun to integrate neuroscience with management and professional practice. Lawyers use brain scans to show the mental capacities of defendants, and jury consultants use neural evidence to predict punishment and retribution in jury decisions (Samson, 2007). Neuromarketing consultants use bran scans to evaluate consumers' cognitive and emotional responses to product features, packaging, and promotional campaigns (Knutson et al., 2007; McClure et al., 2004). Neural studies of politically conservative and liberal voters enable candidates to target voters' cognitive orientations (Westen et al., 2006; Knutson et al., 2006; Amodio et al., 2007).

Can neuroscience inform strategy practice? One area of potential contribution is behavioral self-control (Hare, Camerer, and Rangel, 2009). Behavioral economists have long noted that decision makers behave as though they have multiple selves—for example, a reflective and fairly rational ‘planner-self’ with long time horizons and an impulsive and unreflective ‘doer-self’ with limited capacity for delayed gratification (Thaler and Shefrin, 1981; Schelling, 1984; Ainslee, 1975). In economics, multiple-selves models have been used to explain addiction, procrastination, and self-binding commitments (Elster, 1985; Hoch and Loewenstein, 1991). In general management decisions, poor self-command manifests in problems like temporal myopia, excessive risk taking, ethical malfeasance, and escalations of commitment (Levinthal and March, 1993). In the firm as a whole, poor self-command gives rise to costly organization structures, controls, and incentives (Postrel and Rumelt, 1992).

Multiple-selves theories are consistent with general frameworks of neural organization, such as the triune brain model, and automatic (X-system) versus reflective (C-system) processing. The question for strategy practice is whether executives can control the C-system in a way that down regulates negative emotions in X-system structures like the amygdala. Neural evidence is beginning to emerge, and three areas—affect labeling, reappraisal, and mindfulness—have attracted the most attention.

Some psychologists believe that people can control negative feelings by the technique of ‘affect labeling’—that is, by writing their negative feelings on paper (Wilson and Schooler, 1991). However, the underlying psychological mechanisms of this method remained unclear. Neuroscience has begun to shed new light on the neural origins and impacts of affect labeling. For example, Hariri, Bookheimer, and Mazziotta (2000) found that affect labeling reduced activity in the amygdala, and Lieberman et al. (2007) found that writing negative emotions on paper activated an area of PFC (right ventrolateral PFC) which, in turn, led to a dampening of negative response in the amygdala. Moreover, studies show that affect labeling is more effective than other techniques. For example, trying to suppress negative emotions does not dampen the amygdala, and talking about negative emotions can make the situation worse by heightening arousal in the amygdala, insula, and cingulate cortex (Goldin et al., 2008; Ochsner and Gross, 2005; Gross and John, 2003).

These results are suggestive, but affect labeling does not address the deep and persistent emotional pressures facing senior managers in large organizations. A more substantial method of self-regulation involves reframing problems into new emotional contexts—for example, reframing a new market entrant as both threat and opportunity, or viewing global expansion from the perspective of the host country. This method, known as reappraisal, allows people to detach themselves from anxieties, resentments, and other negative emotions that inhibit creative problem solving (Gross, 1998). Reappraisal involves more complex mental operations than affect labeling (Lieberman et al., 2007), and neural studies show that reappraisal engages more areas of PFC, while down-regulating amygdala arousal using right ventrolateral PFC (Ochsner et al., 2004; Schaefer et al., 2003).

Executive judgment derives from experience, intuition, tacit knowledge, emotional maturity, and sensitivity to ambiguity and context (Vickers,1965; Priem and Cycyota 2001; Tichy and Bennis, 2007; Kahneman and Klein, 2009). Weber and Johnson (2009) linked judgment to a cluster of psychological processes—memory, attention, learning, and emotional processing—associated with cognitive mindfulness. In psychology, mindfulness implies the capacity to override automatic cognition by engaging with alternative points of view (Langer, 1997). In organization studies, mindfulness does not imply the denial of routines or automatic cognition, but the capacity to deploy them in strategic context (Weick, Sutcliffe, and Obstfeld, 1999; Levinthal and Rerup, 2006).

Research on mindfulness has grown dramatically in recent years, and has produced a subindustry of popular books, institutes, and executive seminars (Carroll, 2007). In a review of theory and research, Brown, Ryan, and Cresswell (2007) concluded that clinical and experimental mindfulness interventions nearly always improve short-term cognition and well-being, but that further research, with the aid of brain scanning and other neural methods, is needed to establish their lasting effects. Neuroimaging studies so far suggest that, whereas control subjects engage brain regions associated with subjective emotional response, trained mindfulness practitioners engage regions such as dorsolateral PFC and somatosensory cortex, which support emotional regulation and external sense perception (Farb et al., 2007; Farb et al., 2010). Neural research will play a key role in establishing whether managers can improve long-term emotional regulation through learned mindfulness (Rock,2009).

The Case against Neurostrategy

Many observers predict a bright future for interdisciplinary neuroscience. In law, Chorvat and McCabe (2004: 1735) predicted that neuroscience will ‘tell us how to significantly enhance compliance with law at a minimal cost and to encourage better forms of social interaction.

RG: Is there a potential for enhancing compliance with the law to such an extent that humans can be made into law-abiding automatons? Not to worry: If mindfulness is taught to the masses in the public education system, the experience thus far gained in the clinical world suggests anything but flesh-and-blood robotics. If anything, it suggests movement up Kohlberg’s six-level scale of morality for most, albeit with increased awareness among the sociopathic cognoscenti of how to better manipulate those who do not move up that scale.

This research will probably completely change the way we view nearly every area of law.’ In economics, Zak (2004: 1746) argued that “neuroeconomics provides a unified framework to measure physiological activity during the process of choice, and in doing so opens a window into human nature.' In executive leadership, Rock and Schwartz (2007: 2–3) wrote that ‘scientists have gained a new, far more accurate view of human nature and behavior change…Managers who understand the recent breakthroughs in cognitive science can lead and influence mindful change.’

At the same time, some social scientists remain unconvinced. For example, Gul and Pesendorfer (2008) argued that neuroscience cannot test economic models because economic models make no predictions about the brain. Economists typically concern themselves with observed conditions and choices—for example, the impact of a tax increase on savings—and not with intervening processes. In summarizing the challenge facing neuroeconomists, Bernheim (2009: 38) argued that ‘most economists are not convinced by vague assertions that a deeper understanding of decision making processes will lead to better models of choice.’

Similar suspicions could be raised about neurostrategy. It could be argued, for example, that neurostrategy cannot answer strategy questions because strategic management asks no questions about the brain. On the other hand, such objections seem to beg the main question, which is whether strategy should be asking questions about the brain. Moreover, the analogy from economics to strategy is imperfect. Strategy researchers have always been concerned with intervening decision processes, giving them equal weight with strategies and outcomes (Hofer and Schendel, 1978; Fredrickson and Mitchell, 1984). If neuroscience gives genuine insight into the mechanisms of strategic choice, then it has direct relevance to strategy research.

A more serious concern is that neuroscience is reductionist and, therefore, unhelpful in explaining collective behavior. Although strategic management deals with general managers and other individuals, most of its key phenomena—market entry, acquisition, international expansion, etc.—occur at the level of the firm, strategic group, or industry. Strategy has traditionally taken the firm and industry as its primary units of analysis (Rumelt et al., 1994), and its leading theoretical influences—industrial organization, institutional theory, the resource-based view, evolutionary views, etc.—make few or no assumptions about individual psychology.

Another aggregation problem is that strategy constructs may not be localizable in the brain. In social psychology, Willingham and Dunn (2003) distinguished between the first-order constructs of cognitive psychology (e.g., attention, memory) and the second-order constructs of social psychology that have first-order constructs embedded in them (e.g., stereotyping, conformity). There is no ‘stereotyping lobe’ in the brain, even though stereotyping remains an essential construct in social psychology. By analogy, researchers in neurostrategy will not find brain regions devoted to market entry or resource allocation. According to Willingham and Dunn (2003: 668), ‘the concepts that social psychologists use have a theoretical integrity of their own and should not be abandoned in favor of constructs that may be localizable but that will not be functional in a social theory…Social psychology should reserve its right to develop theoretical constructs that may not be localizable.’

If strategy constructs do not map conveniently onto the brain, there is a risk that neurostrategy could divert scarce financial and human resources from more productive uses. Dovidio et al. (2008) argued, for example, that large investments in neuroimaging research on racial discrimination can divert social researchers from macro-level studies of racism's cultural and social origins. The authors also cautioned social scientists not to be seduced by the impressive explanatory reductionism of hard science, arguing that neural data, especially high-resolution brain scans, have a presentational allure that masks logical inconsistencies. The authors cited experiments by Weisberg et al. (2008) in which researchers described psychological phenomena to neuroscience students and naïve subjects and then explained them using either irrelevant neuroscience data or no neuroscience data. Both the students and naïve subjects found irrelevant neural data more convincing than no neural data.

A significant problem in data interpretation is reverse inference: the practice of using neural measures such as blood oxygenation levels to infer mental states for which a particular region of the brain is ‘known’—for example, using amygdala signals to infer fear or insula signals to infer disgust. As Poldrack (2006) noted, the fact that fMRI experiments elicit a BOLD signal in the brain does not imply that subjects actually experienced psychological events associated with that part of the brain.2 For example, the amygdala is associated not only with fear, but also with bodily movements and the perception of sharp corners and musical tones; and the insula is associated not only with disgust, but also with empathy, pain, spatial learning, pitch perception, and speech production (Phelps, 2009). As Phelps (2009: 247) pointed out: ‘although reverse inference is a powerful technique for generating hypotheses and ideas that inspire additional studies or measurements, its use as a primary technique for determining a role for emotion is questionable.’

In 2008, a working paper by Edward Vul and colleagues, entitled ‘Voodoo correlations in social neuroscience,’ caused a major academic stir that soon spilled into the popular press. The paper, later published as ‘Puzzlingly high correlations in fMRI studies of emotion, personality, and social cognition’ (Vul et al., 2009), charged that social neuroscientists had reported correlations incommensurate with the degree of statistical reliability in their underlying measures. The authors argued that researchers who link psychological measures with BOLD signals could seldom observe statistical correlations greater than 0.70, yet studies reported correlations exceeding 0.80 and, in some cases, 0.95. The authors concluded that ‘a disturbingly large, and quite prominent, segment of fMRI research on emotion, personality, and social cognition is using seriously defective research methods and producing a profusion of numbers that should not be believed’ (Vul et al., 2009: 285).

The Vul et al. (2009) paper set off a chain of replies, rejoinders, and clarifications (e.g., Lieberman, Berkman, and Wager, 2009; Lindquist and Gelman, 2009). Lieberman et al. (2009) objected to both the tone and substance of the claims and argued that the paper was itself methodologically flawed. Poldrack and Mumford (2009: 212) also cited flaws in the paper, but wrote, ‘we believe that the paper by Vul et al., despite its shortcomings, has done a service to the fMRI community by highlighting the need for methodological care and the potential for bias that can arise with some forms of analysis. We hope that the field will take these lessons to heart and ensure that fMRI results are never again open to the claim of voodoo.’ These issues are still being debated and they show the need for vigilance in correlating neural data with independent measures of executive judgment or social cognition.

RG: For those intrigued with such issues in the scientific world and how effectively they can be treated in an operational framework of honesty, openmindedness and adherence to rational empiricism, see Halgin.

In social psychology, Willingham and Dunn (2003: 664) posed the following question: ‘Consider what a critic might say: ‘So the amygdala is active when people experience fear. So what? Why are we better off knowing it is the amygdala rather than the caudate?” The ‘so what’ question raises a key challenge to the value of neural data in the behavioral sciences. Psychologists knew about fear long before the advent of fMRI scanners, and the fact that fear correlates with blood signals in the amygdala, though of great interest to neuroscientists, may have no consequences for theory or practice in psychology. By analogy, fMRI experiments in strategic management might tell us that market entry decisions activate the PFC and ACC, but can they tell us anything new about strategy theory or practice? For example, we already know that markets attract excess entry due to the overconfidence of potential entrants, most of whom believe their abilities are above average (Camerer and Lovallo, 1999). In fMRI studies, overconfidence will give a consistent pattern of neural activations—say, in the ACC and striatum—and this would be neurally interesting. But a skeptic could still ask ‘so what?’ If we already knew that entrants chose suboptimally (excess entry) and we knew why (overconfidence), what did we learn from neuroscience?

RG: I am very surprised at the author’s decision to turn away from this topic before addressing why it is that functional brain mapping is so useful to clinicians. The long and short of it is this: It’s not the location by itself that is relevant, it’s any particular location’s neural linkages – both incoming and outgoing – to other locations in the brain that matters. The up- and down-links to and from the various limbic components known to be involved in one thing or another to and from specific cortical sites known to be involved in one thing or another. Now were talking.

RG: For most neuropsychologists, the concept of linkage is yesterday’s news; for many neurostratigists – including those who deal with suicidal borderlines, starving anorexics, hope-to-die alkies, and activity-obsessed manics – it may be on the order of Nobel Prize stuff. The current crop of clinicians is being trained to do the mindfulness do for no other reason that the neuropsychologists have a better grip with each passing day on those linkages and how either “thickening” or “densifying” them – as opposed to “thinning them out” and “weakening” them – is the stuff that affective relief, relapse prevention and behavioral change is quite literally made of (see Cozolino, Gazzaniga, Huttenlocher, Kaszniak, LeDoux, Panksepp, and Siegel).

From an epistemological point of view, Bennett and Hacker (2003) raised a problem known as the mereological fallacy, the fallacy of ascribing to part of something what can only be true of the whole. According to Bennett and Hacker (2003), brains do not think, feel, see, or believe—these are activities performed by whole human beings and not by their parts, and we cannot ascribe them to brains or nerve cells. According to Bennett and Hacker (2003: 70–71), ‘we recognize when a person asks a question and when another answers it. But do we have any conception of what it would be for a brain to ask a question or answer one? These are all attributes of human beings. Is it a new discovery that brains also engage in such human activities? Or is it a linguistic convention, introduced by neuroscientists, psychologists, and cognitive scientists, extending the ordinary use of these psychological expressions for good theoretical reasons? Or, more ominously, is it a conceptual confusion? Might it be the case that there is simply no such thing as the brain’s thinking or knowing, seeing or hearing, believing or guessing…that is, that these forms of words make no sense?’3

The Future of Neurostrategy

The sometimes vehement tone of the neuroskeptics can be interpreted either as a reaction against exaggerated claims in the scientific and popular press or as evidence that neuroscience has captured the attention of social scientists and must be taken seriously. In either case, the debate will not be resolved by arguments. In the short run, neuroscience will continue to ride a steep growth curve in the social sciences, and its long run contributions will be assessed on a timescale of decades.

What does it all mean for strategic management? Taking an optimistic view, one could argue that strategy is well positioned to benefit from neuroscience for two reasons. First, behavioral strategy has always taken a cognitive view of executive judgment and decision making; whether researchers focus on strategic decision biases or cognitive schema, neural evidence can be interpreted through existing theoretical paradigms. Second, there is a lot of neural evidence available. Strategy researchers interested in competitive positioning have access to neural studies on social norms and punishment in competitive interactions (Knoch et al., 2010); researchers interested in decision making under risk have access to studies on the roles of trust (Baumgartner et al., 2009) and reputation (Izuma, Saito, and Sadato, 2008); researchers interested in loss aversion and reference point framing have access to neural data on prospect theory (Fox and Poldrack, 2009). In short, behavioral neuroscience has left a large trove of neural evidence to be mined for insights in strategic management, and neuroeconomics in particular has acted as a silent benefactor to behavioral strategy.

In future years, strategy researchers will find that neuroscience is increasingly called upon to resolve debates in behavioral strategy. Behavioral strategists have good reasons to familiarize themselves with the relevant neuroscience and to explore how neural methods can assist in construct validation, theory testing and improved strategy practice. Many strategy researchers who focus on firms and industries may prefer to take a ‘wait and see’ attitude toward brain research, and this is understandable. But researchers who do not keep informed of developments in behavioral neuroscience will find themselves facing theoretical claims and empirical data they do not understand.

RG: The state of the science of functional brain mapping has already reached the point where most therapists and many clinical psychologists schooled before the mid-1990s are quite evidently behind the curve in therapeutic practice. The rational-emotive or cognitive behaviorist who graduated in the 1980s is often quite mystified by all this brain scan stuff and metaphorically rather like the computer programmers of the same era who are now falling behind in the competitive race for new work because of all the new JavaScript plug-ins. Continuing education programs are available, but most of them barely scratch the surface of the implications involved, and fly right over the heads of the many wall-eyed clinicians I have observed in seminar audiences conducted by the likes of Louis Cozolino, Mike Gazzaniga, Alfred Kaszniak, Joseph LeDoux, Jak Panksepp and others.

Some behavioral strategists may want to become actively involved in empirical neuroscience. Linking neuroscience with strategic management [RG: and therapeutic intervention] involves a steep learning curve and long lead times in resource accumulation and interdisciplinary relationship building. Before applying neural evidence to strategy problems, researchers need to avoid duplicating prior efforts by understanding the current state of play in neuroeconomics and related fields. At the same time, they need to create links with researchers in disciplines like economics and experimental psychology, which have strong communities of neuroscience expertise and cumulative research agendas in behavioral neuroscience.

Behavioral strategists should also familiarize themselves with research methods in neuroscience. Although much of the attention has fallen on brain imaging, neuroscientists use a wide range of technologies and methods. For example, transcranial magnetic stimulation (TMS) temporarily disrupts neural firing in a specific part of the brain, allowing researchers to determine whether the region is causally necessary to the task at hand. Behavioral neuroscientists increasingly use multi-method designs—for example, Blankenburg et al. (2010) combined TMS with fMRI scanning to study the effects of parietal cortex on attention processing in the visual cortex, and Hsu et al. (2005) combined fMRI scanning with a lesion method to study risk and ambiguity. It is also possible to link fMRI evidence with non-neural methods, such as hormone ratios or electromyography (EMG), which detects electrical potentials in muscle tissue—for example, Chapman et al. (2009) found that moral disgust in an ultimatum game activated the same facial muscles as bad tastes. Even when using single methods, neuroscientists often view their work in relation to cumulative meta-streams of research that embrace diverse methods. For example, a recent EEG study using ultimatum games to study social compliance and punishment behavior (Knoch et al., 2010) cited prior work on this problem using fMRI scanning (Spitzer et al.,2007) and transcranial direct current stimulation (tDCS) (Knoch et al., 2008). In short, research in neurostrategy will require an understanding of multiple methods and how they interact in the accumulation of experimental evidence.

On the ultimate question of whether strategic management needs neuroscience, it is tempting to answer ‘yes and no.’ On the positive side, neuroscience brings new methods and ideas to a fast-growing segment of the strategy field—behavioral strategy—that has natural links with psychology and behavioral neuroscience. Behavioral strategists have much to gain from collaborating with neuroscientists, and ignoring neuroscience involves risk of obsolescence. On the negative side, behavioral strategy is not a large segment of the strategic management field and had not given rise to its own interest group in the first 30 years of the Strategic Management Society.4 For researchers focused on firm- and industry-level problems, neuroscience may remain peripheral in the foreseeable future, though researchers will probably seek ways to achieve closer integration between traditional and behavioral strategy.

There is another important but less obvious question to consider: Does neuroscience need strategic management? This question matters for two reasons. First, it asks whether strategic management has its own research agenda in neuroscience, apart from the agendas of neuroeconomics or other fields. Although this is necessarily uncertain, it is a question that needs asking sooner rather than later. Second, strategy researchers who want to conduct empirical neuroscience must show neuroscientists that strategy brings something new and interesting to their field—that is, that strategic management gives neuroscientists access to social science expertise and research insights they cannot get from economics, law, politics, or marketing. If strategy offers nothing new to neuroscience, then the future of neurostrategy is severely limited.

RG: Given the prospects of gaining competitive advantage via the manipulation of the neurobiology of the masses, it’s hard for me to think that the business sector will not throw considerable sums of grant money at those who can provide that competitive advantage.

The remainder of this section identifies topic areas in which strategy may offer something new to neuroscience. The discussion is exploratory, and some of these topics could arise in one form or another in other fields. However, strategic management has at least two distinctive features with direct implications for empirical neuroscience: its mission of linking research to strategy practice and its emphasis on executive judgment and decision making in the context of the firm. From the time of its founding, strategic management has defined the internally differentiated firm as a distinctive psychological context for research on judgment and decision making (Simon, 1947; Cyert and March, 1963). Decision making in firms seldom means an individual making a discrete choice, but involves complex judgments in a climate of goal conflict, group bargaining, politics, and compromise. Implementation is costly and nontrivial and requires managers to motivate actors not involved in the decision. Strategic decisions entail large resource commitments with consequences for stakeholders beyond the decision makers, including employees, communities, governments, and investors. On the whole, the decision environment of the firm poses psychological questions that are in some ways distinctive to the field of strategic management.

The next discussion identifies research topics suggested by the psychological context of strategic organization. For one of these topics (group decision making), the discussion gives a detailed illustration of a potential collaboration in neurostrategy. For the remainder, the topics are mentioned without further detail.

Group decision making

Group processes are studied in many fields, including politics, sociology, social psychology, and organizational behavior (Kerr and Tindale,2004). Group phenomena such as social identity, self-categorization, and ingroup bias may have evolved from ancestral kinship relations, reciprocal altruism, or cultural evolution—for example, groups with strong pro-social norms may have increased their survival prospects in intergroup competition through more vigilant defense of ingroup values and resources (Mesoudi, 2009). In behavioral neuroscience, researchers have investigated the neural correlates of outgroup discrimination, conformity, and related phenomena (Amodio, 2008).

Strategic management researchers focus on group processes that influence strategic decisions in firms. In this area, strategy researchers have discipline-specific expertise and a set of distinctive research questions. For example, decisions in large firms rarely fall to a lone decision maker, but involve a top management team comprised of senior executives representing product divisions or functional areas (Hambrick and Mason, 1984). These executives bargain for resources and identify in various ways with the goals of the firm, the subunits to which they are accountable, and their own private aspirations. This makes it difficult for top management teams to reach optimal decisions for the firm and raises key questions about strategy process and practice.

Some of these questions have been studied in behavioral experiments, such as how top management team members juggle the interests of the firm with those of the divisions or functions they represent. Blake (1959) called this the problem of ‘organizational statesmanship,’ or ‘loyalty versus logic’ (Blake and Mouton, 1961), and social psychologists ran many experiments to examine what happens when people try to optimize a joint decision while bargaining for resources on behalf of constituents. For example, Blake and Mouton (1961) and Benton and Druckman (1974) found that people bargain more competitively when representing constituents, and Duck and Fielding (2003) found that constituents prefer representatives who vigorously defend the group's position, even at the expense of other groups or the joint optimum.

These findings are interesting, but would be more useful to strategy researchers if they showed the mental states of constituents and representatives. This would allow researchers not only to explain what happened, but to predict behavior in experimental manipulations and real decision contexts. A top management team member might show loyalty to constituents for many reasons: psychological identification with subunit goals, perceived accountability to constituents, or disgust with the firm; and constituents might choose subunit loyalty over firm statesmanship out of self-interest, social comparison, ingroup bias, or identification with their representative. These conditions can be hard to adjudicate behaviorally, and the corresponding mental states can only be inferred.

This is the kind of strategy problem where neuroscience can make a difference. For example, it is possible to modify a trust game so that, rather than bargaining for themselves, subjects bargain on behalf of one or more constituents who can either be known to the subject (for tests of social identification) or unknown (for tests of accountability) and who either share in the subject's payoffs or do not share. The research design goes beyond existing trustee-based studies, involving a stylized version of behavioral experiments on constituent representation, with repeated iterations and modifications for fMRI scanning. Previous studies have established a baseline for the neural encoding of cooperation, competition, and trust in interactive experiments using prisoner's dilemmas, ultimatum games, and trust games (Fehr and Camerer, 2007), and results can be compared with these baselines. For example, it is known that the neural processing of subjective rewards gives a different pattern of brain activations from the pattern associated with moral reasoning, or of regarding another person as part of the self (Dovidio et al.,2008). The problem of constituent representation has many applications in strategy and organization, and neural methods offer a viable way of advancing this stream of research.

Attention

Attention is a shared topic of interest in strategic management (Ocasio, 1997) and cognitive neuroscience (Posner, 2004). In strategy, attention raises questions in problem identification (Starbuck and Milliken, 1988; Lyles, 1981); problem solving (Newell and Simon, 1972; Bower, 1967); resource allocation (Bower, 1970; Ansoff, 1965); strategic issue diagnosis (Dutton, Fahey, and Narayanan, 1983); and organizational mindfulness (Levinthal and Rerup, 2006; Weick and Sutcliffe, 2006). Strategy researchers interested in executive or group attention will find that these topics offer many points of contact with cognitive neuroscience.

Exploration and exploitation

Exploration and exploitation have been studied in animal, machine, and human learning (Krebs and Kacelnik, 1984; Kaelbling, Littman, and Moore, 1996; Cohen, McClure, and Yu, 2007; Daw et al., 2006; Montague, King-Casas, and Cohen, 2006). Neural studies suggest that an area of the brain stem (the nucleus locus coeruleus) controls neurotransmitters that regulate the balance of exploration and exploitation (Aston-Jones and Cohen, 2005). In strategic management, exploration and exploitation refer to the tension between an organization's capacity to acquire new resources and its capacity to consolidate and operative effectively with existing resources (March, 1991; Sidhu, Commandeur, and Volberda, 2007). Using neural methods, it may be possible for strategy researchers to show how these individual and collective conceptions are merged in organizational decision-making.

Decision making with uncertain implementation

In neuroscience experiments, the choices are often difficult, but implementation is usually trivial (e.g., pushing a button). In firms, implementation is usually more difficult than decision making, requiring motivation, resource mobilization, and major project implementation. Strategic decisions are often implemented partially, unsuccessfully, or not at all. Foreknowledge of uncertain implementation changes the psychological context of decision making—for example, by increasing ambiguity—and offers new opportunities for linking strategic management with behavioral neuroscience.

Corporate and competitive strategy

Research in corporate strategy deals with issues such as diversification, economies of scope, strategic alliances, and international expansion. The theory of dominant logic links corporate scope with executive cognition by attributing poor conglomerate performance to constraints on the cognitive schema of top executives (Prahalad and Bettis, 1986). Cognitive views of corporate strategy have clear links to behavioral neuroscience and offer many opportunities for collaborative research. The same is true for theories of competitive strategy that place the origins of competitive behavior in the cognitive schema of top managers (Baden-Fuller, Porac, and Thomas, 1989; Reger and Huff, 1993; Hodgkinson and Johnson, 1994). For example, neural methods would deepen our understanding of executives' perceptions of industries and strategic groups and of the psychology of competitive versus cooperative strategies.

Firm routines and incentives

When costs and rewards are separated in time, individual decisions are subject to pathologies like impulsivity, procrastination, and addiction (Fudenberg and Levine, 2006; Gul and Pesendorfer, 2001; Akerlof 1991; Loewenstein 1988). Neural studies suggest that temporal discounting increases as people regard their future selves as distinct from their present selves (Ersner-Hershfield et al., 2009). In strategic management, temporal discounting has been used to explain the structural features of firms—such as routines, hierarchy, incentives, and formal planning—which may emerge as solutions to the pathologies of individual self-control (Postrel and Rumelt, 1992). Habitual behavior and routines, as contrasted with goal-directed behavior, play prominent roles both in strategic learning in firms (Nelson and Winter, 1982) and in cognitive neuropsychology (Rangel, Camerer, and Montague, 2008; Lieberman, 2007), offering many joint opportunities for exploring the neural foundations of strategic behavior.

RG: For those reading the paper for clinical insights, the relevance pretty much ends at this point.

Leadership and entrepreneurship

In strategy practice, many people believe that innovative, risk-bearing entrepreneurs think and act differently than experienced managers of large corporations (Baron, 2007). Others believe that visionary and charismatic leaders think differently than less inspiring managers (Conger and Kanungo, 1987). Leadership research has already produced collaborations with neuroscientists and offers many ways of integrating neuroscience with strategy practice (Rock, 2009).

Decision making with advice

Executives often solicit external advice from firms like McKinsey and Boston Consulting Group. Consulting firms claim to add value by giving reputational weight to the firm's decisions, by taking an objective view of the firm, and by employing proprietary problem-solving processes. Research on the comparative thought processes of external consultants and internal executives raises questions at the intersection of neuroscience, strategy research, and strategy practice. As technologies evolve, field researchers in neurostrategy will study such questions using technologies such as EEG and TMS, which do not restrict subjects to large and immovable scanners.

In raising these topics, the point is not that strategy researchers should immediately pursue them, but that productive collaborations with neuroscientists require distinctive research questions that can be addressed with neural evidence. Many scholars will find that their research questions do not require neural evidence or that the evidence already exists—for example, questions on moral choice, reputation, and social norms are being addressed in neuroeconomics. Rather than undertaking neurostrategy research, the next step is to engage seriously enough with behavioral neuroscience to determine whether a collaboration is necessary. Broadly speaking, a strategy topic does not require an empirical research program in neurostrategy unless it passes the following tests: (1) Does it address a core problem in strategic management research or practice? (2) Does it raise compelling new questions for neuroscientists? (3) Has it been neglected in other fields and is it likely to remain neglected? (4) Will neural evidence add to our understanding—and, if so, how (through construct validation, theory testing, or informing strategy practice)?

As a final point, strategy researchers should situate their neurostrategy problems within the theoretical conventions of neuroscience. Neuroscientists tend to evaluate theory from an evolutionary point of view, asking whether constructs and causal mechanisms could plausibly derive from considerations of survival, reproduction, or fitness. For example, a neural capacity for exploration and exploitation could have emerged from the survival value of foraging and storing resources in unstable environments; reference point framing could emerge from hierarchy and scarcity in animal and human competition; and impulsivity could survive as an evolutionary remnant of a time of short life expectancies and the absence of property rights to protect resources from expropriation. Neurostrategy questions that can be framed within evolutionary arguments are more likely to have theoretical legitimacy in neuroscience.

Concluding Remarks

Neuroscience has left an imprint on economics, law, marketing, and other disciplines and will continue to influence the social sciences. In strategic management, neuroscience offers new opportunities for strategy researchers to validate constructs, test theories, measure variables, and generate ideas, and it may offer ways to improve strategy practice. At the same time, neuroscience faces hard challenges in theory and measurement and has struggled to prove its capacity to solve traditional problems in the social sciences. On balance, researchers in behavioral strategy should explore the potential contributions of neurostrategy, even if the majority of strategy researchers remain on the sidelines.

Strategy researchers can engage with behavioral neuroscience by evaluating its existing contributions to their research questions, identifying topic areas for neural research, and building relationships and institutional resources to support research in neurostrategy. With time, these relationships will lead to arrangements such as collaborative funded research projects, joint research seminars, and joint doctoral scholarships in neurostrategy. Even if neurostrategy remains a narrow specialization within the field of strategic management, it has the potential, on a longer time scale, to transform behavioral strategy. For researchers interested in the psychological foundations of strategic management, it offers exciting new opportunities at the frontiers of theory development and empirical discovery.

Acknowledgements

The author gratefully acknowledges the financial support of the Saïd Business School Foundation. The author benefited from discussions with Mark Buckley, Mark Baxter, Joseph Ledoux, Matthew Rushworth, Tim Behrens, Robert Rogers, Kate Watkins, Peter Hacker, and Daniel Robinson. The author also thanks Special Issue Editor Craig Fox and three anonymous referees for their helpful comments during the review process.

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1
If A is purely self-interested and believes B is the same, A will propose a large sum for A and just enough for B so that B's share is positive—that is, $ 9.99 to A and $ .01 to B. If B is purely self-interested, B will accept any positive offer.
2
BOLD is the acronym for ‘blood oxygenation level dependent effect,’ the ratio of oxygenated to deoxygenated blood cells, which is the quantity measured in fMRI scans.
3
Bennett and Hacker’s (2003) critique draws on a comment by Wittgenstein (1958: section 281) in Philosophical Investigations: ‘Only of a human being and what resembles (behaves like) a human being can one say: it has sensations; it sees, is blind; hears, is deaf; is conscious or unconscious.’ Not all predicates are limited in this way—e.g., it is not logically absurd to claim that a person is sunburned and her arm is sunburned; or that she is in Europe and her brain is in Europe. The critique applies to psychological predicates: ‘it makes no sense to ascribe psychological predicates (or their negations) to the brain, save metaphorically…The resultant combination of words does not say anything that is false; rather, it says nothing at all, for it lacks sense’ Bennett and Hacker (2003: 71). For a materialist reply, see Dennett (2007).
4
In 2010, the SMS interest groups were: (1) competitive strategy; (2) corporate strategy and governance; (3) global strategy; (4) strategy process; (5) knowledge and innovation; (6) practice of strategy; and (7) entrepreneurship and strategy.

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Commentary © 2012 by Rodger Garrett; all rights reserved. Links are fine. Please contact not_moses@fastmail.fm with comments or questions. Thank you.

Book Review: Trapped in the Mirror

2011-12-30T15:15:00.000-08:00

3.0 out of 5 starExcellent for Problem Identification, but Not a Recovery Manual, December 30, 2011

Excellent for Problem Identification... but Not a Recovery Manual

Rodger Garrett "SighKoBlahGrr" (Loma Linda, CA USA) - See all my reviews
(REAL NAME)

This review is from: Trapped in the Mirror: Adult Children of Narcissists in their Struggle for Self by Elan Golomb at http://www.amazon.com/Trapped-Mirror-Children-Narcissists-Struggle/dp/0688140718/ref=cm_cr_pr_product_top

Trapped... is a work of its time. Which is to say, the era of discovery rather than the later era of what to do about it. It is also a view of the problem as much from within, as from outside of, the paradigm. In that regard, it reads much like the flood of codependency books from the decade that preceded it: a lot of identification and recognition, but only limited experimentation with, and sense of efficacy about, the techniques required to resolve the various issues and move outside of what author Tara Brach calls "the trance."

I scanned the one-, two- and three-star commentaries on the book's amazon.com page and found most to represent the all-or-nothing thinking that's at the root of this and most other psychological problems. If the book is not all good, it's all bad. Which is far from the case. Much as Mellody Beattie's early work on codependency edifies the problem, Golomb's work here does a truly excellent job of clarifying the dynamics of the sadomasochistic, dominance-and-submission, authoritarian-leader-and-good-little-soldier nature of relationships with self-obsessed, self-righteous, self-involved parents.

But Beattie had come from addiction counseling and saw codependency as an addiction (it is), and suggested the widely used 12 Step approach. Golomb comes from neo-Freudian psychodynamicism, a fine method if one has the time and money, but one that will require a lot of both... and one that does not lend itself to any sort of one-size-fits-all approach, much less bibliotherapy, because the psychodynamic method is so case-specific.

Golomb's work recalls Jules Henry's stunning Pathways to Madness and Ronald Laing & Aaron Esterson's equally remarkable Sanity, Madness and the Family, as well as Donald Jackson's The Etiology of Schizophrenia; all from a much earlier time, and all much more clinical. Golomb's approach is a far more reader-friendly (and a lot less upsetting).

It is clear that certain, dogmatically rule-bound, religious traditions tend to produce miniature cults of personality like those described by authors Robert J. Lifton, Margaret Thaler Singer, Edgar Schein, Mark Galanter and Kathleen Taylor. Dad and/or Ma are the guru(s); the kids (and often one of the parents) are the supplicant -- and very much trapped -- door mats and victims.

Having worked with many adult children of such families, it is clear to me that the organizational dynamics of cults described by those authors are almost always present to some degree in such families of origin. (Moreover, many cult members were set up to tolerate such cult dynamics by their experiences with narcissistic parents.)

I have recommended Trapped... to a number of people who found it edifying at their early (usually "contemplation/consideration" after moving up from "denial/pre-contemplation") stage of recovery. In all cases, it assisted their advance to the "identification/acceptance" stage, but did little or nothing to move them on to "commitment/action." How could it?

Most adult children of narcissistic parents will find help in one of the more sophisticated and empirical-research-informed 12 Step programs: Adult Children of Alcoholics / Dysfunctional Families (ACA), which has small AA-like groups throughout North America and Northern Europe.

ACA has a recently published book of its own which describes the dynamics in less vivid detail than Golomb's book, but goes on to provide a 12-Step-cum-cognitive-behavioral-therapy approach to recovery. I've seen that method produce results for dozens who dedicated themselves to working through those steps, though many with more severe personality disorders of their own typically require professional help.

Many ACA members display mild to moderate symptoms of post-traumatic stress disorder including being hypervigilant for narcissistic abuse and primed to hair-trigger fight, flight, freak or freeze responses. I have seen several benefit from the cutting edge treatments like dialectical behavior therapy, acceptance and commitment therapy, mindfulness-based cognitive therapy and self-talk identification, questioning and revision.

Most counselors and therapists understand that one has to "meet the patient where the patient is." If the patient is still in denial/pre-contemplation, he's probably not sitting in your office unless he got a "nudge from the judge." But if the patient has begun to wonder why he or she is so anxious, depressed, codependent and/or angry towards a critically judgmental, ego-battering, self-obsessed parent, Trapped... looks to me like it can be counted upon to open the door to willingness a bit wider. And at $5.00 a copy, it's pretty cost effective.

My response to one of eight emails in response to this post in 16 hours (half of which were overnight):

"I asked myself in 1992 if my inheritance was worth putting up with the ma from hell. It wasn't. I am happy to this day that my cousin wound up with it all. And that neither I nor my adoptive ma had to put up with our codependent reactivity to each other.

"There are moments here and there when my cult-urally contrived mind thinks that I was "selfish" and that I 'should' have done otherwise. Like I said, there are moments...

"Some people, much as Golomb describes at the end of her book, can find a way to be the good, little, God-fearing, commandments-obeying, orthodox Jewish children of an abusive parent until the parent expires. But I am a 'football player' about stuff like this: If I bring my team on to the field of play and they don't, we can't really have a game."

Severe Addiction as Self-Harm through the lens of ACT's Functional Contextualism

2011-12-27T23:10:00.000-08:00

Functional contextualism (a.k.a. functional analysis of behavior)* is bedrock to the conduct of Acceptance and Commitment Therapy (ACT), and rarely is it more crucially applied than in the context of self-harm by patients with borderline personality disorder.

While the article by Gratz quoted below confines self-harm more strictly than most addiction therapists would (e.g.: severe addictive behaviors as “suicide on the installment plan”), the concepts of functional contextualism and self-harm, as well as the two lists of functional purposes of self-harming behaviors are broadly applicable to understanding the behavioral motives of all manner of addicts in the denial / pre-contemplation and contemplation / consideration phases of addiction treatment.

Thanks to Wiley-Blackwell for making Gratz’s article available at no charge.

*see Hayes, Strosahl & Wilson, p. 18, and Hayes, Follette & Linehan, p.11.

Risk Factors for and Functions of Deliberate Self-Harm: An Empirical and Conceptual Review (excerpts)

Kim L. Gratz
Clinical Psychology: Science and Practice
Volume 10, Issue 2, pages 192–205, June 2003

http://onlinelibrary.wiley.com/doi/10.1093/clipsy.bpg022/full

FUNCTIONS OF DELIBERATE SELF-HARM

Linehan's (1993) description of the development of BPD also suggests the potential function of self-harm behavior. Specifically, Linehan suggests that the way emotional vulnerability and invalidating environments interact to influence the development of self-harm is through their impact on emotion dysregulation. For instance, invalidating environments during childhood may contribute to the development of emotion dysregulation by failing to teach effective regulatory strategies for managing emotional arousal and tolerating emotional distress (Linehan, 1993). Moreover, childhood trauma in the form of physical abuse, sexual abuse, or both may contribute to chronic hyper-arousal and, consequently, increased risk for emotion dysregulation (given that high levels of arousal are more difficult to regulate; see Eisenberg, Cumberland, & Spin-rad, 1998; Flett, Blankstein, & Obertynski, 1996). In addition, emotional vulnerability in the form of emotional reactivity and intensity may also contribute to emotion dysregulation (see Calkins & Johnson, 1998; Eisenberg et al., 1998; Melnick & Hinshaw, 2000;Thompson, 1994), as more intense emotions pose a greater challenge for emotion regulation (Flett et al., 1996). Thus, the interaction of these factors increases the likelihood of emotion dys-regulation, which, in turn, increases the risk for deliberate self-harm (as self-harm may function to regulate painful emotions that cannot be tolerated; see Linehan, 1993).

Although Linehan's (1993) theoretical work offers the most detailed and comprehensive description of the emotion regulating function of self-harm behavior, other researchers have also conceptualized self-harm as an emotion regulation strategy (see Haines & Williams, 1997; van der Kolk, 1996)—a conceptualization supported by clinical and empirical literature. Given the relative dearth of empirical research on the functions of self-harm, most of the extant literature on this topic is clinical in nature, consisting of clinical observations and the nonsystematic description of the self-reported functions of self-harming clients. This clinical literature indicates that deliberate self-harm may function in one or more of the following ways:

(1) to relieve anxiety;
(2) to release anger;
(3) to relieve unpleasant thoughts and feelings;
(4) to release tension;
(5) to relieve feelings of guilt, loneliness, alienation, self-hatred, and depression;
(6) to externalize and concretize emotional pain;
(7) to provide an escape from emotional pain;
(8) to provide a sense of security;
(9) to provide a sense of control;
(10) to self-punish;
(11) to set boundaries with others;
(12) to terminate depersonalization and derealization;
(13) to end flashbacks; and
(14) to stop racing thoughts

(Connors, 1996; Coons & Milstein, 1990; Favazza, 1989b, 1992; Favazza, DeRosear, & Conterio, 1989; Greenspan & Samuel, 1989; Kennerley 1996; Lyons, 1991;Shapiro, 1987). Although no data are available on the number of ways in which self-harm may function for any given individual, researchers have suggested that self-harm is likely an overdetermined behavior, serving multiple functions simultaneously (Suyemoto, 1998).

Empirical literature is consistent with this clinical literature. For instance, Favazza and Conterio (1989) examined the self-reported functions of self-harm among a community sample of 240 self-selected females with a history of this behavior. Among these participants, self-harm functioned to facilitate relaxation, control racing thoughts, and relieve feelings of depression, loneliness, and derealization. However, the authors did not specify whether the participants were allowed to describe (by means of an open-ended question) the functions of their self-harm behavior, or whether they were forced to choose from a list of alter natives provided by the researchers—a factor that may have implications for the validity of the results.

Briere and Gil (1998) also examined the functions of self-harm among a group of 93 self-identified (predominantly female) individuals with a history of this behavior (the vast majority of whom also had a history of sexual abuse). These individuals were asked to select the functions of their self-harm from a list of reasons commonly provided by self-harming clients for this behavior. The participants selected a wide variety of functions for their behavior, including self-punishment, distraction from and release of painful feelings, management of stress, reduction of tension, release of anger, and enhancement of feelings of self-control (each endorsed by more than 70% of the self-harming individuals). A factor analysis performed on the reasons for self-harm cited by more than 20% of the participants resulted in nine factors, leading the researchers to conclude that the self-harm behavior of the participants in their study functioned to:

(1) decrease dissociative symptoms such as depersonalization,
(2) prevent flashbacks and upsetting memories,
(3) reduce stress and tension,
(4) express distressing emotions,
(5) provide a sense of safety and protection,
(6) reduce anger,
(7) punish the individual,
(8) show others that the individual needed help, and
(9) protect the individual from hurting others.

Briere and Gil's (1998) use of a close-ended questionnaire to assess the functions of self-harm may be premature in light of the relative lack of empirical research on the functions of this behavior. Results of a qualitative study that used open-ended interviews to assess the functions of self-harm behavior (Gratz, 2000) may help elaborate upon their findings. Despite the study's limited sample (21 college students with a self-identified history of self-harm behavior), the results were comparable to those reported by Briere and Gil (1998), as well as Favazza and Conterio (1989).

Specifically Gratz (2000) found that the most frequently described function of self-harm was to relieve unwanted feelings, reported by 76% of the participants. These participants reported that self-harm relieved feelings of stress, anger, frustration, sadness, emotional upset, tension, anxiety, grief, emotional pain, and being overwhelmed.

Consistent with the aforementioned clinical literature, participants also reported that self-harm externalized emotional pain, thereby making the pain more physical and tangible, and thus less abstract and easier to understand. Participants also noted that self-harm provided an escape, a way to forget about worries and fears, and a way to divert attention from painful internal experiences. According to participants’ reports, self-harm also functioned to express feelings of self-hatred, to self-punish, to provide a sense of control, and to prove something to the individuals (e.g., that they were capable of doing something or that they were tough enough to endure pain). Finally, for six participants (29%), self-harm functioned as a way to communicate with others, including showing others that they were hurting and setting boundaries with others.

Interestingly, and somewhat inconsistent with the clinical and empirical data already described, one of the most frequently cited functions of self-harm within the general literature in this area is the elicitation of a caring response from others (Conterio & Lader, 1998; Favazza, 1992)—a function often described as a means of manipulating or coercing others into providing love or attention (Barstow, 1995; Feldman, 1988;Schwartz et al, 1989). This is the function that historically has been attributed to most self-harm behavior, contributing to the common belief that individuals who engage in this behavior are manipulative and attention seeking (Feldman, 1988; Tantam & Whittaker, 1992). However, researchers have recently begun to address the fact that this negative belief about the function of self-harm is most likely a misconception.

First, self-harm is often a private and secretive act, with many individuals choosing to conceal this behavior from others (Conterio & Lader, 1998; Favazza, 1992). In these instances the purpose of this behavior could not possibly be to manipulate others or gain attention, suggesting that, at the very least, the function of self-harm is not always interpersonal in nature. Also, some researchers argue that even in the case of individuals who harm themselves in the presence of others, it may not be accurate to conceptualize their behavior as manipulative. According to Linehan (1993), who thoughtfully argues against conceptualizing the parasuicidal (including self-harming) behavior of individuals with BPD as manipulative, the fact that the self-harm behavior of an individual may influence others does not mean that this was the intent of the behavior, as “function does not prove intention” (p. 17).

Linehan's (1993) argument is very similar to Levenkron's (1998) discussion of “secondary gain” (p. Ill), in which eliciting a caring response or influencing others is not the intent or primary goal of the behavior but may end up reinforcing the behavior nonetheless. The benefit of framing the interpersonal function of self-harm behavior in this way is that doing so separates the conscious intent of the behavior from the unintended but still possibly reinforcing outcome of the behavior, consequently challenging the stereotype that self-harm behavior and the individuals who engage in it are manipulative.

Moreover, within the empirical research on the functions of self-harm, the elicitation of a caring response from others is not the most frequently cited function of self-harm among self-harming individuals themselves. For example, Gratz (2000) found that less than one third of participants (n= 6) reported that self-harm functioned to get the attention of others, and half of these participants (n= 3) seemed unsure as to whether this was actually one of the functions of their behavior. Conversely, self-harm was also described by three participants as a means to push people away and make others leave them alone.

Similarly, Briere and Gil (1998) found that although 40% of their sample reported engaging in self-harm to get attention or help from others, the majority of self-harming individuals (more than 70%) endorsed the intrapersonal functions of self-punishment, enhancement of self-control, and relief from painful feelings, stress, tension, and anger. Favazza and Conterio (1989) do not report that obtaining the care or attention of someone was one of the functions of self-harm described by the participants in their study; however, it is unclear whether this function was even an option provided to participants. Related to this topic, though, only 20% of the participants in their study endorsed the statement that they liked the attention resulting from self-harm.

Although clinical and empirical data lend support to Linehan's (1993) theory that self-harm serves an emotion regulating function, knowing the particular way in which self-harm may operate to regulate emotions would add depth to an understanding of its function (considering that emotion regulation strategies may take a variety of forms that are more or less adaptive). One emerging construct that may be particularly useful for understanding the specific form of emotion regulation that self-harm most often takes is experiential avoidance (i.e., attempts to alter the form or frequency of unwanted internal experiences, including emotions, thoughts, memories, and bodily sensations; Hayes, Wilson, Gifford, Follette, & Strosahl, 1996).

Because experiential avoidance is a particular type of emotion regulation strategy with commonly associated short-and long-term consequences (including the reduction of distress and subsequent negative reinforcement of the behavior in the short-term and paradoxical, dysregulating effects in the long-term; see Hayes, Strosahl, & Wilson, 1999; Hayes et al., 1996), it may offer a useful conceptual framework for understanding the function of self-harm. In fact, examination of the functions of self-harm reported by research participants and clients suggests that this behavior does often function as a form of experiential avoidance (as it is often used to escape, avoid, or alter emotions or thoughts).

From Fight or Flight to Freak and Fry

2011-12-11T23:10:00.000-08:00

An Argument for PTSD as the Pathological Expression of HPA & ANS Excitotoxic / Allostatic Overload of the Limbic System: Too Much of a Good Thing is Not a Good Thing.

Neurobiology of the Stress Response: Contribution of the Sympathetic Nervous System To the Neuroimmune Axis in Traumatic Injury

Molina, Patricia E
Department of Physiology, Louisiana State University Health Sciences Center, New Orleans, Louisiana

Shock: Injury, Inflammation, and Sepsis: Laboratory and Clinical Approaches, Vol. 24, No. 1, July 2005, pp 3-10

http://journals.lww.com/shockjournal/fulltext/2005/07000/neurobiology_of_the_stress_response__contribution.2.aspx

RG: I have run across other material in the PTSD literature suggesting that overproduction and/or over-long production of pro-inflammatory cytokines is a principle factor in the excitotoxicty of dendritic receptor sites in the limbic system of PTSD sufferers. I am utilizing this state-of-the-art-in-2005 description of what was known at that time about the functions of the hypothalamo-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS) as a platform to introduce what I have learned elsewhere about excitotoxity to provide an explanation of the micro-neurobiology of PTSD as I have been able to see it in the computer-adied tomography of PTSD sufferers. I would like to invite any and all who have superior grasp of the topic to weigh in with comments, factual corrections, etc. I am indebted to Dr. Molina and to Lippincott, Williams and Williams for making the article available for this usage. RG, December 2011.

Abstract

Acute injury produces an immediate activation of neuroendocrine mechanisms aimed at restoring hemodynamic and metabolic counter-regulatory responses. These counter-regulatory responses are mediated by the systemic and tissue-localized release of neuroendocrine-signaling molecules known to affect immune function. This has led to the recognition of the importance of neuroendocrine-immune modulation during acute injury as well as throughout the recovery period. The period immediately after acute injury is characterized by upregulation of proinflammatory cytokine expression leading to a later period of generalized immunosuppression. The course and progression of the host recovery from traumatic injury and the integrity of its response to a secondary challenge is directly related to the effective control of the immediate proinflammatory responses to the initial insult. Among the neuroendocrine mechanisms involved in restoring homeostasis, the sympathetic nervous system plays a central role in mediating acute counter-regulatory stress responses to injury. In addition to its recognized cardiovascular, hemodynamic, and metabolic effects, the neurotransmitters released by the sympathetic nervous system have been shown to affect immune function through specific adrenergic receptor-mediated pathways. In turn, cells of the immune system and their products have been shown to influence peripheral and central neurotransmission, leading to the conceptualization of a bidirectional neuroimmune communication system. The reflex activation of this bidirectonal neuroimmune pathway in response to injury, integrated with the parasympathetic nervous system, and opioid and glucocorticoid pathways responsible for orchestrating the counterregulatory stress response, results in dynamic regulation of host defense mechanisms vital for immune competence and tissue repair. This review provides the biological framework for the integration of our understanding of the neuroendocrine mechanisms involved in mediating the stress response and their role in modulating immune function during and after traumatic injury.

INTRODUCTION

Despite considerable advancement in the development of treatment modalities, our understanding of the processes involved in control of inflammatory responses is incomplete (in 2005). Recently, the importance of neuroendocrine mechanisms has gained recognition, leading to the redefinition of our traditional views of the factors controlling inflammatory responses. Because uncontrolled as well as impaired inflammatory responses can lead to deleterious outcomes, it is imperative to develop the appropriate knowledge base and conceptualization of the control mechanisms involved. Inflammatory responses are not exclusive to chronic or infectious conditions, but have also been identified after acute stress such as that resulting from traumatic injury. Among the etiological factors directly involved in triggering the pro-inflammatory response associated with traumatic injury are tissue hypo-perfusion, hypoxia, infection, and burn (1, 2).

The contribution of neuroendocrine mechanisms to the dynamic regulation of the magnitude and tissue specificity of inflammatory responses has been recognized by several investigators. Considerable attention has been given to the effectiveness of parasympathetic nerve stimulation in suppressing the magnitude of the pro-inflammatory response, leading to coining of the term inflammatory reflex (3). Interestingly, the stress response to injury is associated with suppressed parasympathetic nervous system activity and prevalence of the activation of the other arm of the autonomic nervous system-the sympathetic nervous system. Furthermore, systemic and tissue release of norepinephrine and epinephrine, the principal neurotransmitters of the sympathetic nervous system, exert marked cellular responses on cells of the immune system. Thus, as we increase our understanding of the role of neuronal pathways in modulating the inflammatory response, it is important to integrate the role and contribution of both arms of the autonomic nervous system in the regulation of the inflammatory responses.

Dissecting the relative contribution of the sympathetic nervous system to modulation of immune responses during traumatic injury requires an analysis of conditions under which this arm of the autonomic nervous system is activated: its anatomical interactions with immune competent cells and the functional consequences of this interaction as they affect the regulation of the host response. We begin by providing an overview of the neurobiology of the stress response, and we go on to describe how the organism responds to stress and the neuro-circuitry that is involved, as well as how the efferent autonomic and neuro-endocrine pathways involved in mediating the peripheral responses to stress modulate immune function.

CONDITIONS UNDER WHICH THE SYMPATHETIC NERVOUS SYSTEM IS LIKELY TO BE INVOLVED IN CONTROL OF INFLAMMATION

Alterations in the environment or acute insults to an individual that require adaptation involve the synchronized interaction of multiple neuronal and endocrine pathways geared at restoring homeostasis and ensuring the fundamental survival, growth, and reproductive functions of the host (Fig. 1). The integrated hemodynamic, metabolic, behavioral, and immune responses that allow adaptation of the host are referred to as the stress response (4). Central to the integration of this reflex neuro-endocrine response are the hypothalamo-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS). Their activation in response to stress is centrally integrated, particularly at the level of the periventricular nucleus of the hypothalamus and the locus ceruleus. In parallel to activation of the SNS response, the parasympathetic nervous system tone responsible for vegetative functions is suppressed. Several additional neuro-endocrine pathways are simultaneously activated, which, in turn, form redundant and feedback circuits (feed-forward or negative feedback), contributing to a synchronized cascade of efferent neuro-endocrine signals targeted to increase the host's ability to respond to the stress signal. Despite the multiple and intricate interconnected pathways, the two pathways at the core of the stress system wiring are the HPA axis and the SNS system.

The core function of the HPA and SNS pathways is central to the host's adaptation to acute challenges by ensuring energy substrate mobilization, cardiovascular and hemodynamic compensation, increasing awareness, and subsequently by contributing to host immune function and tissue repair (5). Signals sent to other brain regions, including those that are not directly involved in the immediate restoration of vital functions during acute stress, affect additional behavioral and physiological responses such as sleep, growth, reproduction, and mood. Although the short-term activation of these stress response mechanisms is vital by providing substrate availability to sustain increased metabolic demands of the individual, prolonged duration and increased magnitude of their activity leads to deleterious effects on metabolism (6), immune function (7), reproduction (8), and cardiovascular function (9). Similarly deleterious is the impaired activation or lack of responsiveness of the HPA and autonomic nervous systems, as in the case of the critically ill patient. Thus, the overall appropriate and controlled activation and termination of the neuroendocrine responses that mediate the necessary physiological functions involved in maintaining and restoring homeostasis in the event of illness, trauma, surgery, or fasting are of critical importance.

Using hemorrhagic shock as a model of acute stress, one can dissect the role of the SNS and identify its role as a key component of the neuroendocrine response to stress (Fig. 1). The hemorrhage-induced decreases in mean arterial blood pressure lead to decreased stretch of the baroreceptors in the carotid sinus and aortic arch this decreased firing from baroreceptors initiates afferent signals to the CNS. These afferent signals include visceral peptidergic projections (to oxytocin neurons in the hypothalamus), and signals from the nucleus tractus solitarius relayed via A1 (noradrenergic) and C1 (adrenergic) cells of the ventrolateral medulla (targeting hypothalamic arginine vasopressin and corticotrophin-releasing hormone [CRH] neurons). Additional afferent signals to the hypothalamus are relayed through neurotransmitters other than catecholamines, including glutamate and γ-amino butyric acid. The integration of these afferent signals occurs predominantly at the level of the periventricular nucleus (10), triggering a cascade of intra- and extra-hypothalamic neurochemical events. These signals are relayed via classical transmitters, as well as numerous neuropeptides, including CRH, opioids, neuropeptide Y and galanin, and gaseous neuromodulators like nitric oxide and carbon monoxide, many of which are co-localized with classical transmitters and may act in concert with them at the level of individual PVN neurons. Clearly, multiple neurochemical pathways are simultaneously activated and integrated during the compensatory response to acute blood loss.

In parallel to central relay signals dictating the CNS response to acute stress, descending autonomic visceromotor (11) (brainstem and spinal projections) cell groups (12) are activated as well (Fig. 1). The resulting efferent or descending signals are primarily directed to restoring hemodynamic and metabolic homeostasis, ensuring adequate perfusion and oxygenation of tissues, as well as energy substrate mobilization to sustain the increased demands of the organism during this fight or flight response. These descending projections control heart rate and blood pressure (13) and make contact with sympathetic and parasympathetic preganglionic neurons in the intermediolateral nucleus of the thoracic and lumbar spinal cord. In addition, these neuronal pathways are capable of stimulating cells of the immune system directly through neurotransmitter release in the parenchyma of lymphoid organs (14), and indirectly through neurotransmitter and hormonal release into the circulation. Several lines of evidence indicate that these neurotransmitters and neuromodulators exert significant effects on the inflammatory/immune response, affecting the ability of the host to repair tissue damage and produce an adequate host defense from infections. Thus, descending autonomic neuronal pathways control vital hemodynamic and metabolic functions while also modulating several aspects of the immune system.

THE CNS SIGNALS THE IMMUNE SYSTEM THROUGH NEURONAL AND HORMONAL PATHWAYS

Catecholamines are among the neurotransmitters that affect immune responses humorally through circulating adrenal-derived epinephrine, as well as locally through neuronal release of norepinephrine. Studies have provided anatomical evidence of CNS-lymphoid organ connection through autonomic and sensory fibers in immune tissues such as the bone marrow, thymus, spleen, and lymph nodes (Fig. 2). This sympathetic innervation of lymphoid organs is found across species and has been confirmed by specific immunohistochemistry for tyrosine hydroxylase. In the bone marrow, myelinated and nonmyelinated fibers with immunoreactivity to tyrosine hydroxylase, vasoactive intestinal peptide, and neuropeptide Y are distributed with vascular plexuses where they may influence hemopoiesis and cell migration (15). In the lungs, noradrenergic nerve fibers supply tracheobronchial smooth muscle and glands. In addition, nerve fibers have also been demonstrated throughout the different compartments of bronchus-associated lymphoid tissue, e.g., under the epithelium, in the smooth muscle layer, along the vasculature, and between immune cells of bronchus-associated lymphoid tissue parenchyma, forming close contacts with mast cells, cells of the macrophage/monocyte lineage, and/or other lymphoid cells (16). In the thymus, noradrenergic nerve fibers have been localized in the subcapsular, cortical, and corticomedullary regions, associated with blood vessels and intralobular septa, occasionally branching into the cortical parenchyma where they reach close proximity to thymocytes.

Among the organs that have received the most attention because of the technical feasibility of surgical and chemical manipulation to investigate the role of neuroimmunomodulation is the spleen. Fluorescence histochemistry has demonstrated noradrenergic nerve fibers entering the spleen with the splenic artery and then further distributing with the central artery, with the capsular and trabecular systems, and into the parenchyma where they distribute among T lymphocytes and along a macrophage zone at the marginal sinus. The origin of sympathetic neural innervation in rat spleen is predominantly the superior mesenteric/celiac ganglion. More recent and sophisticated techniques have allowed visualization of noradrenergic fiber distribution into B cell follicles, particularly during development. Thus, T and B lymphocytes as well as macrophages have been identified to be located at sites adjacent to tyrosine hydroxylase-positive nerve fibers, where they are exposed to neuronal norepinephrine release (17). Similar patterns of innervation have been described for cervical, mesenteric, and popliteal lymph nodes, as well as Peyer's patch and lymphoid tissue associated with the appendix. Noradrenergic nerves have been visualized entering the lymph nodes at the hilus with the vasculature and distributed throughout the medullary cords among mixed populations of lymphocytes and macrophages, and in the subcapsular region. These fibers contribute to innervation of the paracortical and cortical regions, regions abundant with T lymphocytes. In addition to the innate distribution of neuronal fibers in close proximity with cells of the immune system, the local production of neuropeptides by cells of the immune system has also been recognized as a mechanism through which neuroimmunomodulation of localized inflammation can take place (18). The enzymatic capacity of immune cells to synthesize, store, and release neurotransmitters like norepinephrine has added an autocrine neuroimmune mechanism not considered in this review, but worth further investigation.

Thus, in lymphoid tissues, lymphocytes and macrophages are located at sites adjacent to neuronal fibers, exposing them to local release of neuropeptides forming synaptic-like neuroimmune interactions, allowing modulation of localized inflammatory responses through direct neural release and humoral neuroendocrine mediators. The local release of neuroendocrine mediators coupled with specific receptor expression in immune cells establishes a functional neuroimmune connection capable of modulating various responses, including cytokine production, neutrophil chemotaxis, phagocytosis, and reactive oxygen species production and release.

WHAT IS THE FUNCTIONAL SIGNIFICANCE OF THESE NEUROENDOCRINE-IMMUNE INTERACTIONS?

The functional significance of neuroimmune synaptic interactions has been demonstrated by several studies. Catecholamines and adrenergic agonists in particular have been demonstrated to exert important regulatory functions on macrophages as well as on B and T lymphocyte cytokine production, proliferation, and antibody secretion (19). In vivo studies have shown that catecholamines affect dendritic cell function, enhancing myelopoiesis and suppressing lymphopoiesis through specific adrenergic receptor mechanisms (20) (but just as insufficient length or amount of catecholamine delivery would fail to adequately enhance myelopoiesis and suppress lymphopoiesis, catecholamine delivery over too long a timespan will induce excitotoxicity at the dendritic entry points and “blow the system.” Overproduction or over-extended production of cytokines is not desirable). In vitro studies have demonstrated that catecholamines inhibit lipopolysaccharide (LPS)-induced macrophage production of tumor necrosis factor (TNF) (21), interleukin (IL)-12 (22), and macrophage inhibitory protein 1α (23) and enhance LPS-stimulated release of IL-10 (24), while suppressing nitrite production (25). The contribution of adrenergic regulation of cytokine production is also evident by the increased TNF-α production by peritoneal macrophages obtained from sympathectomized mice (26).

The conclusions reached by some studies appear to be conflictive, part of which can be explained by differential effects mediated by the specific receptor subtypes, as well as by the differential cellular response. Catecholamines act on their target cells through binding to cell surface adrenergic receptors. (This is pretty likely where “excitotoxicity” occurs as the result of prolonged hammering upstream on the sympathetic branch of the ANS.) Reports indicate that α- and β-adrenergic receptors are expressed in immune cells, with β-adrenergic receptors having a wider expression in these cells (27). β-Adrenergic receptors belong to the family of G protein-coupled receptors that when activated by ligand binding, lead to elevation of intracellular cAMP and activation of protein kinase A. Like other ligand-mediated cAMP elevations, catecholamines suppress TNF, IL-1, and IL-6, and enhance IL-10 production via this mechanism. In contrast, results from in vitro experiments indicate that catecholamine effects mediated through α-adrenergic receptors can enhance TNF message and IL-12 expression (28). Given that expression of β-adrenergic receptors predominates in cells of the immune system, adrenergic effects would favor an anti-inflammatory effect over one of proinflammation. However, overall, it would be an in vivo systemic response that would provide more relevant information on the contribution of the sympathetic nervous system to control of inflammation.

The overall suppressive effect of norepinephrine in proinflammatory mediator release has been demonstrated in studies conducted in our laboratory in which alveolar- and spleen-derived macrophages isolated from naive rats were challenged with LPS in the presence of norepinephrine (10 nM). In this setting, adrenergic stimulation resulted in marked suppression of LPS-induced TNF release from both cell types. Other laboratories have observed similar anti-inflammatory effects of norepinephrine on astrocyte activation and production of TNF (29). Additional mechanisms to that of suppression of cytokine production were identified in those studies. Removal of norepinephrine resulted in enhanced amyloid-induced inflammation (bingo; as per the previous note) attributed to decreased intracellular IκB. Overall, noradrenergic depletion potentiated β-amyloid-induced cortical inflammation and neuronal cell death (30) (which is precisely what happens the fight-or-flight response is maintained for too long and heads into freak and fry), providing evidence that the role of noradrenergic innervation is not limited to control of an acute inflammatory response.

The functional effects of catecholamines on cells of the immune system have been confirmed in healthy human volunteers (31). Furthermore, the relevance of this control mechanism and the implications for its dysregulation have been demonstrated by the rapid systemic release of IL-10 and the high incidence of infection in patients with sympathetic storm from acute accidental or iatrogenic brain trauma (32). (I’ll suggest here that the same sort of sympathetic storm occurs as the result of cognitive priming of the HPA as the result of excessive core valuing of perfectionism and the anxiety it produces because we can see virtually identical, fMRI-visible “hot links” between the same cortical, limbic and brain stem locations.) Similar stress-induced induction of IL-10 expression has been reported for myocardial infarction patients and after traumatic brain injury. Several investigators have documented the exaggerated SNS activation during these periods of critical illness, particularly in patients with head injury. (Well; I just wonder where those head injuries are in a PTSD sufferer: Would they be in the emotion-modulating, neural downlinks to the limbic area from the media pre-frontal and parietal corteces? And would they be microscopic? Would they be "microlesions" at the level of "fried" receptor sites? Would they be demonstrations of chronic over-potentiation or de-potentiation of specific neurosteroidal transferences at synaptic junctions?) Although the detrimental effects of sustained and exaggerated SNS activation on cardiovascular and metabolic homeostasis have been recognized, attention should be brought to the likelihood of immune dysregulation as well. Moreover, the potential immunomodulatory effects of pharmacotherapy used in these critically ill patients needs to be further examined (33).

Thus, sympathoexcitatory pathways exert direct effects on cells of the immune system affecting cytokine expression, lymphocyte function, and cytotoxic activity (Fig. 2). In addition, as described below, the cells of the immune system as well as the inflammatory mediators released by them communicate with the CNS through direct and indirect mechanisms.

THE IMMUNE SYSTEM COMMUNICATES TO THE CNS, FORMING A FEEDBACK LOOP

The neuroimmune bidirectional network is comprised of a descending pathway that links the CNS to peripheral immune tissues and a parallel afferent arm linking the immune system with the CNS. The integrity of this loop allows for communication between the CNS and the peripheral immune system, integrating neuronal and immune signals in the periphery as well as in the CNS. The synaptic-like neural connection with lymphoid tissues modulates multiple cellular processes in the immune system through the local release of neuropeptides, neurotransmitters, and neurohormones. Cells from the immune system express functional receptors and the respective signal-transduction pathway components for several neuroendocrine mediators, allowing cellular functional responses to agonist stimulation. Similarly, cells in the CNS are capable of synthesizing, secreting, and responding to inflammatory and immune-related molecules. There is considerable evidence that the peripheral immune system can signal the brain to elicit a sickness response during infection and inflammation (Fig. 3). Peripheral immune molecules such as cytokines influence CNS actions (34) through various mechanisms, including cytokine entry into the brain through a saturable transport mechanism or through areas that lack the blood-brain barrier as well as through activation of afferent neurons of the vagus nerve. Although active transport is required for some cytokines to enter the brain (35), others gain access into the brain through fenestrated capillaries in different regions of the CNS. These sites are relatively devoid of a blood-brain barrier such as the structures lining the anteroventral border of the third ventricle, including the organum vasculosum of the lateral terminalis and subfornical organ, the median eminence, and the posterior lobe of the pituitary. Their capillaries do not form tight junctions and are thus far more readily penetrable via the paracellular route. Passage of cytokines through these areas is thought to produce localized effects in neuronal structures in the immediate vicinity directly or indirectly (36). Thus, CNS signaling by cytokines may not even require their active transport into the CNS. Signaling may be relayed through classical neurotransmitters or through lipid mediators produced and released in these areas devoid of the blood-brain barrier. Brain microvessels have been shown to respond to cytokine stimulation by producing prostaglandins (PGE2), which can then in turn affect CNS neurotransmission. Other investigators have shown that there is a median eminence site of action at which peripherally stimulated IL-6 possesses CRH-releasing activity. Additionally, evidence suggests that the peripheral production of proinflammatory cytokines may signal the brain through stimulation of vagal afferents (37). Vagal afferent signaling by peripheral immune mediators has been documented to contribute to HPA activation, fever, sleep, norepinephrine turnover, and sickness behavior (38, 39) (so guess what happens if PTSD-type recycling of emotional agitation continues unabated: Would the enteric nervous system in the gut that senses such agitation shoot relentless signaling up the vagus nerve causing the feedback looping of “fight or flight” and turn it into “frying” the dendrites along the entire chain of axonal projections from the amygdala in the limbic system?). The mechanisms involved in the interaction between peripheral cytokines and vagal fibers is still under investigation. Functional cytokine receptors have not been identified in abdominal vagal afferents (aka the enteric nervous system). However, abdominal paraganglia, which are in close proximity to and synapse with vagal fibers, specifically bind biotinylated IL-1ra. Moreover, localized perivagal cytokine production by may also contribute to this signaling mechanism (40). Thus, several mechanisms can be identified that are participant of the signaling from the peripheral immune system to the CNS, closing the bidirectional neuroendocrine loop (precisely as I suggested above).

How these are affected during injury and disease has not been fully investigated. However, several lines of evidence would suggest that pathological conditions would be likely to alter blood-brain barrier permeability, enhancing the access of peripheral immune cells or their products to the CNS (41). This afferent signaling pathway to the CNS in response to peripheral inflammatory challenges functions as a feedback mechanism modulating behavioral and biological responses during disease (Fig. 4). This bidirectional neuroimmune interaction creates a circuit of responses that can be considered an inflammatory reflex because of the immediate effects produced by the release of these neuroendocrine and immune mediators into the periphery, as well as the ability of the CNS of rapidly integrating afferent signals conducted by peripheral nerves. The integrity of such circuit is critical in host protection and adaptation to systemic challenges such as traumatic injury and infection.

RELEVANCE OF THE NEUROIMMUNE REFLEX

Understanding the relevance of neuroimmunomodulation to overall control of inflammatory responses during specific pathological conditions requires a model that resembles a clinical presentation in which the nervous system as well as the immune system are challenged accordingly and in which the outcome from neuroimmune interaction affects the host response. Studies in our laboratory have used hemorrhagic shock in conscious, unrestrained rodents to elucidate the contribution of the SNS to modulation of host response. This model allows for the determination of neuroendocrine activation and the concordant inflammatory response of the host in the absence of anesthetics or sedatives that can alter the efferent neural pathways that are immediately triggered by hypotension and that mediate the restoration of hemodynamic, metabolic, and host defense counterregulatory responses. (I'll suggest here that further research will reveal that over-long proinflammatory response may semi-permanently alter the efferent neural pathways to produce a manifestation of chronic PTSD symptoms.)

Controlled inflammation during a period after injury is essential for tissue repair and maintenance of immune competence (42). The regulated initiation and termination of this tissue proinflammatory response is under neuroendocrine control through direct neurotransmitter release at the target organ, as well as indirectly through humoral factors, including catecholamines, neuropeptides, and glucocorticoids among a few. Although the early post-traumatic inflammatory response is directed to repair tissues and establish immune competence, an increased magnitude and duration of this response is associated with delayed restoration of homeostasis and increased tissue injury leading to multiple organ failure (43) (which seems to agree with the suggested made above).

Several lines of evidence indicate that the early proinflammatory cytokine upregulation contributes to the development of this syndrome by synergistic actions or by priming or predisposing the host to subsequent injury. Thus the pro/anti-inflammatory cytokine balance, which should mediate tissue repair and recovery, if uncontrolled, can produce tissue injury on one spectrum and immunosuppression on the other extreme (44). Hence, the relevance of understanding the mechanisms involved in control of the magnitude and duration of this response.

NEUROIMMUNOMODULATION IN STRESS

The counter-regulatory response to acute and prolonged illness involves the release of catecholamines in high concentrations into the systemic circulation through the sympathoadrenal activation as well as into specific tissue beds through noradrenergic discharge from sympathetic nerve terminals (45). This activation of the SNS is much more evident under conditions of acute traumatic injury, particularly those involving the brain (46) (and it is my observation-based contention that such “acute traumatic injury” includes the microscopic injuries done to neural pathways in the limbic system over time by alcoholism, drug addiction, obsessive hyper-stimulation and/or chronic anxiety). Our working hypothesis is that this sudden and massive release of circulating and tissue catecholamines can affect the magnitude of tissue cytokine response and, consequently, can impact the integrity of subsequent host defense mechanisms. Several clinical observations would support this association. However, demonstration of the role of the SNS in regulation of immune responses during injury is best done in an experimental setting. Using traumatic injury as a trigger for moderate inflammation, we have examined the contribution of tissue norepinephrine content to the inflammatory response after hemorrhagic shock in chronically instrumented conscious unrestrained rodents.

NORADRENERGIC SUPPRESSION OF THE HEMORRHAGE-INDUCED INCREASE IN LUNG TNF

To test the role of tissue norepinephrine, animals were chronically pretreated with small doses of the neurotoxin 6-hyroxy-dopamine (6-OHDA) before hemorrhagic shock (47). Once accumulated in neurons, 6-OHDA undergoes auto-oxidation, causing the degeneration of catecholamine-containing neurons. Enhanced specificity for noradrenergic neurons is achieved through repeated small dose administration. Because 6-OHDA does not penetrate through the blood-brain barrier, the effects of its peripheral administration can be attributed to peripheral noradrenergic nerve endings. Noradrenergic tone was effectively removed by the destruction of noradrenergic nerve terminals (which is pretty much what I see on on scans that seems to occur over time in the limbic tissues as the result of substance and/or behavioral abuse, as well as relentless anxiety), manifested by depletion of norepinephrine stores (80%-90%) in peripheral tissues, including lung and spleen. This removal of tissue norepinephrine stores resulted in an exacerbated rise in lung TNF expression after hemorrhagic shock and fluid resuscitation. These results strongly suggested that during the acute stress produced by hemorrhagic shock, control of the early proinflammatory response is partly under suppressive effects of localized noradrenergic tone. Because norepinephrine is the predominant neurotransmitter released from postganglionic sympathetic nerve terminals, these studies provided evidence of SNS contribution to the regulation of the magnitude of the early proinflammatory response to injury.

Other investigators have reported similar exacerbation of the inflammatory response after liver injury in chemically sympathectomized mice (48). Moreover, studies by Le Tulzo et al. (1) have demonstrated that β-adrenergic blockade increased hemorrhage-induced NF-κB activation and enhanced the hemorrhage-induced proinflammatory cytokine expression in the lung. Evidence supporting a direct anti-inflammatory effect of sympathetic nerve stimulation on cellular responses has been provided by in vitro studies in isolated perfused spleens. In this setting, electrical stimulation of sympathetic nerves inhibits stimulated TNF secretion via β-adrenergic pathways (49). Taken together, these data suggest that overall, tissue norepinephrine exerts anti-inflammatory effects, serving as a brake in the inflammatory cascade, controlling and regulating the magnitude and profile of cytokine responses (but when the limbic system is itself subjected to the excitotoxifying effects of hyper-stimulation over a long period of time, the ANS balance begins to erode, the HPA just "diesels" in epinephrine flood leading to adrenal fatigue syndrome, and there are insufficient amounts of norepinephrine available to “apply the brakes”). Thus, activation of the SNS (autonomous in the case of hemorrhagic shock and stimulated in the case of electrical stimulation) suppresses tissue proinflammatory responses.

The adrenergic effects on immune function appear to be differentially mediated by the specific adrenergic receptor subtypes. The anti-inflammatory effects of norepinephrine appear to be mediated via β2-adrenergic receptors. Le Tulzo et al. (1) showed that although β-blockade enhanced lung proinflammatory cytokine expression, contrasting effects were observed after α-adrenergic antagonist administration before hemorrhagic shock. Their results indicate that α-adrenergic blockade prevents the elevation in mRNA levels of IL-1α, TNF-α, and TGF-β1, the increase in IL-1β protein, as well as the activation of nuclear factor (NF)-κB in intraparenchymal pulmonary mononuclear cells produced by blood loss. Those results suggested that although adrenergic stimulation through the α-adrenergic receptor favored a proinflammatory response, stimulation through the β-adrenergic receptor suppressed or controlled inflammation. This concept of balanced adrenergic control of cytokine production dependent on the specific adrenergic receptor is supported by studies in isolated perfused liver (I have not yet seen studies of the same phenomenon in the limbic system, but see no physiological reason to think it would not exist anywhere else in a body connected to the HPA). In this setting, norepinephrine upregulates TNF production and induces IL-12 through α2-adrenergic receptor-mediated mechanisms (50). These were intriguing findings and their interpretation was complex, as Le Tulzo's (1) studies were performed in anesthetized mice, potentially affecting neural activation during hemorrhage. Furthermore, no assessment was made of the impact of adrenergic blockade on the hemodynamic response to blood loss, a potentially confounding factor to the magnitude of tissue hypoperfusion and thus localized regulation of tissue responses.

Dissecting the contribution of the specific adrenergic receptors involved in modulating proinflammatory responses to hemorrhagic shock is not simple. Results from our studies suggest that the distinction between the adrenergic receptor modulation of tissue cytokine production after hemorrhage can not be clearly demarcated in an in vivo, unanesthetized rodent model of fixed pressure hemorrhage. In vivo administration of adrenergic antagonists can effectively alter the hemodynamic response to blood loss and can affect the severity of the hypotensive response achieved by removal of a given blood volume. Studies from our laboratory show that propranolol pretreatment (1 mg/kg 30 min prehemorrhage) does not produce significant alteration in the tissue expression of TNF, IL-6, and IL1α after hemorrhagic shock and fluid resuscitation. Furthermore, no marked alterations in the hemodynamic response to blood loss and fluid resuscitation were observed in those studies. In contrast, pretreatment with the α-adrenergic receptor antagonist phenoxybenzamine (2.5 mg/kg) before hemorrhagic shock did not produce significant alteration in the magnitude of the tissue cytokine response observed. However, it significantly lowered the blood volume removed required to produce hypotension (mean arterial blood pressure of 40 mmHg). Therefore, α-adrenergic blockade resulted in comparable hemorrhage-induced upregulation in tissue cytokine expression to that elicited by greater blood loss.

Taken together, these results led to the conclusion that depletion of tissue noradrenergic stores removes the inhibitory control on hemorrhage-induced TNF upregulation in the lung. Interestingly, this effect does not appear to be indiscriminate, as no upregulation in IL-6 response was observed in chemically sympathectomized hemorrhaged animals. In contrast, α-adrenergic receptor antagonist-pretreated animals showed an accentuated lung IL-6 response to a given blood loss without affecting the magnitude of the TNF response. Overall, these observations indicate that sympathetic regulation exerts differential adrenergic receptor-mediated effects affecting the balance of cytokine profile expression, supporting a role for sympathetic regulation of immediate tissue cytokine responses to hemorrhagic shock. We speculate that because of the central role of SNS activation during the immediate response to injury, neuroimmune modulation mediated by the SNS during hemorrhagic shock is likely to affect outcome during the postinjury period.

CONCLUSION

SNS activation is central to the integrated stress response. The SNS has significant anatomical and functional interaction with cells of the immune system and plays an important role in control of the magnitude of early inflammatory response to injury by ensuring expression of adequate cytokine balance. These sympathetic neural pathways exert direct effects on cells of the immune system, affecting cytokine expression, lymphocyte function, and cytotoxic activity. In turn, the inflammatory mediators released communicate with the CNS through stimulation of sensory and vagal afferents or by crossing the blood-brain barrier through active transport mechanisms or by taking advantage of areas with fenestrated capillaries, allowing easy access to the median eminence and hypothalamo-pituitary structures. In the CNS, these immune-derived mediators such as cytokines and chemokines modulate neurotransmission, affecting activation of descending autonomic and neuroendocrine pathways. Thus, the system is designed as a neuroendocrine-immune feedback loop in which direct neural activation of lymphoid tissues effects cellular responses, forming a reflex arch, and establishing bidirectional communication.

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© 2011 by Rodger Garrett for the commentary; all rights reserved. Links are fine. Please contact not_moses@fastmail.fm with comments or questions. Thank you.

Book Review: Radical Acceptance

2011-12-11T15:12:00.000-08:00

The Words About the Words may Get in the Way

Rodger Garrett (Loma Linda, CA USA) - See all my reviews

This review is from: Radical Acceptance: Embracing Your Life With the Heart of a Buddha by Tara Brach, New York: Bantam Dell, 2004.

While it will seem (to some) "odd" to say that almost everyone would benefit from reading virtually anything Brach (or Linehan, or Hayes, or Strosahl, or Segal, or Kabat-Zinn, or Tolle, or, or, or) has to say on the general topic mindfulness and the meditation skills that foster it, and then criticize such work...

I do have a problem with a little part of what they say. (Or maybe it's more about how they say it.)

And it is this: While it is clear to me from reading their material that Brach and the rest understand the relevance of words and verbal processes to core beliefs, values, idea(l)s, principles, assumptions, convictions, rules and verbally codified attitudes that directly affect appraisals, evaluations, interpretations, assessment, analyses, judgments of, and attributions of meaning to, our emotional experiences; these authors may appear to the less instructed to suggest that language is itself the problem and should be excluded as quickly as possible after being noticed, acknowledged and allowed to float down the metaphorical stream.

(I know: really long sentence.)

In my own studies of cognitive-affective-experiential-behavioral process, however, it looks to me like while words do in fact "get in the way," we do better to honor and radically accept them as the powerful players in our emotions and actions that they in fact are. Coming from decades of work in the Ellis / Beck / Dyer / Meichenbaum / Seligman / Young / Wessler modes of CBT, my newer studies of neurobiological processing of experience (in my case, with Begley, Cozolino, Gazzaniga, Kaszniak, LeDoux, Panksepp, Rock, Schore, Siegel and many others) simply does not square with a language-rejecting approach to therapy for depression, anxiety, stress, mania, PTSD, what-have-you.

And a careful reading of Brach et al, does not square with it, either. I surely "get" the essential, fundamental, vital notion of the mindfulness-based crowd that "the words get in the way," and that one does well to utilize the Buddhist practices to get past them.

But my own experience in working with many people on addiction, depression, anxiety, etc., is that their core beliefs, values, etc. are the problem. They are mis-interpreting reality because of their common cult-ural beliefs, etc. And those core constructions of verbally represented, rather than actual, directly experienced reality will have to be identified, questioned, reviewed and either rejected or reframed to allow for a different set of interpretations, appraisals, evaluations and what have you.

Now. I agree with the DBT, ACT and MBCT crowd that wordless meditation is a necessary component of the healing process. But I do not agree that it is an entirely sufficient one. And here's why: I have -- for more than 35 years -- observed legions of vipassana (Brach's favorite) and other Asian-method meditators who are still very disconnected from reality and unable to behave functionally or effectively in intimate relationships, in the workplace and with their families of origin.

I have written elsewhere about the "three-legged stool" of 1) self-talk identification, questioning and revision; 2) narrative examination, clarification, revision and reconstruction; and 3) mindfulness (including the meditation crucially required to access it). I see that veteran DBT therapist and writer Matthew McKay and several confederates have developed a new (late 2011) New Harbinger series workbook entitled Mind and Emotions: A Universal Treatment for Emotional Disorders. That book operates from the combined, efficacy-research-proven principles I distilled above into the three-legged stool.

This is very much not, however, any sort "dis job" on Brach's work. Without it, we'd all be considerably less edified. Mental health professionals will do their patients a major favor by making RA a required, bibliotherapuetic adjunct.

(c) 2011 by Rodger Garrett; all rights reserved. Links are okay. Please inquire or comment to not_moses@fastmail.fm. Thank You.