Saturday, October 26, 2013

A Developmental Perspective on Intersubjectivity from Birth Onward (Daniel N. Stern)


Daniel N. Stern was the author of The Interpersonal World Of The Infant A View From Psychoanalysis And Developmental Psychology (2000/1985), one of the most profound books on the healthy and unhealthy development of the infant available. Stern's model is in line with current trends in postmodern psychoanalysis - it's based in attachment theory, relationality, intersubjectivity, and neuroscience. 

Along with Allan Schore, Stern is must reading for anyone who wants to understand the development and pathologies of development in children - the foundation for trauma therapy.

Stern passed away in 2012 - among his other books are The Present Moment in Psychotherapy and Everyday Life (Norton Series on Interpersonal Neurobiology) (2010) and Diary Of A Baby: What Your Child Sees, Feels, And Experiences (1992), told from the baby's point of view.

50 Jahre SFI - A Developmental Perspective on Intersubjectivity from Birth on (Daniel N. Stern)

Published on May 22, 2013

50 Jahre Sigmund-Freud-Institut - 50 Jahre "Forschen und Heilen"

Daniel N. Stern (Boston/Genf)
A developmental perspective on intersubjectivity from birth on

Festakt zum 50-jährigen Bestehen des Sigmund-Freud-Instituts am 24. April 2010 auf dem Campus Westend der Goethe Universität Frankfurt am Main.

Neuron-Glia Interaction as a Possible Glue to Translate the Mind-Brain Gap

Hmmmm . . . . I'm not sure what I think of this article. The mere fact that they use the terms Id, Ego, and Super Ego lead me to suspect that the authors are very poorly trained in contemporary psychology models, especially post-Freudian psychoanalysis.

Still, looking at the interactions between glia and neurons may be a worthy path to a better understanding of how the body-brain generates the emergence of mind.

Neuron-glia interaction as a possible glue to translate the mind-brain gap: a novel multi-dimensional approach toward psychology and psychiatry

Takahiro A. Kato [1,2], Motoki Watabe [3] and Shigenobu Kanba [1]
1. Department of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
2. Innovation Center for Medical Redox Navigation, Kyushu University, Fukuoka, Japan
3. Department of Management, School of Business, Monash University, Sunway, Malaysia

Neurons and synapses have long been the dominant focus of neuroscience, thus the pathophysiology of psychiatric disorders has come to be understood within the neuronal doctrine. However, the majority of cells in the brain are not neurons but glial cells including astrocytes, oligodendrocytes, and microglia. Traditionally, neuroscientists regarded glial functions as simply providing physical support and maintenance for neurons. Thus, in this limited role glia had been long ignored. Recently, glial functions have been gradually investigated, and increasing evidence has suggested that glial cells perform important roles in various brain functions. Digging up the glial functions and further understanding of these crucial cells, and the interaction between neurons and glia may shed new light on clarifying many unknown aspects including the mind-brain gap, and conscious-unconscious relationships. We briefly review the current situation of glial research in the field, and propose a novel translational research with a multi-dimensional model, combining various experimental approaches such as animal studies, in vitro & in vivo neuron-glia studies, a variety of human brain imaging investigations, and psychometric assessments.

Full Citation: 
Kato TA, Watabe M and Kanba S (2013) Neuron-glia interaction as a possible glue to translate the mind-brain gap: a novel multi-dimensional approach toward psychology and psychiatry. Frontiers in Psychiatry: Neuropsychiatric Imaging and Stimulation; 4:139. doi: 10.3389/fpsyt.2013.00139


Neurons and synapses have long been the dominant focus of neuroscience, thus the pathophysiology of psychiatric disorders has come to be understood within the neuronal doctrine. However, the majority of cells in the brain are not neurons but glial cells including astrocytes, oligodendrocytes, and microglia. Traditionally, neuroscientists regarded glial functions as simply providing physical support and maintenance for neurons. Thus, in this limited role glia had been long ignored (1). Recently, glial functions have been gradually investigated, and increasing evidence has suggested that glial cells perform important roles in various brain functions. Digging up the glial functions and further understanding of these crucial cells, and the interaction between neurons and glia may shed new light on clarifying many unknown aspects including the mind-brain gap, and conscious-unconscious relationships. In addition, glial pathophysiology may explain the possible implications for the pathogenesis of major psychiatric disorders. The complexity of these aspects has yet to be well investigated. To explore these physiological and pathological aspects, novel translational methods should be applied with a multi-dimensional approach. Herein, we will briefly review the current situation of glial research in the field, and propose a novel translational research with a multi-dimensional model, combining various experimental approaches such as animal studies, in vitro & in vivo neuron-glia studies, a variety of human brain imaging investigations, and psychological/psychiatric assessments.

Glial Roles and Pathology in Psychiatric Disorders

Recent biological studies have been revealing the important roles of glial cells in the process of neuropsychiatric disorders. 


Astrocytes are the most prevalent cell type in human brain and contribute to the homeostasis of the brain by regulation of neuronal metabolism, modulation of CNS inflammation, and direct/indirect synaptic transmission such as MNDA receptors (2, 3). Astrocyte dysfunction has been critical for various neurological disorders (4). Recent studies have shown abnormal expression of glial fibrillary acid protein (GFAP) – a prototypical marker of astrocyte – in postmortem brain of patients with schizophrenia and major affective disorders (57). In addition, recent rodent studies have suggested that astrocytes modulate anxious and depressive behaviors (8, 9). On the other hand, direct modulating effects of antidepressants have also been revealed (1013). Thus, astrocytes have been supposed to be a novel therapeutic target against various psychiatric disorders such as major affective disorders and bipolar disorders (14, 15).


Oligodendrocytes contribute to brain development and homeostasis in the brain by formulating myelin around axons, supporting neuronal networks in the brain. Recently, novel oligodendrocyte functions have been revealed such as monitoring neuronal activities via myelin-forming oligodendrocytes (16) and modulating the conduction velocity of action potentials along axons in the rat hippocampus (17). Dysfunctions of oligodendrocytes have been indicated in psychiatric disorders, especially schizophrenia and major affective disorders, from a series of genetic studies (18, 19), postmortem studies (2022), and diffusion tensor imaging (DTI) studies (2327). A novel animal model of schizophrenia has been developed by treating a copper chelator, which induces oligodendrocyte dysfunction and white matter abnormality as demyelination and schizophrenia-related behaviors (28, 29). Cuprizone caused marked behavioral changes (working memory deficit) indicated by the results of Y-maze task, which showed an increase in the number of arm entries and a decrease in alternation behavior. These cuprizone-induced behavioral changes were effectively prevented by chronic administration of quetiapine, an atypical antipsychotic, which also diminished demyelination (28). On the other hand, recent rodent studies have revealed the interaction between oligodendrocyte dysfunction and social behaviors. Makinodan et al. reported that oligodendrocyte dysfunction is formed by early-period social isolation and this maladaptive environment induces working memory deficit associated with prefrontal cortex (PFC) function in later life (30). Liu et al. reported that protracted social isolation of adult mice induces behavioral, transcriptional, and ultrastructural changes in oligodendrocytes of the PFC and impairs adult myelination (31).


Microglia are unique glial cells of mesodermal origin in the brain that act as “brain macrophage”; immunological/inflammatory players by moving around and releasing cytokines and free radicals (32, 33). Thus, microglia have proved to play important roles in various brain pathologies such as neurodegenerative diseases and neuropathic pain via inducing inflammation and oxidative stress (3436). Recently, microglia have been revealed to have direct contact with synapses and have proved to play crucial roles in neuronal development through synaptic pruning (3739). Postmortem studies have shown microglial activation in the brain of patients with schizophrenia and major affective disorders, especially suicide victims (4042). In addition, positron emission tomography (PET) imaging studies using the peripheral benzodiazepine receptor bindings has shown that microglia are activated in patients with schizophrenia (4345) and autism (46). On the other hand, minocycline, an antibiotic with inhibitory effects on microglial cells, has been reported to have therapeutic effects on schizophrenia and unipolar psychotic depression (4749). In addition, rodent in vitro studies have proved the novel effect of psychotropic drugs (atypical antipsychotics such as risperidone and aripiprazole, and antidepressants such as paroxetine and sertraline, both selective serotonin reuptake inhibitors) directly on microglia by suppressing release of inflammatory cytokines and free radicals (5054). Thus, microglia are suggested to play key roles in psychiatric disorders (53, 55, 56).

In the brain, neurons, astrocytes, oligodendrocytes, and microglia are mutually communicating with each other, by direct-contacting or via neurotransmitters and other various small molecules (57), and dysfunction of neuron-glia communication may induce pathological conditions not only in neurodegenerative diseases (58) but also in psychiatric conditions such as psychosis, depression, and anxiety. The above-mentioned recent findings strongly suggest that glial cells contribute to psychiatric disorders, while the underlying mechanisms have not been clarified.

Possible Glial Roles in Human Mental Functions

Until recently, the actual roles of glia in mental activities, especially for healthy humans, have not been investigated. As the first step to clarify this unexplored field, we have started to conduct a series of social decision-making experiments with healthy human subjects using minocycline, a microglial inhibitor (5961). Healthy Japanese adult males made a monetary decision about whether or not to trust an anonymous partner after a 4-day oral administration of minocycline. Our first trial revealed that the minocycline group showed a positive correlation between their monetary score in trust game and their evaluation scores of others’ trustworthiness in a questionnaire (Yamagishi’s General Trust Scale), but surprisingly the placebo group did not (60). It would be rational to consider the monetary and questionnaire score to be positively correlated because both scores measure the other’s trustworthiness, but there was no positive correlation with the placebo group. The questionnaire is measuring only conscious-level decision-making, on the other hand the monetary score is measuring the final decision-making affected by not only the conscious but also the unconscious; suggesting that some unconscious noisy factors seem to be affecting the placebo group. Treatment with minocycline, a microglial inhibitor, has shown the positive correlation. Therefore, this first trial has indicated that microglial activation may cause “unconscious noises” against appropriate social decision-making, and inhibiting microglial activity may reduce such noise (60). In a next trial with larger samples, we additionally measured the effects of anxiety and personality as candidates for “noise” factors, by using Temperament and Character Inventory (TCI) and State-Trait Anxiety Inventory (STAI) (59). The monetary score in trust game was significantly lower in the minocycline group. Interestingly, participants’ ways of decision-making were significantly shifted; certain personality traits (cooperativeness, reward dependence, and self-directedness) proved to be the main modulating factors of decision-making in the placebo group, on the other hand the minocycline group was mainly modulated by state anxiety and trustworthiness. Our results of the second trial suggest that minocycline led to more situation-oriented decision-making, possibly by suppressing the effects of personality traits, and furthermore that personality and social behaviors might be modulated by microglia. Interestingly, cooperativeness has proved to be the most influential factor in the process of decision-making in the placebo group of Japanese participants (59). It is widely known that cooperativeness and cooperative behaviors have been highly respected and emphasized aspects in Japanese society. Thus, of course, these aspects are ingrained during childhood by various sociocultural experiences within family relationships, schools, and other areas of society in Japan. Early-life events may activate human microglia, establish a certain neurosynaptic connection, and this formation may determine personality and personality-oriented social behaviors in later life (59, 62). If these experiments are conducted in other countries with different sociocultural backgrounds, other personality traits may be identified.

In addition, we have recently reported a possible outcome that minocycline, a microglial inhibitor, also reduces the risk of the “honey trap” during economic exchanges between males × females (61). Males tend to cooperate with physically attractive females without careful evaluation of their trustworthiness. In our experiment, young healthy male participants made risky choices (whether or not to trust female partners, identified only by photograph, who had decided in advance to exploit the male participants). The results show that trusting behavior in male participants significantly increased in relation to the perceived attractiveness of the female partner, but attractiveness did not impact trusting behavior in the minocycline group (61). These novel effects of minocycline may highlight the unknown roles microglia play in deeper human mental activities; microglia may modulate our unconscious drives in various social settings. The above-mentioned findings shed new light on the dark side of microglial social/mental functions in humans, especially highlighting the role of microglia for the unconscious. In the same way that Sigmund Freud, the founder of psychoanalysis, proposed that our behaviors must be controlled by the unconscious world, microglia may unconsciously control our behaviors. How do microglia act as fundamental mediators between the conscious and the unconscious world? What do neurobiological mechanisms justify their eventual role in bridging the gap between neuroscience and psychoanalysis? Answers to the above questions are not yet clear, but we have recently proposed a hypothesis creating a link between Freud’s unconscious drives such as the death drive and microglial activation (62). For example, microglial maladaptive over-activation in a certain brain region may activate human aggressive behaviors as a result of destructive drives [For the details, please see our recent article; Ref. (62)]. In the brain, not only microglia but also other glia such as astrocytes and oligodendrocytes exist, thus complicated neuron-glia interactions may modulate our mental activities including the unconscious (Figure 1). Further research should be applied to clarify these unresolved questions.

Figure 1. The mind-brain gap from a novel glial neuropsychoanalytic perspective. The interaction between the mind and the brain has not been well understood. Freud, the founder of psychoanalysis, proposed the conception of mind structure models consisting of the following three components: the ID (unconscious/instinctual drives), the EGO (the exclusive apparatus of the conscious mind), and the SUPER-EGO (which represses the id in order to avoid any disruptions of rational thought). The existence and the significances of these mental components may be explained by future understandings of the neuron-glia interactions. The hypothetical interaction between the ID (unconscious drives) and microglia has already been proposed in our recent theoretical paper (62).
After Freud’s theory of unconscious roles in behaviors which was initially identified in the 1980s (63), Pribram and his colleagues have developed this theory in terms of a better articulated model of neural computation (64, 65). In addition, recent neuropsychoanalytic movements have been updating Freud’s theory with modern sophisticated methods of cognitive neuroscience (6672). Thus, these recent approaches have been revealing the underlying mechanisms of implicit processing in a variety of information-processes including the social processes using rodent experiments. At present, the link underlying mechanisms between neuron-glia interactions and the conscious-unconscious relationship is largely unsolved, and few experimental methods have been developed to test these unknown brain mechanisms at either the microscopic or macroscopic level. Unconscious processing needs to be given a greater focus in terms of brain mechanisms. One possible solution is the novel ontogenetic approach; called “optogenetics” (7376). Optogenetics is a revolutionary technique involving taking a light-activated gene (called a channel rhodopsin) targeted into a single neuron type. This technique enables to clarify direct interaction between activation of specific neuron in specific region by light and the resulting outcomes such as behaviors and emotional reactions at rodent level. A recent study has interestingly shown that activation of specific neurons in hippocampus produce a false memory in mice (77). Further technological developments in modulating glial cells by light and in activating both neurons and glial cells at the same time, by multiple fluorescent lights, may shed new light on resolving unknown roles of glia and neuron-glia interaction in behaviors and the conscious-unconscious. Functional roles and pathological contributions of astrocyte, oligodendrocyte, and/or microglia in conscious or unconscious processes have not been well understood, and we hypothesize that each cell may differently contribute to these physical and/or pathological processes in different brain regions such at the brainstem, limbic, or thalamocortical region, respectively. Future developments in optogenetics may clarify these unknown aspects.

Limitation and Future Perspectives of Neuro-Glia Research on Psychology and Psychiatry

To explore the above-mentioned hypothesis, further translational research is needed. Several limitations should be made note of at the present stage. At first, rodent studies focusing on the unconscious are limiting. Even if the unconscious exists in rodents, it seems to be impossible to measure the unconscious in rodents devoid of human language capabilities. Therefore, to uncover the unconscious mechanisms, we have no alternative method except examining actual human subjects. We have no specific drugs to modulate glial cells utilized in human, and minocycline is reported to have other brain functions in addition to microglial inhibition (78, 79). On the other hand, some brain imaging techniques enable us to explore the unknown roles of glial cells such as DTI technique and PET imaging using the peripheral benzodiazepine receptor bindings, while the specificities of these imaging methods are not at satisfactory levels (80). On the other hand, we can reconsider previous findings of brain imaging experiments. Functional MRI (fMRI) is a brain imaging procedure measuring brain activity by detecting associated changes in blood flow (81, 82). Outcomes of fMRI have long been believed to monitor solely neuronal activities, because cerebral blood flow and neuronal activation have been thought to be almost equivalent. However, not only neuronal activities but also glial activities, especially astrocyte activities, rely on cerebral blood flow. Therefore, at least to some extent, brain activities expressed by fMRI may be showing a part of glial activation. In addition, MR spectroscopy (MRS) is one of the novel imaging approaches to measure dynamic brain functions focusing on metabolomics including glia-related molecules. For example, myo-inositol, which can be measured by MRS, is regarded as a marker of astrocyte activity (83). These imaging methods and combination of these imaging techniques may shed new light on clarifying unknown roles of glia in psychiatric disorders (84, 85). For example, activated microglia-derived myelin damage has been indicated in the pathophysiology of schizophrenia by rodent experimental models (28, 29, 86, 87), while it is not confirmed in human subjects. Combination of human DTI and PET may clarify the mutual interaction between microglial activation and myelin damage in schizophrenia patients. On the other hand, connectivity of each brain region has been important in the understanding of the roles of brain functions from the era of Hughlings Jackson. fMRI studies have revealed the importance of these aspects (88, 89), and the recent development of DTI is showing us the significance of more complicated brain networks focusing on not only neurons but also glial cells such as oligodendrocytes (90, 91).

Finally, we propose the multi-dimensional approach to clarify the underlying brain mechanisms of mental functions including the unconscious (Figure 2). Based on our discussion, we believe that not only neurons but also glial cells have a vital role in the process of mental activities, a novel approach focusing on neuron-glia interactions should be applied. Combination of brain imaging techniques focusing on both neurons and glial cells should be applied (24, 26, 27, 4346, 9294). The most significant limitation in human brain research is that we cannot obtain living brain cells, including glial cells, from living human subjects from an ethical perspective. Presently, we can apply an alternative method; human brain cells such as neuronal cells can be established from somatic cells (not from the brain) such as skin fibroblasts by utilizing the gene-modification technique of induced pluripotent stem (iPS) cells. In addition, recently, neuronal cells are more easily established from directly conversion of human skin fibroblasts, called induced neuronal (iN) cells (9599). Novel methods of establishing glial cells are strongly warranted based on iPS or direct conversion techniques in the near future. Multi-dimensional aspects of same human subjects, from genes, blood, brain imaging, psychometrics, social function, unconscious functions, psychodynamic assessments to molecular functions of somatic tissue-derived neuronal and glial cells, should be investigated and analyzed together (Figure 2). This approach may explore the novel roles of glial cells in various human mental activities including the unconscious. The application of this method for psychiatric patients should also be encouraged in the establishment of novel diagnostic methods and novel therapies.
Figure 2. A novel multi-dimensional approach toward psychology & psychiatry.

Conflict of Interest Statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


This work was supported by Grant-in-Aid for Scientific Research on (1) Innovative Areas “Glia Assembly” (No. 25117011) of The Ministry of Education, Culture, Sports, Science, and Technology, Japan, (2) the Japan Society for the Promotion of Science (No. 24650227), and (3) the Health and Labor Sciences Research Grant No. [H 24-Seishin-Jitsuyouka (Seishin)-Ippan-001].

References available at the Frontiers site.

Friday, October 25, 2013

The Wright Show - Robert Wright Talks with Joshua Greene (author of Moral Tribes)

On last week's episode of The Wright Show, Robert Wright spoke with Joshua Greene about his new book, Moral Tribes: Emotion, Reason, and the Gap Between Us and Them (Oct, 2013). Here is a synopsis of the book from Amazon:
October 31, 2013  
A pathbreaking neuroscientist reveals how our social instincts turn Me into Us, but turn Us against Them—and what we can do about it

Our brains were designed for tribal life, for getting along with a select group of others (Us) and for fighting off everyone else (Them). But modern times have forced the world’s tribes into a shared space, resulting in epic clashes of values along with unprecedented opportunities. As the world shrinks, the moral lines that divide us become more salient and more puzzling. We fight over everything from tax codes to gay marriage to global warming, and we wonder where, if at all, we can find our common ground.

A grand synthesis of neuroscience, psychology, and philosophy, Moral Tribes reveals the underlying causes of modern conflict and lights the way forward. Greene compares the human brain to a dual-mode camera, with point-and-shoot automatic settings (“portrait,” “landscape”) as well as a manual mode. Our point-and-shoot settings are our emotions—efficient, automated programs honed by evolution, culture, and personal experience. The brain’s manual mode is its capacity for deliberate reasoning, which makes our thinking flexible. Point-and-shoot emotions make us social animals, turning Me into Us. But they also make us tribal animals, turning Us against Them. Our tribal emotions make us fight—sometimes with bombs, sometimes with words—often with life-and-death stakes.

An award-winning teacher and scientist, Greene directs Harvard University’s Moral Cognition Lab, which uses cutting-edge neuroscience and cognitive techniques to understand how people really make moral decisions. Combining insights from the lab with lessons from decades of social science and centuries of philosophy, the great question of Moral Tribes is this: How can we get along with Them when what they want feels so wrong to Us?

Ultimately, Greene offers a set of maxims for navigating the modern moral terrain, a practical road map for solving problems and living better lives. Moral Tribes shows us when to trust our instincts, when to reason, and how the right kind of reasoning can move us forward.

A major achievement from a rising star in a new scientific field, Moral Tribes will refashion your deepest beliefs about how moral thinking works and how it can work better.
Here's the talk.

The Wright Show

Oct 23, 2013 | Robert Wright & Joshua Greene

Robert Wright (, The Evolution of God, Nonzero) and Joshua Greene (Harvard University)

Recorded: Oct 22 Posted: Oct 23, 2013
Download: wmv | mp4 | mp3 | fast mp3

Links Mentioned

Joshua's new book, "Moral Tribes"
Bob's review of the book
Daniel Kahneman's book, "Thinking, Fast and Slow"
Bob's book, "The Moral Animal"

Empowering A Generation: An Educational Outreach Video for Young Leaders

This new video features the Spiral Dynamics model (Don Beck version), as well as the work of integral theorist Ervin Laszlo. It was posted by Mary Ann Thompson-Frenk, Co-Founder/President of The Memnosyne Institute, Executive Committee Member of NEXUS Global Youth Summit, President of John Philp Thompson Foundation, and Vice-Chair of Giordano Bruno University. Thompson-Frenk helped negotiate the first alliance in 300 years between the Hopi/Navajo nations.

Empowering A Generation: an educational outreach video for young leaders

Published on Oct 18, 2013


"Empowering A Generation" is a FREE educational outreach video designed to empower young 20something/30something leaders created by The Memnosyne Foundation, Nexus: Global Youth Summit, and The Club of Budapest - Americas (COBA) for the members of Nexus Youth Summit, but provides material relevant for anyone interested in learning how they can make a difference in an increasingly interconnected world.

A special thanks goes to Don E. Beck, Ervin Laszlo, Mitch Fine, and Michael Gosney for their expertise and to Tina Hui, Javier I. Kinney, and Mikuak Rai for their participation in making this video a reality!

Revised Ethical Principles Have Profound Implications for Psychological Research

This comes from the PLOS Blogs - it is a summary of the new standards for research involving human subjects, whether medical or psychological, as issued by the World Medical Association in the Declaration of the Helsinki Ethical Principles for Medical Research Involving Human Subjects, published open access in the Journal of the American Medical Association (JAMA).

Very interesting . . . .

Revised Ethical Principles Have Profound Implications for Psychological Research

By James Coyne PhD
Posted: October 20, 2013

The World Medical Association has just released the latest revision of Declaration of the Helsinki Ethical Principles for Medical Research Involving Human Subjects. You can find the full document open access here.

Released on the fiftieth anniversary of the original declaration, the seventh revision will serve as the basis for regulating research involving human subjects. It will also provide the principles for evaluating research protocols submitted to what are called Institutional Review Boards (IRBs) in the United States and to similar bodies elsewhere and as the basis for judging the ethics of investigator behavior.

Manuscripts submitted for publication will have to declare that any research being reported has been reviewed by such bodies and is consistent with the revised Declaration of Helsinki.

The second paragraph of the document notes that it is addressed primarily to physicians, but that others who are involved in medical research are encouraged to adopt the same principles. Based on the reception of past versions of the Declaration of Helsinki, it can be expected that the review of psychological research, whether or not is conducted in medical settings or with medical patients, will be held to the same standards.

The revised standards thus have profound implications for the conduct of psychological research.

One provision is that the design of every research study be preregistered in a publicly accessible place before the first research participant is even enrolled. The requirement is that investigators will have to commit themselves publicly to basic features of their designs, including numbers of research participants enrolled and the primary outcomes on which the efficacy of the invention will be evaluated. They are allowed to make subsequent revisions, but any revisions have to be recorded, along with a preservation of what was originally proposed.

Preregistration of randomized clinical trials (RCTs) has already been a requirement for subsequent publication of results in many journals. If there is no preregistration of a clinical trial, there will be no consideration for publication. But requirement has been inconsistently adopted as a condition for publication in psychology journals and inconsistently enforced.

Granting agencies increasingly require that research they fund involving RCTs will be preregistered, but many psychological intervention studies are simply noncompliant. Checking published randomized clinical trials of psychological interventions, one finds that more recent ones are registered, but that often the outcomes reported in the published papers differ from what is reported in the registration. Alternatively, the registration involves designation of a primary outcome that could be assessed by a full range of measures, without stating which measure will be used. Researchers thus assess psychological distress with the BDI, the CES-D, the distress thermometer, adjective checklists, and a battery of self-reported anxiety measures. They then pick the measures that make the intervention looked most effective. This is the source of rampant selective reporting of outcomes and confirmatory bias. The proportion of clinical trials that report negative outcomes continues to decline, and there’s little doubt that this stems from selective reporting, not improvement in the design and evaluation of interventions.

What is radical is that the revised Declaration of Helsinki extends the ethical requirement that trials be registered to cover all research, not just randomized clinical trials.

Does that mean that all social psychology lab studies and even correlational observational studies be registered? The revised declaration seems to be requiring that, but it would be difficult to imagine the requirement taking hold anytime soon.

It remains to be seen just in what form this expansion of registration will be accommodated, but it has profound implications for transparency and replicability of psychological research. Even if the revised declaration is not enforced to the letter in psychological research, it will set new standards for this research’s evaluation.

The demand for replicability of psychological research will now be facilitated by investigators having to preregister the details of their designs ahead of time, at least for expanded range of designs. We can expect investigators still tried to find wiggle room, but it will be harder to simplify designs after research has been initiated or completed by dropping whole cells or experimental conditions when their inclusion embarrasses the interpretation that investigators are trying to promote.

Another expansion of the Declaration of Helsinki that is relevant to psychological research is the elaboration of the ethical requirements for dissemination, i.e., publication, of research.

Paragraph 36 states
Researchers, authors, sponsors, editors and publishers all have ethical obligations with regard to the publication and dissemination of the results of research. Researchers have a duty to make publicly available the results of their research on human subjects and are accountable for the completeness and accuracy of their reports. All parties should adhere to accepted guidelines for ethical reporting. Negative and inconclusive as well as positive results must be published or otherwise made publicly available. Sources of funding, institutional affiliations and conflicts of interest must be declared in the publication. Reports of research not in accordance with the principles of this Declaration should not be accepted for publication.
Again, it is unclear how long it will take and what form these requirements will be implemented.

Authors, editors, and publishers of journals have a lot invested in the current practices of suppressing and spinning negative findings. But now those of us who oppose such practices can raise ethical issues when authors spin findings or journals continue to protect their impact factor by publishing only positive studies.

In recent months, draft versions of the revised declaration have already been made available for comment. There has already been some debate, and the recent release of the final document in JAMA was accompanied by some critical commentary. We can be confident that once professional psychological associations become aware of the new requirements for psychological research, there will be intense controversy over whether psychologists should adopt the standards or even whether they have any choice.

Let’s have no illusions. There are a lot vested interests in current editorial practices, but now we are better armed to challenge them, with an ethical code that declares that what we want is not only best practices, it is what is ethical. That in itself is a game changer.

This work, unless otherwise expressly stated, is licensed under a Creative Commons Attribution 3.0 Unported License.

About James Coyne PhD

James C. Coyne, Ph.D. is Professor of Psychology in the Department of Psychiatry, Director, Behavioral Oncology Research of the Abramson Cancer Center, and a Senior Fellow at the Leonard Davis Institute for Health Economics, all at the Perelman Medical School of University of Pennsylvania. Additionally, he is Professor of Health Psychology, University of Groningen Medical Center (UMCG), the Netherlands. Previously, he served on the faculties of University of California, Berkeley and University of Michigan School of Medicine. Dr. Coyne has been elected a Fellow of the American Psychological Association, Society of Behavioral Medicine, and Academy of Behavioral Medicine. His critical commentaries have challenged whether psychosocial intervention extends the survival of cancer patients, whether recommended and mandated depression programs improve patient outcomes, and whether meta analyses of behavioral medicine commissioned by professional organizations are valid and credible. A 2008 systematic review and meta-analysis in JAMA of screening for depression among cardiovascular patients was designated by BMJ as one of the eight top papers of the year. He is known for presenting and defending controversial positions and for promoting reform of the clinical and health psychology journals. He is the co-author or editor of a number of books including the 2009 Screening for Depression in Clinical Settings: An Evidence-Based Review (Oxford University Press) with Alex Mitchell.

Thursday, October 24, 2013

Evidence for the Effectiveness of Jungian Psychotherapy: A Review of Empirical Studies


This article comes from a Special Issue of Behavioral Sciences: Analytical Psychology: Theory and Practice. This is the first article I have seen that examines the efficacy of Jungian psychodynamic psychotherapy, which Jung had named Analytical Psychotherapy.

Just for clarification, these are some of the characteristics of Psychodynamic therapy models, which can be quite diverse, although all of them believe to some extent in early attachment issues as a foundation for later mental health issues. To be clear, I disagree with some of the items in the list below, which comes from Wikipedia:
Although psychodynamic psychotherapy can take many forms, commonalities include:[3]
  • An emphasis on the centrality of intrapsychic and unconscious conflicts, and their relation to development. [The conflict model has fallen out of favor since Kohut developed his Self Psychology model in the 1970s, which looks more toward the interpersonal or relational dysfunctions as the source of psychological issues.]
  • Seeing defenses as developing in internal psychic structures in order to avoid unpleasant consequences of conflict. [Defense mechanisms are now seen more as coping strategies to navigate psychologically painful traumas.]
  • A belief that psychopathology develops especially from early childhood experiences.
  • A view that internal representations of experiences are organized around interpersonal relations.
  • A conviction that life issues and dynamics will re-emerge in the context of the client-therapist relationship as transference and counter-transference.
  • Use of free association as a major method for exploration of internal conflicts and problems. [This is more a part of the psychoanalytic tradition.]
  • Focusing on interpretations of transference, defense mechanisms, and current symptoms and the working through of these present problems.
  • Trust in insight as critically important for success in therapy.

Typically when one sees the term "empirically-based therapy" or "evidence-based practice," what is being referred to is some form of cognitive therapy, often Cognitive Behavioral Therapy (CBT) or Dialectical Behavioral Therapy (DBT). However, as Jonathan Shedler demonstrated in his 2010 article, The Efficacy of Psychodynamic Therapy, psychodynamic therapies are as effective as CBT in the short term and more effective than CBT in the long-term.

Here is the abstract to the Shedler article, originally published in Scientific American Mind:
Empirical evidence supports the efficacy of psychodynamic therapy. Effect sizes for psychodynamic therapy are as large as those reported for other therapies that have been actively promoted as “empirically supported” and “evidence based.” In addition, patients who receive psychodynamic therapy maintain therapeutic gains and appear to continue to improve after treatment ends. Finally, nonpsychodynamic therapies may be effective in part because the more skilled practitioners utilize techniques that have long been central to psychodynamic theory and practice. The perception that psychodynamic approaches lack empirical support does not accord with available scientific evidence and may reflect selective dissemination of research findings.

Si it's good to see another model of psychodynamic therapy has proven itself to be "evidence-based" and beneficial for clients.

Full Citation:
Roesler, C. (2013, Oct 24). Evidence for the Effectiveness of Jungian Psychotherapy: A Review of Empirical Studies. Behavioral Sciences; 3(4): 562-575. doi:10.3390/bs3040562

Evidence for the Effectiveness of Jungian Psychotherapy: A Review of Empirical Studies

Christian Roesler 1,2
1. Clinical Psychology, Catholic University of Applied Sciences, Karlsstraße 63, 79104 Freiburg, Germany 
2. Faculty of Psychology, University Basel, Switzerland


Since the 1990s several research projects and empirical studies (process and outcome) on Jungian Psychotherapy have been conducted mainly in Germany and Switzerland. Prospective, naturalistic outcome studies and retrospective studies using standardized instruments and health insurance data as well as several qualitative studies of aspects of the psychotherapeutic process will be summarized. The studies are diligently designed and the results are well applicable to the conditions of outpatient practice. All the studies show significant improvements not only on the level of symptoms and interpersonal problems, but also on the level of personality structure and in every day life conduct. These improvements remain stable after completion of therapy over a period of up to six years. Several studies show further improvements after the end of therapy, an effect which psychoanalysis has always claimed. Health insurance data show that, after Jungian therapy, patients reduce health care utilization to a level even below the average of the total population. Results of several studies show that Jungian treatment moves patients from a level of severe symptoms to a level where one can speak of psychological health. These significant changes are reached by Jungian therapy with an average of 90 sessions, which makes Jungian psychotherapy an effective and cost-effective method. Process studies support Jungian theories on psychodynamics and elements of change in the therapeutic process. So finally, Jungian psychotherapy has reached the point where it can be called an empirically proven, effective method.

Download PDF Full-Text [230 KB, uploaded 24 October 2013]

Sleep and Immunity / Insufficient Sleep - Health Matters (UCTV)

By now, most of us have heard that getting insufficient sleep can cause weight gain, likely due to the increase in stress hormones. New research also shows that lack of sleep harms the immune system and trigger an inflammatory response.

Below are two different perspectives on the same issue. First up is a video of a talk from Sean P.A. Drummond, PhD, director of the Behavioral Sleep Medicine Program and Cognitive Behavioral Interventions Program in the VA San Diego Healthcare System on how insufficient sleep is damaging to our health.

Below that is a research review of a new article from PLOS ONE on the ways insufficient sleep harms not only our metabolic system, but also damages our immune system and causes inflammation (linked to nearly all diseases).

Insufficient Sleep - Health Matters (UCTV)

Published on Oct 23, 2013 

The CDC has declared insufficient sleep to be a national health epidemic. Why are we not getting enough and how can we change our behaviors? Sean P.A. Drummond, PhD, director of the Behavioral Sleep Medicine Program and Cognitive Behavioral Interventions Program in the VA San Diego Healthcare System, joins host Dr.David Granet to discuss the ramifications of insufficient sleep and ways to improve your sleep health. Series: "Health Matters" [10/2013]
 * * * * *

Here is an excellent overview of a new article from the open access journal PLOS ONE

New biological links between sleep deprivation and the immune system discovered

Posted By News On October 23, 2013
Population-level studies have indicated that insufficient sleep increases the risk of cardiovascular diseases and type 2 diabetes. These diseases are known to be linked to inflammatory responses in the body.

University of Helsinki researchers have now shown what kinds of biological mechanisms related to sleep loss affect the immune system and trigger an inflammatory response. They identified the genes which are most susceptible to sleep deprivation and examined whether these genes are involved in the regulation of the immune system. The study was published in the journal PLOS ONE on 23 October 2013.

Conducted at the sleep laboratory of the Finnish Institute of Occupational Health, the study restricted the amount of sleep of a group of healthy young men to four hours per night for five days, imitating the schedule of a normal working week. Blood samples were taken before and after the sleep deprivation test. White blood cells were isolated from the samples, and the expression of all genes at the time of the sampling was examined using microarrays. The results were compared with samples from healthy men of comparable age who had been sleeping eight hours per night for the week.

"We compared the gene expression before and after the sleep deprivation period, and focused on the genes whose behaviour was most strongly altered," explains researcher Vilma Aho. "The expression of many genes and gene pathways related to the functions of the immune system was increased during the sleep deprivation. There was an increase in activity of B cells which are responsible for producing antigens that contribute to the body's defensive reactions, but also to allergic reactions and asthma. This may explain the previous observations of increased asthmatic symptoms in a state of sleep deprivation."

The amount of certain interleukins, or signalling molecules which promote inflammation, increased, as did the amount of associated receptors such as Toll-like receptors (TLR). On the gene level, this was apparent in the higher-than-normal expression of the TLR4 gene after sleep loss. CRP level was also elevated, indicating inflammation.

Sleep loss causes changes to the system that regulates our immune defence. Some of these changes appear to be long-term, and may contribute to the development of cardiovascular diseases and type 2 diabetes. (Photo Credit: Vilma Aho / Univ. of Helsinki)

The researchers also wanted to examine the impact that long-term sleep deprivation could have on the immune system. For this follow-up study, they used material from the national FINRISKI health survey. Participants in this population study underwent blood tests but also answered questions about their health, for example whether they were getting enough sleep.

The researchers compared participants who believed they were sleeping sufficiently with those who felt that they were not sleeping enough. Some of the gene-level changes observed in the experimental working week sleep restriction study were repeated in the population sample. These results may help explain the connection between shorter sleep and the development of inflammatory diseases, such as cardiovascular disease and diabetes, which has been established in epidemiological studies.

"These results corroborate the idea that sleep does not only impact brain function, but also interacts with our immune system and metabolism. Sleep loss causes changes to the system that regulates our immune defence. Some of these changes appear to be long-term, and may contribute to the development of diseases that have been linked to sleep deprivation in epidemiological research," Aho states.

"Our results corroborate the idea that sleep does not only impact brain function, but also interacts with our immune system and metabolism", researcher Vilma Aho states. (Photo Credit: Linda Tammisto / University of Helsinki)
* * * * *

Partial Sleep Restriction Activates Immune Response-Related Gene Expression Pathways: Experimental and Epidemiological Studies in Humans

Vilma Aho equal contributor, Hanna M. Ollila equal contributor, Ville Rantanen, Erkki Kronholm, Ida Surakka, Wessel M. A. van Leeuwen, Maili Lehto, Sampsa Matikainen, Samuli Ripatti, Mikko Härmä, Mikael Sallinen, Veikko Salomaa, Matti Jauhiainen, Harri Alenius, Tiina Paunio, Tarja Porkka-Heiskanen


Epidemiological studies have shown that short or insufficient sleep is associated with increased risk for metabolic diseases and mortality. To elucidate mechanisms behind this connection, we aimed to identify genes and pathways affected by experimentally induced, partial sleep restriction and to verify their connection to insufficient sleep at population level. The experimental design simulated sleep restriction during a working week: sleep of healthy men (N = 9) was restricted to 4 h/night for five nights. The control subjects (N = 4) spent 8 h/night in bed. Leukocyte RNA expression was analyzed at baseline, after sleep restriction, and after recovery using whole genome microarrays complemented with pathway and transcription factor analysis. Expression levels of the ten most up-regulated and ten most down-regulated transcripts were correlated with subjective assessment of insufficient sleep in a population cohort (N = 472). Experimental sleep restriction altered the expression of 117 genes. Eight of the 25 most up-regulated transcripts were related to immune function. Accordingly, fifteen of the 25 most up-regulated Gene Ontology pathways were also related to immune function, including those for B cell activation, interleukin 8 production, and NF-κB signaling (P<0.005). Of the ten most up-regulated genes, expression of STX16 correlated negatively with self-reported insufficient sleep in a population sample, while three other genes showed tendency for positive correlation. Of the ten most down-regulated genes, TBX21 and LGR6 correlated negatively and TGFBR3 positively with insufficient sleep. Partial sleep restriction affects the regulation of signaling pathways related to the immune system. Some of these changes appear to be long-lasting and may at least partly explain how prolonged sleep restriction can contribute to inflammation-associated pathological states, such as cardiometabolic diseases.

Full Citation:

Aho V, Ollila HM, Rantanen V, Kronholm E, Surakka I, et al. (2013, Oct 23). Partial Sleep Restriction Activates Immune Response-Related Gene Expression Pathways: Experimental and Epidemiological Studies in Humans. PLoS ONE 8(10): e77184. doi:10.1371/journal.pone.0077184

Omnivore - Topics in Contemporary Psychology

From Bookforum's Omnivore blog, here is a tasty collection of links on topics in contemporary psychology. Here are three interesting and interrelated articles (linked to in the collection) on the science (or not) of psychology:

Topics in contemporary psychology

Oct 23 2013

Wednesday, October 23, 2013

"Profit from the Positive" - Margaret Greenberg & Senia Maymin | Talks at Google

Margaret Greenberg & Senia Maymin stopped by Talks at Google to promote their new book, Profit from the Positive: Proven Leadership Strategies to Boost Productivity and Transform Your Business. Their book translates scientific research on positive psychology into practical tools we can apply to how we manage ourselves, how we lead, and how we influence our colleagues. Sounds interesting.

Margaret Greenberg & Senia Maymin, "Profit from the Positive" | Talks at Google

Published on Oct 21, 2013

Think back to a moment when you got a piece of really good news.

You felt unstoppable, productive, elated.

Now imagine that feeling at work. Imagine bringing that positivity to your teams and unlocking new heights of productivity and satisfaction.

Join us for translation of scientific research on positive psychology into practical tools we can apply to how we manage ourselves, how we lead, and how we influence our colleagues.

Margaret H. Greenberg and Senia Maymin, Ph.D., will discuss their new book, Profit from the Positive: Proven Leadership Strategies to Boost Productivity and Transform Your Business (McGraw-Hill).

In this session, the authors will share memorable tools that are ingeniously fast and simple. You will walk out saying, "Why didn't I know this before?"
  • Introduction by Mary Kate Stimmler of Pi Lab
  • Hosted by Debbie Newhouse and Dolores Bernardo
  • Authors@Google and Google Manager Programs
~ "Greenberg and Maymin--pioneers in the application of Positive Psychology to organizations--have built an exciting and important bridge...." — Adam Grant, Wharton professor and New York Times bestselling author of Give and Take

Stephanie Keller - Why Patients Choose Psychotherapy or Sertraline: From a Clinical Trial of PTSD Treatment

Interesting study - more than 63% of the subjects chose psychotherapy over meds. Good to see.
The most common reasons cited for preferring one treatment to another concerned the mechanism of treatment (eg, I need to talk about the trauma; 45.5%); the efficacy profile of the treatment (eg, medication will help me; 31.5%); and health concerns (eg, I don’t want side effects from medication; 18%).
Here is the brief article from Psychiatry Weekly.

Why Patients Choose Psychotherapy or Sertraline: From a Clinical Trial of PTSD Treatment

October 21, 2013
Stephanie Keller, MA
- Doctoral Candidate; Department of Psychological Sciences, Case Western Reserve University, OH

First published in Psychiatry Weekly, Volume 8, Issue 21, October 21, 2013


Why do some psychiatric patients prefer a particular treatment modality—or modalities—to another? This question is particularly conspicuous in the context of treating posttraumatic stress disorder (PTSD), for which several psychotherapy protocols show robust evidence of efficacy and exactly two medications—sertraline and paroxetine—have received FDA approval. Numerous lines of research have looked at whether patient preferences for PTSD treatment are shaped by the type of trauma experienced, ethnicity, sex, psychiatric comorbidity, previous PTSD treatment, and perceptions of how or why a treatment is believed to work.

A group of PTSD researchers, led by Dr. Norah Feeny, of Case Western Reserve University, and Dr. Lori Zoellner at the University of Washington, recently conducted the first study of what shapes treatment preferences in a treatment-seeking sample of patients with a primary diagnosis of PTSD.

“We want to understand what shapes people’s preferences for either psychotherapy (prolonged exposure therapy) or medication (sertraline) for PTSD,” explains Stephanie Keller, who co-authored the study. “Prolonged exposure is currently one of the strongest evidence-based treatments for PTSD, and sertraline is approved by the FDA for treating PTSD. At this point, there are no conclusive trials as to whether one is more effective than the other for PTSD in general.”

"Surprisingly, practical reasons, such as time, logistics, and costs associated with treatment were the least commonly cited reasons (4.5%) for preferring one treatment to another."


The present study included a sample of 200 treatment-seeking individuals with a primary diagnosis of chronic PTSD. The sample was composed predominantly of women (75.5%) with a mean age of 37.4 years (SD=11.3 years) who were white (65.5%) and who were not college educated (70%). Nearly half (48.5%) of the sample reported an annual income of <$20,000. The types of target-traumas reported by this sample included adult sexual assault (31%) adult non-sexual assault (22.5%), and childhood assault (24%). Only 2.5% of the sample reported combat/war-related trauma.

Subjects were presented with a standardized videotaped rationale for prolonged exposure therapy and sertraline. Each video discussed the efficacy profile of each treatment, its known side effects, and the mechanisms through which it is believed to work. “These individuals were part of a doubly-randomized preference trial, so they would potentially receive one of the treatments that we asked them to choose between,” says Ms. Keller. “After we presented the participants with the rationale for each treatment, we asked them which treatment they preferred, and to then list their top 5 reasons for that preference.”

The “Why” Behind Treatment Preferences

Subjects’ reasons for their particular treatment preference were grouped in categories similar to those delineated in earlier studies. The most common reasons cited for preferring one treatment to another concerned the mechanism of treatment (eg, I need to talk about the trauma; 45.5%); the efficacy profile of the treatment (eg, medication will help me; 31.5%); and health concerns (eg, I don’t want side effects from medication; 18%).

“I think what we found most surprising was that practical reasons, such as time, logistics, and costs associated with treatment were the least commonly cited reasons (4.5%) for preferring one treatment to another,” says Ms. Keller. “An additional, somewhat surprising, finding was that age, sex, income, education, time since trauma, and severity of psychopathology did not reliably predict treatment preferences.”


Overall, when asked why they preferred either psychotherapy (prolonged exposure) or medication (sertraline) to treat their PTSD symptoms, participants cited both mechanism (eg, I need to talk about my traumatic event) and efficacy (eg, I believe medication will reduce my PTSD) as the two most common reasons that guided their decision.

“These findings can help guide treatment providers when discussing potential treatment options with their patients who have PTSD,” says Ms. Keller. “Explaining the mechanisms of these treatments, that is, how we believe these treatments exert their effect, can help patients to make an educated decision when deciding between psychotherapy or medication for their PTSD symptoms.”

Although practical reasons, such as the time or cost associated with treatment, were not commonly cited reasons for treatment preference, clinicians may want to have a discussion about these factors with their patients, in order to possibly reduce the likelihood of treatment drop-out.

“Overall,” says Ms. Keller, “it seems that patients want a treatment that will address the issues that they believe led to their symptoms of PTSD.”

Disclosure: This research was supported by NIMH grants awarded to Drs. Feeny and Zoellner (R01 MH066347, R01 MH066348).

This interview was conducted on September 26, 2013 by Lonnie Stoltzfoos


Chen JA, Keller SM, Zoellner LA, Feeny NC. “How will it help me?” Reasons underlying treatment preferences between sertraline and prolonged exposure in posttraumatic stress disorder. J Nerv Ment Dis. 2013;201:691-697.

Ed Cohen - Gut Wisdom, Or Why We Are More Intelligent than We Know


In the past few days I have posted an episode of NPR's Radiolab on Guts and another article on the gut microbes (the microbiome) that may be a powerful driver of evolution. And here, from Somatosphere, is another article on "guts," this one by a man living with Crohn's Disease.

Since Cohen mentions the enteric nervous system, and that 90-95% of the serotonin production in the human body occurs in the gut:
Approximately 90% of the human body's total serotonin is located in the enterochromaffin cells in the alimentary canal (gut), where it is used to regulate intestinal movements.[7][8] The remainder is synthesized in serotonergic neurons of the CNS, where it has various functions. These include the regulation of mood, appetite, and sleep. Serotonin also has some cognitive functions, including memory and learning. Modulation of serotonin at synapses is thought to be a major action of several classes of pharmacological antidepressants.
Drugs which block 5-HT2C receptors (several antidepressants) make the body unable to recognize when it is no longer hungry or otherwise in need of nutrients, and are associated with increased weight gain, one of the common side effects of these drugs, as well as the atypical antipsychotics.

If we want to avail ourselves of the natural intelligence of the enteric nervous system (the gut), drugs that affect serotonin are likely to make that more than a little challenging.

Gut Wisdom, Or Why We Are More Intelligent than We Know

By Ed Cohen

Gut feeling. Go with your gut. Gut of the problem. By default I’m a gut guy. At the age of thirteen I was diagnosed with acute Crohn’s Disease. For the next ten years I was borderline incontinent. Then I had a small bowel occlusion that resulted in complications precipitating a near death experience after which several feet of festering small intestine were excised from my viscera. Since then I’ve been living with the guts I have left. Needless to say I’ve had a few opportunities to reflect on “the gut” over the last forty years.

In evolutionary terms, the gut localizes and intensifies a paradox familiar to all living organisms: to live entails being simultaneously open and bounded. Francisco Varela succinctly defined this vital conundrum when he described “the intriguing paradoxicality proper to an autonomous identity: the living system must distinguish itself from its environment, while at the same time maintaining its coupling; this linkage cannot be detached since it is against this very environment from which the organisms arises, comes forth.”[i] In order to maintain this distinctive coupling, the permeable cell membrane has been as continuously conserved through the course of evolution as the crystalline DNA molecule, suggesting that the organism’s lively paradox constitutes an irreducible tension from which the living stretches itself out in time and space. Be that as it may, the gut contains this lively paradox in the most literal way: it folds the outside inward in order to keep the perturbations entailed by that paradox contained. In other words, it helps us hold our shit together. And by incorporating the open/bounded situation of the living, the gut constitutes the paradox that we are. If the gut is the way the outside lives inside of us — which of course in a topological sense it must be — then we are twisted around our guts, rather than our guts being twisted up inside of us, no matter how often we might feel the latter to be the case.

Single celled organisms don’t have guts. Guts evolve in multi-celled beings in order to govern the complex flows of nutrients and toxins that pervade the cellular world. The more convoluted the flows become the more the gut matters. Some argue that the first creatures to develop organized nervous systems were worms. Guts with brains. It’s hard to imagine, then, why people were so surprised when the enteric nervous system, the so-called “brain-in-the-gut,” was “discovered” at the end of the twentieth century. Yet, until then, for as long as anatomists had been dissecting human viscera they managed to miss this possibility. Oops. And how did the enteric nervous system finally come to our attention? Psycho-pharmacologists began prescribing SSRIs to people with depression and they noticed that one of the side effects was constipation. But why should a drug that helps us hold our shit together literally hold our shit together? It turns out the gut has all the same neuro-receptors and makes all the same neuro-transmitters as the brain does (and more recently the same has been found to be the case for the heart). Indeed the gut makes 95% of all the serotonin in the human body.[ii] So now bioscience finally acknowledges what non-scientists have been saying for quite some time: the gut has a mind of its own. Quelle surprise. After all, what does “gut wisdom” mean besides this? Seems like now that we are finally giving the gut its due, we’re finding out that we are more intelligent than we ever knew.

Perhaps the motto of gut wisdom, then, ought to be: We are more than we know, for when it comes from the gut, intelligence does not take the form of knowledge. When Kant proposed his motto for the Enlightenment: Sapere Aude—Dare to Know, he ensconced a precept that privileged knowing over not-knowing as a properly human goal, the path to “maturity” as he would have it. In the two centuries since, this precept garnered the not-unself-interested backing of neuroscience, which invested heavily in an egregious cephallocentrism that has swelled the heads of many humanoid researchers. The intelligence of the gut, however, has a more humble ambition. Our guts do not seek to distinguish us from other living beings; they do not affirm human specialness as a species imperative. Rather they remind us that “specialness,” insofar as it pertains to “species” in general, does not make us different from one another or from other life forms; the special is what we all have in common. The titles of two of the greatest children’s books of recent years, Everyone Poops and the equally important, The Gas We Pass, suggest that this is a lesson that all children can learn. Our guts remind us that we are not only a species, but also a kind of organism, the kind whose guts mediate our relations to each other and to the world, and thereby contain the vital paradox that we are. If we begin to appreciate that we are this kind of being, then our guts may help us to appreciate that kindness, even more than specialness, is a lively virtue — a virtue which our guts have known for quite some time.

~ Ed Cohen teaches Modern Thought in the Women’s and Gender Studies Department at Rutgers University. His most recent book is A Body Worth Defending: Immunity, Biopolitics and the Apotheosis of the Modern Body (Duke 2009). He is currently writing a new gut wrenching opus entitled Shit Happens: Ruminations on Living with Crohn’s Disease.

[i] Francisco Varela. “Organism: A Meshwork of Selfless Selves.” In Alfred Tauber, ed. Organism and the Origins of Self. Boston: Kluwer Academic Publishers, 1991. 85. 
[ii] Adam Hadhazy. “Think Twice: How the Gut’s “Second Brain” Influences Mood and Well-Being.” Scientific American Online. Accessed December 21, 2012.

Image: “Repair in progress,” Thirteen of Clubs, flickr.