Understanding Gender Nonconforming Children (Diane Rehm Show)

This segment of the Diane Rehm Show aired last Thursday (Sept. 5, 2013), and although it has taken me a few days to get it posted, it's a good show. Andrew Solomon's book,  Far From the Tree: Parents, Children and the Search for Identity (2012) is worth the read even if you have no interest in transgender children.

Understanding Gender Nonconforming Children

• Listen
• Transcript

Guest Host: Susan Page

Thursday, September 5, 2013 

 

This undated publicity image released by Broadway Books shows author Lori Duron, right, and her son, the inspiration for Duron's book "Raising My Rainbow: Adventures in Raising a Fabulous, Gender Creative Son," at their California home. (AP Photo/Broadway Books)

Throughout history, there have always been people who defied gender norms. Research shows gender identity is formed in early childhood. Kids as young as 2 or 3 years old can already show strong preferences to play with and dress like the opposite gender. Girls who want to play sports and wear pants are mostly accepted as “tomboys” but boys who want to play with dolls or dress in pink and purple face a tougher road. They are often bullied by peers and rejected by parents and relatives. A few of these children will grow into transgender adults where they will face more disapproval, even as society becomes more open. Guest host Susan Page and a panel of experts discuss gender nonconforming children and the challenges they present for parents and schools. 

Guests

• Lori Duron: writer, consultant and blogger; author of "Raising My Rainbow: Adventures in Raising a Fabulous, Gender Creative Son."
• Andrew Solomon: writer and lecturer on psychology, politics and the arts; author of "Far From the Tree: Parents, Children and the Search for Identity."
• Dr. Edgardo Menvielle: psychiatrist and director of gender nonconforming youth program, Children's National Medical Center in Washington, D.C.
• Allyson Robinson: transgender advocate and consultant. 

Related Links

Raising My Rainbow Blog 

Related Items

Raising My Rainbow: Adventures in Raising a Fabulous, Gender Creative Son 

Far From the Tree: Parents, Children and the Search for Identity 

Read An Excerpt

Excerpted from "Raising My Rainbow: Adventures in Raising a Fabulous, Gender Creative" by Lori Duron. Copyright © 2013 by Lori Duron. Published by Broadway Books, an imprint of the Crown Publishing Group, a division of Random House LLC, a Penguin Random House Company. 

Excerpted from;Raising My Rainbow: Adventures in Raising a Fabulous, Gender Creative Son by Lori Duron

Biological Psychiatry and the New Science of Mind (Yeah, Not So Much)

At Frontiers in Theoretical and Philosophical Psychology, Henrik Walter (Research Division of Mind and Brain, Department of Psychiatry and Psychotherapy, Charité Universitaetsmedizin Berlin, Germany; Berlin School of Mind and Brain, Humboldt University) offers a theory article on a proposed third wave of biological psychiatry. From Walter's abstract:

A look at current conceptualizations in biological psychiatry as well as at some discussions in current philosophy of mind on situated cognition, reveals that the thesis, that mental brain disorders are brain disorders has to be qualified with respect to how mental states are constituted and with respect to multilevel explanations of which factors contribute to stable patterns of psychopathological signs and symptoms.

Full Citation: 
Walter H. (2013, Sep 5). The third wave of biological psychiatry. Frontiers in Theoretical and Philosophical Psychology; 4:582. doi: 10.3389/fpsyg.2013.00582

As a little bit of background, Walter offers a brief sketch of each of the first two waves of biological psychiatry:

The first wave in the second half of the nineteenth century can be best understood as a new research agenda. It was not so much characterized by the idea that the mental and the nervous system are closely linked – this was already believed by ancient philosophers – but rather by the ambition to uncover the relation between mind and brain by doing systematic research linking neuropathology and mental disorder and by using the experimental method in animals and humans. Wilhelm Griesinger (1817–1868), one of the most important figures of this first wave, famously declared: mental disorders are disorders of the brain.

And . . .

The second wave of biological psychiatry started only in the second half of the twentieth century and was, according to Shorter, driven by two new discoveries. The first was genetics, which could show that severe mental disorders, in particular schizophrenia, have a strong genetic component. The second was the discovery of efficient medication for various mental disorders (1949 lithium, 1952 chlorpromazin, 1957 imipramin, 1958 haloperidol, 1963 diazepam). They quickly became a major pillar of psychiatric treatment and contributed strongly to the opening and later disappearance of the large mental asylums in the second half of the last century. Soon, the concept of a neurochemical imbalance of neurotransmitters became the favored explanatory model for psychiatric disorders.

Walter argues that there have been two recent (in the last two decades) developments that signal the transition into a Third Wave - (1) the advances in if the molecular neurosciences, and (2) the development and advances in the fields of cognitive neuroscience and neuroimaging. In support of the first point:

It became increasingly clear that the effects of psychiatric drugs are not primarily exerted via the level of neurotransmitters in the synaptic cleft, but that there is up- and down-regulation of receptors, effects on intracellular cascades, and even regrowth of neurons in the hippocampus. The picture of the neurobiological changes underlying psychiatric disorders and treatment thus became much more complex and differentiated and it became apparent that different levels of brain organization are important which interact in a complex way. 

In support of his second point:

With the first human study published in 1991, fMRI has today become a major research tool in psychology as well as in psychiatry. This development could not have taken place without a large increase in computational power. In fact, computational neuroscience which tries to develop mathematical models of brain function, has become an important tool in explaining neurocognitive processes and recently the program of computational psychiatry has begun to evolve (Montague et al., 2012). Further methods and technologies have become available to investigate the interplay of genetics, experience and environment in the etiology and neural explanation of psychiatric disorders like imaging genetics, epigenetics, optogenetics, or deep brain stimulation.

Rightly, Walter comments in this section of the paper on the ways popular media reporting misrepresents the findings from these new technologies (he offers as examples: “love is in the ACC,” “the God spot,” “gene for schizophrenia discovered”). With this over-reach in interpreting results, the new field of critical neuroscience (see [article] Slaby, 2010, Steps towards a Critical Neuroscience, Phenomenology and the Cognitive Sciences, 9(3); or [book] Slaby and Choudhury, 2011, Critical Neuroscience: A Handbook of the Social and Cultural Contexts of Neuroscience). 

The Third Wave

Walter offers a concise definition of his proposed third wave as it relates to mental disorders in this single sentence:

According to the third wave of biological psychiatry, mental disorders are relatively stable prototypical, dysfunctional patterns of experience and behavior that can be explained by dysfunctional neural systems at various levels. 

Representative of this model (Walter calls it a paradigmatic example) is Thomas Insel's research domain criteria (RDoC), the development of which he has overseen in his role as Director of the National Institutes of Mental Health (NIMH). Insel generated a lot of discussion when he announced that the NIMH would not be using the American Psychiatric Association's the DSM-5, claiming that:

the weakness (of DSM-5) is its lack of validity. Unlike our definitions of ischemic heart disease, lymphoma, or AIDS, the DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure. In the rest of medicine, this would be equivalent to creating diagnostic systems based on the nature of chest pain or the quality of fever. Indeed, symptom-based diagnosis, once common in other areas of medicine, has been largely replaced in the past half century as we have understood that symptoms alone rarely indicate the best choice of treatment (Insel, 2013, Transforming Diagnosis).

Rather than using the DSM categories as the "gold standard," Insel argues that we need to move away from the symptom-based approach that has been dominant for more than 100 years in Western psychology and, instead, seek to understand the causal explanatory structures that underlay the symptoms.

Walter offers this summary of the basic philosophy of the RDoC model:

RDoC can be regarded as a generalization of these initiatives being constructed for application to all mental disorders. It is based on three central assumptions: (1) mental disorders are presumed to be disorders of brain circuits. (2) Tools of neuroscience, including neuroimaging, electrophysiology and new methods for measuring neural connections can be used to identify dysfunctions of neural circuits. (3) Data from genetics research and clinical neuroscience will yield biosignatures that will augment clinical signs and symptoms for the purposes of clinical intervention and management.

These three central objectives smell a lot like a methodology for developing pharmaceutical interventions (which is my belief). However, there are also environmental and developmental factors considered as orthogonal dimensions (a way to graphically display large amounts of information) that will inform the neurological findings derived from the RDoC organization structure.

In this case, the data is organized as a 2-dimensional schema:

One dimension includes constructs that represent five core domains of mental functioning: Negative valence systems, positive valence systems, cognitive systems, systems for social processes and attention/arousal systems. Each of these domains includes subconstructs (around five). For example the negative valence systems include: active threat (“fear”), potential threat (“anxiety”), sustained threat, loss and frustrative non-reward. To take another example: the cognitive systems domain comprises attention, perception, working memory, declarative memory, language behavior, and cognitive (effortful) control. The second dimension consists of units of levels of organization on which the constructs can be measured. These levels are defined as follows: genes, molecules, cells, circuits, physiology, behavioral, self-reports, and paradigms. The “circuits” unit of analysis refers to measures that can index the activity of neural circuits, either through functional neuroimaging or through recordings previously validated as circuit indices (e.g., fear-potentiated startle). “Physiology” refers to well-established measures that have been validated by assessing various constructs, but that do not measure brain circuit activity directly (e.g., heart rate, cortisol). “Behavior” may refer either to systematically observed behavior or to performance on a behavior task such a working memory.

As powerful as is the NIMH (grant proposals not adhering to their new framework will not be funded), there are still many researchers, including neuroscientists, who offer objections to the RDoC model. Here is a summary of the four most common objections to the third wave perspective, as suggested by Walter:

(1) It could still be argued that the framework favors the neurobiological over other factors, as it entails the idea that psychiatric disorders are brain disorders. It will make no difference if you call psychiatric disorders “disorders of the brain” or “disorders of brain circuits” and thus do not justice to the mental within the concept of mental disorders. 
(2) The third wave does not include a solution to the normativity problem, namely the question of when a constellation of psychological signs and symptoms is already a disorder or when it is still part of “normal experience,” so it will still promote a medicalization of life problems. 
(3) Even if we somehow could solve the first two problems, it might be argued that a focus on the brain will lead to inefficient resource allocation because the outcome for patients is not worth the effort be put in. History has shown that all general claims that we will in the near future know “the” causes of mental disorders have failed, and the continuous failure of neurobiology (with some exceptions) to sufficiently explain or predict mental disorders shows that it cannot account for such complex phenomena. 
(4) We should rather focus on the well-known psychosocial factors contributing to the development or sustainment of psychiatric disorders which are much more relevant in practice.

I tend to agree with these basic objections. Fundamentally, the third wave model (and especially the RDoC) is premised on the unproven and highly questionable proposition that the mind is equivalent to the brain.

To his credit, Walter addresses this fundamental issue, that all we need to do in understanding the mind is look at the brain. He brings in the philosophical idea of situated cognition:

There is not yet a consistent or complete theory of situatedness, rather there are several strands of research and theorizing that can be subsumed under the catchword “the 4Es”: the embodied, extended, embedded and enacted mind (Lyre and Walter, 2013). The main idea is that in order to understand what cognition (the mental) is, it is necessary to take into account that cognitive capacities of a system may depend on the fact that those systems (our brains) are (i) embodied, i.e., coupled to our bodily constitution and that it therefore is necessary to regard the bodily realization of cognitive abilities as an integral part of the cognitive architecture; (ii) situationally embedded, i.e. are dependent in a specific way on their environment, i.e., cognitive systems exploit the specific circumstances of their environmental context in order to increase their performative abilities, (iii) extended, i.e., extend over the boundaries of our body into the technological or social environment and thus are constituted not only by internal factors but also by external, environmental factors and (iv) enacted, i.e., arise only by the active interaction of an autonomous systems with its environment (Walter, 2010).

I have long been arguing that all four of these types of situatedness are essential to any definition of mind or consciousness. If we do not even know how the mind is generated, and why, how can we ever begin to say that specific brain  circuits or brain states are pathological?

The New Science of Mind?

In an opinion article in the Sunday (Sept. 8, 2013) New York Times, Dr. Eric Kandel (2000 Nobel Prize in Physiology or Medicine for his research on the physiological basis of memory storage in neurons) outlines his perspective on the currently emerging "new science of mind."

In the first part of the article, Kandel outlines four key findings that have emerged over the course of our increasing exploration of neuroscience and the brain-based correlates of mental distress:

• First, the neural circuits disturbed by psychiatric disorders are likely to be very complex.
• Second, we can identify specific, measurable markers of a mental disorder, and those biomarkers can predict the outcome of two different treatments: psychotherapy and medication.
• Third, psychotherapy is a biological treatment, a brain therapy. It produces lasting, detectable physical changes in our brain, much as learning does.
• And fourth, the effects of psychotherapy can be studied empirically. Aaron Beck, who pioneered the use of cognitive behavioral therapy, long insisted that psychotherapy has an empirical basis, that it is a science. Other forms of psychotherapy have been slower to move in this direction, in part because a number of psychotherapists believed that human behavior is too difficult to study in scientific terms. 

Numbers three and four here are crucial to any forward movement we are going to make in our understanding of non-invasive ways to alter unhealthy psychological functioning. Unfortunately, he goes on in the second half of the article to espouse the mainstream materialist view, although he stops just short of saying the brain = mind.

This new science of mind is based on the principle that our mind and our brain are inseparable.

Inseparable? Yes - when the brain dies, we cease to exist. But identical? No.

There really is a new science of mind, but it is not the RDoC model of Thomas Insel and the NIMH, nor is it the third wave of biological psychiatry. Rather, it is a field known as interpersonal neurobiology, proposed and named by Daniel Siegel and co-developed with Allan Schore, with support form Louis Cozolino, Marco Iacoboni, Stephen Porges, Pat Ogden, Daniel Stern, and Diana Fosha.

From Dan Siegel's personal site, here is a long definition of interpersonal neurobiology:

About Interpersonal Neurobiology

An Introduction to Interpersonal Neurobiology

An Interdisciplinary Field:  Seeking Similar Patterns 

Daniel J. Siegel, M.D. is a pioneer in the field called interpersonal neurobiology (The Developing Mind, 1999) which seeks the similar patterns that arise from separate approaches to knowledge. This interdisciplinary field invites all branches of science and other ways of knowing to come together and find the common principles from within their often disparate approaches to understanding human experience. Sciences contributing to this exciting field include the following: 

• Anthropology
• Biology (developmental, evolution, genetics, zoology)
• Cognitive Science
• Computer Science
• Developmental Psychopathology
• Linguistics
• Neuroscience (affective, cognitive, developmental, social)
• Mathematics
• Mental Health
• Physics
• Psychiatry
• Psychology (cognitive, developmental, evolutionary, experimental, of religion, social, attachment theory, memory)
• Sociology
• Systems Theory (chaos and complexity theory)

Interpersonal neurobiology weaves research from these areas into a consilient framework that examines the common findings among independent disciplines.  This framework provides the basis of interpersonal neurobiology. The mind is defined and its components necessary for health are illuminated.  

The Mindsight Approach Exists Within the Field of Interpersonal Neurobiology 

Under the umbrella of interpersonal neurobiology, Dr. Siegel’s mindsight approach applies the emerging principles of interpersonal neurobiology to promote compassion, kindness, resilience, and well-being in our personal lives, our relationships, and our communities. At the heart of both interpersonal neurobiology and the mindsight approach is the concept of “integration” which entails the linkage of different aspects of a system—whether they exist within a single person or a collection of individuals.  Integration is seen as the essential mechanism of health as it promotes a flexible and adaptive way of being that is filled with vitality and creativity. The ultimate outcome of integration is harmony. The absence of integration leads to chaos and rigidity—a finding that enables us to re-envision our understanding of mental disorders and how we can work together in the fields of mental health, education, and other disciplines, to create a healthier, more integrated world.
 
Integration:  At the Core of Our Well-Being 

Integration is at the heart of both interpersonal neurobiology and Dr. Siegel’s mindsight approach. Defined as the linkage of differentiated components of a system, integration is viewed as the core mechanism in the cultivation of well-being. In an individual’s mind, integration involves the linkage of separate aspects of mental processes to each other, such as thought with feeling, bodily sensation with logic. In a relationship, integration entails each person’s being respected for his or her autonomy and differentiated self while at the same time being linked to others in empathic communication.

What Does Integration Mean for the Brain? 

For the brain, integration means that separated areas with their unique functions, in the skull and throughout the body, become linked to each other through synaptic connections. These integrated linkages enable more intricate functions to emerge—such as insight, empathy, intuition, and morality. A result of integration is kindness, resilience, and health. Terms for these three forms of integration are a coherent mind, empathic relationships, and an integrated brain.

Focus Your Attention:  Actually Change Your Brain 

This highly integrative field is not a division of one particular area of research, but rather is an open and evolving way of knowing that invites all domains of both academic and reflective explorations of reality into a collective conversation about the nature of the mind, the body, the brain, and our relationships with each other and the larger world in which we live. This emerging approach is fundamental to exploring a range of human endeavors, including the fields of mental health, education, parenting, organizational leadership, climate change intervention, religion, and contemplation. Knowing about the way the focus of attention changes the structure and function of the brain throughout the lifespan opens new doors to healing and growth at the individual, family, community, and global levels.

"Inspire to Rewire" 

 By combining the exciting new findings of how awareness can shape the connections in the brain toward integration together with the knowledge of how interpersonal relationships shape our brains throughout the lifespan, we can actively “inspire each other to rewire” our internal and interpersonal lives toward integration. 

 Dr. Siegel edits the Norton Series on Interpersonal Neurobiology, from W.W. Norton Publishers. For counselors and psychotherapists, this series offers some of the most useful books available.


When Dr. Kandel mentioned that psychotherapy is a biological approach because it literally can change and even rewire the brain, he was referring primarily to Aaron Beck's cognitive behavioral therapy (CBT). I have not seen any evidence that CBT can effectively rewire the brain, but there is a growing body of evidence that suggests that depth psychology, specifically psychodynamic and relational psychoanalytic approaches, can rewire the brain through the repair of faulty attachments schemas.

If we are to be healthy and functional human beings, we will by necessity be in relationship with others.

Relational-needs are present throughout the entire life cycle from early infancy to old age. People do not outgrow their need for relationship. These needs are the basis of our humanness. Even as adults we attach to others because we perceive them as being able to satisfy our variety of needs. (Erskine, Attachment, Relational-Needs, and Psychotherapeutic Presence, 2011).

Relational psychoanalysis is based on the premise that much of who we are as human beings is formed by our relationships to primary caregivers, our environment, and our peers. By this measure, then, dysfunction is based in unhealthy relationships and/or coping strategies in one of these areas. The psychotherapeutic process is also a relationship, and it is in the relationship more than the theory employed that allows for healing to occur.

According to Mikulincer and Shaver (2007, Attachment in Adulthood: Structure, Dynamics, and Change), some clients (many more so in trauma work) experience relational bonds with their therapists that are similar to infant attachment bonding patterns.

Specifically, some clients: (i) regard their therapist as stronger and wiser; (ii) seek proximity through emotional connection and regular meetings; (iii) rely upon their therapist as a safe haven when they feel threatened; (iv) derive a sense of felt security from their therapist, who serves as a secure base for psychological exploration; and (v) experience separation anxiety when anticipating loss of their therapist. [Cited in Mallinckrodt, 2010, Journal of Social and Personal Relationships; 27(2)]

In concluding the article, which has turned out to be much longer than I had anticipated, here is a video of David Wallin talking about Attachment in Psychotherapy (2007).

  Attachment in Psychotherapy from Books Inc on FORA.tv

Adrian D. Nelson - The Study of Fundamental Consciousness Entering the Mainstream

Christof Koch, working alongside Francis Crick, spent a couple of decades seeking the neural correlates of consciousness, and established himself as a leader in the study of consciousness and the ways the brain creates the mind. Yet, for all the discoveries and advances in our understanding of the brain, the how of converting sensory experience into subjective sensations remains a mystery.

Philosopher of mind David Chalmers has distinguished between the easy problem of consciousness and the hard problem of consciousness. The "easy problem" is essentially the area in which Koch and Crick were working - identifying the what, the neural correlates of consciousness.

Finding the neural correlates of consciousness is a problem of the same general type as finding the neural correlates of anything—language or memory, for instance. Neuroscience has made great progress in solving such problems in the past. Finding the brain regions and processes that correlate with consciousness is simply a matter of directing an existing research strategy from areas of previous success (language, memory) onto a different aspect of mental functioning (consciousness).

Solms, Mark; Turnbull, Oliver. (2010-09-07). Brain and the Inner World: An Introduction to the Neuroscience of Subjective Experience (Kindle Locations 799-802).

This approach seeks to understand which brain regions and/or processes correlated with conscious experience, and identifying where in the brain they reside. The "hard problem" is the why and the how.

In his own work, Koch is careful to distinguish between neural correlates of consciousness and a theory of consciousness.

It should be noted that discovering and characterizing the Neural Correlates of Consciousness in brains is not the same as a theory of consciousness. Only the latter can tell us why particular systems can experience anything, why they are conscious, and why other systems - such as the enteric nervous system or the immune system - are not. However, understanding the Neural Correlates of Consciousness is a necessary step toward such a theory. (Koch, C. Neural Correlates of Consciousness, Scholarpedia entry)

In his most recent book, Consciousness: Confessions of a Romantic Reductionist (2012), Koch admits his openness to non-materialist explanations of consciousness, including the possibility that consciousness is a fundamental feature of the universe. In this interview from The Atlantic, he goes a little further:

I was surprised to see your book invoke Pierre Teilhard de Chardin, the Jesuit priest and paleontologist who believed the universe is becoming more conscious as it gets more complex. Most scientists write off Teilhard as a religious apologist.

Koch: Most scientists don't even know about him. He had this idea about evolution where he argued that from very simple micro molecules to single cell organisms to multi-cell organisms to simple animals to complex animals to us is the emergence of complexity. He observed that the universe was getting more and more complex, and he postulated this would continue. Essentially, he postulated something like the Internet. He called it the "noosphere" -- the sphere of knowledge that covers the entire planet and is heavily interconnected. He died in 1955, long before any of this emerged, and he postulated that human society would evolve into a very complicated entity that would become self-conscious. He thought this would happen on other planets and throughout the entire universe, and the universe in some weird state would become self-conscious. It's all totally speculative, but I do like some of these ideas. I see a universe that's conducive to the formation of stable molecules and to life. And I do believe complexity is associated with consciousness. Therefore, we seem to live in a universe that's particularly conducive to the emergence of consciousness. That's why I call myself a "romantic reductionist."

The article below, from the Collective Evolution blog, offers a little overview of how the study of consciousness is changing in fundamental ways.

The Study of Fundamental Consciousness Entering the Mainstream

August 8, 2013 by Adrian D. Nelson



The world-renowned neuroscientist Christof Koch, spent decades working alongside the co-discoverer of the DNA molecule, Francis Crick. For decades these two men searched for the neurobiological basis of consciousness. They discovered many insights into cognition and the functioning of perception, yet the central enigma, the nature of consciousness itself, remained mysteriously elusive.

In 2009, Koch shocked the scientific community by publishing his conviction that consciousness probably isn’t just in brains, but is a fundamental feature of reality. This is a view known to philosophers as ‘panpsychism.’ The theory that Koch is now dedicating his research to is called ‘Integrated Information Theory’ or ‘IIT.’ It is the brainchild of neuroscientist Giulio Tononi of the University of Wisconsin-Madison.

In explaining his theory, Tononi asks us to consider a simple light sensitive photo diode like those found in a digital camera. A simple diode might respond to just two states: light or dark. We could present our diode with any number of images, yet regardless of the picture, the diode conforms to one of only two possible states. Is it light, or is it dark?

Now consider yourself looking at the same picture, lets say, of the Eiffel Tower on a beautiful spring day in Paris. For us, looking at this image results in a reduction from a near infinity of possible states. Not an image of the Andromeda galaxy, not a childhood picture of your mother, not cells dividing in a Petri dish and so on. Because of the vast number of images we are capable of recognizing, each one is highly informative. For Tononi, the vast amount of information capable of being integrated in the brain means that we have a comparatively huge capacity for consciousness.

Tononi’s theory, that consciousness is born out of networks with high degrees of integrated information, has novel ways of being tested in the laboratory.

In studies with sleeping participants, Tononi and his colleagues used transcranial magnetic stimulation to send a ripple of activity through the cortex of sleeping participants. The researchers found that when dreaming, this ripple reverberated through the cortex longer than when participants were in stages of dreamless sleep. This demonstrated that during dreaming, when the brain is conscious, the cortex has a higher degree of integration.

In another experiment, the researchers built tiny robots known as ‘animats’ that they placed into mazes. The animats used simple integrated networks capable of evolving over sequential generations. To their surprise, the greater the degree of integration that the animats evolved, the quicker they were able to escape the mazes. For Tononi this finding suggested that consciousness may play a more central role in evolution than had previously been thought.

The mathematical value of integrated information in a network is known as phi. But Tononi’s theory, now the topic of serious mainstream discussion, has an extraordinary implication. Phi didn’t just occur in brains, it is a property of any network with a total informational content greater than its individual parts. Every living cell, every electronic circuit, even a proton consisting of just three elementary particles have a value of phi greater than zero. According to Integrated Information Theory, all of these things possess something, albeit but a glimmer of ‘what it is like’ to be them. Tononi states:

“Consciousness is a fundamental property, like mass or charge. Wherever there is an entity with multiple states, there is some consciousness. You need a special structure to get a lot of it but consciousness is everywhere, it is a fundamental property.”

Integrated information theory is in its infancy and there are still many questions it must face. Did the information of brains operate at the level of the neuron, or the protein, or something deeper still? The electromagnetic field of the brain, as observed by psi researcher Dean Radin, is always re-establishing its quantum connection to the entire universe. Could a much richer informational interaction exist than has yet been imagined?

Physicists such as John Wheeler have laid the groundwork for a radical new understanding of reality, in which matter, the laws and constants of nature, and indeed the entire universe is best described, not in terms of physical objects, but through the play and display of a fundamental dynamic information.

Quantum mechanics suggests that the entire physical universe is potentially interconnected at a deep level of nature. So is the total informational content of the universe integrated in some deep sense? Is it in a mysterious way conscious of itself?

As spiritual traditions throughout the ages have long asserted, instead of isolated and separate experiencing beings, we may experience on behalf of the greater evolving system in which we find ourselves.

In Koch’s highly anticipated 2012 book, ‘Consciousness – Confessions of a Romantic Reductionist’, he states:

“I do believe that the laws of physics overwhelmingly favored the emergence of consciousness. The universe is a work in progress. Such a belief evokes jeremiads from many biologists and philosophers but the evidence from cosmology, biology and history is compelling.”

Regardless of the validity of Tononi’s theory, today increasing numbers of scientists and academics are convinced that the existence of consciousness simply cannot be sensibly denied. The study of fundamental consciousness is now entering the mainstream. This movement consists of thinkers in and outside of the mind sciences. Yet despite their different academic backgrounds, they are united by two common convictions: that consciousness is an intrinsic rather than incidental emergence in the universe, and that any complete account of reality must include an explanation of it.

Sources:

Koch, C. (2009, August 18). A complex theory of consciousness: Is complexity the secret to sentience, to a panpsychic view of consciousness? Scientific American.

Tononi, G. (2008). Consciousness as integrated information: A provisional manifesto. Biological Bulletin, 215(3), 216-242.

Edlund, J. A., Chaumont, N., Hintze, A., Koch C., Tononi G., & Adami, C. (2011). Integrated information increases with fitness in the evolution of animats. PLoS Computational Biology, 7(10).

Radin, D. I. (2006). Entangled Minds: Extrasensory experiences in quantum reality. New York: Simon & Schuster.

Koch, C. (2012). Consciousness: Confessions of a Romantic Reductionist. MIT Press Books.

David Dobbs - The Social Life of Genes (on Epigenetics)

This is an exceptionally well-written science article on the field of epigenetics, the ways in which experience, feelings, thoughts, people, and our environment can flip on/off switches in our genes (gene expression).

When it comes down to it, really, genes don’t make you who you are. Gene expression does. And gene expression varies depending on the life you live.

Every biologist accepts this. That was the safe, reasonable part of [Gene] Robinson’s notion. 

But this limited perspective did not account for genetic changes he was seeing in the bees he was studying. He believed there was more going on - that social environment could alter large portions of the genome, not just specific genes.

Robinson, however, suspected that environment could spin the dials on “big sectors of genes, right across the genome”—and that an individual’s social environment might exert a particularly powerful effect. Who you hung out with and how they behaved, in short, could dramatically affect which of your genes spoke up and which stayed quiet—and thus change who you were.

This was provocative - and similar ideas espoused by E.O. Wilson had made him the target of criticism by materialist scientists since the publication of Sociobiology: The New Synthesis in 1975. The criticism became ridicule and personal attacks earlier this year when Wilson released The Social Conquest of Earth.


Wilson argued that our innate, biological need for group membership - not just family, but clan - can be both a blessing and a curse.

Another researcher, Steven Cole, whose background was in psychology (UC Santa Barbara), and then in social psychology, epidemiology, virology, cancer, and genetics at UCLA, speculated that the gene’s ongoing, real-time response to incoming environmental information

is where life works many of its changes on us. The idea is both reductive and expansive. We are but cells. At each cell’s center, a tight tangle of DNA writes and hands out the cell’s marching orders. Between that center and the world stand only a series of membranes.

Here is more:

“We think of our bodies as stable biological structures that live in the world but are fundamentally separate from it. That we are unitary organisms in the world but passing through it. But what we’re learning from the molecular processes that actually keep our bodies running is that we’re far more fluid than we realize, and the world passes through us.”

One of his important findings:

“We typically think of stress as being a risk factor for disease,” said Cole. “And it is, somewhat. But if you actually measure stress, using our best available instruments, it can’t hold a candle to social isolation. Social isolation is the best-established, most robust social or psychological risk factor for disease out there. Nothing can compete.

This is an excellently written, well-researched article - and this is the future of medicine. It's well worth your time to read - via Pacific Standard Magazine.

The Social Life of Genes 

Your DNA is not a blueprint. Day by day, week by week, your genes are in a conversation with your surroundings. Your neighbors, your family, your feelings of loneliness: They don’t just get under your skin, they get into the control rooms of your cells. Inside the new social science of genetics.

September 3, 2013 • By David Dobbs

(ILLUSTRATION: JEREMY DIMMOCK) 

A few years ago, Gene Robinson, of Urbana, Illinois, asked some associates in southern Mexico to help him kidnap some 1,000 newborns. For their victims they chose bees. Half were European honeybees, Apis mellifera ligustica, the sweet-tempered kind most beekeepers raise. The other half were ligustica’s genetically close cousins, Apis mellifera scutellata, the African strain better known as killer bees. Though the two subspecies are nearly indistinguishable, the latter defend territory far more aggressively. Kick a European honeybee hive and perhaps a hundred bees will attack you. Kick a killer bee hive and you may suffer a thousand stings or more. Two thousand will kill you.

Working carefully, Robinson’s conspirators—researchers at Mexico’s National Center for Research in Animal Physiology, in the high resort town of Ixtapan de la Sal—jiggled loose the lids from two African hives and two European hives, pulled free a few honeycomb racks, plucked off about 250 of the youngest bees from each hive, and painted marks on the bees’ tiny backs. Then they switched each set of newborns into the hive of the other subspecies.

Robinson, back in his office at the University of Illinois at Urbana-Champaign’s Department of Entomology, did not fret about the bees’ safety. He knew that if you move bees to a new colony in their first day, the colony accepts them as its own. Nevertheless, Robinson did expect the bees would be changed by their adoptive homes: He expected the killer bees to take on the European bees’ moderate ways and the European bees to assume the killer bees’ more violent temperament. Robinson had discovered this in prior experiments. But he hadn’t yet figured out how it happened.

He suspected the answer lay in the bees’ genes. He didn’t expect the bees’ actual DNA to change: Random mutations aside, genes generally don’t change during an organism’s lifetime. Rather, he suspected the bees’ genes would behave differently in their new homes—wildly differently.

This notion was both reasonable and radical. Scientists have known for decades that genes can vary their level of activity, as if controlled by dimmer switches. Most cells in your body contain every one of your 22,000 or so genes. But in any given cell at any given time, only a tiny percentage of those genes is active, sending out chemical messages that affect the activity of the cell. This variable gene activity, called gene expression, is how your body does most of its work. 

Sometimes these turns of the dimmer switch correspond to basic biological events, as when you develop tissues in the womb, enter puberty, or stop growing. At other times gene activity cranks up or spins down in response to changes in your environment. Thus certain genes switch on to fight infection or heal your wounds—or, running amok, give you cancer or burn your brain with fever. Changes in gene expression can make you thin, fat, or strikingly different from your supposedly identical twin. When it comes down to it, really, genes don’t make you who you are. Gene expression does. And gene expression varies depending on the life you live.

Every biologist accepts this. That was the safe, reasonable part of Robinson’s notion. Where he went out on a limb was in questioning the conventional wisdom that environment usually causes fairly limited changes in gene expression. It might sharply alter the activity of some genes, as happens in cancer or digestion. But in all but a few special cases, the thinking went, environment generally brightens or dims the activity of only a few genes at a time.

Robinson, however, suspected that environment could spin the dials on “big sectors of genes, right across the genome”—and that an individual’s social environment might exert a particularly powerful effect. Who you hung out with and how they behaved, in short, could dramatically affect which of your genes spoke up and which stayed quiet—and thus change who you were.

Robinson was already seeing this in his bees. The winter before, he had asked a new post-doc, Cédric Alaux, to look at the gene-expression patterns of honeybees that had been repeatedly exposed to a pheromone that signals alarm. (Any honeybee that detects a threat emits this pheromone. It happens to smell like bananas. Thus “it’s not a good idea,” says Alaux, “to eat a banana next to a bee hive.”)

To a bee, the pheromone makes a social statement: Friends, you are in danger. Robinson had long known that bees react to this cry by undergoing behavioral and neural changes: Their brains fire up and they literally fly into action. He also knew that repeated alarms make African bees more and more hostile. When Alaux looked at the gene-expression profiles of the bees exposed again and again to alarm pheromone, he and Robinson saw why: With repeated alarms, hundreds of genes—genes that previous studies had associated with aggression—grew progressively busier. The rise in gene expression neatly matched the rise in the aggressiveness of the bees’ response to threats.

Robinson had not expected that. “The pheromone just lit up the gene expression, and it kept leaving it higher.” The reason soon became apparent: Some of the genes affected were transcription factors—genes that regulate other genes. This created a cascading gene-expression response, with scores of genes responding.

This finding inspired Robinson’s kidnapping-and-cross-fostering study. Would moving baby bees to wildly different social environments reshape the curves of their gene-expression responses? Down in Ixtapan, Robinson’s collaborators suited up every five to 10 days, opened the hives, found about a dozen foster bees in each one, and sucked them up with a special vacuum. The vacuum shot them into a chamber chilled with liquid nitrogen. The intense cold instantly froze the bees’ every cell, preserving the state of their gene activity at that moment. At the end of six weeks, when the researchers had collected about 250 bees representing every stage of bee life, the team packed up the frozen bees and shipped them to Illinois.

There, Robinson’s staff removed the bees’ sesame-seed-size brains, ground them up, and ran them through a DNA microarray machine. This identified which genes were busy in a bee’s brain at the moment it met the bee-vac. When Robinson sorted his data by group—European bees raised in African hives, for instance, or African bees raised normally among their African kin—he could see how each group’s genes reacted to their lives.

Robinson organized the data for each group onto a grid of red and green color-coded squares: Each square represented a different gene, and its color represented the group’s average rate of gene expression. Red squares represented genes that were especially active in most of the bees in that group; the brighter the red, the more bees in which that gene had been busy. Green squares represented genes that were silent or underactive in most of the group. The printout of each group’s results looked like a sort of cubist Christmas card.

When he got the cards, says Robinson, “the results were stunning.” For the bees that had been kidnapped, life in a new home had indeed altered the activity of “whole sectors” of genes. When their gene expression data was viewed on the cards alongside the data for groups of bees raised among their own kin, a mere glance showed the dramatic change. Hundreds of genes had flipped colors. The move between hives didn’t just make the bees act differently. It made their genes work differently, and on a broad scale.

What’s more, the cards for the adopted bees of both species came to ever more resemble, as they moved through life, the cards of the bees they moved in with. With every passing day their genes acted more like those of their new hive mates (and less like those of their genetic siblings back home). Many of the genes that switched on or off are known to affect behavior; several are associated with aggression. The bees also acted differently. Their dispositions changed to match that of their hive mates. It seemed the genome, without changing its code, could transform an animal into something very like a different subspecies.

These bees didn’t just act like different bees. They’d pretty much become different bees. To Robinson, this spoke of a genome far more fluid—far more socially fluid—than previously conceived. 

Gene Robinson, an entomologist at the University of Illinois, found that when European honeybees are raised among more aggressive African killer bees, they not only start to become as belligerent as their new hive mates—they come to genetically resemble them. (PHOTO: COURTESY OF GENE ROBINSON)

ROBINSON SOON REALIZED HE was not alone in seeing this. At conferences and in the literature, he kept bumping into other researchers who saw gene networks responding fast and wide to social life. David Clayton, a neurobiologist also on the University of Illinois campus, found that if a male zebra finch heard another male zebra finch singing nearby, a particular gene in the bird’s forebrain would “re up—and it would do so differently depending on whether the other finch was strange and threatening, or familiar and safe.

Others found this same gene, dubbed ZENK ramping up in other species. In each case, the change in ZENK’s activity corresponded to some change in behavior: a bird might relax in response to a song, or become vigilant and tense. Duke researchers, for instance, found that when female zebra finches listened to male zebra finches’ songs, the females’ ZENK gene triggered massive gene-expression changes in their forebrains—a socially sensitive brain area in birds as well as humans. The changes differed depending on whether the song was a mating call or a territorial claim. And perhaps most remarkably, all
of these changes happened incredibly fast—within a half hour, sometimes within just five minutes.

ZENK, it appeared, was a so-called “immediate early gene,” a type of regulatory gene that can cause whole networks of other genes to change activity. These sorts of regulatory gene-expression response had already been identified in physiological systems such as digestion and immunity. Now they also seemed to drive quick responses to social conditions.

One of the most startling early demonstrations of such a response occurred in 2005 in the lab of Stanford biologist Russell Fernald. For years, Fernald had studied the African cichlid Astatotilapia burtoni, a freshwater fish about two inches long and dull pewter in color. By 2005 he had shown that among burtoni, the top male in any small population lives like some fishy pharaoh, getting far more food, territory, and sex than even the No. 2 male. This No. 1 male cichlid also sports a bigger and brighter body. And there is always only one No. 1.

I wonder, Fernald thought, what would happen if we just removed him?

So one day Fernald turned out the lights over one of his cichlid tanks, scooped out big flashy No. 1, and then, 12 hours later, flipped the lights back on. When the No. 2 cichlid saw that he was now No. 1, he responded quickly. He underwent massive surges in gene expression that immediately blinged up his pewter coloring with lurid red and blue streaks and, in a matter of hours, caused him to grow some 20 percent. It was as if Jason Schwartzman, coming to work one day to learn the big office stud had quit, morphed into Arnold Schwarzenegger by close of business.

These studies, says Greg Wray, an evolutionary biologist at Duke who has focused on gene expression for over a decade, caused quite a stir. “You suddenly realize birds are hearing a song and having massive, widespread changes in gene expression in just 15 minutes? Something big is going on.”

This big something, this startlingly quick gene-expression response to the social world, is a phenomenon we are just beginning to understand. The recent explosion of interest in “epigenetics”—a term literally meaning “around the gene,” and referring to anything that changes a gene’s effect without changing the actual DNA sequence—has tended to focus on the long game of gene-environment interactions: how famine among expectant mothers in the Netherlands during World War II, for instance, affected gene expression and behavior in their children; or how mother rats, by licking and grooming their pups more or less assiduously, can alter the wrappings around their offspring’s DNA in ways that influence how anxious the pups will be for the rest of their lives. The idea that experience can echo in our genes across generations is certainly a powerful one. But to focus only on these narrow, long-reaching effects is to miss much of the action where epigenetic influence and gene activity is concerned. This fresh work by Robinson, Fernald, Clayton, and others—encompassing studies of multiple organisms, from bees and birds to monkeys and humans—suggests something more exciting: that our social lives can change our gene expression with a rapidity, breadth, and depth previously overlooked.

Why would we have evolved this way? The most probable answer is that an organism that responds quickly to fast-changing social environments will more likely survive them. That organism won’t have to wait around, as it were, for better genes to evolve on the species level. Immunologists discovered something similar 25 years ago: Adapting to new pathogens the old-fashioned way—waiting for natural selection to favor genes that create resistance to specific pathogens—would happen too slowly to counter the rapidly changing pathogen environment. Instead, the immune system uses networks of genes that can respond quickly and flexibly to new threats.

We appear to respond in the same way to our social environment. Faced with an unpredictable, complex, ever-changing population to whom we must respond successfully, our genes behave accordingly—as if a fast, fluid response is a matter of life or death.

ABOUT THE TIME ROBINSON was seeing fast gene expression changes in bees, in the early 2000s, he and many of his colleagues were taking notice of an up-and-coming UCLA researcher named Steve Cole.

Cole, a Californian then in his early 40s, had trained in psychology at the University of California-Santa Barbara and Stanford; then in social psychology, epidemiology, virology, cancer, and genetics at UCLA. Even as an undergrad, Cole had “this astute, fine-grained approach,” says Susan Andersen, a professor of psychology now at NYU who was one of his teachers at UC Santa Barbara in the late 1980s. “He thinks about things in very precise detail.”

In his post-doctoral work at UCLA, Cole focused on the genetics of immunology and cancer because those fields had pioneered hard-nosed gene-expression research. After that, he became one of the earliest researchers to bring the study of whole-genome gene-expression to social psychology. The gene’s ongoing, real-time response to incoming information, he realized, is where life works many of its changes on us. The idea is both reductive and expansive. We are but cells. At each cell’s center, a tight tangle of DNA writes and hands out the cell’s marching orders. Between that center and the world stand only a series of membranes.

“Porous membranes,” notes Cole.

“We think of our bodies as stable biological structures that live in the world but are fundamentally separate from it. That we are unitary organisms in the world but passing through it. But what we’re learning from the molecular processes that actually keep our bodies running is that we’re far more fluid than we realize, and the world passes through us.”

Cole told me this over dinner. We had met on the UCLA campus and walked south a few blocks, through bright April sun, to an almost empty sushi restaurant. Now, waving his chopsticks over a platter of urchin, squid, and amberjack, he said, “Every day, as our cells die off, we have to replace one to two percent of our molecular being. We’re constantly building and re-engineering new cells. And that regeneration is driven by the contingent nature of gene expression.

“This is what a cell is about. A cell,” he said, clasping some amberjack, “is a machine for turning experience into biology.”

When Cole started his social psychology research in the early 1990s, the microarray technology that spots changes in gene expression was still in its expensive infancy, and saw use primarily in immunology and cancer. So he began by using the tools of epidemiology—essentially the study of how people live their lives. Some of his early papers looked at how social experience affected men with HIV. In a 1996 study of 80 gay men, all of whom had been HIV-positive but healthy nine years earlier, Cole and his colleagues found that closeted men succumbed to the virus much more readily.

He then found that HIV-positive men who were lonely also got sicker sooner, regardless of whether they were closeted. Then he showed that closeted men without HIV got cancer and various infectious diseases at higher rates than openly gay men did. At about the same time, psychologists at Carnegie Mellon finished a well-controlled study showing that people with richer social ties got fewer common colds.

Something about feeling stressed or alone was gumming up the immune system—sometimes fatally.

“You’re besieged by a virus that’s going to kill you,” says Cole, “but the fact that you’re socially stressed and isolated seems to shut down your viral defenses. What’s going on there?”

He was determined to find out. But the research methods on hand at the time could take him only so far: “Epidemiology won’t exactly lie to you. But it’s hard to get it to tell you the whole story.” For a while he tried to figure things out at the bench, with pipettes and slides and assays. “I’d take norepinephrine [a key stress hormone] and squirt it on some infected T-cells and watch the virus grow faster. The norepinephrine was knocking down the antiviral response. That’s great. Virologists love that. But it’s not satisfying as a complete answer, because it doesn’t fully explain what’s happening in the real world.

“You can make almost anything happen in a test tube. I needed something else. I had set up all this theory. I needed a place to test it.”

His next step was to turn to rhesus monkeys, a lab species that allows controlled study. In 2007, he joined John Capitanio, a primatologist at the University of California-Davis, in looking at how social stress affected rhesus monkeys with SIV, or simian immunodeficiency virus, the monkey version of HIV. Capitanio had found that monkeys with SIV fell ill and died faster if they were stressed out by constantly being moved into new groups among strangers—a simian parallel to Cole’s 1996 study on lonely gay men.

Capitanio had run a rough immune analysis that showed the stressed monkeys mounted weak antiviral responses. Cole offered to look deeper. First he tore apart the lymph nodes—“ground central for infection”—and found that in the socially stressed monkeys, the virus bloomed around the sympathetic nerve trunks, which carry stress signals into the lymph node.

“This was a hint,” says Cole: The virus was running amok precisely where the immune response should have been strongest. The stress signals in the nerve trunks, it seemed, were getting either muted en route or ignored on arrival. As Cole looked closer, he found it was the latter: The monkeys’ bodies were generating the appropriate stress signals, but the immune system didn’t seem to be responding to them properly. Why not? He couldn’t find out with the tools he had. He was still looking at cells. He needed to look inside them.

Finally Cole got his chance. At UCLA, where he had been made a professor in 2001, he had been working hard to master gene-expression analysis across an entire genome. Microarray machines—the kind Gene Robinson was using on his bees—were getting cheaper. Cole got access to one and put it to work.

Thus commenced what we might call the lonely people studies.

First, in collaboration with University of Chicago social psychologist John Cacioppo, Cole mined a questionnaire about social connections that Cacioppo had given to 153 healthy Chicagoans in their 50s and 60s. Cacioppo and Cole identified the eight most socially secure people and the six loneliest and drew blood samples from them. (The socially insecure half-dozen were lonely indeed; they reported having felt distant from others for the previous four years.) Then Cole extracted genetic material from the blood’s leukocytes (a key immune-system player) and looked at what their DNA was up to.

He found a broad, weird, strongly patterned gene-expression response that would become mighty familiar over the next few years. Of roughly 22,000 genes in the human genome, the lonely and not-lonely groups showed sharply different gene-expression responses in 209. That meant that about one percent of the genome—a considerable portion—was responding differently depending on whether a person felt alone or connected. Printouts of the subjects’ gene-expression patterns looked much like Robinson’s red-and-green readouts of the changes in his cross-fostered bees: Whole sectors of genes looked markedly different in the lonely and the socially secure. And many of these genes played roles in inflammatory immune responses.

Now Cole was getting somewhere.

Normally, a healthy immune system works by deploying what amounts to a leashed attack dog. It detects a pathogen, then sends inflammatory and other responses to destroy the invader while also activating an anti-inflammatory response—the leash—to keep the inflammation in check. The lonely Chicagoans’ immune systems, however, suggested an attack dog off leash—even though they weren’t sick. Some 78 genes that normally work together to drive inflammation were busier than usual, as if these healthy people were fighting infection. Meanwhile, 131 genes that usually cooperate to control inflammation were underactive. The underactive genes also included key antiviral genes.

This opened a whole new avenue of insight. If social stress reliably created this gene-expression profile, it might explain a lot about why, for instance, the lonely HIV carriers in Cole’s earlier studies fell so much faster to the disease.

But this was a study of just 14 people. Cole needed more.

Over the next several years, he got them. He found similarly unbalanced gene-expression or immune-response profiles in groups including poor children, depressed people with cancer, and people caring for spouses dying of cancer. He topped his efforts off with a study in which social stress levels in young women predicted changes in their gene activity six months later. Cole and his collaborators on that study, psychologists Gregory Miller and Nicolas Rohleder of the University of British Columbia, interviewed 103 healthy Vancouver-area women aged 15 to 19 about their social lives, drew blood, and ran gene-expression profiles, and after half a year drew blood and ran profiles again. Some of the women reported at the time of the initial interview that they were having trouble with their love lives, their families, or their friends. Over the next six months, these socially troubled subjects took on the sort of imbalanced gene-expression profile Cole found in his other isolation studies: busy attack dogs and broken leashes. Except here, in a prospective study, he saw the attack dog breaking free of its restraints: Social stress changed these young women’s gene-expression patterns before his eyes. 

Gene-expression microarray printouts (this one comes from a study of autistic versus non-autistic people) depict snapshots of activity across a genome. Red squares represent genes that are more active, green squares represent genes that are less active. (PHOTO: PUBLIC DOMAIN)

IN EARLY 2009, COLE sat down to make sense of all this in a review paper that he would publish later that year in Current Directions in Psychological Science. Two years later we sat in his spare, rather small office at UCLA and discussed what he’d found. Cole, trimly built but close to six feet tall, speaks in a reedy voice that is slightly higher than his frame might lead you to expect. Sometimes, when he’s grabbing for a new thought or trying to emphasize a point, it jumps a register. He is often asked to give talks about his work, and it’s easy to see why: Relaxed but animated, he speaks in such an organized manner that you can almost see the paragraphs form in the air between you. He spends much of his time on the road. Thus the half-unpacked office, he said, gesturing around him. His lab, down the hall, “is essentially one really good lab manager”—Jesusa M. Arevalo, whom he frequently lists on his papers—“and a bunch of robots,” the machines that run the assays.

“We typically think of stress as being a risk factor for disease,” said Cole. “And it is, somewhat. But if you actually measure stress, using our best available instruments, it can’t hold a candle to social isolation. Social isolation is the best-established, most robust social or psychological risk factor for disease out there. Nothing can compete.”

This helps explain, for instance, why many people who work in high-stress but rewarding jobs don’t seem to suffer ill effects, while others, particularly those isolated and in poverty, wind up accruing lists of stress-related diagnoses—obesity, Type 2 diabetes, hypertension, atherosclerosis, heart failure, stroke.

Despite these well-known effects, Cole said he was amazed when he started finding that social connectivity wrought such powerful effects on gene expression.

“Or not that we found it,” he corrected, “but that we’re seeing it with such consistency. Science is noisy. I would’ve bet my eyeteeth that we’d get a lot of noisy results that are inconsistent from one realm to another. And at the level of individual genes that’s kind of true—there is some noise there.” But the kinds of genes that get dialed up or down in response to social experience, he said, and the gene networks and gene-expression cascades that they set off, “are surprisingly consistent—from monkeys to people, from five-year-old kids to adults, from Vancouver teenagers to 60-year-olds living in Chicago.”

COLE’S WORK CARRIES ALL kinds of implications—some weighty and practical, some heady and philosophical. It may, for instance, help explain the health problems that so often haunt the poor. Poverty savages the body. Hundreds of studies over the past few decades have tied low income to higher rates of asthma, flu, heart attacks, cancer, and everything in between. Poverty itself starts to look like a disease. Yet an empty wallet can’t make you sick. And we all know people who escape poverty’s dangers. So what is it about a life of poverty that makes us ill?

Cole asked essentially this question in a 2008 study he conducted with Miller and Edith Chen, another social psychologist then at the University of British Columbia. The paper appeared in an odd forum: Thorax, a journal about medical problems in the chest. The researchers gathered and ran gene-expression profiles on 31 kids, ranging from nine to 18 years old, who had asthma; 16 were poor, 15 well-off. As Cole expected, the group of well-off kids showed a healthy immune response, with elevated activity among genes that control pulmonary inflammation. The poorer kids showed busier inflammatory genes, sluggishness in the gene networks that control inflammation, and—in their health histories—more asthma attacks and other health problems. Poverty seemed to be mucking up their immune systems.

Cole, Chen, and Miller, however, suspected something else was at work—something that often came with poverty but was not the same thing. So along with drawing the kids’ blood and gathering their socioeconomic information, they showed them films of ambiguous or awkward social situations, then asked them how threatening they found them.

The poorer kids perceived more threat; the well-off perceived less. This difference in what psychologists call “cognitive framing” surprised no one. Many prior studies had shown that poverty and poor neighborhoods, understandably, tend to make people more sensitive to threats in ambiguous social situations. Chen in particular had spent years studying this sort of effect.

But in this study, Chen, Cole, and Miller wanted to see if they could tease apart the effect of cognitive framing from the effects of income disparity. It turned out they could, because some of the kids in each income group broke type. A few of the poor kids saw very little menace in the ambiguous situations, and a few well-off kids saw a lot. When the researchers separated those perceptions from the socioeconomic scores and laid them over the gene-expression scores, they found that it was really the kids’ framing, not their income levels, that accounted for most of the difference in gene expression. To put it another way: When the researchers controlled for variations in threat perception, poverty’s influence almost vanished. The main thing driving screwy immune responses appeared to be not poverty, but whether the child saw the social world as scary.

But where did that come from? Did the kids see the world as frightening because they had been taught to, or because they felt alone in facing it? The study design couldn’t answer that. But Cole believes isolation plays a key role. This notion gets startling support from a 2004 study of 57 school-age children who were so badly abused that state social workers had removed them from their homes. The study, often just called “the Kaufman study,” after its author, Yale psychiatrist Joan Kaufman, challenges a number of assumptions about what shapes responses to trauma or stress.

The Kaufman study at first looks like a classic investigation into the so-called depression risk gene—the serotonin transporter gene, or SERT—which comes in both long and short forms. Any single gene’s impact on mood or behavior is limited, of course, and these single-gene, or “candidate gene,” studies must be viewed with that in mind. Yet many studies have found that SERT’s short form seems to render many people (and rhesus monkeys) more sensitive to environment; according to those studies, people who carry the short SERT are more likely to become depressed or anxious if faced with stress or trauma.

Kaufman looked first to see whether the kids’ mental health tracked their SERT variants. It did: The kids with the short variant suffered twice as many mental-health problems as those with the long variant. The double whammy of abuse plus short SERT seemed to be too much.

Then Kaufman laid both the kids’ depression scores and their SERT variants across the kids’ levels of “social support.” In this case, Kaufman narrowly defined social support as contact at least monthly with a trusted adult figure outside the home. Extraordinarily, for the kids who had it, this single, modest, closely defined social connection erased about 80 percent of the combined risk of the short SERT variant and the abuse. It came close to inoculating kids against both an established genetic vulnerability and horrid abuse.

Or, to phrase it as Cole might, the lack of a reliable connection harmed the kids almost as much as abuse did. Their isolation wielded enough power to raise the question of what’s really most toxic in such situations. Most of the psychiatric literature essentially views bad experiences—extreme stress, abuse, violence—as toxins, and “risk genes” as quasi-immunological weaknesses that let the toxins poison us. And abuse is clearly toxic. Yet if social connection can almost completely protect us against the well-known effects of severe abuse, isn’t the isolation almost as toxic as the beatings and neglect?

The Kaufman study also challenges much conventional Western thinking about the state of the individual. To use the language of the study, we sometimes conceive of “social support” as a sort of add-on, something extra that might somehow fortify us. Yet this view assumes that humanity’s default state is solitude. It’s not. Our default state is connection. We are social creatures, and have been for eons. As Cole’s colleague John Cacioppo puts it in his book Loneliness, Hobbes had it wrong when he wrote that human life without civilization was “solitary, poor, nasty, brutish, and short.” It may be poor, nasty, brutish, and short. But seldom has it been solitary.

“A cell,” Steve Cole said, clasping some amberjack, “is a machine for turning experience into biology.”

TOWARD THE END OF the dinner I shared with Cole, after the waiter took away the empty platters and we sat talking over green tea, I asked him if there was anything I should have asked but had not. He’d been talking most of three hours. Some people run dry. Cole does not. He spoke about how we are permeable fluid beings instead of stable unitary isolates; about recursive reconstruction of the self; about an engagement with the world that constantly creates a new you, only you don’t know it, because you’re not the person you would have been otherwise—you’re a one-person experiment that has lost its control.

He wanted to add one more thing: He didn’t see any of this as deterministic.

We were obviously moving away from what he could prove at this point, perhaps from what is testable. We were in fact skirting the rabbit hole that is the free-will debate. Yet he wanted to make it clear he does not see us as slaves to either environment or genes.

“You can’t change your genes. But if we’re even half right about all this, you can change the way your genes behave—which is almost the same thing. By adjusting your environment you can adjust your gene activity. That’s what we’re doing as we move through life. We’re constantly trying to hunt down that sweet spot between too much challenge and too little.

“That’s a really important part of this: To an extent that immunologists and psychologists rarely appreciate, we are architects of our own experience. Your subjective experience carries more power than your objective situation. If you feel like you’re alone even when you’re in a room filled with the people closest to you, you’re going to have problems. If you feel like you’re well supported even though there’s nobody else in sight; if you carry relationships in your head; if you come at the world with a sense that people care about you, that you’re valuable, that you’re okay; then your body is going to act as if you’re okay—even if you’re wrong about all that.”

Cole was channeling John Milton: “The mind is its own place, and in itself can make a heaven of hell, a hell of heaven.”

Of course I did not realize that at the moment. My reaction was more prosaic.

“So environment and experience aren’t the same,” I offered.

“Exactly. Two people may share the same environment but not the same experience. The experience is what you make of the environment. It appears you and I are both enjoying ourselves here, for instance, and I think we are. But if one of us didn’t like being one-on-one at a table for three hours, that person could get quite stressed out. We might have much different experiences. And you can shape all this by how you frame things. You can shape both your environment and yourself by how you act. It’s really an opportunity.”

Cole often puts it differently at the end of his talks about this line of work. “Your experiences today will influence the molecular composition of your body for the next two to three months,” he tells his audience, “or, perhaps, for the rest of your life. Plan your day accordingly.”