Neuroplasticity, psychosocial genomics, and the biopsychosocial paradigm in the 21st century.
Abstract: The biopsychosocial perspective is a foundation of social work theory and practice. Recent research on neuroplasticity and psychosocial genomics lends compelling support to this perspective by elucidating mechanisms through which psychosocial forces shape neurobiology. Investigations of neuroplasticity demonstrate that the adult brain can continue to form novel neural connections and grow new neurons in response to learning or training even into old age. These findings are complemented by the contributions of psychosocial genomics, a field of scientific inquiry that explores the modulating effects of experience on gene expression. Findings from these new sciences provide external validation for the biopsychosocial perspective and offer important insights into the manifold means by which socioenvironmental experiences influence neurobiological structure and function across the life course.

KEY WORDS: biopsychosocial; gene-environment interaction; neuroplasticity; psychotherapy
Article Type: Report
Subject: Human growth (Genetic aspects)
Human growth (Social aspects)
Neuroplasticity (Genetic aspects)
Neuroplasticity (Social aspects)
Authors: Garland, Eric L.
Howard, Matthew Owen
Pub Date: 08/01/2009
Publication: Name: Health and Social Work Publisher: National Association of Social Workers Audience: Academic; Professional Format: Magazine/Journal Subject: Health; Sociology and social work Copyright: COPYRIGHT 2009 National Association of Social Workers ISSN: 0360-7283
Issue: Date: August, 2009 Source Volume: 34 Source Issue: 3
Topic: Event Code: 290 Public affairs
Geographic: Geographic Scope: United States Geographic Code: 1USA United States
Accession Number: 204610807
Full Text: Like sand on a beach, the brain bears the footprints of the decisions we have made, the skills we have learned, the actions we have taken.

--Sharon Begley, 2007

Social work professionals in the 21st century have adopted the biopsychosocial paradigm. This paradigm, first articulated by the physician George Engel (1977), holds that humans are dynamic systems whose functioning depends on the holistic integration of biological, psychological, and social factors; indeed, according to the biopsychosocial model, these factors are fundamentally interrelated and interdependent. Although Engel rejected the reductionism of the dominant biomedical model of his era, which assumed that molecular biological processes (for example, genes, biochemistry) immutably dictated physiology and behavior, a simpleminded biological determinism nonetheless took root, becoming widely and uncritically accepted. At its inception, there was scant evidence to support Engel's biopsychosocial perspective; however, scientific discoveries of the past decade have provided important new findings validating and elaborating the biopsychosocial paradigm.

Over the past decade, two fields of empirical investigation, neuroplasticity and psychosocial genomics, have offered important findings that may lead to a paradigm shift in our conceptions of psyche and soma and the modes of their interrelationships. These two fields mutually inform one another, depicting interpenetrating biopsychosocial relationships on different scales: Neuroplasticity research describes how neurons within the brain proliferate and grow new connections across the life span, whereas psychosocial genomics describes the processes by which psychological and social experiences activate or deactivate genes, thereby driving the development of new neural pathways. The interplay of these sciences reflects a vision of humans as inherently resilient; psychosocial factors appear to stimulate gene expression within neurons, resulting in alterations to the structure and function of the brain. Discoveries from both fields reveal that experience and learning can contribute to positive change, even at the neurobiological and structural levels.

Social work academicians have embraced the biopsychosocial perspective, yet many are perhaps not fully aware of recent developments in genomic and neurobiological research that have implications for social work and the biopsychosocial perspective. This research provides insights into the very substrates of biopsychosocial change. Thus, we review recent neuroplasticity and psychosocial genomics research and their implications for current understanding and application of the biopsychosocial perspective.


Basic Neurotransmission

The human brain is a complex, self-organizing, biological system, consisting of trillions of interconnected nerve cells called neurons. The operation of neurons results in two distinct forms of information processing: signaling and integration. Each neuron propagates signals via action potentials, electrochemical currents that travel the length of its axon. This current leads to the release of neurotransmitters that traverse synapses, the gaps between neurons. These chemical messages are received via specialized receptor cells at the ends of numerous, tree-like branches of the receiving neuron, called dendrites. The stimulation of dendritic receptors by neurotransmitters leads to integration, whereby large amounts of information from many neurons are summed before reaching a threshold to fire the action potential down the next axon. In this manner, perceptual information from the external environment and the internal milieu of the body is transmitted and processed in the brain, leading to cognition, emotion, and behavior--the essence of human experience.

Origins of Neuroplasticity Research

The brains of infants and children are known to be plastic, undergoing spurts of neuronal development in response to stimulus exposure during critical periods (Mundkur, 2005). This development consists of the genesis of neurons, increased connectivity between extant neurons, and the routing of new synaptic connections between previously unrelated neurons. However, before 1998, it was widely accepted that neuronal connections in the adult brain were immutable; the neurons that populated a given brain area were thought to be fixed in accordance with whatever form and function the genetic code prescribed for that region (Begley, 2007). In addition, the conventional wisdom at the time--that no new neurons could be generated after injury or insult to the brain--was held with conviction on the part of leading neuroscientists.

However, on discovery of the growth of new neural tissue, or neurogenesis, in the adult human hippocampus, a brain region responsible for memory (Eriksson et al., 1998), the dogma of the "hardwired brain" was formally repudiated. This finding complemented earlier evidence from primate studies demonstrating that novel sensory experience and learning of new behaviors triggers neuronal growth in the somatosensory and motor cortices, areas of the brain subserving tactile perception and limb movement (Jenkins, Merzenich, Ochs, Allard, & Guic-Robles, 1990; Nudo, Milliken, Jenkins,& Merzenich, 1996). Subsequent to the discovery of neurogenesis in the adult human brain, neuroscience has pursued this fine of investigation with vigor, aided by advances in brain imaging techniques such as magnetic resonance imaging (MRI).

Neuroplasticity Research Findings

The growth of neurons has been documented in the brains of adults exposed to a variety of experiences. For instance, violinists evidence neural growth in the portion of their somatosensory cortex devoted to their fingering hand through hours of musical practice (Elbert, Pantev, Wienbruch, Rockstroh, & Taub, 1995); people engaged in the practice of juggling evidence similar growth (Draganski et al., 2004). In addition to such physical training, mental practice may promote neuroplasticity: Neurogenesis can occur in the motor cortex simply through the act of imagining playing the piano (Pascual-Leone, Amedi, Fregni, & Merabet, 2005). Similarly, taxicab drivers develop the areas of their brains involved in spatial relationships by memorizing the labyrinthine streets and avenues of the cities in which they work (Maguire et al., 2000). Although the underlying mechanisms are different, neuroplasticity research suggests that challenging learning experiences can lead to the development of brain tissue in a manner analogous to the ways that physical exercise can lead to the development of muscle tissue.

One area of research that has found significant evidence of mental training leading to neuroplastic modifications in brain activity focuses on the study of meditation. Meditation, although greatly varying in technique and purpose across the diverse spiritual and cultural traditions in which it is used, may be generally defined as the intentional practice whereby one grasps "the handle of cognition" to cultivate a competent use of one's own mental capacities, gaining agency over thought and emotion (Depraz, Varela, & Vermersch, 2003). Such intentional mental training has been shown to induce functional neurobiological changes.

A study by Lutz, Greischar, Rawlings, Ricard, and Davidson (2004) found marked alterations in the synchronization of neurons as an effect of long-term training in Buddhist loving-kindness meditation, a practice that is thought by some practitioners to promote a state of unconditional compassion and benevolence. Neural synchrony of the type observed in this study may be indicative of coherent and integrated psychological functioning (Williams et al., 2005). The synchronization of brain activity found in some of the practitioners sampled, whose experience ranged between 10,000 and 50,000 hours spent in meditation, was higher than any previously reported in the literature. Such increased neural synchrony was observed not only during the meditative state, but also when the practitioners were not meditating, suggesting that long-term mental practice can induce lasting, trait-level changes, possibly mediated by structural modifications to the brain (Begley, 2007).

Other research has documented changes in neurobiological function as a result of mindfulness meditation, the practice of cultivating a present-centered, metacognitive awareness, "a naturalistic state wherein consciousness transcends its content to rest upon the dynamics of its own processes" (Garland, 2007, p. 5). A recent study by Slagter et al. (2007) compared the attentional performance of a group of experienced meditators participating in a three-month mindfulness meditation retreat with that of members of a novice control group who received a one-hour meditation class and were asked to meditate 20 minutes daily for one week. Relative to controls, experienced meditators evidenced significant improvements in attentional performance that correlated with alterations in brain activity. This cognitive enhancement was maintained three months after formal meditation practice, providing suggestive evidence that mental training can stimulate neuroplastic changes in the adult human brain (Slagter et al., 2007).

Although the work of Slagter et al. (2007) and Lutz et al. (2004) provides tentative support for meditation-induced neuroplasticity, neither study examined structural brain changes per se. However, two structural MRI investigations comparing the brains of experienced meditators with those of control subjects matched in sex, age, race, and years of education found that years of meditation experience correlated with increased cortical thickness in brain areas where visceral attention (for example, right anterior insula) and self-awareness (for example, left superior temporal gyrus) have been localized (Holzel et al., 2008; Lazar et al., 2005). These empirical investigations of meditation suggest that mental training may stimulate structural alterations reflective of neuroplasticity.

Clinical Implications of Neuroplasticity Research

The finding that experience and training can lead to the development of new neural connections has key implications. For example, people suffering from what was once thought to be permanent brain injury, as in the case of stroke, can heal through rehabilitation designed to stimulate the damaged area (Taub et al., 2006). However, although largely speculative, it is possible that neuroplasticity may undergird not only rehabilitation of physical illness but that of select psychological disorders as well, mediating natural recovery from mental illness in some cases and improvements related to psychosocial interventions. At present, it has been demonstrated that psychotherapy can induce functional changes in brain activation. For example, a brain imaging study found that people with obsessive-compulsive disorder (OCD) who were treated with a mindfulness-oriented form of cognitive-behavioral therapy (CBT) exhibited functional changes in the orbital frontal cortex and striatum, two brain structures found to be overactive in OCD (Schwartz & Begley, 2002). Other studies have demonstrated psychotherapy-related alterations in brain circuits involved in depression (for example, Goldapple et al., 2004; Martin, Martin, Rai, Richardson, & Royall, 2001). CBT has also been associated with changes in frontal and temporal brain regions of people suffering from panic disorder (Prasko et al., 2004). Such intervention-related changes in both psychosocial function and neural activity may correlate with neuroplastic alterations to the brain; critically, a combined functional and structural MRI study of practice-induced increases in gray matter found that increased task-specific brain activation led to the remodeling of one of the same neural structures (dorsolateral occipital cortex) that was activated by the practice and learning of the task (Ilg et al., 2008).

Neuroplasticity research on psychosocial interventions has just begun. A recent longitudinal study of CBT for women with chronic fatigue syndrome found increases in gray matter of the lateral prefrontal cortex after 16 sessions of CBT (de Lange et al., 2008). Increases in gray matter volume correlated with enhanced cognitive processing speed, suggesting that the neuroplasticity evoked by psychotherapy played a causal role in rehabilitation of cognitive performance after cerebral atrophy resulting from chronic fatigue.

Indeed, neuroplasticity may be the biological mechanism through which psychosocial interventions exert at least some of their therapeutic effects. During psychotherapy, when the client recalls negative or painful life experiences, the clinician may assist in reframing the context so that the experience takes on new meaning (de Shazer, 1988). For instance, in the treatment of people who have experienced traumas such as rape, therapy may help clients to envision themselves as survivors rather than victims. Such reframing or reappraisal may be a critical component of successful biopsychosocial outcomes (Folkman, 1997; Garland, Gaylord, & Park, 2009; Penley, Tomaka, & Wiebe, 2002). Some theorists hypothesize that the process of recalling, reconstructing, and reframing memories of past trauma during psychotherapy is mediated by the reorganization and genesis of neurons (Centonze, Siracusano, Calabresi, & Bernardi, 2005; Rossi, 2005a).This hypothesis is founded on evidence that the formation of new long-term memories results from neuroplastic changes in the brain structure known as the hippocampus. Hippocampal changes appear within hours of significant learning experiences (McGaugh, 2000), such as those that can occur during psychotherapy.

Neuroplasticity is mediated at the cellular level through activity-dependent gene expression, the mechanism by which neurons secrete growth factors leading to the "activation of gene transcription in the nucleus that support[s] synaptic connections.... Thus, with every new experience, the brain slightly rewires its physical structure and this rewiring is mediated through the signaling cascade" (Mundkur, 2005, p. 856). Hence, to understand neuroplasticity, we must consider the domain of psychosocial genomics.


Basic Epigenetics

In the 21st century, there is broad agreement that the genome is the basis of human life and a precondition for psychosocial experience. Nevertheless, the question of the respective roles of nature and nurture in human experience and the manner of their interaction in select contexts remains contentious, despite the more than half-century since Watson and Crick (1953) identified DNA as the building block of biological processes.

The DNA code of the human genome does not determine protein synthesis in a one-to-one fashion; instead, genes are subject to epigenetic processes (that is, modifications that do not occur because of changes in the basic genetic sequence of amino acids but, instead, result from biological and environmental influences on the expression of genes as proteins) (Eisenberg, 2004). During gene expression, the genetic code serves as a "blueprint" that guides the construction of proteins from amino acids. However, this construction process is modulated by signals from the internal and external environments, which steer and modify the manner in which basic organic molecules are organized into anatomy and physiology. Although genes prescribe protein synthesis, there is substantial variability in the manner in which they are expressed.

A single genotype, the genetic blueprint of an organism, can be expressed in a multiplicity of distinct physiological and behavioral forms, known as phenotypes. This is evident in Eisenberg's (2004) example of phenylketonuria, a disorder that when untreated may lead to severe mental retardation, psychosis, and seizures. If children with this genetic abnormality are kept on a postnatal diet low in the amino acid phenyalanine, they do not develop these disorders. Hence, although the genotype for phenylketonuria does not change, its phenotypic expression is modified by the environment (that is, nutrition) to which the individual has been exposed. The mechanisms by which such different phenotypes are expressed are just beginning to be understood, but they appear to involve the regulatory effect of internal and external environmental signals on stress hormones, which in turn modify gene transcription processes (Kandel, 1998; Rossi, 2004).

Learning and Other Psychosocial

Experiences May Modulate Gene Expression

In addition to physical environmental forces, learning experiences in the social environment can alter gene expression (McCutcheon, 2006). The bidirectional relationship of nature and nurture, genes and environment, was first demonstrated in a series of path-breaking studies of maternal care in rats (Francis, Champagne, Liu, & Meaney, 1999; Liu et al., 1997). In these studies, an inverse relationship was found between the number of stress hormone receptors in a rat's hippocampus and its tendency to exhibit stress reactions. The number of these receptors is dictated by the genotype of the rat. Highly stress-reactive rats give low levels of maternal care to their offspring, who, in turn, exhibit high stress reactivity and later provide low levels of maternal care to their offspring. However, these studies revealed that hormonal and behavioral stress reactions of rat pups, as well as the numbers of their stress hormone receptors, are modulated by the licking, grooming, and nursing behaviors of their mothers. Even if a rat were born with a genotype coding for fewer stress hormone receptors, if it was reared by an adoptive mother providing high levels of maternal care, its genes produced more stress receptors, making it calmer, less reactive to stressors, and more apt to provide maternal care to its offspring. These findings offer some evidence that social behavior may be inherited and transduced via gene expression into neuroplastic alterations in brain structure, leading to psychobiological learning and change.

The notion that social experience can lead to changes in gene expression was voiced most prominently by Nobel laureate Eric Kandel (1998), who regarded this observation as the core component of a new paradigm for psychiatry. Kandel (1998) summarized the current state of biological thinking with regard to the relation between social experiences and neurobiology, observing that

This powerful claim, although supported by over a decade of rigorous research, has rarely been directly tested. However, advances in psychoendoneuroimmunology, the study of how mental processes affect the immune system, have clearly shown the effects of psychological and social factors on human physiological functions that indirectly involve the genetic replication of cells (Ray, 2004). Such alterations of biological function may be mediated through experience-dependent gene expression, the process whereby social--environmental signals turn genes "on" and "off," leading to alterations in protein synthesis that ultimately result in physiological changes (Pinaud, 2004).

Psychosocial Genomic Hypotheses

Although our genes provide a basic outline for development, environmental influences such as social experiences shape gene expression and ultimately make us unique individuals. This interaction is the essence of what Rossi (2002) has termed "psychosocial genomics," the interdisciplinary study of the processes by which gene expression is modulated by psychological, social, and cultural experiences. Practitioners might profit from knowing more about this new science, for according to Kandel (1998),

Thus, it is conceivable that psychosocial interventions, the tools of social work practice, may produce alterations in gene expression, leading, in some cases, to measurable neurobiological changes. Because stress can affect neurogenesis through alterations in gene expression and transcription (Glaser et al., 1990; Warner-Schmidt & Duman, 2006), ultimately leading to dysregulation of affect (Post, 1992), psychosocial interventions designed to reduce distress and improve mood may affect brain structure and function through this pathway. Muenke (2008) has recently suggested that the therapeutic effects of stress-reduction techniques might be mediated by changes in gene expression. In line with this hypothesis, a recent study of a meditative breathing practice found increased gene expression of the immune factors glutathione S-transferase, Cox-2, and HSP-70 in practitioners relative to controls (Sharmaa et al., 2008). Although this study supports the psychosocial genomic hypothesis, its cross-sectional design does not allow for confident inferences about causality. However, in light of this potential shortcoming, it is noteworthy that another study identified changes in the expression of 1,561 genes involved in the stress response before and after exposure to eight weeks of meditation training (Dusek et al., 2008). Although controlled psychosocial genomic research is uncommon, there are a growing number of psychosocial intervention studies that do measure physiological outcomes such as blood levels of cortisol or immune factors. For instance, stress reduction interventions have been shown to increase numbers of immune cells and decrease numbers of cells associated with allergic reactivity (Castes et al., 1999) and to improve antibody response to the flu vaccine (Davidson et al., 2003). Intervention-related changes in such biological markers may serve as indirect measures of alterations in gene expression.

The new scientific paradigm outlined earlier provides a perspective on how the biopsychosocial constitutions of practitioners and clients might interact in the act of therapy:

When a therapist speaks to a patient and the patient listens, the therapist is not only making eye contact and voice contact, but the action of neuronal machinery in the therapist's brain is having an indirect, and, one hopes, long-lasting effect on the neuronal machinery in the patient's brain; and quite likely, vice versa. Insofar as our words produce changes in our patient's mind, it is likely that these psychotherapeutic interventions produce changes in the patient's brain. From this perspective, the biological and sociopsychological approaches are joined. (Kandel, 1998, p. 466)

The union of neuroplasticity and psychosocial genomics research represents a synthesis of the social and biological sciences that is nonreductive: It does not dismiss human experience as the product of a neural machine, predetermined by its genetic blueprint. Instead, it is integrative, inclusive, and holistic; this unitary approach reveals the power of thought and emotion, society and culture to affect not only our phenomenological experience but our very neurobiological structure and function. In sharp contrast to genetic determinism, this new paradigm envisions individuals as having the innate potential for agency over the tripartite dimensionality of their biopsychosocial selves.


The social work profession's historical emphasis on the social environment as the context for individual well-being is supported by research over the past decade. Neuroplasticity and psychosocial genomic research indicate that socioenvironmental forces have the potency to alter human well-being through their effects on neurobiology. Social experience may be transduced through the activation of neurons, leading to modifications in the phenotypic expression of genes and eventuating in structural changes to the brain. Although genes and neurobiology may be the substrates of vulnerability to environmental stressors, they are also, in all likelihood, the substrates of resilience (Cicchetti, 2003; Cicchetti & Blender, 2006).

The sciences of neuroplasticity and psychosocial genomics may provide new empirical bases for social work interventions. Biological measures of change can and should be used to enhance the evaluation of social intervention research. Given the current funding climate and priorities of the National Institutes of Health, research programs designed to evaluate social work practice may be more likely to obtain grant support if interventions studied are evaluated with physiological outcome measures, including those assessing gene expression and neuroplasticity. In time, a given practice may be deemed "evidence based" when, among other criteria, it is shown to result in plastic brain changes or altered gene expression associated with improved biopsychosocial functioning.

Currently, there is a paucity of empirical support for this new paradigm in studies with humans. An abundance of research on higher mammals indicates that experience can trigger gene expression leading to neuroplasticity. As referenced earlier, several studies on humans indicate that learning and training have led to neurogenesis and the reorganization of neural networks. Despite developments in these lines of research, science has only begun to examine the effects of psychosocial interventions on brain structure and function. More research must be conducted in this emerging field, and the social work profession, with its expertise in addressing social problems and enhancing human well-being, can make a vital contribution to this endeavor.

Brain imaging and gene assays may be used to detect the neuroplastic and genomic effects of psychosocial interventions. Technologies such as MRI, functional MRI, and positron emission tomography are capable of assessing the neurophysiological changes associated with psychosocial interventions (Kumari, 2006). Reductions in psychiatric symptoms may be reflected in the alterations in brain metabolism and structure revealed by these imaging technologies. DNA microarray technologies, which can evaluate messenger RNA production in cells and thereby determine which genes are activated (Mirnics, Middleton, Lewis, & Levitt, 2001; Raychaudhuri, Sutphin, Chang, & Altman, 2001), have been used to assess alterations in gene expression related to posttraumatic stress disorder (Segman et al., 2005), social aggression (Berton et al., 2006), and depression (Evans et al., 2004). DNA microarrays may become more widely used to measure biological effects of psychosocial interventions in the not too distant future (Rossi, 2005b).

Nevertheless, the funding and specialized training necessary to perform brain imaging and DNA microarrays decreases the likelihood that social work researchers working in isolation could leverage these technologies for biopsychosocial research. Consequently, future psychosocial intervention research could involve interdisciplinary teams of social workers, neuroscientists, and molecular biologists, with data from the biological sciences complemented by the insights of social work research. Alternatively, other more accessible biological markers, such as stress hormone levels in saliva, could be measured as a proxy for physiological change induced by psychosocial interventions. For example, salivary cortisol assays are a relatively inexpensive form of assessment that can be done by many university laboratories. Social work investigators could add this measure to their intervention research protocols.

Whether the impact of psychosocial interventions can be traced at the neuronal, genomic, or grosset levels of physiological response, biological markers will only be meaningful as a complement to self-report and collateral measures of change. Indeed, Engel's (1977) biopsychosocial paradigm is rooted in the philosophical principle of complementarity (Freedman, 1995); instead of the "either/or" mentality of dualistic reductionism, biopsychosocial research should embrace a "both/and" logic whereby reports of subjective experience garnered through validated instruments and qualitative interviews are correlated with biological and behavioral data. Such research can add value to social work as a primary mental health and allied health profession and lead to the implementation of interventions with demonstrable physiological, psychological, and behavioral benefits.


Over the past decade, neuroplasticity research has enriched the biopsychosocial perspective by demonstrating that psychosocial experiences not only influence neurobiological processes but may actually change the structure of the adult brain. These structural changes consist of increased arborization of neurons, enhanced synaptic connectivity, and even the genesis of new neural tissue. Although neuroplasticity research is in its infancy, recent findings suggest that the effects of psychosocial experiences such as learning and mental training on cognitive, emotional, and behavioral functions may be mediated by alterations to the architecture of the brain.

In turn, experience-dependent modifications to neural tissue may be driven by epigenetic processes (that is, changes in gene expression produced by environmental determinants).The human environment is constantly conditioned by social experiences, which, when transduced by the nervous system into electrochemical signals, may modulate protein synthesis in the nuclei of nerve cells, ultimately leading to changes in the replication and growth of neurons. Social experience can change gene expression, leading to the restructuring of the brain through neuroplasticity. Although tentative at present, empirical investigations of the psychosocial genomic hypothesis will likely proliferate over the next decade.

These new biopsychosocial sciences are consistent with a view of human beings as holistic, recursive systems structurally coupled with their environments in a process of mutual change (Maturana & Varela, 1987). Intentionality and volition can generate changes in the structure of the brain, the very organ assumed to produce such mental phenomena (Schwartz & Begley, 2002). With this finding, it is evident that human experience is not driven solely from the bottom up by neurobiology and genetics. Instead, there is growing evidence that psychosocial experience can exert a macrodeterministic, top-down force on our biology. In the philosophy of emergent interactionism, Roger Sperry (1987), Nobel laureate neuroscientist, described macrodeterminism as a higher order, molar level of organization that determines and conditions the activity of lower order, nested subcomponents. Hence, human beings, who are at one level assemblies of organ systems comprising aggregates of cells, which are in turn composed of organic molecules made up of subatomic particles, are not merely the sum of these physical elements. Instead, the consciousness that emerges from the interaction of these components can act back upon its physical substrate. Thought, emotion, and action trigger neural activity, which can lead to a reorganization of the brain, shaping future psychosocial experience. From this perspective, we are not the passive products of neurophysiology and heredity; rather, through our behavior in the social environment, we become active agents in the construction of our own neurobiology and, ultimately, our own lives.

This new paradigm may reveal the empirical foundation of that most central of social work principles--the idea that people have the power to transcend and transform their limitations into opportunities for growth and well-being.

Original manuscript received September 4, 2007

Final revision received December 9, 2008

Accepted January 29, 2009


Begley, S. (2007). Train your mind, change your brain: How a new science reveals our extraordinary potential to transform ourselves. New York: Ballantine Books.

Berton, O., McClung, C.A., Dileone, R.J., Krishnan, V., Renthal, W., Russo, S.J., et al. (2006, February 10). Essential role of BDNF in the mesolimbic dopamine pathway in social defeat stress. Science, 311, 864-868.

Castes, M., Hagel, I., Palenque, M., Canelones, P., Corao, A., & Lynch, N. R. (1999). Immunological changes associated with clinical improvement of asthmatic children subjected to psychosocial intervention. Brain, Behavior, and Immunity, 13, 1-13.

Centonze, D., Siracusano, A., Calabresi, P., & Bernardi, G. (2005). Removing pathogenic memories: A neurobiology of psychotherapy. Molecular Neurobiology, 32, 123-132.

Cicchetti, D. (2003). Foreword. In S. S. Luthar (Ed.), Resilience and vulnerability: Adaptation in the context of childhood adversities (pp. xix-xxvii). Cambridge, England: Cambridge University Press.

Cicchetti, D., & Blender, J. A. (2006). A multiple-levels-of-analysis perspective on resilience: Implications for the developing brain, neural plasticity, and preventive interventions. In B. M. Lester, A. Masten, & B. McEwen (Eds.), Resilience in children: Annals of the New York Academy of Sciences (Vol. 1094, pp. 248-258). New York: New York Academy of Sciences.

Davidson, R.J., Kabat-Zinn, J., Schumacher, J., Rosenkranz, M., Muller, D., Santorelli, S. F., et al.

(2003). Alterations in brain and immune function produced by mindfulness meditation. Psychosomatic Medicine, 65, 564-570.

de Lange, F. P., Koers, A., Kalkman, J. S., Bleijenberg, G., Hagoort, P., van der Meer, J. W., & Toni, I. (2008). Increase in prefrontal cortical volume following cognitive behavioural therapy in patients with chronic fatigue syndrome. Brain, 131, 2172-2180.

Depraz, N., Varela, F., & Vermersch, P. (2003). On becoming aware. Philadelphia: John Benjamins. de Shazer, S. (1988). Clues: Investigating solutions in brief therapy. New York: W.W. Norton.

Draganski, B., Gaser, C., Busch, V., Schuierer, G., Bogdahn, U., & May, A. (2004, January 22). Neuroplasticity: Changes in grey matter induced by training. Nature, 427, 311-312.

Dusek, J. A., Otu, H. H., Wohlhueter, A. L., Bhasin, M., Zerbini, L. F., Joseph, M. G., et al. (2008). Genomic counter-stress changes induced by the relaxation response. PloS ONE, 3(7), e2576, doi: 10.1371/journal.pone.0002576

Eisenberg, L. (2004). Social psychiatry and the human genome: Contextualising heritability. British Journal of Psychiatry, 184, 101-103.

Elbert, T., Pantev, C., Wienbruch, C., Kockstroh, B., & Taub, E. (1995, October 13). Increased cortical representation of the fingers of the left hand in string players. Science, 270, 305-307.

Engel, G. L. (1977, April 8).The need for a new medical model: A challenge for biomedicine. Science, 196, 129-136.

Eriksson, P. S., Perfilieva, E., Bjork-Eriksson, T., Alborn, A. M., Nordborg, C., Peterson, I3. A., & Gage, F. H. (1998). Neurogenesis in the adult human hippocampus. Nature Medicine, 4, 1313-1317.

Evans, S. J., Choudary, P. V., Neal, C. R., Li, J. Z., Vawter, M. P., Tomita, H., et al. (2004). Dysregulation of the fibroblast growth factor system in major depression. Proceedings of the National Academy of Sciences USA, 101, 15506-15511.

Folkman, S. (1997). Positive psychological states and coping with severe stress. Social Science & Medicine, 45, 1207-1221.

Francis, D. D., Champagne, F. A., Liu, D., & Meaney, M. J. (1999). Maternal care, gene expression, and the development of individual differences in stress reactivity. In N. E. Adler, M. Marmot, B. S. McEwen, & J. Stewart (Eds.), Socioeconomic status and health in industrial nations: Social, psychological, and biological pathways: Annals of the New York Academy of Sciences (Vol. 896, pp. 66-84). New York: New York Academy of Sciences.

Freedman, A. M. (1995). The biopsychosocial paradigm and the future of psychiatry. Comprehensive Psychiatry, 36, 397-406.

Garland, E. L. (2007). The meaning of mindfulness: A second-order cybernetics of stress, metacognition, and coping. Complementary Health Practice Review, 12, 15-30.

Garland, E. L., Gaylord, S., & Park, J. (2009).The role of mindfulness in positive reappraisal. Explore, 5, 37-44.

Glaser, K., Kennedy, S., Lafuse, W. P., Bonneau, R. H., Speicher, C., Hillhouse, J., & Kiecolt-Glaser, J. K. (1990). Psychological stress-induced modulation of interleukin 2 receptor gene expression and interleukin 2 production in peripheral blood leukocytes. Archives of General Psychiatry, 47, 707-712.

Goldapple, K., Segal, Z., Garson, C., Lau, M., Bieling, P., Kennedy, S., & Mayberg, H. (2004). Modulation of cortical-limbic pathways in major depression: Treatment-specific effects of cognitive behavior therapy. Archives of General Psychiatry, 61, 34-41.

Holzel, B. K., Ott, U., Gard, T., Hempel, H., Weygandt, M., Morgen, K., & Vaitl, D. (2008). Investigation of mindfulness meditation practitioners with voxel-based morphometry. Social Cognitive and Affective Neuroscience, 3, 55-61.

Ilg, R., Wohlschlager, A. M., Gaser, C., Liebau, Y., Dauner, R., Woller, A., et al. (2008). Gray matter increase induced by practice correlates with task-specific activation: A combined functional and morphometric magnetic resonance imaging study. Journal of Neuroscience, 28, 4210-4215.

Jenkins, W. M., Merzenich, M. M., Ochs, M. T., Allard, T., & Guic-Robles, E. (1990). Functional reorganization of primary somatosensory cortex in adult owl monkeys after behaviorally controlled tactile stimulation. Journal of Neurophysiology, 63, 82-104.

Kandel, E. R. (1998).A new intellectual framework for psychiatry. American Journal of Psychiatry, 155, 457-469.

Kumari, V. (2006). Do psychotherapies produce neurobiological effects? Acta Neuropsychiatrica, 18, 61-70.

Lazar, S.W., Kerr, C. E., Wasserman, R. H., Gray, J. R., Greve, D. N., Treadway, M. T., et al. (2005). Meditation experience is associated with increased cortical thickness. NeuroReport, 16, 1893-1897.

Liu, D., Diorio, J., Tannenbaum, B., Caldji, C., Francis, D., Freedman, A., et al. (1997, September 12). Maternal care, hippocampal glucocorticoid receptors, and hypothalamic-pituitary-adrenal responses to stress. Science, 277, 1659-1662.

Lutz, A., Greischar, L. L., Rawlings, N. B., Ricard, M., & Davidson, R.J. (2004). Long-term meditators self-induce high-amplitude gamma synchrony during mental practice. Proceedings of the National Academy of Sciences USA, 101, 16369-16373.

Maguire, E. A., Gadian, D. G., Johnsrude, I. S., Good, C. D., Ashburner, J., Frackowiak, R. S., & Frith, C. D. (2000). Navigation-related structural change in the hippocampi of taxi drivers. Proceedings of the National Academy of Sciences USA, 97, 4398-4403.

Martin, S., Martin, E., Rai, S., Richardson, M., & Royall, R. (2001). Brain blood flow changes in depressed patients treated with interpersonal psychotherapy or venlafaxine hydrochloride: Preliminary findings. Archives of General Psychiatry, 58, 641-648.

Maturana, H., &Varela, F. (1987). The tree of knowledge: The biological roots of human understanding. Boston: Shambala.

McCutcheon, V. (2006).Toward an integration of social and biological research. Social Service Review, 80, 159-178.

McGaugh, J. L. (2000, January 14). Memory--A century of consolidation. Science, 287, 248-251.

Mirnics, K., Middleton, E A., Lewis, D. A., & Levitt, P. (2001).The human genome: Gene expression profiling and schizophrenia. American Journal of Psychiatry, 158, 1384.

Muenke, M. (2008, October). A paradigm shift in genetics: How hypnosis influences our genes. Paper presented at the 59th Annual Workshops and Scientific Program of the Society for Clinical and Experimental Hypnosis, King of Prussia, PA.

Mundkur, N. (2005). Neuroplasticity in children. Indian Journal of Pediatrics, 72, 855-857.

Nudo, R. J., Milliken, G. W., Jenkins, W. M., & Merzenich, M. M. (1996). Use-dependent alterations of movement representations in primary motor cortex of adult squirrel monkeys. Journal of Neuroscience, 16, 785-807.

Pascual-Leone, A., Amedi, A., Fregni, E, & Merabet, L. B. (2005).The plastic human brain cortex. Annual Reviews of Neurosdence, 28, 377-401.

Penley, J. A., Tomaka, J., & Wiebe, J. S. (2002). The association of coping to physical and psychological health outcomes: A meta-analytic review. Journal of Behavioral Medicine, 25, 551-603.

Pinaud, R. (2004). Experience-dependent immediate early gene expression in the adult central nervous system: Evidence from enriched-environment studies. International Journal of Neuroscience, 114, 321-333.

Post, R. M. (1992). Transduction of psychosocial stress into the neurobiology of recurrent affective disorder. American Journal of Psychiatry, 149, 999-1010.

Prasko, J., Horacek, J., Zalesky, R., Kopecek, M., Novak, T., Paskova, B., et al. (2004).The change of regional brain metabolism (18FDG PET) in panic disorder during the treatment with cognitive behavioral therapy or antidepressants. Neuro Endocrinology Letters, 25, 340-348.

Ray, O. (2004).The revolutionary health science of psychoendoneuroimmunology: A new paradigm for understanding health and treating illness. In R. Yehuda & B. McEwen (Eds.), Biobehavioral stress response: Protective and damaging effects: Annals of the New York Academy of Sciences (Vol. 1032, pp. 35-51). New York: New York Academy of Sciences.

Raychaudhuri, S., Sutphin, P. D., Chang, J. T., & Altman, R. B. (2001). Basic microarray analysis: Grouping and feature reduction. Trends in Biotechnology, 19, 189-193.

Rossi, E. L. (2002). Psychosocial genomics: Gene expression, neurogenesis, and human experience in mind-body medicine. Advances in Mind--Body Medicine, 18(2), 22-30.

Rossi, E. L. (2004). Stress-induced alternative gene splicing in mind-body medicine. Advances in Mind-Body Medicine, 20(2), 12-19.

Rossi, E. L. (2005a).The ideodynamic action hypothesis of therapeutic suggestion: Creative replay in the psychosocial genomics of therapeutic hypnosis. European Journal of Clinical Hypnosis, 6(2), 2-12.

Rossi, E. L. (2005b). Prospects for exploring the molecular-genomic foundations of therapeutic hypnosis with DNA microarrays. American Journal of Clinical Hypnosis, 48(2-3), 165-182.

Schwartz, J. M., & Begley, S. (2002). The mind and the brain: Neuroplasticity and the power of mental force. New York: HarperCollins.

Segman, R. H., Shefi, N., Goltser-Dubner, T., Friedman, N., Kaminski, N., & Shalev, A. Y. (2005). Peripheral blood mononuclear cell gene expression profiles identify emergent post-traumatic stress disorder among trauma survivors. Molecular Psychiatry, 10, 500-513.

Sharmaa, H., Dattaa, E, Singha, A., Sena, S., Bhardwajb, N., Kochupillaib,V., & Singh, N. (2008). Gene expression profiling in practitioners of Sudarshan Kriya. Journal of Psychosomatic Research, 64, 213-218.

Slagter, H. A., Lutz, A., Greischar, L. L., Francis, A. D., Nieuwenhuis, S., Davis, J. M., & Davidson, R.J. (2007). Mental training affects distribution of limited brain resources. PLoS Biology, 5(6),Article e138. Retrieved December 28, 2007, from ?request=getdocument&doi=10.1371/journal.pbio.0050138 Sperry, R. (1987). Structure and significance of the consciousness revolution. Journal of Mind and Behavior, 8, 37-456.

Taub, E., Uswatte, G., King, D. K., Morris, D., Crago, J. E., & Chatterjee, A. (2006). A placebo-controlled trial of constraint-induced movement therapy for upper extremity after stroke. Stroke, 37, 1045-1049.

Warner-Schmidt, J. L., & Duman, R. S. (2006). Hippocampal neurogenesis: Opposing effects of stress and antidepressant treatment. Hippocampus, 16, 239-249.

Watson, J. D., & Crick, E H. (1953, May 30). Genetical implications of the structure of deoxyribonucleic acid. Nature, 171, 964-967.

Williams, L. M., Grieve, S. M., Whitford, T. J., Clark, C. R., Gur, R. C., Goldberg, E., et al. (2005). Neural synchrony and gray matter variation in human males and females: Integration of 40 Hz gamma synchrony and MRI measures. Journal of Integrative Neuroscience, 4, 77-93.

Eric L. Garland, MSW, LCSW, is a doctoral candidate, and Matthew Owen Howard, PhD, is Frank A. Daniels, Jr. Distinguished Professor of Human Services Policy, School of Social Work, University of North Carolina at Chapel Hill. The development of this article was supported by National Center for Complementary and Alternative Medicine Grant T32ATO03378; a grant from the George H. Hitchings Fund for Health Research and Science Education of the Triangle Community Foundation, Durham, NC; a Francisco J. Varela Research Grant from the Mind and Life Institute, Boulder, CO; and an Armfield-Reeves Innovation Grant from the University of North Carolina at Chapel Hill School of Social Work. Address correspondence to Eric L. Garland, University of North Carolina at Chapel Hill, 19 Copper Hill Court, Durham, NC 27713; e-mail:
the regulation of gene expression by social
   factors makes all bodily functions, including
   all functions of the brain, susceptible to social
   influences. These social influences will be biologically
   incorporated in the altered expressions
   of specific genes in specific nerve cells of specific
   regions of the brain. These socially influenced
   alterations are transmitted culturally (p. 461).

insofar as psychotherapy or counseling is effective
   and produces long-term changes in behavior,
   it presumably does so though learning, through
   producing changes in gene expression that alter
   the strength of synaptic connections and structural
   changes that alter the anatomical pattern
   of nerve cells of the brain (p. 460)
Gale Copyright: Copyright 2009 Gale, Cengage Learning. All rights reserved.