The effect of exercise on depression, anxiety, and other mood states

Byrne, A. & Byrne, D.G. (1993). The effect of exercise on depression, anxiety, and other mood states. Journal of Psychosomatic Research, 37, 565-574.

This review supports the claim that exercise treatments are associated with positive psychological benefits for both clinical and non-clinical populations. Although most of the studies employed aerobic interventions, some studies even showed positive improvements associated with non-aerobic exercise (e.g. weight lifting). However, all of these results need to be interpreted with caution as the result of methodological limitations and indirect evidence. If future studies were to show unequivocally positive psychological gains are caused by exercise interventions, including exercise for people with affective disorders will undoubtedly have a number of advantages since it is time and cost effective by comparison to psychotherapy and pharmacotherapy, comes with few side effects if done correctly, and may even by used to prophylactically prevent the occurrence of future affective episodes.

Repeated stress induces dendritic spine loss in the rat medial prefrontal cortex

Radley, J.J. et al. (2005). Repeated stress induces dendritic spine loss in the rat medial prefrontal cortex. Cerebral Cortex, 16, 313-320.

The medial prefrontal cortex (mPFC) plays an important role in higher cognitive processes and in the regulation of stress-induced HPA axis activity. This study investigated the effect of stress on dendritic spine density in the mPFC. Rats were restrained for 6 hours daily for 21 days with wire mesh. Following the 21 days of stress, stressed rats weighed less than controls, had a 20% decrease in overall apical dendritic length, a 16% decrease in apical dendritic spine density, and hence an estimated 33% reduction in the total number of axospinous synapses on apical dendrites of pyramidal neurons in the mPFC. These morphological changes may have a significant impact on the functional properties of this region. Clinically, mPFC dysfunction is associated with PTSD and depression. One potential neuroanatomical substrate relevant to these disorders is the mPFC-amygdala circuit. Normally, the mPFC may inhibit amygdala output through its connections on the GABAergic intercalated cells at the border of the lateral and central nuclei of the amygdala. Experimental lesions of the mPFC support this, leading to an enhancement of amygdala-dependent behaviors such as emotionality and fear conditioning. Future studies are needed to investigate the extent to which these morphological changes from chronic stress are reversible.

Prolonged Exposure Treatment for PTSD following 9/11

Kazi, A., Freund, B., & Ironson, G. (2008). Prolonged Exposure Treatment for Posttraumatic Stress Disorder following the 9/11 attack with a person who escaped from the Twin Towers. Clinical Case Studies, 7, 100-116.

This article chronicles the progress of one 9/11 survivor through the cognitive-behavioral therapy intervention of prolonged exposure (PE) therapy to address her PTSD and depressive symptomatology. This treatment consists of (1) imaginal exposure, and (2) in vivo exposure. It is designed to elicit emotional processing until the detrimental traumatic memories and avoidances have habituated (desensitized). After 15 sessions this client improved 75% as measured by a composite index. However, there was residual symptomatology 6 months after therapy ended but measures remained sub-clinical. Progress through treatment can be seen as waxing and waning, but trending towards improvement. Still, in this type of therapy clients must be stressed before they are to feel better. With the prevalence of PTSD at 8% in the US population, clinicians are calling more and more for effective treatment regimes. PE may be a promising candidate.

HPA Axis, neuroendocrine factors, and stress

Tsigos, C. & Chrousos, G.P. (2002). Hypothalamic-pituitary-adrenal axis, neuroendocrine factors, and stress. Journal of Psychosomatic Research, 53, 865-871.

Psychology is concerned with the transactions and interactions we have with the world. Stress research examines how we respond to transactions that are stressful. This paper does a great job to illustrate the complexity of our physiological responses to stressors.

CRH/AVP. The paper begins with our physiological response following detection of a stressor. CRH and AVP are secreted into a special portal system and activate neurons of the paraventricular nuclei (PVN) of the hypothalamus, which primarily kicks off activation of the greater hypothalamic-pituitary-adrenal (HPA) axis.

LC/NE system. The locus ceruleus and other noradrenergic cell groups of the medulla and pons, collectively known as the LC/NE system, serve as a global alarm system, using brain epinephrine to execute autonomic and neuroendocrine responses.

The autonomic axis. The ANS provides rapid response to stress, engaging the SNS and withdrawing the PSNS, and enacting cardiovascular, respiratory, gastrointestinal, renal, and endocrine changes.

The HPA Axis. CRH and AVP normally follow certain circadian rhythms, with increasing pulses seen in the early morning hours and decreasing throughout the day. During acute stress, pulsations in this portal system markedly increase, resulting in release of ACTH from the pituitary into the general bloodstream, which finally results in secretion of cortisol and other glucocorticoids from the adrenal cortex. These corticoids involve the whole body in the organism's response to stress and ultimately contribute to the termination of the response via inhibitory feedback.

Other changes. Concomitant with the aforementioned changes, the sympathetic-adrenomedullary system (SAM) influences the body organs, and vagal and sacral parasympathetic responses are also instantiated mediating our gut responses to stress.

The paper also goes into advanced topics including interactions that exist between the HPA axis and the immune system, interactions between the HPA and the gonadal and growth axes, and interactions between the HPA and metabolism. It also discusses pathologies related to the HPA axis. A spectrum of conditions may be associated with increased and prolonged activation of the HPA axis, including melancholic depression, anorexia nervosa, OCD, panic anxiety, excessive exercising, and childhood sexual abuse. Another group of conditions may be associated with hypoactivation of the stress system, including atypical depression, seasonal depression, and chronic fatigue syndrome. Antalarmin, a CRH-R1 antagonist, was also mentioned as being a potentially important drug to combat HPA axis disorders characterized by HPA and LC/NE hyperactivity in the future.

Plasticity underlying fear conditioning occurs in the BLA

Fanselow, M.S. & LeDoux, J.E. (June 1999). Why we think plasticity underlying Pavlovian fear conditioning occurs in the basolateral amygdala. Neuron, Vol. 23, 229-232.

A debate over the role of the neural plasticity in the amygdala has been ongoing. The 'encoding view' believes that neural plasticity in the basolateral complex of the amygdala (BLA) encodes the emotional component of memories formed during fear conditioning. The 'modulatory view' sees the amygdala as modulating memories stored in other brain regions, not unlike current theories of the hippocampus. This paper believes that the two views are not mutually exclusive, and argues for a synthesized model in which the amygdala is both the site of fear memory encoding and storage and a modulator of memory functions in other structures.

The Emotionally Engaged Analyst

Miller, M.L. (2008). The Emotionally Engaged Analyst: Theories of affect and their influence on therapeutic action. Psychoanalytic Psychology, Vol. 25, No. 1, 3-25.

The article provides a review of affect theories and how they relate to therapy. As Dahl mentions, "the absence of a coherent psychoanalytic theory of emotions is truly remarkable, given clinician's nearly universal belief in the centrality of emotions in every patient's life and treatment".

Two broad categories have predominated thus far. One is the cognitive appraisal theory of emotion which holds that emotions are the conscious or unconscious cognitive appraisal of an arousing stimulus. These cognitive evaluations are formed by assimilating the current event into a stored schema that represents earlier experiences in similar circumstances. Schemas may be processed in subsymbolic, nonverbal symbolic, and verbal symbolic modes. If we are to represent and understand emotional experiences, subsymbolic processes must be integrated with symbolic processes. This idea forms the basis for therapy: enable the patient to metabolize unformulated subsymbolic experiences of emotion into meaningful feelings.

The second category encompasses so-called functional and discrete theories of emotion. These theories hold that the brain is more an emotional organ than a cognitive one, and emotions are seen as a hierarchy of embedded regulatory functions necessary for the automatic adaptive survival of the organism. Emotions are orchestrated in response to significant changes perceived in the internal or external milieu, and responses are executed subcortically. Cortical involvement occurs after subcortical emotional processes have begun; this may later influence the execution of the underlying emotional processes by providing the informational context of the body, the self, and the environment. Feelings, the mental representations of ongoing regulatory processes, do not initiate these emotional processes but are instead the product of them. These theories view the essence of change in psychoanalytic treatment as the remodeling of the nonconscious procedures through which the person adapts to his or her environment.

The dynamic systems theory of emotion, a recent theoretical addition, can be viewed as a combination of the cognitive appraisal schema of emotion and the discrete/functional models of emotion with an emphasis on social interaction. In this model, emotions should be seen not as discrete states of being or constructed interpretive programs but as ongoing, continuous processes influencing and being influenced by the complex context in which they occur. Emotions emerge as three critical component systems (the subcortical arousal system, the cortical interpretive system, and the motor system) dance together. In so doing, emotions, meanings, and actions are continuously modified and negotiated. Viewed in the context of social interaction, another three-way interaction can be seen to take place between each person's own emotional processes, those of the person he or she in interacting with, and the emotional character of the interaction itself. Although all of these components within the individual and without can interact with one another in an infinite number of ways, they have a tendency to self-organize into a finite number of stable patterns which tend to repeat under particular conditions and ultimately define the different emotional states and state transitions a system can take. The goal of therapy is then to engender systemic change, to perturb the system appropriately into allowing transformations in the emotional experience of the client. In a truly interactive system, with multiple internal and external factors contributing to the individual's emotional experience, as one component within the system changes, all other components adjust to that change. As such, the analyst's emotional participation is viewed as an essential component.

Affect Regulation

Schore, A.N. (2002). Dysregulation of the Right Brain: A Fundamental Mechanism of Traumatic Attachment and the Psychopathogenesis of Posttraumatic Stress Disorder, Australian and New Zealand Journal of Psychiatry, 36, 9-30.

This article is by Allan Schore, a doctor in UCLA’s department of Psychiatry and an impressively well-published author. Schore’s style is to assimilate interdisciplinary literature into unified theories of brain function. This review article does well to illustrate his approach by integrating the latest thinking from attachment theory, affective neuroscience, developmental stress research, and infant psychiatry into a theory on post-traumatic stress disorder (PTSD). The article drives home several key points:

(1) The individual response to stressful stimuli may or may not be adaptive.

(2) Current evidence shows that the neural circuitry of the stress system is located in the early developing right brain, the hemisphere that is dominant for affect regulation and inhibitory control.

(3) The development of the right brain is highly experience-dependent, and this experience is primarily mediated by the dyadic attachment relationship that develops between caregiver and infant. Simply put, the mother plays a key role in co-regulating the infant’s postnatally developing nervous system, particularly its stress responses. At a very early age, we thereby rely on and learn strategies from our mothers on self-regulation of emotion. As such, if either the mother or the child is improperly psychobiologically attuned to the body-based states of the self or the other (for whatever reason), this can have detrimental effects on the child’s autoregulatory mechanisms which are still under construction.

(4) This point I will offer more parenthetically. Social stressors are far more detrimental than non-social aversive stimuli. As an example, abuse or neglect would be likely to have a much more deleterious effect on the infant brain than assaults from the nonhuman or inanimate, physical environment. From this, I think one can conclude our brains are more specially honed to social cues than to other types of input.

(5) Due to the shape of the human developmental arc, early experiences in life may be particularly important in shaping an individual’s responsiveness later in life. As developmental effects are almost always cumulative, building on the brick and mortar that has already been laid by previous developmental processes, later growth is “limited by the adequacy of already-formed, underlying networks, and therefore maturation is optimal only if the preceding stages were installed optimally”.

(6) Stress effects are also shown to be cumulative. Whereas acute stress produces short-term and reversible deficits, repeated, prolonged, chronic stress can lead to irreversible or only partially reversible enduring effects.

Add it all up and essentially Shore has conceived of a vignette in which the experiences of the maturing infant can establish inefficient coping mechanisms and individual “dissociation” in times of stress, seen behaviorally even many years later in adulthood. The crux of it… “Optimal attachment experiences allow for the emergence of self-awareness, the ability to sense, attend to, and reflect upon the dynamic changes of one’s subjective self states, but traumatic attachments in childhood lead to self-modulation of painful affect by directing attention away from internal emotional states.” More impressive yet are the 246 citations he makes in an 18-page article!

What is personally interesting to me is the take-away that our development – and in this case, our emotional development – is so unambiguously externally mediated, especially by close parental and familial relationships. (We actually see a reasonable case for the intergenerational transmission of regulation and coping strategies.)

But more importantly, we are essentially “propped” or “wired up” to learn via social mechanisms from people with whom we have intimacy. Said another way, certain parts of the brain may be more receptive to reprogramming by social “interfacing” than by other mechanisms, perhaps even in adulthood. This idea is central to Schore’s thinking on the therapist-patient relationship, which he expounds upon in his three-book-set on Affect Regulation.