Heed the Message, Don’t Shoot the Messenger

VirginIslandsNP_EN-US154535774The messages provided by the stress reaction that something is wrong, or dangerous, or simply requires our attention are often very powerful, even debilitating. Just think of the feeling we get in our gut (seat of the enteric nervous system) when something is not quite right. Even though we might not identify the threat right away, the stress signal activates our body’s defense almost instantaneously and we become fully alert. In the absence of a clearly identifiable threat, or upon identification of a threat that we cannot immediately escape, we may choose to treat stress itself as if it were the enemy. The common phrase, “I have too much stress” should in fact be restated as, “I have people, situations or circumstances that are an emotional, physical or mental threat to my well-being.”

Turning off the stress alert system is possible, especially with the use of powerful drugs or alcohol, at least for time. In fact, this amounts to unscrewing the warning lights on a dashboard so as not to be bothered by what they signal. The stress messenger conveys valuable information in the form of neural signals (mediated by the limbic system), sensations, and subjective feelings. The messenger does its job, the way it should, to ensure our survival. Nevertheless, the repeated stress signals may rise to a high and uncomfortable level of intensity, depending on the perceived dangerousness of the situation. That noxious feeling of being stressed is trying to give us a priority notification, to make sure that certain signals (which represent an important message) grab our full attention. Refusing to heed the signals of stress, or simply shutting them off or ignoring them, is not an appropriate response.

The best use we can make of stress messages is twofold:

  1. Use its intensity and the timing of its occurrence to become aware and acknowledge that a psychological or physical threat exists, and gauge its significance. For example, an immediate physical danger will elicit a more immediate and dramatic body reaction than a psychological threat that may occur in the future.
  2. Identify and address the cause of the stress reaction (which is usually accompanied by more or less severe anxiety) and focus our attention on it, with the aim of confronting, reducing or eliminating the stressor. For example, in a relationship that isn’t quite working the way it should the stress signal is the anxiety and worry over it, the stressor is that painful aspect of the relationship that needs to be confronted, reduced or eliminated.

In short, stress is the message, the stressor is its cause. It is much more productive to focus our efforts on the stressor, rather than just unscrew and throw out the red light bulb.

How Good and Bad Stress Are the Same

MountRotui_EN-US1706638791Eustress (or good stress) and bad stress (acute or chronic) cause the exact same reaction in the human body. Even during voluntary “stressful” activities such as sport or exercise or when we receive unexpected good news, the brain stem, the oldest and more primordial part of the human brain, immediately mobilizes the body’s resources. The brain stem does not know, and one might say does not care, what triggers the sudden demand for additional physical activity. All the brain stem knows, prior to any higher brain intervention such as a decision to be afraid of something, or a decision to exercise, is that more blood is needed immediately to fulfill physical demands that may already be occurring (in the case of exercise or a real and impending threat) or that may be presumed to occur (in the case of perceived danger in a situation).

When the motor areas of the brain and the limbic system become activated by a positive but sudden event, most of the reticular activating system of the brain stem is also mobilized. This activation includes greatly increased stimulation of the vasoconstrictor and cardioacceleratory areas of the vasomotor center of the brain stem. Thus, the increase in arterial pressure permits to keep pace with an expected increase in muscle activity. A similar rise in pressure occurs during negatively stressful situations. The need to prepare to meet the danger posed by the stressor mobilizes the reticular activating system and the vasomotor center of the brain stem.

During dangerous situations (real or perceived), arterial pressure rises to as high as twice its normal value within a few seconds. This dramatic increase can immediately supply blood to any or all muscles of the body needed to respond. This translates into an enormously increased ability to fight against or to flee from the cause of danger. It is indeed a significant survival factor that no conscious decision is needed when this split-second mobilization is required.

The Bipolar Hippocampus

aavanGogh_1888_PontLAngloisA Vanderbilt University study just published in the Archives of General Psychiatry reveals that hippocampal interneurons are modified by bipolar depression. The hippocampus is an important component of the limbic system that acts as the switching center through which incoming sensory signals are retransmitted and initiate behavioral reactions for different purposes. Its importance has been demonstrated empirically: experimental artificial stimulation of the hippocampus can induce a wide variety of behavioral patterns such as pleasure, rage, passivity, or excessive sexual drive. Because of its central function in the modulation of emotions, the hippocampus is believed to have a role in mood disorders such as depression. Numerous postmortem studies conducted on the brain of individuals who were affected by bipolar disorder have shown a decreased density and decreased gene expression of hippocampal interneurons. These findings, however, had not been confirmed by neuroimaging studies of hippocampal volume and function in live subjects—until now.

hippocampal_anatomyTo assess hippocampal volume, neuron number, and interneurons the Vanderbilt study examined sample brain specimens of hippocampi from 14 individuals with bipolar disorder and compared them to those taken from 18 healthy control subjects. The specimens, provided by the Harvard Brain Tissue Resource Center at McLean Hospital, were cut at 2.5-mm intervals and sections from each tissue slice were either Nissl-stained or stained with antibodies against somatostatin or parvalbumin. Messenger RNA was extracted from fixed tissue and real-time quantitative polymerase chain reaction was performed.

The researchers analyzed each sample by measuring the volume of pyramidal and nonpyramidal cell layers, overall neuron number and size, number of somatostatin- and parvalbumin-positive interneurons, and messenger RNA levels of somatostatin, parvalbumin, and glutamic acid decarboxylase 1.

After comparing healthy and unhealthy hippocampal samples, the study showed that the 2 groups did not differ in the total number of hippocampal neurons, but the bipolar disorder group showed reduced volume of the nonpyramidal cell layers, reduced somal volume in cornu ammonis sector 2/3, reduced number of somatostatin- and parvalbumin-positive neurons, and reduced messenger RNA levels for somatostatin, parvalbumin, and glutamic acid decarboxylase 1.

According to the researchers, these results indicate a specific alteration of hippocampal interneurons in bipolar disorder, which is likely to produce a hippocampal dysfunction that can have, among other manifestations, an effect on the onset and severity of bipolar depression.

Optogenetics Discovers Brain Anxiety Circuit

AmygdCingGyrusThe state of heightened apprehension and high arousal in the absence of immediate threat—commonly labeled as acute stress or anxiety—can be a severely debilitating condition. Over 28% of the population suffers from anxiety disorders that contribute to the development of major depressive disorder and substance abuse. Of all the structures of the limbic system, the seat of emotion processing, the amygdala plays a key role in anxiety, although by what exact mechanism still remains unclear. Newly published research carried out by a group of neuroscientists at Stanford University using the novel technique of optogenetics with two-photon microscopy has permitted a much closer exploration of the neural circuits underlying anxiety than ever before. The optogenetics approach facilitates the identification not only of cell types but also the specific connections between cells. The researchers noticed that timed optogenetic stimulation of the basolateral amygdala (BLA) terminals in the central nucleus of the amygdala (CeA) produced a significant, acute, and reversible anxiety-reducing effect. Conversely, selective optogenetic inhibition of the same projection resulted in increased anxiety-related behaviors. These results indicate that specific BLA–CeA projections are the critical circuit elements for acute anxiety control in the brain. The results were published in the March 17 issue of the scientific journal Nature.

A Closer Look at the Amygdala’s BLA and CeA Regions

BasolateralAmygdalaThe amygdalae (amygdaloid nucleus) are two identical almond-shaped brain structures located in each temporal lobe. Each amygdala receives input from the olfactory system, as well as from visceral structures. The amygdala in humans has been confirmed by functional MRI imaging to be the area of the brain that is best correlated with emotional reactions and plays a key role in the brain’s integration of emotional meaning with perception and experience. The emotional aspect of the response of the individual is passed on to the frontal cortex, where “decisions” are made regarding possible responses. In this way, the response of the individual can take into account the emotional aspect of the situation.

Additionally, the amygdala coordinates the actions of the autonomic and endocrine systems and prompts release of adrenaline and other excitatory hormones into the bloodstream. The amygdala is involved in producing and responding to nonverbal signs of anger, avoidance, defensiveness, and fear. The amygdala has been implicated in emotional dysregulation, aggressive behavior, and psychiatric illnesses such as depression. It has also been shown to play an important role in the formation of emotional memory and in temporal lobe epilepsy.

The basolateral amygdala, one of the two structures studied in the recent Stanford research, receives extensive projections from areas of the brain cortex that are specialized for recognizing objects such as faces in central vision. Extensive intrinsic connections within the amygdala
promote further coordination of sensory information.

Biological effects initiated by amygdala include increases or decreases in arterial pressure and heart rate, gastrointestinal motility and secretion, evacuation, pupillary dilation, piloerection, and secretion of various anterior pituitary hormones, especially the gonadotropins and
adrenocorticotropic hormone, which are key agents in the stress reaction. Interestingly, amygdala stimulation can also cause several types of involuntary movement, such as raising the head or bending the body, circling movements, occasionally rhythmical movements, and movements
associated with taste and eating, such as licking, chewing, and swallowing.

LimbicSystemGeographyThe findings also show the involvement of the amygdala’s CeA region in mediating threat-related anxiety and acute fear-related behavioral and hormonal responses. Earlier studies had shown that stimulation of this same area reduces snake fear and pituitary-adrenal activity and that CeA lesions resulted in decreased expression of threat-induced freezing. Additionally, the CeA region of the amygdala was reported as being significantly involved in the consolidation of contextual fear memory, i.e., what permits us to remember so vividly and persistently objects or situations that have caused fear in us in the past.

Stress Hardware Review: Anterior Cingulate

Dolomites_EN-US3033597177The anterior cingulate cortex is a region of the brain that is activated by sensation, cognition, and emotion. It appears to play an important role in autonomic, affective, and cognitive behavior. Because of its position, the anterior cingulate is anatomically and functionally well positioned to integrate information across the physical, intellectual and emotional domains. Important in the stress reaction, the anterior cingulate region is activated during self-regulation of arousal through its connections with the cholinergic basal forebrain. The whole structure, but especially area 32, produces inhibitory inputs that decrease amygdala responsiveness and are helpful in mitigating the effects of fear and in preventing or at least delaying “amygdala hijacks.”

The normal functioning of the anterior cingulate area leads to a normal response to stressful events, which is a psychophysiological arousal or increased emotionality. The normality of the brain response to traumatic stimuli also serves to inhibit feelings of fear when there is no true threat.  Any chemical or structural failure of activation in this area and/or decreased blood flow in the adjacent subcallosal gyrus can lead to an exaggerated response to stress, resulting in significantly higher emotionality and the inability to properly regulate fear. The latter condition provides the inducing cues in anxiety disorders, i.e. increased and persistent fearfulness that is not appropriate for the context.

What the Anterior Cingulate Does

BrodmanBrainAreasPhysically, stimulation of the anterior cingulate (especially in area 24) induces changes in blood pressure, heart rate, respiratory rate, pupillary dilation, skin conductance, thermoregulation, gastrointestinal motility, and changes in adrenal cortical hormone secretion (ACTH). Cognitively, the anterior cingulate cortex plays a leading role in learning new behaviors, whether as a conditioned response to predictors of painful stimuli, as an instrumental response to avoid such stimuli, or in response to reduced reward. Emotionally, the anterior cingulate (along with other structures in the limbic system) mediates emotional responses including fear, agitation, and euphoria, and verbal expression with affective content, such as sighs, cries, and screams.

Neuroimaging studies with powerful fMRI instruments show electrical activation in the rostral–ventral anterior cingulate cortex when individuals under study are asked to recall sad memories or view faces with sad expressions, when they are told to anticipate an upcoming painful electric shock, and when exposed to scenes or words with emotional content. It should come as no surprise that stress-induced activations in the amygdala and orbitofrontal cortex occur simultaneously with those in the anterior cingulate cortex.

Genes, Stress and the Anterior Cingulate

Genetic studies have conclusively demonstrated that the anterior cingulate cortex is highly sensitive to environmental stressors, either physical, psychological, or behavioral. Anoxia (lack of oxygen), maternal separation, amyloid protein expression, and drug abuse all induce hypometabolism, gliosis, and programmed cell death in the anterior cingulate cortex. After prolonged and continued exposure to stress, nerve cells in the anterior cingulate cortex are damaged and killed by excessive stimulation, a process called excitotoxicity.

When the Anterior Cingulate Malfunctions

Several psychiatric disorders are linked with abnormalities in the function of the anterior cingulate cortex. Significantly elevated neurochemical activity in this region of the brain has been observed in obsessive–compulsive disorder, tic disorder, and depression. A normal range of activity is restored with behavioral and pharmacological treatment of these disorders. Other psychiatric disorders that have been associated with abnormal functioning of the anterior cingulate cortex include attention deficit hyperactivity disorder (ADHD) and schizophrenia.

Stress Hardware Update: Limbic System 2.0

LimbicSystemGeographyThe term limbic system designates the entire neuronal circuitry and forebrain structures that control emotional behavior, motivational drives and the processing of present and past sensory experiences. The brain structures of the limbic system are located around the middle edge of the brain. Several limbic structures are involved in determining the affective nature of sensory inputs, i.e., whether the sensations are pleasant or unpleasant. The emotional qualities we attach to the input provided by our five senses are also called reward (when they are pleasing to us and therefore we crave more of them) or punishment (when they are unpleasant and therefore we seek to avoid them), or satisfaction or aversion. Neurobiological research on the functions of the limbic system dating back to its XIX century pioneer Pierre-Paul Broca (1861), later expanded by James Papez (1937), Giuseppe Moruzzi and Horace Magoun (1949), and Ross MacLean (1949, 1952) identified the “reticular” and “limbic” systems as regulating the energizing and expressive roles in the central nervous system.

The limbic system is comprised of numerous structures, the most important of which are the hypothalamus, the amygdala, the hippocampus, the cortex, the cingulate gyrus, the striatum, the pallidum, the thalamus, and Meynert’s nucleus basalis. Each of these structures performs a specific function, and often also serves to receive, transmit and amplify communication within the limbic system, with other areas of the brain, and with other parts of the central nervous system.

The Hypothalamus: The Central Autonomic Controller

A major component of the limbic system is the hypothalamus and its related substructures. The hypothalamus complex controls the internal state of the body, such as temperature, osmolality of the body fluids, appetite and thirst and the regulation of body weight. Despite its very small size of only a few cubic centimeters (which represents less than 1% of the brain mass), the hypothalamic complex has two-way communicating pathways with all levels of the limbic system and is the key structure for higher level coordination of autonomic and endocrine functions. There would not be a stress reaction, with its almost instantaneous activation of physical and psychological defense mechanisms, without the hypothalamus providing the critical signal activation.

The Amygdala: The CPU of Emotional Response

AmygdCingGyrusThe amygdala is a group of nuclei embedded in the anteromedial temporal lobe, which receives input from all five senses. It performs the analysis of form and color and facilitates the recognition of complex stimuli such as human faces. The amygdala can influence heart rate and blood pressure, gut and bowel function, respiratory function, bladder function, and many more instinctive physical reactions. It is in the amygdala and its connection to other limbic structures that the determination of the affective value of sensory stimuli (rewarding or aversive) is made and our mood (or feelings about something) is determined. Stimulation of the amygdala produces the defense reaction that prepares us for fight, flight or freeze, along with complex sensory and experiential phenomena, which may include fear, sensory hallucinations, feelings of deja vu, and memory-related flashbacks and nightmares. The amygdala receives neuronal signals from all portions of the limbic cortex and is the “central processing unit” in which the limbic system produces an emotional response to events, people and situations. The amygdala also interacts with higher brain regions that govern such processes as directed attention, declarative memory, and response inhibition (Davidson, Putnam, & Larson, 2000; LeDoux, 1995).

The Hippocampus: Memory Chips and Orientation

The hippocampus is a highly specialized region of the cerebral cortex, which along with surrounding areas of the parahippocampal gyrus is directly involved in memory processing and spatial orientation. The hippocampus provides the neural mechanism for association of different parameters that is necessary for the moment-to-moment incorporation of experience into our short- and long-term memory banks. Almost any type of input from the five senses causes activation of at least part of the hippocampus, which in turn distributes many outgoing signals to the anterior thalamus, to the hypothalamus, and to other parts of the limbic system, especially through the fornix, a major communicating pathway.

The Orbital and Medial Prefrontal Cortex: Food and Personality

PhineasGageThe cortical areas of the limbic system are divided into two interconnected networks with related but distinct functions. Many of these functions are related to food or eating (e.g., olfaction, taste, visceral afferents, somatic sensation from the hand and mouth, and vision), and neurons in the orbital cortex respond to multisensory stimuli involving the appearance, texture, or flavor of food. Therefore, the orbital and medial prefrontal cortex have the function of evaluating feeding-related sensory information and to stimulate appropriate visceral reactions. More importantly, damage to the ventromedial frontal lobe can produce dramatic behavioral changes, which suggests that the visceral reactions evoked through this cortical area are critical in evaluating alternatives and making choices. As the well-publicized 19th-century case of Mr. Phineas Gage’s accidental head impaling by a steel rod demonstrates, individuals with damage to the ventromedial prefrontal cortex have no problem with their motor or sensory function, their intelligence or cognitive function, but show devastating changes in personality and choice behavior.

The Cingulate Gyrus: The Cement of Society

Intriguing data and ideas have been proposed by several researchers seeking to identify specific functions of the cingulate gyrus. In what has been termed the affiliation/attachment drive theory, Everly (1988) has shown experimentally that the removal of the cingulate gyrus eliminates both affiliative and grooming behaviors. MacLean (1985) has argued that the affiliative drive may be hard-coded in the limbic system and may be the anatomical underpinning of the “concept of family” in humans and primates. The drive toward other-oriented behaviors, such as attachment, nurturing, affection, reliability, and collaborative play, which has been referred to as the “cement of society” (Henry and Stephens, 1977), appears to originate in this relatively small limbic system structure.

The Ventromedial Striatum, Ventral Pallidum, and Medial Thalamus

The nuclei of the ventromedial striatum are also related to reward and reward-related behavior, whereby they inhibit or suppress unwanted behaviors while allowing other behaviors to be freely expressed. The dorsolateral striatum and related areas of the globus pallidus appear to be involved in switching between different patterns of motor behavior, whereas the ventromedial striatum and pallidum may allow changing of stimulus–reward associations when the reward value of a stimulus has changed. These areas are examples of the complexity and redundancies built into limbic system structures that permit multiple iterations of signal transmission and reception, and a much more complex and refined analysis of sensory inputs from the five senses.

Nucleus Basalis (of Meynert)

The nucleus basalis of Meynert is a prominent group of large cells located in the basal forebrain, most of which are involved in the activation of acetylcholine or GABA neurotransmitters, indispensable in activation of the stress reaction and our defense mechanism when a physical or psychological threat is perceived. The magnocellular basal forebrain nuclei are well situated to modulate brain activity in relation to limbic activity.

Disorders of the Limbic System

Although lesions to limbic structures do not necessarily result in sensory or motor deficits, any loss of function in these structures is usually associated with a variety of psychological problems, including depression, bipolar disorder, obsessive–compulsive disorder, and schizophrenia.

Structural changes have been noted in the hippocampal formation, medial thalamus, and prefrontal cortex in schizophrenic subjects. Images obtained through positron emission tomography scans show that the amygdala, prefrontal cortex and medial thalamus are abnormally active in patients suffering from severe unipolar and bipolar depression.

The complete removal of the amygdala and other nearby structures in laboratory settings causes specific changes in animal behavior called the Klüver-Bucy syndrome, whose characteristic symptoms are a complete lack of fear of anything, extreme curiosity about everything, rapid loss of short-term memory, tendency to place everything in the mouth and sometimes even trying to eat solid objects, and a sex drive so strong that it leads to attempts to copulate with immature animals, animals of the wrong sex, or even animals of a different species. Although similar lesions in human beings are rare, afflicted people respond in a manner not too different from that of the affected animal.

When Stress Hurts: Central Nervous System

In establishing the connection between the onset of psychogenic pain and stress, it is important to notice that pain and stress share the same central nervous system (CNS) pathways and structures. In this second post in the series on the close association between psychological stress and psychogenic pain, we’ll take a look at these shared structures.

CNS Structures Mobilized by Pain and Stress

PendulumThe body’s response to pain engages a large number of CNS structures that are often the same as the ones activated by the stress reaction. The afferent pathways that carry pain signals connect to the thalamic nuclei and from there to the somatosensory, insular and anterior cingulate (ACC) portions of the brain cortex. A recent functional MRI (fMRI) study (Keltner et al., 2006) on the effects of pain expectation on pain transmission provides the best evidence for the activation of the rostral ACC (rACC), periaqueductal gray (PAG), and medial prefrontal cortex. This and other imaging studies provide evidence of a bidirectional pain pathway receiving input from the limbic system and the amygdala, converging on the PAG, traveling through the pontomedullar nuclei, and controlling spinal pain transmission neurons (Fields, 2000; Fields & Martin, 2001). As the authors of this study point out, “expectation for a higher intensity noxious stimulus increases subjectively experienced pain intensity in part through the action of a descending pathway that facilitates nociceptive transmission at and/or caudal to the region of the contralateral nucleus cuneiformis (nCF)” (p. 4442). The nCF, in humans and other primates, has a composition similar to the PAG and its neurons project directly into the rostroventral medulla, the hypothalamus and the amygdala, all structures directly involved in modulation of the stress reaction.

PMR_muscle-crampsLikewise, the body’s stress response engages a large number of the same CNS structures, specifically certain subregions of the hypothalamus such as the paraventricular nucleus (PVN), the amygdala, and the periaqueductal grey; and certain cortical brain structures, such as the medial prefrontal cortex and subregions of the anterior cingulate and insular cortices (Maier, 2003). These structures provide output to the pituitary and pontomedullar nuclei, which in their turn stimulate the body’s neuroendocrine secretions, as well as to the hypothalamic-pituitary-adrenal (HPA) axis, the endogenous pain modulation system, and the ascending aminergic pathways. The feedback controlling the stress response is provided by the serotonergic (raphe) and noradrenergic (locus ceruleus) structures and by the levels of glucocorticoids in the blood stream, which provide inhibitory impulses to the medial prefrontal cortex and to the hippocampus. Corticotrophin releasing hormone (CRH) is the fundamental chemical substances mediating the stress response, which is secreted by PVN, amygdala, and locus ceruleus neurons. Acute or chronic stress can temporarily or permanently modify the level of responsiveness and output of the CNS to stress (Bennett et al., 1998).

Sharing Pathways, Sharing Outcomes

With this significant convergence of pathways, neurochemical activity and CNS structure activation, it should come as no surprise that acute stress can provoke physical pain, often in the head, the muscles, and the abdominal region. Equally unsurprising is that pain, especially when sharp and unexpected, is in itself a cause of stress that mobilizes the body into immediate action (think of the hand that immediately goes to cover the cut or the burn). Continuous pain, of any origin, is inherently stressful. Continuous stress can be, and often is, manifested by otherwise unexplained (thus psychogenic) physical pain.

Previously in this series: When Stress Hurts: Psychogenic Pain


  • The Neurochemistry of Psychogenic Pain and Stress
  • Psychological Stressors and the Sudden Appearance of Psychogenic Pain
  • Fibromyalgia, Severe Headaches and Other Stress-Related Misery
  • Medical and Non-Medical Treatments for Stress and Psychogenic Pain

Something Needs to Be Done About Hostility!

Ginetto at Hostility is stressful, both ways. To giver and receiver alike, hostility metes out its toxic charge of badness. Far from being a true relief for frustration, pent-up anger, or unexpressed emotion, a sudden explosion of hostility merely releases a burst of energy and briefly discharges some muscle tension. Beyond these ephemeral effects, it is hard to find a good justification for hostility in everyday situations. So why is it so prevalent?

Two reasons account for hostility’s “popularity.” The first is the genetically programmed aggression instinct, which, in its proper setting and situation, can be useful (in a competitive physical sport like football), or downright vital (in combat situations, to fight off an aggressor, or in other situations of danger when a calm and relaxed demeanor would be clearly out of place). We can be aggressive and hostile by design, but we are also given a brain that helps mitigate the limbic system’s rage of emotions, and the amygdala’s watchfulness against aggressors, real or perceived as they may be.

The second reason for the pervasive presence of hostility is a misfiring of the very structures of the brain that are supposed to help us regulate it. Poor regulation of negative emotions can unleash hostility. Notoriously so, antisocial personalities have little to no self-regulation of hostility and most of the times this lands them in jail. Many more individuals, though, fall short of law-breaking hostility but still exhibit plenty of it in everyday situations (behind the wheel of their car, while waiting in line, with customer service people, with their spouses, children, friends) to make life more stressful for themselves and for anyone they come in contact with.

Steve Slater on At the other end of the spectrum, hostility, while present as a natural emotion, can be sublimated into a more productive and less threatening display of displeasure with someone or a situation.  Well-regulated hostility and aggressive instinct become assertiveness, standing up for one’s right, engaging in an passionate discussion. It can also sublimate into artistic pursuit, an all-out workout at the gym, or humor. A recent example of the latter was portrayed by JetBlue flight attendant Jeff Slater. Justifiably enraged by an unjustifiably aggressive passenger, Mr. Slater regulated down his hostility, expressed himself aloud on the plane’s PA system, grabbed a couple of beers, activated the emergency slide, slid down to the tarmac, ran for his car and drove home.

Hostility and (Bad) Health

Negative emotional states, such as anger and hostility, when they persist over time and become chronic, can negatively impact health. The risk to health comes through a number of mechanisms, including engaging in high-risk behavior (verbally provoking, physically attacking others), loss of social support (no one wants to be with a chronically hostile individual), and social isolation.

Chronic negative emotions also induce a semi-permanent activation of the stress reaction and cause sustained systemic inflammation, both of which increase the risk of disease. Research on hostility and aggressive personality has clearly established a link between these emotional states and heart disease, heart attacks, and cardiac-related mortality. Hostility not only contributes to a higher incidence and increased severity of heart disease, but is also related to symptoms of metabolic syndrome, including insulin resistance.

What Can Be Done?

Taking a page from Mr. Slater’s playbook, humor is one of the highest levels of sublimation that can be achieved in down-regulating aggression and hostility. Other forms of self-regulation of hostility (which incidentally are also ways of dealing with stressful situations in general) can be listed as follows:

  • Anticipation (the ability to anticipate the consequences of hostility and evaluate alternative responses)
  • Affiliation (turning to others for help and support, initiating a dialogue instead of a confrontation)
  • Altruism (taking into account the needs of others, and being able to contain rather than meet their aggression head on)
  • Humor (finding the amusing and the ironic in the situation)
  • Self-assertion (expressing feelings and thoughts directly and openly, but without resorting to verbal or physical violence)
  • Self-observation (reflecting on one’s own reactions and regulating them appropriately, before the explosion occurs)
  • Sublimation (channeling negative feelings into positive behaviors, i.e. taking it out on gym equipment, a good run, a distracting activity)
  • Suppression (intentionally avoiding catastrophic, negative and pessimistic thoughts that can lead to aggression).

Stress, As Seen Through the Eye of Science

Bazille at Stresshacker.comWhen science looks at stress, the focus is on the body/mind interaction or, more precisely, on its psychophysiological mechanisms. Traveling back in time from our present condition to conception, we can see that our genes and the environment in which we grow up (in which our genes are expressed) determine how we respond to stress as adults. Our genetic and environmental differences (the nature or nurture of who we are) help explain how individuals exposed to the same stressful situation can have an entirely different reaction. Some can adapt successfully to the stressor (albeit not without discomfort), while others experience more severe immediate trauma and long-term emotional problems, such as PTSD.

During specific developmental periods, such as infancy, puberty, adolescence, adulthood, or maturity, certain stressors are almost certain to occur and are understood to be typical and appropriate to the process of maturation and change. The earliest such stressor is the effect of caregiving styles, which stems from the parents’ psychological state. An attentive and nurturing style produces vastly different effects on the child’s later adaptation to stress than a harsh, unforgiving or neglectful one. In adolescence, patterns of behavior and emotional reactivity—including the stress reaction—begin to crystallize and become fully set in early adulthood.

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Is Stress Entertainment?

Avatar at The rep is that stress is to be avoided. The reality is otherwise. Stress is avidly watched, read, and heard because, contrary to what we think we believe about it, stress is entertaining. Why?

The truth is, stress sells—in movies, books, quiz shows, talent shows, and crime scene dramas. Not always and not for everyone, to be sure, but in vast numbers of book plots, screenplays, TV storylines, in radio plays, and theater plays, stress reigns supreme.

The surface reason is that stressful situations, when they are happening to someone else as in most forms of entertainment, hold our attention. Peaceful, restful, and relaxing situations, when we watch them happening to someone else, generally do not. There is not much fun in reading about someone having a really quiet day when nothing much is happening, but isn’t it great to watch a-thrill-every-second action on the big screen? Indeed, there is a deeper, genetically programmed reason why stress can be fun.

What’s the Fun in Stress?

To understand what’s happening, we must step back and consider the mechanics of stress. When we perceive a threat (a risk, a danger, a challenge), our mind is instantly alerted by the stress reaction that we experience in the body. Most often, this consists of increased heart beat, elevated blood pressure, muscle tension, and a release of excitatory hormones into the blood stream (cortisol, epinephrine, adrenaline), plus a host of other biological changes that very quickly get us ready for action. Now, what is interesting here is that, in addition to mobilizing the body, the excitatory hormones also generate a certain amount of pleasurable sensations. Is this nature’s little joke, or what?

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iPhone, iPad, iBrain: A Multitasker Paradise?

Multitasking at Here’s a (very) short history of information explosion: oral poetry; carved tablets; papyrus; illuminated manuscripts; printing press; radio; television; computer; iPhone; iPad. At each turn, the volume and quality of available information grew, first geometrically, then exponentially. Availability has now far exceeded the capacity, and some say the need, of the human brain to receive, decode, and make use of the data. Volume has also created an additional stressor that was unknown until the latter part of the 20th century: information overload.

Today more than ever, we are exposed to a far larger volume of sensory input than our senses and brain can process. Billions of individual bits of information compete for our attention, requiring us to rapidly determine which needs to be processed, remembered, or used for action. Information can be just data (it’s now 7:15pm) but it can also carry an emotional value (it’s later than I thought!). Emotion-laden stimuli have a special advantage in the competition for our limited attention resources because the correct evaluation of an emotional stimulus may be critical in determining whether it represents a threat (oh no, I’ll miss the start of the game!) or a reward (good, I wont’ have to sit through the previews). See this post on the value of emotion as information.

In spite of the enormous amount of valuable and potentially interesting information that can be ours just for the asking (or the thumbing), more than 99% will not be accessed, processed or remembered. The greater part of the remaining 1% that makes it to our eyes and ears will be discarded by the brain as irrelevant and unimportant. So we are left with an almost insignificant sliver of information that manages to be retained and used in some way. Pity, one might say. Thank goodness, says I.

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Stress Hardware Reviews: The Hippocampus

clip_image001What brain structures rouse us from inactivity and set in motion our defense mechanisms when a stressor is perceived? Predictably, the brain’s older and more primordial area, the so-called animal brain, where the hypothalamus, the amygdala, the hippocampus, the septum area, the basal ganglia and the thalamus are located. These structures, collectively called the limbic system, are interconnected and work together to initiate motor and other functional activities of the brain that mobilize the body. In this post about stress hardware, we discuss the hippocampus.

Virtually any experience perceived by the five senses appears to cause the activation of at least some part of the hippocampus. The hippocampus in turn redistributes these sensory signals to the thalamus, the hypothalamus, and other parts of the limbic system. Thus, the hippocampus acts as an important switching center through which incoming sensory signals are retransmitted and initiate behavioral reactions for different purposes. Its importance has been demonstrated empirically: experimental artificial stimulation of the hippocampus can induce a wide variety of behavioral patterns such as pleasure, rage, passivity, or excessive sexual drive.

The cells of the hippocampus appear to be especially sensitive to the effects of various stressors. Although not directly involved in the stress response, its ventral regions appear to exercise a regulatory influence on the hypothalamic-pituitary-adrenal (HPA) axis activity and are also a primary target for elevated glucocorticoid levels. The glucocorticoid hormones owe their name to their important effects on blood glucose concentration, which is the principal source of energy of the human cell. They also regulate protein and fat consumption, and the utilization of carbohydrates to produce additional quantities of energy. Cortisol is the principal glucocorticoid. Read more

Stress Hardware Review: The Amygdala


There are things I cannot do. I cannot watch my people suffer. I cannot sit when something must be done. I cannot judge those who are different. There are things I cannot do. Run. Hide. Ignore. There are things I cannot do. But there are certainly things I will do!

Padmé Amidala in Star Wars: Clone Wars

One of the most important structures of the brain’s limbic system is the amygdala, which in Queen Amidala’s imaginary brain produced behavior that was characteristically cool and aloof at times, forceful and passionate at others, but always kept in balance by poise and careful deliberation. An exemplar of good stress management.

amygdala The human amygdala is an almond-shaped double  complex (one on each side of the brain) of multiple small nuclei located immediately beneath the cerebral cortex of the medial anterior pole of each temporal lobe. It has abundant bidirectional connections with the hypothalamus as well as with other areas of the limbic system. The amygdala is understood to be a behavioral awareness area that operates at a semiconscious level. It also appears to project into the limbic system one’s current status in relation to both surroundings and thoughts. The most important function of the amygdala is to make the person’s behavioral response appropriate for each occasion… or not, as the case may be.

What specific stress behaviors are directly regulated by the amygdala? We can only infer, as the Maker did not provide a user manual, through observing what happens when the amygdala is accidentally or intentionally removed. Take the jump to find out.

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