Being
Present
Understanding
Anxiety and Managing Stress
Your heart
races, your palms sweat, your throat clenches, but you have to move forward.
“I just can’t
go in. I get so scared. I can’t even say my name.”
“I always feel
just a little bit on edge.” “I jump
when someone enters the rooms.”
“ I am angry
and just not myself.”
Charles could
no longer do his job because of the after hours social events. Walking into a room of known and new people
made him nervous and sweaty. He always
bolted before he made it to the buffet.
John was
referred by his EAP for emotional outbursts. His anger always seemed right
beneath, if not on top of, the surface. “The house, the kids the job the
parents, the roof.... I just can’t get to
sleep anymore.”
There are many faces to stress and anxiety. There are everyday levels of these energies
that may motivate us to accomplish the things that are necessary and inspire us
to finish the projects that loom before us.
However, these energies become clinical issues when they interfere with
our everyday functioning and quality of life.
They may disturb our eating, our family life, our job performance, our
sleep and dreams. The mechanism of fear
that often protects us from danger breaks out of its protective mode and
immobilizes us. The media has focused
attention on stress and anxiety lately due to the world events and the
economy. People who had previously envisioned
their life with more ease are finding themselves up against major obstacles to
retirement. National security is an ongoing question with the oft-repeated
assurance that there will be another attack.
As we approached the anniversary of Sept 11, we were inundated with
images and stories reflecting the horror and grief of that day. It would probably be less likely to not be
experiencing a fair level of stress and anxiety at this time. The key as a clinician is to decide what
level of intervention and treatment your client might require. With all
successful approaches, dealing with stress in the present, ‘the here and now’,
is critical. It is in the present
moment that any change, if possible, can be made. To decrease stress and anxiety we must decrease our tendencies to
dwell on the past and to worry about the future. Our approach may include psychodynamic techniques to uncover the
past stimuli, but it will be the working on the trauma in the present where the
healing will take place. This concept
sounds far more simplistic than it is to put in practice. “Being present” has been part of many
healing traditions for centuries and people continue to struggle with this
challenge.
To address anxiety and stress we must examine the
effects on the body, mind and spirit.
First we will look briefly at the biology underlying stress and
anxiety. Then, we will proceed to
examine specific life stressors. We will then give resources and ideas for
stress relief that may be included in your practice. Finally, the greater part of this course will anxiety disorders and effective treatments
for them.
The Biology of Stress and Anxiety
Your heart races, your palm sweats, your throat clenches but you
know you have to move forward.
‘I just can’t go in; I get so scared, I can’t even say my
name.”
“I always feel just a little bit on edge.” I jump when someone enters the rooms. I am angry and just not myself.”
These energies derive from a fear response in the brain and body. It is necessary for our survival that we have a healthy fear response that alerts us to any impending danger. It is only when this fear response is attached to some past event reoccurring in one’s memory or unforeseen future worries, that it can become incapacitating in its intensity. It the case of traumatic stress, it may be several months before the anxiety response can settle. In researching the impact of world news on our physical bodies, the suggestion has been made that we, as humans, want to react with action to help when we see human suffering. However, in today’s world the suffering we witness via media is in much larger proportion and more distant lands than we can immediately impact. This can leave the body with a heightened sense of stress and anxiety. With my clients, who are already on overload, I encourage them to take a ‘media fast’ and allow their brains and emotions some ‘down time’.
From The Surgeon General’s Report on Mental Health Chapter 4
Etiology of Anxiety Disorders
The etiology of most anxiety disorders, although not fully understood, has come into sharper focus in the last decade. In broad terms, the likelihood of developing anxiety involves a combination of life experiences, psychological traits, and/or genetic factors. The anxiety disorders are so heterogeneous that the relative roles of these factors are likely to differ. Some anxiety disorders, like panic disorder, appear to have a stronger genetic basis than others (National Institute of Mental Health [NIMH], 1998), although actual genes have not been identified. Other anxiety disorders are more rooted in stressful life events.
It is not clear why females have higher rates than males of most anxiety disorders, although some theories have suggested a role for the gonadal steroids. Other research on women’s responses to stress also suggests that women experience a wider range of life events (e.g., those happening to friends) as stressful as compared with men who react to a more limited range of stressful events, specifically those affecting themselves or close family members (Maciejewski et al., 1999).
What the myriad of anxiety disorders has in common is a state of increased arousal or fear (Barbee, 1998). Anxiety disorders often are conceptualized as an abnormal or exaggerated version of arousal. Much is known about arousal because of decades of study in animals2 and humans of the so-called “fight-or-flight response,” which also is referred to as the acute stress response. The acute stress response is critical to understanding the normal response to stressors and has galvanized research, but its limitations for understanding anxiety have come to the forefront in recent years, as this section later explains.
In common parlance, the term “stress” refers either to the external stressor, which can be physical or psychosocial in nature, as well as to the internal response to the stressor. Yet researchers distinguish the two, calling the stressor the stimulus and the body’s reaction the stress response. This is an important distinction because in many anxiety states there is no immediate external stressor. The following paragraphs describe the biology of the acute stress response, as well as its limitations, in understanding human anxiety. Emerging views about the neurobiology of anxiety attempt to integrate and understand psychosocial views of anxiety and behavior in relation to the structure and function of the central and peripheral nervous system.
Acute Stress Response
When a fearful or threatening event is perceived, humans react
innately to survive: they either are ready for battle or run away (hence the
term “fight-or-flight response”). The nature of the acute stress response is
all too familiar. Its hallmarks are an almost instantaneous surge in heart
rate, blood pressure, sweating, breathing, and metabolism, and a tensing of
muscles. Enhanced cardiac output and accelerated metabolism is essential for
mobilizing fast action. The host of physiological changes activated by a
stressful event is unleashed in part by activation of a nucleus in the brain
stem called the locus ceruleus. This nucleus is the origin of most
norepinephrine pathways in the brain. Neurons using norepinephrine as their
neurotransmitter project bilaterally from the locus ceruleus along distinct
pathways to the cerebral cortex, limbic system, and the spinal cord, among
other projections.
Normally, when someone is in a serene, unstimulated state, the “firing” of neurons in the locus ceruleus is minimal. A novel stimulus, once perceived, is relayed from the sensory cortex of the brain through the thalamus to the brain stem. That route of signaling increases the rate of noradrenergic activity in the locus ceruleus, and the person becomes alert and attentive to the environment. If the stimulus is perceived as a threat, a more intense and prolonged discharge of the locus ceruleus activates the sympathetic division of the autonomic nervous system (Thase & Howland, 1995). The activation of the sympathetic nervous system leads to the release of norepinephrine from nerve endings acting on the heart, blood vessels, respiratory centers, and other sites. The ensuing physiological changes constitute a major part of the acute stress response. The other major player in the acute stress response is the hypothalamic-pituitary-adrenal axis, which is discussed in the next section.
In the 1980s, the prevailing view was that excess discharge of the locus ceruleus with the acute stress response was a major contributor to the etiology of anxiety (Coplan & Lydiard, 1998). Yet over the past decade, the limitations of the acute stress response as a model for understanding anxiety have become more apparent. The first and most obvious limitation is that the acute stress response relates to arousal rather than anxiety. Anxiety differs from arousal in several ways (Barlow, 1988; Nutt et al., 1998). First, with anxiety, the concern about the stressor is out of proportion to the realistic threat. Second, anxiety is often associated with elaborate mental and behavioral activities designed to avoid the unpleasant symptoms of a full-blown anxiety or panic attack. Third, anxiety is usually longer lived than arousal. Fourth, anxiety can occur without exposure to an external stressor.
Other limitations of this model became evident from a lack of support from clinical and basic research (Coplan & Lydiard, 1998). Furthermore, with its emphasis on the neurotransmitter norepinephrine, the model could not explain why medications that acted on the neurotransmitter serotonin (the selective serotonin reuptake inhibitors, or SSRIs) helped to alleviate anxiety symptoms. In fact, these medications are becoming the first-line treatment for anxiety disorders (Kent et al., 1998). To probe the etiology of anxiety, researchers began to devote their energies to the study of other brain circuits and the neurotransmitters on which they rely. The locus ceruleus still participates in anxiety but is understood to play a lesser role.
New Views About the Anatomical and Biochemical
Basis of Anxiety
An exciting new line of research proposes that anxiety engages a
wide range of neurocircuits. This line of research catapults to prominence two
key regulatory centers found in the cerebral hemispheres of the brain—the
hippocampus and the amygdala. These centers, in turn, are thought to activate
the hypothalamic-pituitary-adrenocortical (HPA) axis3
(Goddard & Charney, 1997; Coplan & Lydiard, 1998; Sullivan et al.,
1998). Researchers have long established the contribution of the HPA axis to
anxiety but have been perplexed by how it is regulated. They are buoyed by new
findings about the roles of the hippocampus and the amygdala.
The hippocampus and the amygdala govern memory storage and emotions, respectively, among their other functions. The hippocampus is considered important in verbal memory, especially of time and place for events with strong emotional overtones (McEwen, 1998). The hippocampus and amygdala are major nuclei of the limbic system, a pathway known to underlie emotions. There are anatomical projections between the hippocampus, amygdala, and hypothalamus (Jacobson & Sapolsky, 1991; Charney & Deutch, 1996; Coplan & Lydiard, 1998).
Studies of emotional processing in rodents (LeDoux, 1996; Rogan & LeDoux, 1996; Davis, 1997) and in humans with brain lesions (Adolphs et al., 1998) have identified the amygdala as critical to fear responses. Sensory information enters the lateral amygdala, from which processed information is passed to the central nucleus, the major output nucleus of the amygdala. The central nucleus projects, in turn, to multiple brain systems involved in the physiologic and behavioral responses to fear. Projections to different regions of the hypothalamus activate the sympathetic nervous system and induce the release of stress hormones, such as CRH.4 The production of CRH in the paraventricular nucleus of the hypothalamus activates a cascade leading to release of glucocorticoids from the adrenal cortex. Projections from the central nucleus innervate different parts of the periaqueductal gray matter, which initiates descending analgesic responses (involving the body's endogenous opioids) that can suppress pain in an emergency, and which also activates species-typical defensive responses (e.g., many animals freeze when fearful).
Anxiety differs from fear in that the fear-producing stimulus is either not present or not immediately threatening, but in anticipation of danger, the same arousal, vigilance, physiologic preparedness, and negative affects and cognitions occur. Different types of internal or external factors or triggers act to produce the anxiety symptoms of panic disorder, agoraphobia, post-traumatic stress disorder, specific phobias, and generalized anxiety disorder, and the prominent anxiety that commonly occurs in major depression. It is currently a matter of research to determine whether dysregulation of these fear pathways leads to the symptoms of anxiety disorders. It has now been established, using noninvasive neuroimaging, that the human amygdala is also involved in fear responses. Fearful facial expressions have been shown to activate the amygdala in MRI studies of normal human subjects (Breiter et al., 1996). Functional imaging studies in anxiety disorders, such as PET studies of brain activation in phobias (Rauch et al., 1995), are also beginning to investigate the precise neural circuits involved in the anxiety disorders.
What is especially exciting is that neuroimaging has furnished direct evidence in humans of the damaging effects of glucocorticoids. In people with post-traumatic stress disorder, neuroimaging studies have found a reduction in the size of the hippocampus. The reduced volume appears to reflect the atrophy of dendrites—the receptive portion of nerve cells—in a select region of the hippocampus. Similarly, animals exposed to chronic psychosocial stress display atrophy in the same hippocampal region (McEwen & Magarinos, 1997). Stress-induced increases in glucocorticoids are thought to be responsible for the atrophy (McEwen, 1998). If the hippocampus is impaired, the individual is thought to be less able to draw on memory to evaluate the nature of the stressor (McEwen, 1998).
Neurotransmitter Alterations
There are many neurotransmitter alterations in anxiety
disorders. In keeping with the broader view of anxiety, at least five
neurotransmitters are perturbed in anxiety: serotonin, norepinephrine,
gamma-aminobutyric acid (GABA), corticotropin-releasing hormone (CRH),5
and cholecystokinin (Coplan & Lydiard 1998; Rush et al., 1998). There is
such careful orchestration between these neurotransmitters that changes in one
neurotransmitter system invariably elicits changes in another, including
extensive feedback mechanisms. Serotonin and GABA are inhibitory
neurotransmitters that quiet the stress response (Rush et al., 1998). All of
these neurotransmitters have become important targets for therapeutic agents
either already marketed or in development (as discussed in the section on
treatment of anxiety disorders).
Psychological Views of Anxiety
There are several major psychological theories of anxiety:
psychoanalytic and psychodynamic theory, behavioral theories, and cognitive
theories (Thorn et al., 1999). Psychodynamic theories have focused on symptoms
as an expression of underlying conflicts (Rush et al., 1998; Thorn et al.,
1999). Although there are no empirical studies to support these psychodynamic
theories, they are amenable to scientific study (Kandel, 1999) and some
therapists find them useful. For example, ritualistic compulsive behavior can
be viewed as a result of a specific defense mechanism that serves to channel
psychic energy away from conflicted or forbidden impulses. Phobic behaviors
similarly have been viewed as a result of the defense mechanism of
displacement. From the psychodynamic perspective, anxiety usually reflects more
basic, unresolved conflicts in intimate relationships or expression of anger.
More recent behavioral theories have emphasized the importance of two types of learning: classical conditioning and vicarious or observational learning. These theories have some empirical evidence to support them. In classical conditioning, a neutral stimulus acquires the ability to elicit a fear response after repeated pairings with a frightening (unconditioned) stimulus. In vicarious learning, fearful behavior is acquired by observing others’ reactions to fear-inducing stimuli (Thorn et al., 1999). With general anxiety disorder, unpredictable positive and negative reinforcement is seen as leading to anxiety, especially because the person is unsure about whether avoidance behaviors are effective.
Cognitive factors, especially the way people interpret or think about stressful events, play a critical role in the etiology of anxiety (Barlow et al., 1996; Thorn et al., 1999). A decisive factor is the individual’s perception, which can intensify or dampen the response. One of the most salient negative cognitions in anxiety is the sense of uncontrollability. It is typified by a state of helplessness due to a perceived inability to predict, control, or obtain desired results (Barlow et al., 1996). Negative cognitions are frequently found in individuals with anxiety (Ingram et al., 1998). Many modern psychological models of anxiety incorporate the role of individual vulnerability, which includes both genetic (Smoller & Tsuang, 1998) and acquired (Coplan et al., 1997) predispositions. There is evidence that women may ruminate more about distressing life events compared with men, suggesting that a cognitive risk factor may predispose them to higher rates of anxiety and depression (Nolen-Hoeksema et al., in press).
Please read the following articles on the biology of stress and anxiety.
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It is well known that the early months and years of life are critical for brain development. But the question remains: just how do early influences act on the brain to promote or challenge the developmental process? Research has suggested that many both positive and negative experiences, chronic stressors, and various other environmental factors may affect a young child's developing brain. And now, studies involving animals are revealing in greater detail how this may occur. One important line of research has focused on brain systems that control stress hormones—cortisol, for example.1,2 Cortisol and other stress hormones play an important role in emergencies: they help our bodies make energy available to enable effective responses, temporarily suppress the immune response, and sharpen attention. However, a number of studies conducted in people with depression indicate that excess cortisol released over a long time span may have many negative consequences for health.3,4,5 Excess cortisol may cause shrinking of the hippocampus, a brain structure required for the formation of certain types of memory. In experiments with animals, scientists have shown that a well-defined
period of early postnatal development may be an Striking differences were seen in rat pups removed from their mothers for periods of 3 hours a day, a model of neglect compared to pups that were not separated. After 3 hours, the mother rats tended to ignore the pups, at least initially, upon their return. In sharp contrast to those pups that were greeted attentively by their mothers after a short absence, the "neglected" pups were shown to have a more profound and excessive stress response in subsequent tests. This response appeared to last into adulthood.7,8 The implications of these animal studies are worrisome. However, research is in progress to determine the extent to which the hypersensitive or dysregulated stress response of "neglected" rat pups can be reversed if, for example, foster mothers are provided who will groom the pups more intensely, or if the animals are raised in an "enriched" environment following their separation. An enriched setting may include, for example, a diverse and varied diet, a running wheel, mazes, and changes of toys. Animal investigators are well aware of another kind of long-term change, again rooted in the first days of life. Laboratory rats are often raised in shoebox cages with few sources of stimulation. Scientists have compared these animals to rats raised in an enriched environment and found that the "privileged" rats consistently have a thicker cerebral cortex and denser networks of nerve cells than the "deprived" rats.9,10 Another study recently reported that infant monkeys raised by mothers who experienced unpredictable conditions in obtaining food showed markedly high levels of cortiocotropin releasing factor (CRF) in their cerebrospinal fluid and, as adults, abnormally low levels of cerebrospinal fluid cortisol.11 This is a pattern often seen in humans with post-traumatic stress disorder and depression. 5 The distressed monkey mothers, uncertain about finding food, behaved inconsistently and sometimes neglectfully toward their offspring. The affected young monkeys were abnormally anxious when confronted with separations or new environments. They were also less social and more subordinate as adult animals. It is far too early to draw firm conclusions from these animal studies about the extent to which early life experience produces a long-lived or permanent set point for stress responses, or influences the development of the cerebral cortex in humans. However, animal models that show the interactive effect of stress and brain development deserve serious consideration and continued study. For More Information ----------------------------------- All material in this fact sheet is in the public domain and may be copied or reproduced without permission from the Institute. Citation of the source is appreciated. NIH Publication No. 01-4603 ----------------------------------- References |
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important
determinant of the capacity to handle stress throughout life.Updated: January 01, 2001
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"Stress, the Brain,
and Our Mental and Physical Health"
Bruce S. McEwen, Ph.D.,
is Professor and Head, Harold and Margaret Milliken Hatch Laboratory of
Neuroendocrinology at the Rockefeller University.
Objective physiological evidence demonstrates
that our life experiences impact the health of our brains. The overused
shorthand term for that impact is "stress," as in, "I feel
stressed out."
The autonomic and sympathetic nervous systems
produce the physiologic stress response. The autonomic nervous system produces
catecholamines and regulates the production of cortisol. The sympathetic
nervous system includes the adrenal glands, which produce both adrenaline and
cortisol.
Physical activity, a state of arousal, and
fear stimulate adrenaline production. Cortisol production requires similar
circumstances but a real sense of threat or change, particularly in relation to
unexpected events and strong emotions.
A person speaking before an audience for the
first time may experience increases in adrenaline and cortisol levels, blood
pressure, and heart rate. After several speeches, most people's adrenaline
continues to increase, which is good because they must think on their feet, but
their cortisol levels do not rise. The production of stress hormones is an
adaptive and protective event without which we would not survive very long.
If these systems are overactive for too long,
they can accelerate certain kinds of disease processes. Catecholamine and
adrenaline affect cell surfaces. Cortisol affects cell receptors in the
nucleus, regulating metabolism in the liver and aspects of brain function,
influencing the immune system and cardiovascular function, and impacting heart
rate and blood pressure.
Cortisol increases appetite and helps to
mobilize energy resources, but if we satisfy our appetites with junk food and
do not exercise, we risk developing hypercortisolemia, a factor in promoting
Type II diabetes.
Our behavior dictates the choices we make
about food and exercise just as it influences how we respond to conflict or
negative experiences. Do we always feel hostility and anger? Repeated blood
pressure surges and inadequate buffering in the vascular system accelerate
atherosclerosis, increasing our risk for a myocardial infarction. While none of
us can completely eliminate stress from our lives, modifying our behavior can
change the way we react to it.
Stress also has a negative effect on the
hippocampus. The hippocampus contains receptors for cortisol and plays a role
in shutting off the stress response. Damage to the hippocampus can impact many
systems of the body. Repeated increases of cortisol can and have recently been
shown to impair declarative memory. Exposure to an enriched environment or
learning something new increases neurogenesis in the dentate gyrus of the
hippocampus; stress impairs neurogenesis.
Depressive illness, truly a systemic disorder,
offers a classic example of how stress can physically affect the central nervous
and cardiovascular systems. The hippocampus is plastic and, in the short run,
seems capable of withstanding the effects of chronic stress, albeit with some
impairment of cognitive function. The hippocampus of people with recurrent
depressive illness, however, becomes 10-12 percent smaller over time; using
magnetic resonance imaging (MRI), some researchers have seen evidence that
suggests permanent damage. This hippocampal atrophy seems not to be a function
of age of the subjects but of the duration of the depressive illness.
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. Imaging Emotion in the Brain
In
the last few years, there has been a revolution in the study of emotions. Our
emotions—love, fear, anger, and desire—give coloration and meaning to
everything in life. Our emotions are indispensable whenever we choose to
pursue one goal and not another. The derangement of emotions is what leads to
the profound pain and much of the disability experienced in mental illness.
The emotions were once thought to reside in the heart, but scientists know
now that they originate in the brain. New Imaging Tools
Brain Pathways
Fear
is the emotion that has been most successfully studied. Fear is required for
our survival, but when it is not regulated, it becomes responsible for anxiety disorders
and some of the symptoms of depression.
We have learned that fear depends on very specific circuits in the brain. In
fact, the way that the brain processes emotion is no different from the way
it processes vision or voluntary movements, which also rely on their own
specific circuitry. The
emotion of fear relies on pathways that involve a structure deep in our brains
called the amygdala.
The details of this circuitry have been worked out in rat models; however, a
series of studies that began in 1996 and have become increasingly
sophisticated have demonstrated that showing a fearful face to a normal
subject while scanning his/her brain permits us to see activation of the
amygdala and associated brain pathways. 1,2,3,4
Subsequent experiments have shown that if humans learn a connection between a
neutral signal and something noxious, like a loud buzzing sound, we actually
can observe the brain in the act of storing information about the signal that
predicts danger.5,6,7
We can see that the brain processes information about threat and fear even
when the person is not concentrating on it and may not even consciously
remember seeing the danger signal. Although
this research is still in its early phase, success to date in delineating
specific fear pathways has encouraged the investigations of emotional
pathways in mental illness. We are finding out, for example, whether phobias
hitchhike on the same pathways used by normal fear. Soon we will have
information about other emotions and conditions such as depression. Over
time, these tools will be used to study the effects of medications and psychological
therapies on mental illness. All material in this fact sheet is in the public domain and
may be copied or reproduced without permission from the Institute. Citation
of the source is appreciated. NIH
Publication No. 01-4601 ----------------------------------- References 1 Morris J, Frith C, Perrett D, et al. A
differential neural response in the human amygdala to fearful and happy
facial expressions. Nature, 1996; 383(6603): 812-15. 2 Breiter H, Etcoff N, Whalen P, et al. Response
and habituation of the human amygdala during visual processing of facial
expression. Neuron, 1996; 17(5): 875-87. 3 Whalen P, Rauch S, Etcoff N, et al. Masked
presentations of emotional facial expressions modulate amygdala activity
without explicit knowledge. Journal of Neuroscience, 1998; 18(1):
411-18. 4 Hariri A, Bookheimer S, Mazziotta J.
Modulating emotional responses: effects of a neocortical network on the
limbic system. Neuroreport, 2000; 11(1): 43-8. 5 Buechel C, Dolan R. Classical fear
conditioning in functional neuroimaging. Current Opinion in Neurobiology,
2000; 10(2): 219-23. 6 LaBar K, Gatenby J, Gore J, et al. Human
amygdala activation during conditioned fear acquisition and extinction: a
mixed-trial fMRI study. Neuron, 1998; 20(5): 937-45. 7 Morris J, Ohman A, Dolan R. Conscious and
unconscious emotional learning in the human amygdala. Nature, 1998;
393(6684): 467-70. |
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Updated:
January 01, 2001
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Background: The "fight-or-flight" response is generally regarded as the prototypic human response to stress. Physiologically, it is characterized by sympathetic nervous system activation, which ultimately results in the secretion of chemicals into the bloodstream mobilizing the behavioral response. Whether the response culminates in "fight" or "flight" is thought to depend on whether the threat or stressor is perceived as surmountable. Thus, an appropriate stress response is essential to survival. While this biobehavioral "fight-or-flight" theory has dominated stress research for the past 5 decades, it has been disproportionately based on studies of males. This is because females' greater cyclical variation in neuroendocrine responses presented a confusing and often uninterpretable pattern of results. As a result, the processes involved in stress responses in females are less well understood. Advance: A team of NIMH-supported scientists has formulated a theory that characterizes female responses to stress by a pattern they term "tend-and-befriend," rather than by "fight-or-flight." They believe that female stress responses have selectively evolved to simultaneously maximize the survival of self and offspring. Thus, the "tend-and-befriend" pattern involves females' nurturance of offspring under stressful circumstances, the exhibition of behaviors that protect them from harm (tending), and befriending ---namely, creating and joining social groups for the exchange of resources and to provide protection. They propose that these responses build on the biobehavioral attachment-caregiving processes that depend in part on oxytocin, estrogen and endogenous opioid mechanisms for the down-regulation of sympathetic and hypothalamic-pituitary-adrenocortical (HPA) responses to stress. A substantial neuroendocrine literature from animal studies (rats and nonhuman primates) provides support for these proposed mechanisms. These neuroendocrine models link to humans in that oxytocin, coupled with endogenous opioid mechanisms and other sex-linked hormones, fosters similar maternal and affiliative behaviors in both animals and humans in response to stress. Finally, literature on both human and nonhuman primates evidence substantial female preference to affiliate under stress compared to males. The "tend-and-befriend" pattern likely is maintained not only by sex-linked, neuroendocrine responses to stress, but by social and cultural roles as well. Implications: This interesting, new, theoretical model opens a fresh field of inquiry in stress research that has potential for closing some empirical gaps and addressing gender biases. For example, it examines other neurohormones (e.g., serotonin, prolactin, dopamine, etc.) that also may be implicated in these processes of stress-regulation, but that are not yet well understood in either males or females. It also examines the role of oxytocin in social bonds outside of the basic mother-offspring attachment processes commonly studied. [Biology, Knowledge: Molecular/ Cellular] Taylor SE, Cousino-Klein L, Lewis BP, Gruenewald TL, Gurung RAR, and Updegraff JA: Biobehavioral responses to stress in females: Tend-and-befriend, not fight-or-flight. Psychological Review 107 (3): 411-429, 2000. |
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Updated: June 07, 2001
Continue to Life Stressors Chapter