stress
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(strĕs) 
n.
n.
- Importance, significance, or emphasis placed on something. See synonyms at emphasis.
- Linguistics.
- The relative force with which a sound or syllable is spoken.
- The emphasis placed on the sound or syllable spoken most forcefully in a word or phrase.
- The relative force of sound or emphasis given a syllable or word in accordance with a metrical pattern.
- A syllable having strong relative emphasis in a metrical pattern.
- Accent or a mark representing such emphasis or force.
- Physics.
- An applied force or system of forces that tends to strain or deform a body.
- The internal resistance of a body to such an applied force or system of forces.
- A mentally or emotionally disruptive or upsetting condition occurring in response to adverse external influences and capable of affecting physical health, usually characterized by increased heart rate, a rise in blood pressure, muscular tension, irritability, and depression.
- A stimulus or circumstance causing such a condition.
- A state of extreme difficulty, pressure, or strain: "He presided over the economy during the period of its greatest stress and danger" (Robert J. Samuelson).
- To place emphasis on: stressed basic fire safety.
- To give prominence to (a syllable or word) in pronouncing or in accordance with a metrical pattern.
- To subject to physical or mental pressure, tension, or strain.
- To subject to mechanical pressure or force.
- To construct so as to withstand a specified stress.
stress out Informal.
- To subject to or undergo extreme stress, as from working too much.
[Middle English stresse, hardship, partly from destresse (from Old French; see distress) and partly from Old French estrece, narrowness, oppression (from Vulgar Latin *strictia , from Latin strictus, past participle of stringere, to draw tight; see strait).]
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In psychology, a state of bodily or mental tension resulting from factors that tend to alter an existent equilibrium. Stress is an unavoidable effect of living and is an especially complex phenomenon in modern technological society. It has been linked to coronary heart disease, psychosomatic disorders, and various other mental and physical problems. Treatment usually consists of a combination of counseling or psychotherapy and medication.
For more information on stress, visit Britannica.com.
Generally, environmental events of a challenging sort as well as the body's response to such events. Of particular interest has been the relationship between stress and the body's adaptation to it on the one hand and the body's susceptibility to disease on the other. Both outcomes involve behavioral and brain changes as well as psychosomatic events, that is, changes in body function arising from the ability of the brain to control such function through neural output as well as hormones. One problem is that both environmental events and bodily responses have been referred to interchangeably as stress. It is preferable to refer to the former as the stressor and the latter as the stress response. The stress response consists of a cascade of neural and hormonal events that have short- and long-lasting consequences for brain and body alike. A more serious issue is how an event is determined to be a stressor. One view is to define a stressor as an environmental event causing a negative outcome, such as a disease. Another approach is to view stressors as virtually any challenge to homeostasis and to regard disease processes as a failure of the normal operation of adapative mechanisms, which are part of the stress response. With either view, it is necessary to include psychological stressors, such as fear, that contain implied threats to homeostasis and that evoke psychosomatic reactions. These are reactions that involve changes in neural and hormonal output caused by psychological stress. Psychosomatic reactions may lead to adaptive responses, or they may exacerbate disease processes. Whether the emphasis is on adaptation or disease, it is essential to understand the processes in the brain that are activated by stressors and that influence functions in the body. See also Homeostasis; Psychosomatic disorders.
Among the many neurotransmitter systems activated by stress is noradrenaline, produced by neurons with cell bodies in the brainstem that have vast projections up to the forebrain and down the spinal cord. Stressful experiences activate the noradrenergic system and promote release of noradrenaline; severe stress leads to depletion of noradrenaline in brain areas such as the hypothalamus. This release and depletion of noradrenaline stores results in changes at two levels of neuronal function: phosphorylation is triggered by the second-messenger cyclic AMP and occurs in the presynaptic and postsynaptic sites where noradrenaline is released and where it also acts; synthesis of new protein is induced via actions on the genome. Both processes enhance the ability of the brain to form noradrenaline when the organism is once again confronted with a stressful situation. Other neurotransmitter systems may also show similar adaptive changes in response to stressors. See also Noradrenergic system.
Stress also activates the neurally mediated discharge of adrenaline from the adrenal medulla and of hypothalamic hormones that initiate the neuroendocrine cascade, culminating in glucocorticoid release from the adrenal cortex. Thus, the activity of neurons triggered by stressful experiences, physical trauma, fear, or anger leads to hormone secretion that has effects throughout the body. Virtually every organ of the body is affected by stress hormones. The hypothalamic hormone (corticotrophin-releasing hormone) that triggers the neuroendocrine cascade directly stimulates the pituitary to secrete ACTH. In response to certain stressors, the hypothalamus also secretes vasopressin and oxytocin, which act synergistically with corticotrophin-releasing hormone on the pituitary to potentiate the secretion of ACTH. Various stressors differ in their ability to promote output of vasopressin and oxytocin, but all stressors stimulate release of corticotrophin-releasing hormone. Other hormones involved in the stress response include prolactin and thyroid hormone; the metabolic hormones insulin, epinephrine, and glucagon; and the endogenous opiates endorphin and enkephalin. See also Endorphins.
Of all the hormones in the endocrine cascade initiated by stress, the glucocorticoids are the most important because of their widespread effects throughout the body and in the brain. The brain contains target cells for adrenal glucocorticoids secreted in stress, and receptors in these cells are proteins that interact with the genome to affect expression of genetic information. Thus, the impact of stress-induced activation of the endocrine cascade that culminates in glucocorticoid release is the feedback of glucocorticoids on target brain cells. The effect is to alter the structure and function of the brain cells over a period of time ranging from hours to days.
In the case of noradrenaline, glucocorticoids have several types of feedback effects that modify how the noradrenergic system responds to stress. Glucocorticoids inhibit noradrenaline release, and they reduce the second-messenger response of brain structures such as the cerebral cortex to noradrenaline. Glucocorticoid feedback also affects the serotonin system, facilitating serotonin formation during stress but at the same time altering the levels of several types of serotonin receptors in different brain regions, which has the net effect of shifting the balance within the serotonergic system. Taken together, evidence points to a role of glucocorticoid secretion in leading to restoration of homeostatic balance by counteracting the acute neural events such as increased activity of noradrenaline and serotonin, which are turned on by stressful experiences. Other neurotransmitter systems may also respond to glucocorticoid action. Moreover, the other hormones activated by stress have effects on the brain and body that must be considered. See also Serotonin.
In general, stress hormones are protective and adaptive in the immediate aftermath of stress, and the organism is more vulnerable to many conditions without them. However, the same hormones can promote damage and accelerate pathophysiological changes, such as bone mineral loss, obesity, and cognitive impairment, when they are overproduced or not turned off. This wear-and-tear on the body has been called allostatic load. It is based upon the notion that allostasis is the active process of maintaining stability, or homeostasis, through change, and allostatic load is the almost inevitable cost to the body of doing so.
Stress hormone actions have important effects outside the brain on such systems as the immune response. Glucocorticoids and catecholamines from sympathetic nerves and the adrenal medulla participate in the mobilization and enhancement of immune function in the aftermath of acute stress. These effects improve the body's defense against pathogens but can exacerbate autoimmune reactions. When they are secreted chronically, the stress-related hormones are generally immunosuppressive; such effects can be beneficial in the case of an autoimmune disease but may compromise defense against a virus or bacterial infections. At the same time, glucocorticoids are important agents for containing the acute-phase response to an infection or autoimmune disturbance. In the absence of such containment, the organism may die because of the excessive inflammatory response. See also Immunology.
Besides affecting the immune response, stressors are believed to exacerbate endogenous depressive illness in susceptible individuals. Major depressive illness frequently results in elevated levels of cortisol in the blood. It is not clear whether the elevated cortisol is a cause or strictly a result of the brain changes involved in depressive illness. See also Affective disorders.
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A psychological condition occurring when individuals feel unable to cope with the demands being made on them. They also believe that this failure will have important consequences. This condition is sometimes called distress, to distinguish it from the positive or pleasant aspects of stressful situations (eustress). Stress is usually associated with feeling a lack of control and involvement in the decisions which affect life and work.
The jobs with the highest strain are those in which there is heavy pressure to perform, where hours and procedures are rigid, there is a threat of redundancy, there is little opportunity to learn new skills, and there is little involvement in decision making. Such jobs tend to be the least prestigious. Workers low in the hierarchy tend to experience the most stress. It is unclear how stress affects health, but one possibility is that it disturbs important systems in the body, such as the hormonal, nervous, or immune system.
Although it may not be possible to change jobs, the effects of stress can be relieved by exercise and a healthy diet. Regular aerobic exercise, consisting of a daily 40-minute brisk walk, can reduce anxiety by as much as 14 per cent. In stressful situations, those who exercise regularly tend to have less muscle tension and lower blood pressure than inactive people.
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Stress is a word derived from the Latin word stringere, meaning to draw tight, and was used in the seventeenth century to describe hardship and affliction. During the late eighteenth century (as Hinkle records), stress denoted ‘force, pressure, strain, or strong effort’, referring primarily to an individual, or to the individual's organs or mental powers.
Definitions of strain and load used in physics and engineering eventually began to influence our understanding of how stress affects individuals and their health. Under this concept, external forces (load) are seen as exerting pressure upon an individual, producing strain. Proponents of this view felt that they could measure the stress to which an individual is subjected, in the same way we can measure physical strain on a machine. While this concept looks at stress as an outside stimulus, an alternative concept defines stress as a person's response to a disturbance. As early as 1910, Sir William Osler explored the idea of stress and strain causing ‘disease’, when he saw a relationship between chest pains (angina pectoris) and a hectic pace of life. The idea that environmental forces could actually cause disease rather than just short-term ill health effects, and that people have a natural tendency to resist such forces, was seen in the work of Walter B. Cannon in the 1930s. Cannon studied the effects of stress in animals and people, and in particular studied the ‘fight or flight’ reaction. Through this reaction, people, as well as animals, will choose whether to stay and fight or try to escape when confronting extreme danger. Cannon observed that when his subjects experienced situations of cold, lack of oxygen, or excitement, he could detect physiological changes such as emergency adrenaline secretions. Cannon described these individuals as being ‘under stress’.
One of the first scientific attempts to explain the process of stress-related illness was made in 1946 by physician Hans Selye, who described three stages an individual encounters in stressful situations: (i) alarm reaction, in which an initial phase of lowered resistance is followed by countershock, during which the individual's defence mechanisms become active; (ii) resistance, the stage of maximum adaption and, hopefully, successful return to equilibrium for the individual. If, however, the stress agent continues or the defence mechanism does not work, he will move on to a third stage; (iii) exhaustion, when adaptive mechanisms collapse.
Critics of Selye's work say it ignores both the psychological impact of stress on an individual, and the individual's ability to recognize stress and act in various ways to change his or her situation.
Newer and more comprehensive theories of stress emphasize the interaction between a person and his or her environment, describing it as a response to internal or external pressures which reach levels that strain physical and psychological systems beyond their coping capacities.
In the 1970s Richard S. Lazarus suggested that an individual's stress reaction ‘depends on how the person interprets or appraises (consciously or unconsciously) the significance of a harmful, threatening, or challenging event.’ Lazarus' work disagrees with those who see stress simply as environmental pressure. Instead, the intensity of the stress experience is determined significantly by how well people feel they can cope with an identified threat. Any person who is unsure of his or her coping abilities, or is likely to feel helpless and overwhelmed.
Similarly, Tom Cox and colleagues in the late 1970s rejected the idea of looking at stress as simply either environmental pressures or physiological responses; they suggest that it can best be understood as ‘part of a complex and dynamic system of transaction between the person and his environment’ and criticize the mechanical model of stress: ‘Men and their organizations are not machines … Stress has to be perceived or recognized by man. A machine, however, does not have to recognize the load or stress placed upon it.’
By looking at stress as resulting from a misfit between an individual and his/her particular environment, we can begin to understand why one person seems to flourish in a certain setting, while another suffers. Tom Cummings and Cary Cooper in 1979 explored the stress process in a cybernetic framework as follows:
(i) Individuals, for the most part, try to keep their thoughts, emotions, and relationships with the world in a ‘steady state’.
(ii) Each factor of a person's emotional and physical state has a ‘range of stability’, in which that person feels comfortable. On the other hand, when forces disrupt one of these factors beyond the range of stability, the individual must act or cope to restore a feeling of comfort.
(iii) An individual's behaviour aimed at maintaining a steady state makes up his or her ‘adjustment process’, or coping strategies.
Accordingly, a stress is any force that puts a psychological or physical factor beyond its range of stability, producing a strain within the individual. Knowledge that a stress is likely to occur constitutes a threat to the individual. A threat can cause a strain because of what it signifies to the person.
Stress certainly involves a range of bodily reactions. Man is the product of many thousands of years of evolution, and to survive required a quick physical response to dangers. The body developed the ability to ‘rev-up’ for a short time. Cannon described this mobilization of forces as the ‘fight or flight’ reaction mentioned earlier. Primitive man expended this burst of energy and strength in physical activity, such as a life and death struggle or a quick dash to safety.
Modern man has retained his hormonal and chemical defence mechanisms through the millenia. But for the most part, the lifestyle in the Western world today does not allow physical reaction to the stress agents we face. As Albrecht pointed out, attacking the boss, hitting an insolent customer, or smashing an empty automatic cash dispenser are not solutions allowed by contemporary society. Even the non-aggressive ‘flight’ reaction would hardly be judged appropriate in most situations. The executive who flees from a tense meeting, and the assembly worker who dashes out in the middle of a shift, will likely suffer the consequences of their actions. Our long-evolved defence mechanisms prepare us for dramatic and rapid action, but find little outlet. The body's strong chemical and hormonal responses are then like frustrated politicians: all dressed up with nowhere to go, as Melhuish describes it.
It is this waste of our natural response to stress which may actually harm us. Although scientists do not fully understand this process, our thought patterns regarding ourselves and the situations we are in can trigger widespread physiological changes, acting through the hypothalamus — the part of the brain which co-ordinates a complexity of neural and hormonal mechanisms for taking care of bodily functions. In a situation of challenge, tension, or pressure, the hypothalamus activates both the sympathetic branch of the autonomic nervous system and certain hormone secretions from the pituitary gland. The resulting release of adrenaline and other hormones, together with other actions of sympathetic nerves, enhances the level of arousal and stimulates the cognitive, neural, cardiovascular, and muscular systems, whilst also mobilizing metabolic fuels to provide energy for an increase in muscular activity. These physiological changes are designed to improve the individual's performance: the heart speeds up and beats more strongly; this and widening of muscle blood vessels increase the blood supply of the muscles; breathing rate and depth increase. Blood pressure rises, and less blood flows to the stomach and the intestines, as well as the skin, resulting in the cold hands and feet often associated with a nervous disposition.
All of the body's ‘rev-up’ activity is designed to improve performance. But if the stress which launches this activity continues unabated, researchers believe, the human body begins to weaken as it is bombarded by stimulation and stress-related chemicals. As stress begins to take its toll on the body and mind, a variety of symptoms can result. We have identified physical and behavioural symptoms of stress occurring before the onset of serious stress-related illnesses; these include: insomnia, eating difficulties, breathlessness without exertion, a tendency to sweat with no good reason, frequent intestinal difficulties, loss of sense of humour, constant irritability with people, difficulty with making decisions, suppressed anger, difficulty in concentrating, the inability to finish one task before rushing on to the next, and so on. Many of these symptoms are the prelude to more serious illnesses, in which stress is one of the risk factors. Recent research has shown that the psycho-social or stress risk factors can be found in hypertension, chronic fatigue syndrome, coronary artery disease, mental disorders, and a range of other illnesses; also suppression of immune responses by the stress-related hormones may provide chemical explanations of links between environmental and emotional pressures and susceptibility to diseases.
— Cary L. Cooper
Bibliography
- Albrecht, K. (1979). Stress and the manager. Making it work for you. Prentice-Hall, New Jersey.
- Cooper, C. (ed.) (1996). Handbook of stress, medicine and health. CRC Press, Boca Raton, Florida.
- Hinkle, L. E. (1973). The concept of stress in the biological social sciences. Stress medicine and man 1, 31-48.
- Lazarus, R. E. (1976). Patterns of adjustment. McGraw-Hill, New York.
- Melhuish, A. (1978). Executive health. Business Books, London
See also autonomic nervous system.
Roget's Thesaurus:
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stress
noun
- Special weight placed upon something considered important: accent, accentuation, emphasis. See important/unimportant.
- The act, condition, or effect of exerting force on someone or something: pressure, strain1, tension. See push/pull.
verb
- To accord emphasis to: accent, accentuate, emphasize, feature, highlight, italicize, play up, point up, underline, underscore. See important/unimportant.
Antonyms by Answers.com:
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stress
n
Definition: physical or mental pressure
Antonyms: indifference, relaxation
v
Definition: accentuate, emphasize
Antonyms: attenuate, reduce, relax
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Over the course of evolution, the human mind and body have developed means of handling stressful situations. Over the short term, such stress response pathways are highly adaptive, allowing a person to manage his or her resources in order to navigate the crisis; in some cases, however, these processes go awry and result in pathology. Chronic stress is becoming increasingly problematic in the United States as workers work longer and harder hours. Approximately one-third of all workers report that they are in high-stress jobs, and that not only is stress implicated in 15 percent of all disability claims, the number of stress-related absences is increasing. Such prolonged exposure to stress can also result in consequences in the form of physical illness. Alternatively, a severe acute stressor may result in a stress-response syndrome such as an acute stress disorder or a post-traumatic stress disorder.
In acute stress, the mind and body respond with a fight or flight response that involves activation of the sympathetic nervous system and release of stress hormones such as cortisol. Psychologically, this increases the organism's alertness and response time. Physiologically, these changes provide the organism with the energy needed to meet the emergency. Such intense activation helps the organism in the short term, but prolonged activation of this system creates problems in that it may increase the risk of certain disease states, and, once set into motion, chronic stress responses may be difficult to extinguish. This has led some researchers to investigate potential mediating factors such as personality. For example, a correlation has been established between a personality characterized by hostile competitiveness (type A) and increased risk of myocardial infarction (heart attack).
An acute stressor or psychological trauma, such as a life-threatening circumstance, presents a person with new information that may be difficult to assimilate. In an attempt to adapt, the person will typically alternate between contemplation of the stressor and avoidance of reminders of the event. Such a cycle allows for dose-by-dose psychological processing of the event. Difficulties in adaptation may present as an acute stress disorder that manifests itself as an extreme version of this cycle. People with such a disorder may have intrusive remembrances, nightmares, or even flashbacks of the stress event. These can alternate with emotional numbing, interpersonal alienation, and extreme avoidance of traumatic reminders. A diagnosis of postraumatic stress disorder (PTSD) is made if these symptoms persist longer than one month. Studies suggest that approximately 0.5 percent of men and 1.3 percent of women meet criteria for PTSD over their lifetime. A larger percentage (approximately 15%) of subjects were found to have some symptoms but did not meet criteria for the full disorder.
At present, psychotherapy is the mainstay of treatment for stress response syndromes. A variety of approaches exist, but they share a common goal of assisting the patient with conscious contemplation of the event in such a way that it may be assimilated and anxiety responses extinguished. Care must be taken to create an environment of safety and to avoid retraumatization, which may occur with overly rapid exposure to traumatic memories. Patients experience decreased feelings of guilt and shame as they learn that they responded to the trauma as adequately as possible. Contemplation of the event in therapy may lead to further benefits, including an enhanced understanding of the meaning of the event in the larger context of the individual's life.
Psychopharmacologic treatment may be a useful adjunct for specific symptom clusters such as associated anxiety, depression, and insomnia. The prognosis for treatment is good and is improved if the patient was without preexisting psychiatric comorbidity and if the treatment occurs in close proximity to the event. Brief treatment is frequently helpful in restoring a patient to a baseline level of functioning, but longer-term treatment may be necessary if exposure to the stressor was chronic or occurred in childhood.
Stress response systems have developed in humans as an adaptive mechanism to assist individuals in times of crisis. These systems, however, may also result in physical or psychological pathology. Chronic overactivation of the stress response may predispose an individual to greater risk for physical illnesses such as heart disease. Overly intense exposure to an acute stressor may result in a stress response syndrome with potentially disabling consequences. Treatment is, however, available and may return individuals to their previous level of functioning. A subset of patients even report a sense of enhanced insight into their lives as a result of the trauma.
(SEE ALSO: Mental Health)
Bibliography
Eisendrath, S. J., and Feder, A. (1995). "The Mind and Somatic Illness: Psychological Factors Affecting Physical Illness." In Review of General Psychiatry. ed. H. H. Goldman. Norwalk CT: Appleton & Lang.
Horowitz, M. J. (1997). Stress Response Syndromes: PTSD, Grief and Adjustment Disorders, 3rd edition. Northvale, NJ: Aranson.
Van der Kolk, B. A.; McFarlane, A. C.; and Weisaeth, L. (1996). Traumatic Stress: The Effects of Overwhelming Experience on Mind, Body and Society. New York: Guilford Press.
— JAMES POWERS; STUART J. EISENDRATH
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The force applied to a unit area of a substance measured in newtons per square metre. Compressive stress crushes the rock which may collapse as the air pockets within it are compressed. Tensile stress is a force which tends to pull a rock or soil apart and which may cause fractures and pores to open. A shear stress deforms a rock or soil by one part sliding over another.
The internal forces set up at a point in an elastic material by the action of external forces; expressed in units of force per unit area, e.g., pounds per square inch or kilograms per square millimeter.
1. The magnitude of a distorting force, expressed as force per unit area of the surface on which it is applied. If the stress on an object, such as bone, exceeds the tolerance load, a fracture may occur (see also stress fracture). A compressive stress results from squeezing or pressing objects together; tensile stress results from pulling forces (see tension); and shear stress results from sliding forces (see shear force).
2. Any factor, physical or psychological, that tends to disturb homeostasis and has a detrimental effect on body functions
3. A psychological condition occurring when individuals perceive a substantial imbalance between demands being made on them and their ability to meet those demands, where failure to do so has important consequences. See also distress, eustress, general adaptation syndrome, state anxiety, triad response.
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A physical factor, such as injury, or mental state, such as anxiety, that disturbs the body's normal state of functioning. Stress may contribute to the development of some illnesses, including heart disease and cancer.
Quotes About:
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Stress
Quotes:
"The perfect no-stress environment is the grave. When we change our perception we gain control. The stress becomes a challenge, not a threat. When we commit to action, to actually doing something rather than feeling trapped by events, the stress in our life becomes manageable."
- Greg Anderson
"You don't get ulcers from what you eat. You get them from what's eating you."
- Vicki Baum
"Pressure and stress is the common cold of the psyche."
- Andrew Denton
"When you suffer an attack of nerves you're being attacked by the nervous system. What chance has a man got against a system?"
- Russell Hoban
"In this world without quiet corners, there can be no easy escapes from history, from hullabaloo, from terrible, unquiet fuss."
- Salman Rushdie
"Mental tensions, frustrations, insecurity, aimlessness are among the most damaging stressors, and psychosomatic studies have shown how often they cause migraine headache, peptic ulcers, heart attacks, hypertension, mental disease, suicide, or just hopeless unhappiness."
- Hans Selye
See more famous quotes about Stress
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1. forcibly exerted influence; pressure, e.g. compression, tension.
2. the sum of the biological reactions to any adverse stimulus, physical, mental, or emotional, internal or external, that tends to disturb the homeostasis of an organism. Should these reactions be inappropriate, they may lead to disease states. The term is also used to refer to the stimuli that elicit the reactions, e.g. heat, nutritional, lactational, confinement, transportation. See also psychosomatic disease.
- s. induced diarrhea of the horse — see acute undifferentiated and chronic undifferentiated diarrhea of the horse.
- porcine s. syndrome — see porcine stress syndrome.
- s. reaction — see alarm reaction.
- s.-starvation syndrome — said of sheep. See pregnancy toxemia.
- s. testing — a test for evaluating circulatory response to physical stress produced by exercise. See also exercise testing.
Mosby's Dental Dictionary:
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stress
n
1. a force induced by or resisting an external force; measured in terms of force per unit area. 2. the force of energy directed against a tissue structure or against the function of tissue as the result of injury and trauma associated with fracture, burn, infection, surgical procedure, pharmacologic action, or anxiety states. The response to stress involves local metabolic function, the hormonal activity of the endocrine system regulated by the pituitary gland, and the autonomic and central nervous systems. The stress phenomenon is frequently associated with the general adaptation syndrome. 3. in prosthetic dentistry, forcibly exerted pressure (for example, the pressure of the upper teeth against the mandibular teeth or the pressure contact of a distorted removable partial denture on the supporting teeth or ridge structures).
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Stress (biology)
This article is about the concept of "stress" in relation to biology. For the concept of "stress" in physics and mechanics, see Stress (mechanics).
Stress is a term that is commonly used today but has become increasingly difficult to define. It shares, to some extent, common meanings in both the biological and psychological sciences. Stress typically describes a negative concept that can have an impact on one’s mental and physical well-being, but it is unclear what exactly defines stress and whether or not stress is a cause, an effect, or the process connecting the two. With organisms as complex as humans, stress can take on entirely concrete or abstract meanings with highly subjective qualities, satisfying definitions of both cause and effect in ways that can be both tangible and intangible.
The term stress had none of its contemporary connotations before the 1920s. It is a form of the Middle English destresse, derived via Old French from the Latin stringere, "to draw tight."[1] It had long been in use in physics to refer to the internal distribution of a force exerted on a material body, resulting in strain. In the 1920s and 1930s, the term was occasionally being used in biological and psychological circles to refer to a mental strain, unwelcome happening, or, more medically, a harmful environmental agent that could cause illness. Walter Cannon used it in 1926 to refer to external factors that disrupted what he called homeostasis.[2]
Homeostasis is a concept central to the idea of stress. In biology, most biochemical processes strive to maintain equilibrium, a steady state that exists more as an ideal and less as an achievable condition. Environmental factors, internal or external stimuli, continually disrupt homeostasis; an organism’s present condition is a state in constant flux wavering about a homeostatic point that is that organism’s optimal condition for living. Factors causing an organism’s condition to waver away from homeostasis can be interpreted as stress. A life-threating situation such as a physical insult or prolonged starvation can greatly disrupt homeostasis. On the other hand, an organism’s effortful attempt at restoring conditions back to or near homeostasis, oftentimes consuming energy and natural resources, can also be interpreted as stress. In such instances, an organism’s fight-or-flight response recruits the body’s energy stores and focuses attention to overcome the challenge at hand. The ambiguity in defining this phenomenon was first recognized by Hans Selye in 1926 who loosely described stress as something that "…in addition to being itself, was also the cause of itself, and the result of itself."[3] First to use the term in a biological context, Selye continued to define stress as "the non-specific response of the body to any demand placed upon it." Present-day neuroscientists including Bruce McEwen and Jaap Koolhaas believe that stress, based on years of empirical research, "should be restricted to conditions where an environmental demand exceeds the natural regulatory capacity of an organism."[4] Despite the numerous definitions given to stress, homeostasis appears to lie at its core.
Biology has progressed in this field greatly, elucidating complex biochemical mechanisms that appear to underlie diverse aspects of stress, shining a necessary light on its clinical relevance and significance. Despite this, science still runs into the problem of not being able to settle or agree on conceptual and operational definitions of stress. Because stress is ultimately perceived as a subjective experience, it follows that its definition perhaps ought to remain fluid. For a concept so ambiguous and difficult to define, stress nevertheless plays an obvious and predominant role in the everyday lives of humans and nature alike.
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Biological background
Biology primarily attempts to explain major concepts of stress in a stimulus-response manner, much like how a psychobiological sensory system operates. The central nervous system (brain and spinal cord) plays a crucial role in the body’s stress-related mechanisms. Whether these mechanisms ought to be interpreted as the body’s response to a stressor or embody the act of stress itself is part of the ambiguity in defining what exactly stress is. Nevertheless, the central nervous system works closely with the body’s endocrine system to regulate these mechanisms. One branch of the central nervous system, the sympathetic nervous system, becomes primarily active during a stress response, regulating many of the body’s physiological functions in ways that ought to make an organism more adaptive to its environment. Below is a brief biological background of the neuroanatomy and neurochemistry and how they relate to stress.
Neuroanatomy
Brain
The brain plays a critical role in the body’s perception of and response to stress. However, pinpointing exactly which regions of the brain are responsible for particular aspects of a stress response is difficult and often unclear. Understanding that the brain works in more of a network-like fashion carrying information about a stressful situation across regions of the brain (from cortical sensory areas to more basal structures and vice versa) can help explain how stress and its negative consequences are heavily rooted in neural communication dysfunction. In spite of this, several important brain structures implicated in playing key roles in stress response pathways are described below.
Hypothalamus
The hypothalamus is a small portion of the brain located "below the thalamus" and above the brainstem. One of its most important functions is to help link together the body’s nervous and endocrine systems. This structure has many bidirectional neural inputs and outputs from and to various other brain regions. These connections help regulate the hypothalamus’ ability to secrete hormones into the body’s blood stream, having far-reaching and long-lasting effects on physiological processes such as metabolism. During a stress response, the hypothalamus secretes various hormones, namely corticotropin-releasing hormone, which stimulates the body’s pituitary gland and initiates a heavily regulated stress response pathway.
Amygdala
The amygdala is a small, "almond"-shaped structure located bilaterally, deep within the medial temporal lobes of the brain and is a part of the brain’s limbic system, with projections to and from the hypothalamus, hippocampus, and locus coeruleus, among other areas. Thought to play a role in the processing of emotions, the amygdala has been implicated in modulating stress response mechanisms, particularly when feelings of anxiety or fear is involved.
Hippocampus
The hippocampus is a structure located bilaterally, deep within the medial temporal lobes of the brain, just lateral to each amygdala, and is a part of the brain’s limbic system. The hippocampus is thought to play an important role in memory formation. There are numerous connections to the hippocampus from the cerebral cortex, hypothalamus, and amygdala, among other regions. During stress, the hippocampus is particularly important, in that cognitive processes such as prior memories can have a great influence on enhancing, suppressing, or even independently generating a stress response. The hippocampus is also an area in the brain that is susceptible to damage brought upon by chronic stress.
Locus coeruleus
The locus coeruleus is an area located in the pons of the brainstem that is the principal site of the synthesis of the neurotransmitter norepinephrine, which plays an important role in the sympathetic nervous system’s fight-or-flight response to stress. This area receives input from the hypothalamus, amygdala, and raphe nucleus among other regions and projects widely across the brain as well as to the spinal cord.
Raphe nucleus
The raphe nucleus is an area located in the pons of the brainstem that is the principal site of the synthesis of the neurotransmitter serotonin, which plays an important role in mood regulation, particularly when stress is associated with depression and anxiety. Projections extend from this region to widespread areas across the brain, namely the hypothalamus, and are thought to modulate an organism's circadian rhythm and sensation of pain among other processes.
Spinal cord
The spinal cord plays a critical role in transferring stress response neural impulses from the brain to the rest of the body. In addition to the neuroendocrine blood hormone signaling system initiated by the hypothalamus, the spinal cord communicates with the rest of the body by innervating the peripheral nervous system. Certain nerves that belong to the sympathetic branch of the central nervous system exit the spinal cord and stimulate peripheral nerves, which in turn engage the body’s major organs and muscles in a fight-or-flight manner.
Pituitary gland
The pituitary gland is a small organ that is located at the base of the brain just under the hypothalamus. This gland releases various hormones that play significant roles in regulating homeostasis. During a stress response, the pituitary gland releases hormones into the blood stream, namely adrenocorticotropic hormone, which modulates a heavily regulated stress response system
Adrenal gland
The adrenal gland is a major organ of the endocrine system that is located directly on top of the kidneys and is chiefly responsible for the synthesis of stress hormones that are released into the blood stream during a stress response. Cortisol is the major stress hormone released by the adrenal gland.
In addition to the locus coeruleus existing as a source of the neurotransmitter norepinephrine within the central nervous system, the adrenal gland can also release norepinephrine during a stress response into the body’s blood stream, at which point norepinephrine acts as a hormone in the endocrine system.
Neurochemistry
Corticotropin-releasing hormone
Corticotropin-releasing hormone is the neurohormone secreted by the hypothalamus during a stress response that stimulates the anterior lobe of the pituitary gland by binding to its corticotropin-releasing hormone-receptors, causing the anterior pituitary to release adrenocorticotropic hormone.
Adrenocorticotropic hormone
Adrenocorticotropic hormone is the hormone secreted by the anterior lobe of the pituitary gland into the body’s blood stream that stimulates the cortex of the adrenal gland by binding to its adrenocorticotropic hormone-receptors, causing the adrenal gland to release cortisol.
Cortisol
Cortisol is a steroid hormone, belonging to a broader class of steroids called glucocorticoids, produced by the adrenal gland and secreted during a stress response. Its primary function is to redistribute energy (glucose) to regions of the body that need it most (i.e., the brain and major muscles during a fight-or-flight situation). As a part of the body’s fight-or-flight response, cortisol also acts to suppress the body’s immune system.
Norepinephrine
Norepinephrine is a neurotransmitter released from locus coeruleus when stimulated by the hypothalamus during a stress response. Norepinephrine serves as the primary chemical messenger of the central nervous system’s sympathetic branch that prepares the body for fight-or-flight response.
Serotonin
Serotonin is a neurotransmitter synthesized in the raphe nucleus of the pons of the brainstem and projects to most brain areas. Serotonin is thought to play an important role in mood regulation. Stress-induced serotonin dysfunctions have been associated with anxiety, fear, and depression-like symptoms.
Neuropeptide Y
Neuropeptide Y is a protein that is synthesized in the hypothalamus and acts as a chemical messenger in the brain. Traditionally, it has been thought to play an important role in appetite, feeding behavior, and satiety, but more recent findings have implicated Neuropeptide Y in anxiety and stress, specifically, stress resiliency.[5]
Biological mechanisms
Hypothalamic-pituitary-adrenal (HPA) axis
The HPA axis is a multi-step biochemical pathway where information is transmitted from one area of the body to the next via chemical messengers[disambiguation needed 
]. Each step in this pathway, as in many biochemical pathways, not only passes information along to stimulate the next region but also receives feedback from messengers produced later in the pathway to either enhance or suppress earlier steps in the pathway – this is one way a biochemical pathway can regulate itself, via a feedback mechanism.
When the hypothalamus receives signals from one of its many inputs (e.g., cerebral cortex, limbic system, visceral organs) about conditions that deviate from an ideal homeostatic state (e.g., alarming sensory stimulus, emotionally charged event, energy deficiency), this can be interpreted as the initiation step of the stress-response cascade. The hypothalamus is stimulated by its inputs and then proceeds to secrete corticotropin-releasing hormones. This hormone is transported to its target, the pituitary gland, via the hypophyseal portal system (short blood vessels system), to which it binds and causes the pituitary gland to, in turn, secrete its own messenger, adrenocorticotropic hormone, systemically into the body’s blood stream. When adrenocorticotropic hormone reaches and binds to its target, the adrenal gland, the adrenal gland in turn releases the final key messenger in the cascade, cortisol. Cortisol, once released, has widespread effects in the body. During an alarming situation in which a threat is detected and signaled to the hypothalamus from primary sensory and limbic structures, cortisol is one way the brain instructs the body to attempt to regain homeostasis – by redistributing energy (glucose) to areas of the body that need it most, that is, toward critical organs (the heart, the brain) and away from digestive and reproductive organs, during a potentially harmful situation in an attempt to overcome the challenge at hand.
After enough cortisol has been secreted to best restore homeostasis and the body’s stressor is no longer present or the threat is no longer perceived, the heightened levels of cortisol in the body’s blood stream eventually circulate to the pituitary gland and hypothalamus to which cortisol can bind and inhibit, essentially turning off the HPA-axis’ stress-response cascade via feedback inhibition. This prevents additional cortisol from being released. This is biologically identified as a normal, healthy stress mechanism in response to a situation or stressor – a biological coping mechanism for a threat to homeostasis.
It is when the body’s HPA-axis cannot overcome a challenge and/or is chronically exposed to a threat that this system becomes overtaxed and can be harmful to the body and brain. A second major effect of cortisol is to suppress the body’s immune system during a stressful situation, again, for the purpose of redistributing metabolic resources primarily to fight-or-flight organs. While not a major risk to the body if only for a short period of time, if under chronic stress, the body becomes exceptionally vulnerable to immune system attacks. This is a biologically negative consequence of an exposure to a severe stressor and can be interpreted as stress in and of itself – a detrimental inability of biological mechanisms to effectively adapt to changes in homeostasis.
Immune response
Cortisol can weaken the activity of the immune system. Cortisol prevents proliferation of T-cells by rendering the interleukin-2 producer T-cells unresponsive to interleukin-1 (IL-1), and unable to produce the T-cell growth factor.[35]Cortisol also has a negative-feedback effect on interleukin-1.[36] IL-1 must be especially useful in combating some diseases; however, endotoxic bacteria have gained an advantage by forcing the hypothalamus to increase cortisol levels (forcing the secretion of CRH hormone, thus antagonizing IL-1). The suppressor cells are not affected by glucosteroid response-modifying factor (GRMF),[37] so the effective setpoint for the immune cells may be even higher than the setpoint for physiological processes (reflecting leukocyte redistribution to lymph nodes, bone marrow, and skin). Rapid administration of corticosterone (the endogenous Type I and Type II receptor agonist) orRU28362 (a specific Type II receptor agonist) to adrenalectomized animals induced changes in leukocytedistribution. Natural killer cells are not affected by cortisol.[38]
Effect of stress on the immune system
Stress is the body’s reaction to any stimuli that disturb its equilibrium. When the equilibrium of various hormones is altered the effect of these changes can be detrimental to the immune system.[6] Much research has shown a negative effect stress has on the immune system, mostly through studies where participants were subjected to a variety of viruses. In one study, individuals caring for a spouse with dementia, representing the stress group, saw a significant decrease in immune response when given an influenza-virus vaccine compared to a non-stressed control group.[6][7] A similar study was conducted using a respiratory virus. Participants were infected with the virus and given a stress index. Results showed that an increase in score on the stress index correlated with greater severity of cold symptoms.[6] Studies with HIV have also shown stress to speed up viral progression. Men with HIV were 2–3 times more likely to develop AIDS when under above average stress.[6]
Effects of chronic stress
Chronic stress is defined as a "state of prolonged tension from internal or external stressors, which may cause various physical manifestations–eg, asthma, back pain, arrhythmias, fatigue, headaches, HTN, irritable bowel syndrome, ulcers, and suppress the immune system".[citation needed] Chronic stress takes a more significant toll on your body than acute stress does. It can raise blood pressure, increase the risk of heart attack and stroke, increase vulnerability to anxiety and depression, contribute to infertility, and hasten the aging process. For example, results of one study demonstrated that individuals who reported relationship conflict lasting one month or longer have a greater risk of developing illness and show slower wound healing. Similarly, the effects that acute stressors have on the immune system may be increased when there is perceived stress and/or anxiety due to other events. For example, students who are taking exams show weaker immune responses if they also report stress due to daily hassles.[8]
Mechanisms of chronic stress
Studies revealing the relationship between the immune system and the central nervous system indicate that stress can alter the function of white blood cells involved in immune function, known as lymphocytes and macrophages. People undergoing stressful life events, such as marital turmoil or bereavement, have a weaker lymphoproliferative response. After antigens initiate an immune response, these white blood cells send signals, composed of cytokines and other hormonal proteins, to the brain and neuroendocrine system.[9] Cytokines are molecules involved with cell signaling. Cortisol, a hormone released during stressful situations, affects the immune system greatly by preventing the production of cytokines. During chronic stress, cortisol is over produced, causing fewer receptors to be produced on immune cells so that inflammation cannot be ended. A study involving cancer patient’s parents confirmed this finding. Blood samples were taken from the participants. Researchers treated the samples of the parents of cancer patients with a cortisol-like substance and stimulated cytokine production. Cancer patient parents’ blood was significantly less effective at stopping cytokine from being produced.[10]
Chronic stress and wound healing
The immune system also plays a role in stress and the early stages of wound healing. It is responsible for preparing tissue for repair and promoting recruitment of certain cells to the wound area.[8] Consistent with the fact that stress alters the production of cytokines, Graham et al. found that chronic stress associated with care giving for a person with Alzheimer’s Disease leads to delayed wound healing. Results indicated that biopsy wounds healed 25% more slowly in the chronically stressed group, or those caring for a person with Alzheimer’s disease.[6]
Chronic stress and development
Chronic stress has also been shown to impair developmental growth in children by lowering the pituitary gland's production of growth hormone, as in children associated with a home environment involving serious marital discord, alcoholism, or child abuse.[11]
Chronic stress and memory
Chronic stress is seen to affect parts of the brain where memories are processed through and stored. When people feel stressed, stress hormones get over-secreted, which affects the brain. This secretion is made up of glucocorticoids, including cortisol, which are steroid hormones that the adrenal gland releases.[12]
Stress and visceral fat
Studies of female monkeys at Wake Forest University (2009) discovered that individuals suffering from higher stress have higher levels of visceral fat in their bodies. This suggests a possible cause-and-effect link between the two, wherein stress promotes the accumulation of Visceral fat, which in turn causes hormonal and metabolic changes that contribute to heart disease and other health problems.[13]
Psychological concepts
Eustress
Selye published in 1975 a model dividing stress into eustress and distress.[14] Where stress enhances function (physical or mental, such as through strength training or challenging work), it may be considered eustress. Persistent stress that is not resolved through coping or adaptation, deemed distress, may lead to anxiety or withdrawal (depression) behavior.
The difference between experiences that result in eustress and those that result in distress is determined by the disparity between an experience (real or imagined) and personal expectations, and resources to cope with the stress. Alarming experiences, either real or imagined, can trigger a stress response.[15]
Coping
Main article: Stress management
Responses to stress include adaptation, psychological coping such as stress management, anxiety, and depression. Over the long term, distress can lead to diminished health and/or increased propensity to illness; to avoid this, stress must be managed.
Stress management encompasses techniques intended to equip a person with effective coping mechanisms for dealing with psychological stress, with stress defined as a person's physiological response to an internal or external stimulus that triggers the fight-or-flight response. Stress management is effective when a person uses strategies to cope with or alter stressful situations.
There are several ways of coping with stress[16], such as controlling the source of stress or learning to set limits and to say "No" to some demands that bosses or family members may make.
A person's capacity to tolerate the source of stress may be increased by thinking about another topic such as a hobby, listening to music, or spending time in a wilderness.
Cognitive appraisal
Lazarus[17] argued that, in order for a psychosocial situation to be stressful, it must be appraised as such. He argued that cognitive processes of appraisal are central in determining whether a situation is potentially threatening, constitutes a harm/loss or a challenge, or is benign.
Both personal and environmental factors influence this primary appraisal, which then triggers the selection of coping processes. Problem-focused coping is directed at managing the problem, whereas emotion-focused coping processes are directed at managing the negative emotions. Secondary appraisal refers to the evaluation of the resources available to cope with the problem, and may alter the primary appraisal.
In other words, primary appraisal includes the perception of how stressful the problem is and the seconday appraisal of estimating whether one has more than or less than adequate resources to deal with the problem that affects the overall appraisal of stressfulness. Further, coping is flexible in that, in general, the individual examines the effectiveness of the coping on the situation; if it is not having the desired effect, s/he will, in general, try different strategies.[18]
Clinical symptoms and disorders
Symptoms Signs of stress may be cognitive, emotional, physical, or behavioral.
Cognitive symptoms
- Memory problems
- Inability to concentrate
- Poor judgment
- Pessimistic approach or thoughts
- Anxious or racing thoughts
- Constant worrying
Emotional symptoms
- Moodiness
- Irritability or short temper
- Agitation, inability to relax
- Feeling overwhelmed
- Sense of loneliness and isolation
- Depression or general unhappiness
Physical symptoms
- Aches and pains
- Diarrhea or constipation
- Nausea, dizziness
- Chest pain, rapid heartbeat
- Loss of sex drive
- Frequent colds
Behavioral symptoms
- Eating more or less
- Sleeping too much or too little
- Isolating oneself from others
- Procrastinating or neglecting responsibilities
- Using alcohol, cigarettes, or drugs to relax
- Nervous habits (e.g. nail biting, pacing)
DSM-IV TR
Diagnosis
A renewed interest in salivary alpha amylase as a marker for stress has surfaced. Yamaguchi M, Yoshida H (2005) have analyzed a newly introduced hand-held device called the Cocorometer developed by Nipro Corp., Japan. They state that this can be reliably used to analyze the amylase levels and is definitely a cheaper alternative as compared to the more expensive ELISA kits. The working consists of a meter and a saliva collecting chip, which can be inserted into the meter to give the readings. The levels of amylase obtained have been calibrated according to standard population, and can be categorized into four levels of severity.[19]
See also: Holmes and Rahe stress scale
Measuring stress level independent of differences in people's personalities has been inherently difficult: Some people are able to process many stressors simultaneously, while others can barely address a few. Such tests as the Trier Social Stress Test attempted to isolate the effects of personalities on ability to handle stress in a laboratory environment. Other psychologists, however, proposed measuring stress indirectly, through self-tests.
Because the amount of stressors in a person's life often (although not always) correlates with the amount of stress that person experiences, researchers combine the results of stress and burnout self-tests. Stress tests help determine the number of stressors in a person's life, while burnout tests determine the degree to which the person is close to the state of burnout. Combining both helps researchers gauge how likely additional stressors will make him or her experience mental exhaustion.[20]
Health risk factors
Both negative and positive stressors can lead to stress. The intensity and duration of stress changes depending on the circumstances and emotional condition of the person suffering from it (Arnold. E and Boggs. K. 2007). Some common categories and examples of stressors include:
- Sensory input such as pain, bright light, noise, temperatures, or environmental issues such as a lack of control over environmental circumstances, such as food, air and/or water quality, housing, health, freedom, or mobility.
- Social issues can also cause stress, such as struggles with conspecific or difficult individuals and social defeat, or relationship conflict, deception, or break ups, and major events such as birth and deaths, marriage, and divorce.
- Life experiences such as poverty, unemployment, clinical depression, obsessive compulsive disorder, heavy drinking,[21] or insufficient sleep can also cause stress. Students and workers may face performance pressure stress from exams and project deadlines.
- Adverse experiences during development (e.g. prenatal exposure to maternal stress,[22][23] poor attachment histories,[24] sexual abuse[25]) are thought to contribute to deficits in the maturity of an individual's stress response systems. One evaluation of the different stresses in people's lives is the Holmes and Rahe stress scale.
Generalized anxiety syndrome
The areas of the brain affected by generalised anxiety disorder
During passive activity, patients with generalised anxiety disorder (GAD) exhibit increased metabolic rates in the occipital, temporal and frontal lobes and in the cerebellum and thalamus compared with healthy controls. Increased metabolic activity in the basal ganglia has also been reported in patients with GAD during vigilance tasks. These finding suggest that there may be hyperactive brain circuits in GAD.[26]
The areas of the brain affected in generalised anxiety disorder (advanced)
Patients with generalised anxiety disorder (GAD) exhibit increased metabolic rates in several brain regions compared with healthy controls. Hyperactive neurotransmitter circuits between the cortex, thalamus, amygdala and hypothalamus have been implicated in the disorder. Hypofunction of serotonergic neurones arising from the dorsal raphe nucleus and GABAergic neurones that are widely distributed in the brain may result in a lack of inhibitory effect on the putative GAD pathway. Furthermore, overactivity of noradrenergic neurones arising from the locus coeruleus may produce excessive excitation in the brain areas implicated in GAD.[27]
The septohippocampal circuit
Based on early neuroanatomical observations and studies with psychoactive drugs, the septohippocampal circuit has been proposed as a model for anxiety disorders. The circuit that links the septum, amygdala, hippocampus and fornix is thought to process external stimuli and regulate the behavioural response through wider projections in the brain. Hyperstimulation of this putative ‘behavioural inhibition’ circuit, through dysfunctional noradrenergic and serotonergic neurotransmission, has been implicated in producing anxiety, and increased arousal and attention.[28]
The noradrenaline pathways in generalised anxiety disorder
In generalised anxiety disorder (GAD) there is increased noradrenaline transmission from both the locus coeruleus and the caudal raphe nuclei. The locus coeruleus-noradrenaline system is associated with anxiety and may mediate the autonomic symptoms associated with stress such as increased heart rate, dilated pupils, tremour and sweating.[29]
Serotonergic pathways showing the effects of generalised anxiety disorder
Serotonergic nuclei are found in the rostral and caudal raphe nuclei. Neurones ascend from the rostral raphe nuclei to the cerebral cortex, limbic regions and basal ganglia. The activity of neurones innervating the pre-frontal cortex, basal ganglia and limbic region is decreased in generalised anxiety disorder (GAD). The activity of descending neurones from serotonergic nuclei in the brainstem is unaffected in GAD. This altered neurotransmitter balance contributes towards the feeling of anxiety associated with GAD.[30]
GABAergic pathways showing the effects of generalised anxiety disorder
GABA is the main inhibitory neurotransmitter in the central nervous system (CNS). GABAergic inhibition is seen at all levels of the CNS, including the hypothalamus, hippocampus, cerebral cortex and cerebellar cortex. The activity of GABAergic neurones is decreased in generalised anxiety disorder.[31]
Panic disorder
The areas of the brain affected in panic disorder
There are a number of areas of the brain affected in panic disorder. Decreased serotonin activity in the amygdala and frontal cortex induces symptoms of anxiety, whereas decreased activity in the periaquaductal grey results in defensive behaviours and postural freezing. The locus coeruleus increases norepinephrine release mediating physiological and behavioural arousal, while the hypothalamus mediates the sympathetic nervous system.[32][33][34]
The areas of the brain affected in panic disorder (advanced)
Hyperactive neurotransmitter circuits between the cortex, thalamus, hippocampus, amygdala, hypothalamus and peri-adqueductal grey matter have been implicated in panic disorder. Hypofunction of serotonergic neurones arising from the rostral raphe nucleus may result in a lack of inhibitory effect on the putative panic pathways in the brain. While, overactivity of norepinephrine neurons arising from the locus coeruleus may produce excessive excitation in the regions implicated in panic disorder. Physiological symptoms of the panic response are medicated by the autonomic nervous system through connections with the locus coeruleus and hypothalamus.[32][33][34][35][36]
The serotonin pathways in panic disorder
The principal serotonin centres in the brain are the caudal and rostral raphe nuclei. Transmission of serotonin from the rostral raphe nuclei to the pre-aquaductal grey, amygdala, temporal lobe and limbic cortex is decreased in panic disorder compared with normal. Serotonin transmission to other target regions of the brain remain unchanged.[37]
The norepinephrine pathways in panic disorder
In panic disorder there is increased norepinephrine transmission from both the locus coeruleus and the caudal raphe nuclei. The locus coeruleus-norepinephrine system may have a significant role in processing fear-related stimuli or it may affect fear-related processing by stimulating other regions of the brain implicated in anxiety and fear behaviours i.e. amygdala, hippocampus, hypothalamus, cortex and spinal cord.[38]
General adaptive syndrome
Physiologists define stress as how the body reacts to a stressor, real or imagined, a stimulus that causes stress. Acute stressors affect an organism in the short term; chronic stressors over the longer term.
Alarm is the first stage. When the threat or stressor is identified or realized, the body's stress response is in a state of alarm. During this stage, adrenaline will be produced in order to bring about the fight-or-flight response. The organism's resistance to the stressor drops temporarily below the normal range and some level of shock may be experienced. There is also some activation of the HPA axis, producing cortisol.
Resistance is the second stage. If the stressor persists, it becomes necessary to attempt some means of coping with the stress. Although the body begins to try to adapt to the strains or demands of the environment, the body cannot keep this up indefinitely, so its resources are gradually depleted.
Exhaustion is the third and final stage in the GAS model. At this point, all of the body's resources are eventually depleted and the body is unable to maintain normal function. The initial autonomic nervous system symptoms may reappear (sweating, raised heart rate, etc.). If stage three is extended, long-term damage may result, as the body's immune system becomes exhausted, and bodily functions become impaired, resulting in decompensation.
The result can manifest itself in obvious illnesses such as ulcers, depression, diabetes, trouble with the digestive system, or even cardiovascular problems, along with other mental illnesses.
Phobia
The areas of the brain affected in phobia
There are a number of areas of the brain affected in phobia. Activation of the amygdala causes anticipatory anxiety or avoidance (conditioned fear) while activation of the hypothalamus activates the sympathetic nervous system. Other regions of the brain involved in phobia include the thalamus and the cortical structures, which may form a key neural network along with the amygdala. Stimulation of the locus coeruleus increases noradrenaline release mediating physiological and behavioural arousal.[34]
The noradrenaline pathways in phobia
One hypothesis about the biological basis of phobia suggests that there is an excess of noradrenaline in the principal noradrenergic pathways in the brain and that this causes a down-regulation of post-synaptic adrenergic receptors. Transmission of noradrenaline from the caudal raphe nuclei and the locus coeruleus is increased in phobia.[39]
The serotonin pathways in phobia
The principal serotonin centres in the brain are the caudal and rostral raphe nuclei. Transmission of serotonin from the rostral raphe nuclei to the thalamus, limbic cortex and cerebral cortex is decreased in phobia compared with normal. The other major pathways for serotonin transmission which involve the basal ganglia and cerebellum, and project down the spinal cord, remain unchanged.[40]
Post-traumatic stress disorder (PTSD)
Post-traumatic stress disorder (PTSD) is a severe anxiety disorder that can develop after exposure to any event that results in psychological trauma. This event may involve the threat of death to oneself or to someone else, or to one's own or someone else's physical, sexual, or psychological integrity, overwhelming the individual's ability to cope. As an effect of psychological trauma, PTSD is less frequent and more enduring than the more commonly seen acute stress response. Diagnostic symptoms for PTSD include re-experiencing the original trauma(s) through flashbacks or nightmares, avoidance of stimuli associated with the trauma, and increased arousal – such as difficulty falling or staying asleep, anger, and hypervigilance. Formal diagnostic criteria (both DSM-IV-TR and ICD-10) require that the symptoms last more than one month and cause significant impairment in social, occupational, or other important areas of functioning.
The areas of the brain affected in post-traumatic stress disorder
Sensory input, memory formation and stress response mechanisms are affected in patients with post-traumatic stress disorder (PTSD). The regions of the brain involved in memory processing that are implicated in PTSD include the hippocampus, amygdala and frontal cortex. While the heightened stress response is likely to involve the thalamus, hypothalamus and locus coeruleus.[35][41]
Memory
Cortisol works with epinephrine (adrenaline) to create memories of short-term emotional events; this is the proposed mechanism for storage of flash bulb memories, and may originate as a means to remember what to avoid in the future. However, long-term exposure to cortisol damages cells in the hippocampus; this damage results in impaired learning. Furthermore, it has been shown that cortisol inhibits memory retrieval of already stored information.
Atrophy of the hippocampus in posttraumatic stress disorder
There is consistent evidence from MRI volumetric studies that hippocampal volume is reduced in posttraumatic stress disorder (PTSD). This atrophy of the hippocampus is thought to represent decreased neuronal density. However, other studies suggest that hippocampal changes are explained by whole brain atophy and generalised white matter atrophy is exhibited by people with PTSD.[42][43]
Depression
The areas of the brain affected in depression
Many areas of the brain appear to be involved in depression including the frontal and temporal lobes and parts of the limbic system including the cingulate gyrus. However, it is not clear if the changes in these areas cause depression or if the disturbance occurs as a result of the etiology of psychiatric disorders.[44]
The hypothalamic-pituitary-adrenal (HPA) axis in depression
In depression, the hypothalamic-pituitary-adrenal (HPA) axis is upregulated with a down-regulation of its negative feedback controls. Corticotropin-releasing factor (CRF) is hypersecreted from the hypothalamus and induces the release of adrenocorticotropin hormone (ACTH) from the pituitary. ACTH interacts with receptors on adrenocortical cells and cortisol is released from the adrenal glands; adrenal hypertrophy can also occur. Release of cortisol into the circulation has a number of effects, including elevation of blood glucose. The negative feedback of cortisol to the hypothalamus, pituitary and immune system is impaired. This leads to continual activation of the HPA axis and excess cortisol release. Cortisol receptors become desensitized leading to increased activity of the pro-inflammatory immune mediators and disturbances in neurotransmitter transmission.[45][46][47][48]
The serotonin pathways in depression
Serotonin transmission from both the caudal raphe nuclei and rostal raphe nuclei is reduced in patients with depression compared with non-depressed controls. Increasing the levels of serotonin in these pathways, by reducing serotonin reuptake and hence increasing serotonin function, is one of the therapeutic approaches to treating depression.[49]
The noradrenaline pathways in depression
In depression the transmission of noradrenaline is reduced from both of the principal noradrenergic centres – the locus coeruleus and the caudal raphe nuclei. An increase in noradrenaline in the frontal/prefrontal cortex modulates the action of selective noradrenaline reuptake inhibition and improves mood. Increasing noradrenaline transmission to other areas of the frontal cortex modulates attention.[50]
History in research
However, the novel usage arose out of Selye's 1930s experiments. He started to use the term to refer not just to the agent but to the state of the organism as it responded and adapted to the environment. His theories of a universal non-specific stress response attracted great interest and contention in academic physiology and he undertook extensive research programs and publication efforts.[51]
While the work attracted continued support from advocates of psychosomatic medicine, many in experimental physiology concluded that his concepts were too vague and unmeasurable. During the 1950s, Selye turned away from the laboratory to promote his concept through popular books and lecture tours. He wrote for both non-academic physicians and, in an international bestseller entitled Stress of Life, for the general public.
A broad biopsychosocial concept of stress and adaptation offered the promise of helping everyone achieve health and happiness by successfully responding to changing global challenges and the problems of modern civilization. Selye coined the term "eustress" for positive stress, by contrast to distress. He argued that all people have a natural urge and need to work for their own benefit, a message that found favor with industrialists and governments.[51] He also coined the term stressor to refer to the causative event or stimulus, as opposed to the resulting state of stress.
From the late 1960s, academic psychologists started to adopt Selye's concept; they sought to quantify "life stress" by scoring "significant life events," and a large amount of research was undertaken to examine links between stress and disease of all kinds. By the late 1970s, stress had become the medical area of greatest concern to the general population, and more basic research was called for to better address the issue. There was also renewed laboratory research into the neuroendocrine, molecular, and immunological bases of stress, conceived as a useful heuristic not necessarily tied to Selye's original hypotheses. The US military became a key center of stress research, attempting to understand and reduce combat neurosis and psychiatric casualties.[51]
The psychiatric diagnosis post-traumatic stress disorder (PTSD) was coined in the mid 1970s, in part through the efforts of anti-Vietnam War activists and the anti war group Vietnam Veterans Against the War and Chaim F. Shatan. The condition was added to the Diagnostic and Statistical Manual of Mental Disorders as posttraumatic stress disorder in 1980.[52] PTSD was considered a severe and ongoing emotional reaction to an extreme psychological trauma, and as such often associated with soldiers, police officers, and other emergency personnel. The stressor may involve threat to life (or viewing the actual death of someone else), serious physical injury, or threat to physical or psychological integrity. In some cases, it can also be from profound psychological and emotional trauma, apart from any actual physical harm or threat. Often, however, the two are combined.
By the 1990s, "stress" had become an integral part of modern scientific understanding in all areas of physiology and human functioning, and one of the great metaphors of Western life. Focus grew on stress in certain settings, such as workplace stress, and stress management techniques were developed. The term also became a euphemism, a way of referring to problems and eliciting sympathy without being explicitly confessional, just "stressed out." It came to cover a huge range of phenomena from mild irritation to the kind of severe problems that might result in a real breakdown of health. In popular usage, almost any event or situation between these extremes could be described as stressful.[1][51]
See also
References
Notes
- ^ a b Keil, R.M.K. (2004) Coping and stress: a conceptual analysis Journal of Advanced Nursing, 45(6), 659–665
- ^ W. B. Cannon. ‘‘Physiological regulation of normal states: some tentative postulates concerning biological homeostatics.’’ IN: A. Pettit (ed.). A Charles Richet: ses amis, ses collègues, ses élèves, p. 91. Paris: Éditions Médicales, 1926.
- ^ The Stress of Life, Hans Selye, New York: McGraw-Hill, 1956.
- ^ Koolhaas, J., et al. "Stress revisited: A critical evaluation of the stress concept." Neuroscience and Biobehavioral Reviews 35, 1291–1301, 2011.
- ^ Urban, Janice, et al. (2008). "Neuropeptide Y in the Amygdala Induces Long-Term Resilience to Stress-Induced Reductions in Social Responses But Not Hypothalamic–Adrenal–Pituitary Axis Activity or Hyperthermia" The Journal of Neuroscience, 28(4): 893–903; doi:10.1523/JNEUROSCI.0659-07.2008
- ^ a b c d e Khansari, D., Murgo, A., & Faith, R. (1990). Effects of stress on the immune system. Immunology Today, 11, 170–175.
- ^ Kemeny, M. E. (2007). "Understanding the interaction between psychosocial stress and immune-related diseases: A stepwise progression." Brain, Behavior, and Immunity, 21 (8), 1009–1018.
- ^ a b Graham, J., Christian, L. & Kiecolt-Glaser, J. (2006). Stress, Age, and Immune Function: Toward a Lifespan Approach. Journal of Behavioral Medicine, 29, 389–400.
- ^ Dantzer, R. & Kelley, K. (1989). Stress and immunity: An integrated view of relationships between the brain and the immune system. Life Sciences, 44, 1995–2008.
- ^ Glaser, R. & Kiecolt-Glaser, J. K. (2005). "Stress-induced immune dysfunction: Implications for health." Immunology, 5, 243–251.
- ^ Powell, Brasel, & Blizzard, 1967.
- ^ "Renew-Stress on the Brain". The Franklin Institute. http://www.fi.edu/learn/brain/stress.html.
- ^ Alice Park (2009-08-08). "Fat-Bellied Monkeys Suggest Why Stress Sucks". Time. http://www.time.com/time/health/article/0,8599,1915237,00.html. Retrieved 2009-08-08.
- ^ Selye (1975). "Confusion and controversy in the stress field". Journal of Human Stress 1: 37–44.
- ^ Ron de Kloet, E; Joels, M. & Holsboer, F. (2005). "Stress and the brain: from adaptation to disease". Nature Reviews Neuroscience 6 (6): 463–475. doi:10.1038/nrn1683. PMID 15891777.
- ^ "The Silent Denial of Stress in a Competitive World". The Silent Denial of Stress in a Competitive World. 2012-3-17. http://drshem.com/2012/01/29/the-silent-denial-of-stress-in-a-competitive-world/. Retrieved 2012-3-17.
- ^ Lazarus, R.S. (1966). Psychological Stress and the Coping Process. New York: McGraw-Hill.
- ^ Aldwin, Carolyn (2007). Stress, Coping, and Development, Second Edition. New York: The Guilford Press. ISBN 1-57230-840-0.
- ^ Shankar, A.A.; Dandekar, R.C. "Assessment of stress in patients with Recurrent Aphthous Stomatitis, by salivary alpha amylase using a Cocorometer" dissertation submitted for Oral Pathology to Maharashtra University of Health Sciences, Nashik in December 2009.
- ^ Truby, William. "Stress Test", Stress Test: A self assessment, December, 2009.
- ^ Glavas, M.M.; Weinberg, J. (2006). "Stress, Alcohol Consumption, and the Hypothalamic-Pituitary-Adrenal Axis". In Yehuda, S.; Mostofsky, D.I.. Nutrients, Stress, and Medical Disorders. Totowa, NJ: Humana Press. pp. 165–183. ISBN 978-1-58829-432-6.
- ^ Davis et al. (June 2007). Prenatal Exposure to Maternal Depression and Cortisol Influences Infant Temperament. Journal of the American Academy of Child & Adolescent Psychiatry, v46 n6 p737.
- ^ O'Connor, Heron, Golding, Beveridge & Glover. (June 2002). Maternal antenatal anxiety and children's behavioural/emotional problems at 4 years. Br J Psychiatry. 180:478–9.
- ^ Schore, Allan (2003). Affect Regulation & the Repair of the Self. New York: W.W. Norton. ISBN 0-393-70407-6.
- ^ Michael D. DeBellis, George P. Chrousos, Lorah D. Dorn, Lillian Burke, Karin Helmers, Mitchel A. Kling, Penelope K. Trickett, and Frank W. Putnam. Hypothalamic—Pituitary—Adrenal Axis Dysregulation in Sexually Abused Girls
- ^ J Clin Psychiatry 2001;62(Suppl. 11):22–27.
- ^ J Clin Psychiatry 2001;62(Suppl. 11):22–27
- ^ L’Encéphale 1983;IX:161B–166B.
- ^ Anxiolytics and sedative-hypnotics. In: Essential Psychopharmacology. Neuroscientific basis and practical applications. Stahl S. Cambridge, UK: Cambridge University Press, 1996: 167–215.
- ^ Psychiatr Clin North Am 2001;21:75–97.
- ^ J Clin Psychiatry 2001;62:22–27.
- ^ a b J Clin Psychiatry 1997;58(suppl. 2):4–11.
- ^ a b J Clin Psychiatry 1998;59(suppl. 8):24–28.
- ^ a b c Am J Psychiatry 2000;157:493–505.
- ^ a b Current Opinions in Neurobiology 2000;10:211–218.
- ^ J Clin Psychiatry 2000;61(Suppl. 5):24–29.
- ^ J Clin Psychiatry 1997;58(Suppl. 2):4–11.
- ^ J Clin Psychiatry 1997;58(Suppl. 2):4–11.
- ^ Drug treatments for obsessive compulsive disorder, panic disorder, and phobia. In: Essential Psychopharmacology. Neuroscientific basis and practical applications. Stahl S. Cambridge, UK: Cambridge University Press, 1996: 216–248.
- ^ Drug treatments for obsessive compulsive disorder, panic disorder, and phobia. In: Essential Psychopharmacology. Neuroscientific basis and practical applications. Stahl S. Cambridge, UK: Cambridge University Press, 1996: 216–248.
- ^ J Clin Psychiatry 2000;61(Suppl. 5):24–29.
- ^ Biol Psychiatry 2002;52:119–125.
- ^ Semin Clin Neuropsychiatry 2001;6:113–145.
- ^ Depression. What happens in the brain? www.brainexplorer.org Accessed 20th May 2002.
- ^ Primary Care Companion J Clin Psychiatry 2001;3:151–155.
- ^ Metabolism 2002;51:5–10.
- ^ Neuroendocrinol 2001;13:1009–1023.
- ^ Br Med Bull 1996;52:597–617.
- ^ Neural plasticity and disorders of the nervous system. In: Neuroscience at a glance, Barker RA and Barasi S with Neal MJ. London, England, 1999:105–121.
- ^ Neurotransmitters and psychiatric disorders. In: Psychiatric disorders with a biochemical basis. Donaldson D. Carnthorn, UK: The Parthenon Publishing Group Inc, 1998: 45–55.
- ^ a b c d Viner, R. (1999) Putting Stress in Life: Hans Selye and the Making of Stress Theory. Social Studies of Science, Vol. 29, No. 3 (June 1999), pp. 391–410
- ^ Shalev, Arieh Y.; Yehuda, Rachel; Alexander C. McFarlane (2000). International handbook of human response to trauma. New York: Kluwer Academic/Plenum Press. ISBN 0-306-46095-5.; on-line.
External links
Introductory
 |
Look up stress in Wiktionary, the free dictionary. |
- The American Institute of Stress
- University of Massachusetts Medical School Stress Reduction Program
- "Research on Work-Related Stress", European Agency for Safety and Health at Work (EU-OSHA)
- "Working on Stress", European Agency for Safety and Health at Work (EU-OSHA)
- "Taming Stress", Scientific American, September 2003
- Self help guide (NHS Direct)
Bibliography
- Carlson, N.R. & Heth, C.D. (2007). Psychology the science of behaviour. 4th ed. Upper Saddle River, New Jersey: Pearson Education, Inc., 527.
- Petersen, C.; Maier, S.F.; Seligman, M.E.P. (1995). Learned Helplessness: A Theory for the Age of Personal Control. New York: Oxford University Press. ISBN 0-19-504467-3
- Seligman, M.E.P. (1975). Helplessness: On Depression, Development, and Death. San Francisco: W.H. Freeman. ISBN 0-7167-2328-X
- Seligman, M.E.P. (1990). Learned Optimism. New York: Knopf. (Reissue edition, 1998, Free Press, ISBN 0-671-01911-2).
- Holmes, T.H. and Rahe, R.H. (1967). The social readjustments rating scales. Journal of Psychosomatic Research 11:213–218.
This entry is from Wikipedia, the leading user-contributed encyclopedia. It may not have been reviewed by professional editors (see full disclaimer)
Translations:
Top
Stress
Dansk (Danish)
n. - stress, pres, tryk, betoning, eftertryk, vigtighed, belastning, spænding
v. tr. - betone, fremhæve, lægge vægt på, lægge eftertryk på, stresse
idioms:
- lay stress on lægge vægt på, lægge tryk på, understrege, betone, fremhæve
Nederlands (Dutch)
spanning, nadruk, klemtoon, beklemtonen, drukken, onder druk zetten, testen (door extra veel te eisen)
Français (French)
n. - tension, stress, insistance, (Génie Civ, Phys) effort, (Ling, Phon) accentuation, accent
v. tr. - insister sur, mettre l'accent sur, (Ling, Mus) accentuer, (Génie Civ, Tech) soumettre (qch) à des efforts, faire travailler (métal)
idioms:
- lay stress on insister sur, placer l'accent sur
Deutsch (German)
v. - betonen, belasten, überanstrengen
n. - Nachdruck, Betonung, Spannung, Streß, Belastung
idioms:
- lay stress on Wert legen auf
Ελληνική (Greek)
v. - τονίζω, υπογραμμίζω, δίνω έμφαση σε, καταπονώ, κουράζω, ζορίζω, (καθομ.) προκαλώ άγχος
n. - (γραμμ., μτφ.) τονισμός, τόνος, ένταση, έμφαση, υπερένταση, άγχος, στρες, κόπωση, καταπόνηση
idioms:
- lay stress on δίνω έμφαση σε, υπογραμμίζω
Italiano (Italian)
accentuare, accento, tensione, risalto, stress
idioms:
- lay stress on sottolineare
Português (Portuguese)
v. - salientar
n. - acento (m), fadiga (f), pressão (f), importância (f)
idioms:
- lay stress on acentuar
Русский (Russian)
давление, напряжение, ударение, значение, усилие, стресс, ставить ударение, подчеркивать, подвергать действию внешней силы, создавать или вызывать напряжение, стресс
idioms:
- lay stress on придавать (чему-л.) особое значение
Español (Spanish)
n. - acento, acentuación, tensión, ansiedad, énfasis, insistencia, estrés
v. tr. - acentuar, enfatizar, recalcar, insistir en
idioms:
- lay stress on hacer hincapié en, dar importancia a
Svenska (Swedish)
v. - stressa, utsätta för stress
n. - stress, påfrestningar
中文（简体）(Chinese (Simplified))
重压, 压力, 逼迫, 着重, 重读, 强调
idioms:
- lay stress on 把重点放在, 在...上用力
中文（繁體）(Chinese (Traditional))
n. - 重壓, 壓力, 逼迫
v. tr. - 著重, 重讀, 強調
idioms:
- lay stress on 把重點放在, 在...上用力
한국어 (Korean)
n. - 강조, 강세, 변형 작용
v. tr. - 강조하다, ~임을 강조하다, 압력을 가하다
idioms:
- lay stress on ~을 역설하다
日本語 (Japanese)
n. - 圧迫, 緊張, ストレス, 圧力, 緊迫, 力, 強調, 重視, 強勢
v. - 強調する, 強勢を置く
العربيه (Arabic)
(فعل) أكد, شدد على (الاسم) ضغط, وطأة, تأكيد, اجهاد
עברית (Hebrew)
n. - לחץ, מתיחות, מצוקה, מתח נפשי, דגש, חשיבות, משקל, נגינה, טעם, הטעמה
v. tr. - הדגיש, הטעים
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