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Stress (biology)

From Wikipedia, the free encyclopedia

This article is about biological stress. For stress in physics and mechanics, see Stress (mechanics).

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Stress is defined as an organism's total response to an environmental condition or stimulus, also known as a stressor. Stress typically describes a negative condition that can have an impact on an organism's mental and physical well-being.

|Contents |
| [hide] |
|1 Ambiguity of the word |
|1.1 Biological background |
|2 Neuroanatomy |
|2.1 Brain |
|2.1.1 Hypothalamus |
|2.1.2 Amygdala |
|2.1.3 Hippocampus |
|2.1.4 Locus coeruleus |
|2.1.5 Raphe nucleus |
|2.2 Spinal cord |
|2.3 Pituitary gland |
|2.4 Adrenal gland |
|3 Neurochemistry |
|3.1 Corticotropin-releasing hormone |
|3.2 Adrenocorticotropic hormone |
|3.3 Cortisol |
|3.4 Norepinephrine |
|3.5 Serotonin |
|3.6 Neuropeptide Y |
|4 Biological mechanisms |
|4.1 Hypothalamic-pituitary-adrenal (HPA) axis |
|4.2 Immune response |
|4.2.1 Effect of stress on the immune system |
|4.2.2 Effects of chronic stress |
|4.2.3 Mechanisms of chronic stress |
|4.2.4 Chronic stress and wound healing |
|4.2.5 Chronic stress and development |
|4.2.6 Chronic stress and memory |
|4.2.7 Stress and visceral fat |
|5 Psychological concepts |
|5.1 Eustress |
|5.2 Coping |
|5.3 Cognitive appraisal |
|6 Clinical symptoms and disorders |
|6.1 Symptoms |
|6.2 DSM-IV TR |
|6.2.1 Diagnosis |
|6.2.2 Health risk factors |
|6.3 Generalized anxiety syndrome |
|6.4 Panic disorder |
|6.5 General adaptation syndrome |
|6.6 Phobia |
|6.7 Post-traumatic stress disorder (PTSD) |
|6.8 Depression |
|7 History in research |
|8 See also |
|9 References |
|9.1 Notes |
|9.2 Bibliography |
|10 External links |

[edit]Ambiguity of the word

The term stress had none of its contemporary connotations before the 1920s. It is a form of the Middle English destresse, derived viaOld 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 or 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 moving about a homeostatic point that is that organism’s optimal condition for living. Factors causing an organism’s condition to diverge too far from homeostasis can be interpreted as stress. A life-threatening 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.

[edit]Biological background

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Biology primarily attempts to explain major concepts of stress in a stimulus-response manner, much like how a psychobiologicalsensory 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’sendocrine 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.

[edit]Neuroanatomy

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[edit]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.

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Human brain (hypothalamus=red, amygdala=green, hippocampus/fornix=blue, pons=gold, pituitary gland=pink)

[edit]Hypothalamus

The hypothalamus is a small portion of the brain located below the thalamus and above thebrainstem. 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.

[edit]Amygdala

The amygdala is a small, "almond"-shaped structure located bilaterally, deep within themedial 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.

[edit]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.

[edit]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 neurotransmitternorepinephrine, 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.

[edit]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 neurotransmitterserotonin, 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.

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Human spinal cord

[edit]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.

[edit]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

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Adrenal gland

[edit]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.

[edit]Neurochemistry

[edit]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.

[edit]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.

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Cortisol

[edit]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.

Cortisol is synthesized from cholesterol in the adrenal cortex.[5] Its primary function is to increase blood sugar through gluconeogenesis, suppress the immune system and aid in fat and protein metabolism.[6]

[edit]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.

[edit]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.

[edit]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.[7]

[edit]Biological mechanisms

[edit]Hypothalamic-pituitary-adrenal (HPA) axis

Main article: Hypothalamic–pituitary–adrenal axis

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Basic hypothalamic–pituitary–adrenal axis summary (corticotropin-releasing hormone=CRH, adrenocorticotropic hormone=ACTH).

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-responsecascade. 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.

[edit]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]

[edit]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.[8] 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.[8][9] 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.[8] 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.[8]

[edit]Effects of chronic stress

Main article: Chronic stress

Chronic stress is defined as a "state of prolonged tension from internal or external stressors, which may cause various physical manifestations – e.g., 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.[10]

[edit]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.[11] 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.[12]

[edit]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.[10] 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.[8]

[edit]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.[13]

[edit]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 aresteroid hormones that the adrenal gland releases.[14]

[edit]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.[15]

[edit]Psychological concepts

[edit]Eustress

Selye published in 1975 a model dividing stress into eustress and distress.[16] 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.[17]

[edit]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,[18] such as controlling the source of stress or learning to set limits and to say "no" to some of the 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.

[edit]Cognitive appraisal

Lazarus[19] 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 secondary 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.[20]

[edit]Clinical symptoms and disorders

[edit]Symptoms

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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 • Increased frequency of urination • Indigestion • Changes in blood glucose • Nausea, dizziness • Chest pain, rapid heartbeat • Loss of sex drive • Frequent colds • Irregular periods.
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)

[edit]DSM-IV TR

[edit]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.[21]

See also: Holmes and Rahe stress scale and Stress (psychological)

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.[22]

[edit]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,[23] 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,[24][25] poor attachment histories,[26] sexual abuse)[27] 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.

[edit]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.[28]

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.[29]

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.[30]

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.[31]

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.[32]

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.[33]

[edit]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 periaqueductal gray 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.[34][35][36]

The areas of the brain affected in panic disorder (advanced)

Hyperactive neurotransmitter circuits between the cortex, thalamus, hippocampus, amygdala, hypothalamus and periaqueductal gray 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.[34][35][36][37][38]

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.[39]

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.[40]

[edit]General adaptation syndrome

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A diagram of the General Adaptation Syndrome model.

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, which is divided into two phases: the shock phase and the antishock phase.[41]

• Shock phase: During this phase, the body can endure changes such ashypovolemia, hypoosmolarity, hyponatremia, hypochloremia,hypoglycemia—the stressor effect. This phase resembles Addison's disease. The organism's resistance to the stressor drops temporarily below the normal range and some level of shock (e.g. circulatory shock) may be experienced. • Antishock phase: When the threat or stressor is identified or realized, the body starts to respond and is in a state of alarm. During this stage, the locus coeruleus/sympathetic nervous system is activated and catecholamines such as adrenaline are being produced, hence the fight-or-flight response. The result is: increased muscular tonus, increased blood pressure due to peripheral vasoconstriction and tachycardia, and increased glucose in blood. There is also some activation of the HPA axis, producing glucocorticoids (cortisol, aka the S-hormone or stress-hormone).
Resistance is the second stage and increased secretion of glucocorticoids play a major role, intensifying the systemic response—they have lypolytic, catabolic and antianabolic effects: increased glucose, fat and aminoacid/protein concentration in blood. Moreover, they cause lymphocytopenia, eosinopenia, neutrophilia and polycythemia. In high doses, cortisol begins to act as a mineralocorticoid (aldosteron) and brings the body to a state similar to hyperaldosteronism. 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.

The third stage could be either exhaustion or recovery:

• Recovery stage follows when the system's compensation mechanisms have successfully overcome the stressor effect (or have completely eliminated the factor which caused the stress). The high glucose, fat and aminoacid levels in blood prove useful for anabolic reactions, restoration of homeostasis and regeneration of cells. • Exhaustion is the alternative third 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 (prolonged vasoconstriction results in ischemia which in turn leads to cell necrosis), as the body's immune system becomes exhausted, and bodily functions become impaired, resulting indecompensation.
The result can manifest itself in obvious illnesses, such as peptic ulcer and general trouble with the digestive system (e.g. occult bleeding, melena, constipation/obstipation), depression, diabetes, or even cardiovascular problems (angina pectoris), along with other mental illnesses.

[edit]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.[36]

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.[42]

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.[43]

[edit]Post-traumatic stress disorder (PTSD)

See article: Posttraumatic stress disorder

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[pic]

Regions of the brain associated with stress and posttraumatic stress disorder[44]

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 intrusion, avoidance and hyperarousal -- re-experiencing the original trauma(s) through "flashbacks" or nightmares (intrusion), emotional numbing or 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 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.[37][45]

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.[46][47]

[edit]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.[48]

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.[49][50][51][52]

The serotonin pathways in depression

Serotonin transmission from both the caudal raphe nuclei and rostral 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.[53]

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.[54]

[edit]History in research

The current usage of the word stress 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.[55]

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.[55] 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 immunologicalbases 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.[55]

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 theDiagnostic and Statistical Manual of Mental Disorders as posttraumatic stress disorder in 1980.[56] 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 sympathywithout 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][55]

[edit]See also

|Amygdala hijack |Psychological resilience |
|Burnout (psychology) |Self-medication |
|Compassion fatigue |Stress (disambiguation) |
|Chronic stress |Stress management |
|Defense Physiology |Trier Social Stress Test |
|Depression (differential diagnoses) |Workplace stress |
|Grief |Work-life balance |
|Hypothalamic-pituitary-adrenal axis |Xenohormesis |

[edit]References

[edit]Notes

1. ^ a b Keil, R.M.K. (2004) Coping and stress: a conceptual analysis Journal of Advanced Nursing, 45(6), 659–665 2. ^ 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. 3. ^ The Stress of Life, Hans Selye, New York: McGraw-Hill, 1956. 4. ^ Koolhaas, J., et al. "Stress revisited: A critical evaluation of the stress concept." Neuroscience and Biobehavioral Reviews 35, 1291–1301, 2011. 5. ^www.drexelmed.edu/documents/pharmacology_physiology/clinks/gpharmhandouts/Adrenal%2520Steroids%2520Grad%2520Pharm%25202004.doc+cortisol+synthesized:site:.edu&hl=en&gl=ca&pid=bl&srcid=ADGEESiAqyJW2OGe1cmfb6-waOqyfkOCarFccQftB22AsbmLy0vZ6PcJeoDFZi1eJ59-hOJwmYYG1iqpPWipjyYL5n5HvIPMsmu974Jlz_n01DEqF9ElTXFbs_xTkJLLoqwVHMX3t7Cq&sig=AHIEtbTiUJxhId53GcDB111z4lNO4_RTcQ 6. ^ Measurement of Cortisol: Introduction to the hypothalamic - pituitary - adrenocortical axis. Nancy A. Nicolson, 2007 7. ^ 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 8. ^ a b c d e Khansari, D., Murgo, A., & Faith, R. (1990). Effects of stress on the immune system. Immunology Today, 11, 170–175. 9. ^ 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. 10. ^ 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. 11. ^ 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. 12. ^ Glaser, R. & Kiecolt-Glaser, J. K. (2005). "Stress-induced immune dysfunction: Implications for health." Immunology, 5, 243–251. 13. ^ Powell, Brasel, & Blizzard, 1967. 14. ^ "Renew-Stress on the Brain". The Franklin Institute. 15. ^ Alice Park (2009-08-08). "Fat-Bellied Monkeys Suggest Why Stress Sucks". Time. Retrieved 2009-08-08. 16. ^ Selye (1975). "Confusion and controversy in the stress field".Journal of Human Stress 1: 37–44.doi:10.1080/0097840X.1975.9940406. PMID 1235113. 17. ^ 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. 18. ^ "The Silent Denial of Stress in a Competitive World". The Silent Denial of Stress in a Competitive World. 2012-03-17. Retrieved 2012-03-17. 19. ^ Lazarus, R.S. (1966). Psychological Stress and the Coping Process. New York: McGraw-Hill. 20. ^ Aldwin, Carolyn (2007). Stress, Coping, and Development, Second Edition. New York: The Guilford Press. ISBN 1-57230-840-0. 21. ^ 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. 22. ^ Truby, William. "Stress Test", Stress Test: A self assessment, December, 2009. 23. ^ 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. 24. ^ 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. 25. ^ 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. 26. ^ Schore, Allan (2003). Affect Regulation & the Repair of the Self. New York: W.W. Norton. ISBN 0-393-70407-6. 27. ^ 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 28. ^ J Clin Psychiatry 2001;62(Suppl. 11):22–27. 29. ^ J Clin Psychiatry 2001;62(Suppl. 11):22–27 30. ^ L’Encéphale 1983;IX:161B–166B. 31. ^ Anxiolytics and sedative-hypnotics. In: Essential Psychopharmacology. Neuroscientific basis and practical applications. Stahl S. Cambridge, UK: Cambridge University Press, 1996: 167–215. 32. ^ Psychiatr Clin North Am 2001;21:75–97. 33. ^ J Clin Psychiatry 2001;62:22–27. 34. ^ a b J Clin Psychiatry 1997;58(suppl. 2):4–11. 35. ^ a b J Clin Psychiatry 1998;59(suppl. 8):24–28. 36. ^ a b c Am J Psychiatry 2000;157:493–505. 37. ^ a b Current Opinions in Neurobiology 2000;10:211–218. 38. ^ J Clin Psychiatry 2000;61(Suppl. 5):24–29. 39. ^ J Clin Psychiatry 1997;58(Suppl. 2):4–11. 40. ^ J Clin Psychiatry 1997;58(Suppl. 2):4–11. 41. ^ Pathology: Medical student's library ISBN 978-83-61047-18-6http://books.google.rs/books?id=Pvk0MoLNjgYC&lpg=PA272&ots=PuqI645Scs&dq=antishock%20phase%20general%20adaptive%20syndrome&pg=PA272#v=onepage&q=antishock%20phase%20general%20adaptive%20syndrome&f=false 42. ^ 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. 43. ^ 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. 44. ^ "NIMH · Post Traumatic Stress Disorder Research Fact Sheet". National Institutes of Health. 45. ^ J Clin Psychiatry 2000;61(Suppl. 5):24–29. 46. ^ Biol Psychiatry 2002;52:119–125. 47. ^ Semin Clin Neuropsychiatry 2001;6:113–145. 48. ^ Depression. What happens in the brain? www.brainexplorer.org Accessed 20th May 2002. 49. ^ Primary Care Companion J Clin Psychiatry 2001;3:151–155. 50. ^ Metabolism 2002;51:5–10. 51. ^ Neuroendocrinol 2001;13:1009–1023. 52. ^ Br Med Bull 1996;52:597–617. 53. ^ 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. 54. ^ Neurotransmitters and psychiatric disorders. In: Psychiatric disorders with a biochemical basis. Donaldson D. Carnthorn, UK: The Parthenon Publishing Group Inc, 1998: 45–55. 55. ^ a b c d Viner, R. (1999) Putting Stress in Life: Hans Selyeand the Making of Stress Theory. Social Studies of Science, Vol. 29, No. 3 (June 1999), pp. 391–410 56. ^ 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.

[edit]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.

[edit]External links

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• 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)
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...Section A – English assignment Summary of Bad stress, good stress. Texts 2 Bad Stress, Good Stress by Sacha Bonsor is an article about the issue of coping with stress. Sacha Bonsor writes about Piers Morgan and his aggressive attitude while being put under pressure and being stressed. Sacha Bonsor also writes that stress has become a too common word and that it is an overrated expression in the modern language, which she develops further with the raising statistics of stress from the UK economy. The article also mentions that those people who are able to cope with stress have high levels of what academics and psychologist call “psychological flexibility”. And for those people who cannot handle stress is it possible to teach them how to handle stress effectively. Clare Harris, a lecturer at the Praxis Centre for Developing Personal Effectiveness, says that the crux of the problem is to recognize stress that often manifests itself by taking out one’s tension on others. Yet a certain amount of tension is not only good for us but also vital to our well-being. Comment on the statement: “If you want to live long and healthily, don’t settle into routines” Routines can both be good for you and bad for you. You can say that a routine is like a schedule for your actions in life but you don’t always need to have schedules in your life. People will always make routines in their lives because it’s safe. When you have a routine in your life, you have a picture of what is going...

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...Introduction Stress definition: Stress is pressure from unusual demands, constraints, or opportunities. In other words; stress is a state of tension encountered by an individual(s) facing great unexpected requirements, constraints, or opportunities. The things that cause the stress are called stressors. There are two types of stressors: • Direct stressors that can be traced directly from the workplace. A list of common stressors includes the following: • Task demands: being asked to do too much or being asked to do too little. • Role ambiguities: not knowing what one is expected to do or how work performance is evaluated. • Role conflicts: feeling unable to satisfy multiple, possibly conflicting, performance expectations. • Ethical dilemmas: being asked to do things that violate the law or personal values. • Interpersonal problems: experiencing bad relationships or working with others who do not get along. • Career developments: moving too fast and feeling stretched; moving too slowly and feeling plateau. • Physical setting: being bothered by noise, lack of privacy, pollution, or other unpleasant working conditions. • Indirect stressors that can be driven from non-work and personal factors. • Personal factors: such as personal needs, and capabilities. • Economic difficulties And a lot more. Discussion From the above introduction, and in order to manage the stress, I have to know first where is the stress coming from, and...

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...head: Stress Living a Stress-Free Life Is it possible to attain a stress free life? Is this a reasonable question to ask? A stress free life seems unimaginable and unattainable. We listen to our doctors whom give us loads of information relating to stress and tell us how to successfully balance your work and home life so that your life can be free from stress, but is there any real way to overcome stressors. If you were to ask 10 people what their definition of stress was I am sure you would get 10 different answers from all 10 different people. The reason for this is because stress varies from person to person and how each person copes with it also tends to vary. To understand stress and how it impacts our physical and mental lives, we must educate ourselves on stress, the effects of stress, the causes of stress, the symptoms of stress and how to manage and cope with stress. Stress can be very debilitating and could impact various aspects of our everyday lives if it is not dealt with and managed effectively. I have been through various bouts of stress throughout my life and I have found different ways to combat it which will be explained later in this research paper. As part of my research, I will define stress, the effects of stress, the cause of stress, the symptoms of stress and how to manage and cope with stress, as well as my own personal experience relating to stress. The ideal solution for everyone is to understand stress so when...

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...What are some of the effects of stress for both the individual concerned and for organisations that the individual is part of? To what extent should a manager feel responsible for trying to help reduce this stress? Over the years stress has been defined in many different ways. . Originally it was perceived as pressure from the environment it was conceived of as pressure from the environment, then as strain within the person. The generally accepted definition today is one of interaction between the situation and the individual. It is the psychological and physical state that results when the resources of the individual are not sufficient to cope with the demands and pressures of the situation. Thus, stress is more likely in some situations than others and in some individuals than others. Stress can undermine the achievement of goals, both for individuals and for organisations (box 1). Organizational stress can have a profound effect on production and motivation in the workplace. Worries about job security or the demands of a heavy workload increase stress levels and cause a variety of emotional and physical ailments. When stress factors, or stressors, are coupled with ineffective or uncaring management, stress can become a problem that extends to the entire department or company. Identifying signs of organizational stress is the first step in designing a strategy to address problems(small business) The consequences and symptoms of stress first become visible at the individual...

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...CHAPTER 1 : INTRODUCTION 1.1 BACKGROUND OF STUDY 1.2.1 Definition of Stress According to Jay W. Marks (2011) , Stress is a feeling that’s created when we react with particular events or problems. It’s the body’s way of rising to a challenge and preparing to meet a tough situation with focus, strength and heightened alertness. In general, stress is related to both external and internal factors. External factors include physical environment – including job, relationship with others, home, challenges, difficulties and expectations you’re confronted with on a daily basis. Internal factors determine your body ability to respond to or deal with the external stress-inducing factors. Stress is simply a fact of nature. The individual responds to stress in ways that affect the individual as well as their environment. 1.2.2 Symptoms of Stress According to the article Understanding Stress by Melinda Smith, Robert Segal and Jeanne Segal (November 2012) , Stress is a common problem among people nowadays especially for the women. There are many signs or symptoms of stress. It is divided into four group that is – Cognitive Symptoms, Emotional Symptoms, Physical Symptoms and Behavioral Symptoms. Firstly is the Cognitive Symptoms. The symptoms are : i. Memory problem ii. Inability to concentrate iii. Poor judgement iv. Constant worrying v. Anxious thoughts Next is the Emotional Symptoms : ...

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...COURSEWORK STRESS IN UNIVERSITY STUDENTS: Investigating problem solving coping, wishful thinking coping, anxiety and depression as predictors of coursework stress. ANN-MARIE ROY Contact: aroy11@caledonian.ac.uk COURSEWORK STRESS STUDY ANN-MARIE ROY ABSTRACT The aim of the present study was to investigate students’ perceived university coursework stress and whether the use of wishful thinking or problem-focused coping was related to anxiety and depression levels. The method of investigation was a four-part questionnaire. Participants were 81 Glasgow Caledonian University students. There were two hypotheses: 1) problem solving copers will score lower on the Hospital Anxiety and Depression scale. 2) Those high in perceived coursework stress and who reveal wishful thinking strategies will have higher anxiety and depression scores. A multiple regression revealed partial support for both hypotheses – problem strategies had no relationship to coursework stress but wishful thinking and anxiety were both positive predictors of stress; however, contrary to hypothesis 2 depression revealed a strong negative association with stress. The conclusion from this study is that wishful thinkers are also more likely to be anxious; problem focused copers are not anxious, depressed or stressed; stressed students do not suffer from depression. The last finding is possibly because coursework stress is a transient stressor not severe enough to trigger depression. 2 COURSEWORK STRESS...

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...UBS 2012-2014 STUDY OF STRESS LEVEL AMONG PEOPLE AND THEIR PERCEPTION TOWARDS STRESS SUBMITTED BY PULKIT NEHRU, MBA BIOTECH, 3RD SEMESTER. TABLE OF CONTENTS Certificate………………………………………………………………………………………...I Acknowledgement……………………………………………………………………………..II Executive Summary…………………………………………………………………………..III Chapter 1: Background of Industry and Company………………………………………1 1.1 Operations…………………………………………………………………………………...2 1.2 Research and Development………………………………………………………….…….3 1.3 Products……………………………………………………………………………………...4 1.4 Motivation of Study………………………………………………………………………….8 Chapter 2: Introduction……………………………………………………………………….9 2.1 The Dynamics of Stress……………………………………………………………………9 2.2 Stress Can be Positive……………………………………………………………………10 2.3 Stress throughout Evolution………………………………………………………….…..11 2.4 Causes of Stress………………………………………………………………………..…12 2.5 Stress and its Impact……………………………………………………………………...15 2.6 Ways to Overcome Stress………………………………………………………………..24 Chapter 3: Research Methodology………………………………………………………..39 Chapter 4: Data Analysis……………………………………………………………………41 Chapter 5: Conclusions…………………………………………………………………..…90 5.1 Limitations of the Study…………………………………………………………………...95 Chapter 6: Bibliography……………………………………………………………………..96 Chapter 7: Appendix…………………………………………………………………………98 CERTIFICATE I hereby certify that this project report entitled “Study of stress level among the people and their perception towards it and its impact” has been prepared by me under the guidance...

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...away from stress. Stress is the response of our body due to events that disrupt our normal functioning in society. Sometimes the response of stress in the body is the production of chemicals that produce more energy in the body. This can be beneficial because we can put the energy to better use and do something positive in return. But this can also be a bad thing if the stress is caused by something emotional and there is nothing to take out the extra energy being produced. There are many things that can cause stress. It can be cause by something physical like fear for something or by something emotional like worry for the family. These are called stressors. Some major causes of stress are survival stress. This is caused when we are found in dangerous situations the energy produced is used to survive the situation or to escape it all together. Then there is internal stress, this people make themselves stressed over things that they can’t control. There is also environmental stress; this is caused by things around us that make us stress out, for example the family pressuring you over a situation or an important decision you have to take. Fatigue and over work are also stressors. It is important for people to know how to handle stress for it may lead to health problems, reduce productivity in tasks performed. Some common health problems related to stress are high blood pressure, heart diseases, ulcers or even diabetes. There are certain techniques that can reduce stress. Some of...

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