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18.7: Hormonal Regulation of Stress - Biology

18.7: Hormonal Regulation of Stress - Biology


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When a threat or danger is perceived, the body responds by releasing hormones that will ready it for the “fight-or-flight” response. The effects of this response are familiar to anyone who has been in a stressful situation: increased heart rate, dry mouth, and hair standing up.

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Interactions of the endocrine hormones have evolved to ensure the body’s internal environment remains stable. Stressors are stimuli that disrupt homeostasis. The sympathetic division of the vertebrate autonomic nervous system has evolved the fight-or-flight response to counter stress-induced disruptions of homeostasis. In the initial alarm phase, the sympathetic nervous system stimulates an increase in energy levels through increased blood glucose levels. This prepares the body for physical activity that may be required to respond to stress: to either fight for survival or to flee from danger.

However, some stresses, such as illness or injury, can last for a long time. Glycogen reserves, which provide energy in the short-term response to stress, are exhausted after several hours and cannot meet long-term energy needs. If glycogen reserves were the only energy source available, neural functioning could not be maintained once the reserves became depleted due to the nervous system’s high requirement for glucose. In this situation, the body has evolved a response to counter long-term stress through the actions of the glucocorticoids, which ensure that long-term energy requirements can be met. The glucocorticoids mobilize lipid and protein reserves, stimulate gluconeogenesis, conserve glucose for use by neural tissue, and stimulate the conservation of salts and water. The mechanisms to maintain homeostasis that are described here are those observed in the human body. However, the fight-or-flight response exists in some form in all vertebrates.

The sympathetic nervous system regulates the stress response via the hypothalamus. Stressful stimuli cause the hypothalamus to signal the adrenal medulla (which mediates short-term stress responses) via nerve impulses, and the adrenal cortex, which mediates long-term stress responses, via the hormone adrenocorticotropic hormone (ACTH), which is produced by the anterior pituitary.

Short-Term Stress Response

When presented with a stressful situation, the body responds by calling for the release of hormones that provide a burst of energy. The hormones epinephrine (also known as adrenaline) and norepinephrine (also known as noradrenaline) are released by the adrenal medulla. How do these hormones provide a burst of energy? Epinephrine and norepinephrine increase blood glucose levels by stimulating the liver and skeletal muscles to break down glycogen and by stimulating glucose release by liver cells. Additionally, these hormones increase oxygen availability to cells by increasing the heart rate and dilating the bronchioles. The hormones also prioritize body function by increasing blood supply to essential organs such as the heart, brain, and skeletal muscles, while restricting blood flow to organs not in immediate need, such as the skin, digestive system, and kidneys. Epinephrine and norepinephrine are collectively called catecholamines.

Watch this Discovery Channel animation describing the flight-or-flight response.

A link to an interactive elements can be found at the bottom of this page.

Long-Term Stress Response

Long-term stress response differs from short-term stress response. The body cannot sustain the bursts of energy mediated by epinephrine and norepinephrine for long times. Instead, other hormones come into play. In a long-term stress response, the hypothalamus triggers the release of ACTH from the anterior pituitary gland. The adrenal cortex is stimulated by ACTH to release steroid hormones called corticosteroids. Corticosteroids turn on transcription of certain genes in the nuclei of target cells. They change enzyme concentrations in the cytoplasm and affect cellular metabolism. There are two main corticosteroids: glucocorticoids such as cortisol, and mineralocorticoids such as aldosterone. These hormones target the breakdown of fat into fatty acids in the adipose tissue. The fatty acids are released into the bloodstream for other tissues to use for ATP production. The glucocorticoidsprimarily affect glucose metabolism by stimulating glucose synthesis. Glucocorticoids also have anti-inflammatory properties through inhibition of the immune system. For example, cortisone is used as an anti-inflammatory medication; however, it cannot be used long term as it increases susceptibility to disease due to its immune-suppressing effects.

Mineralocorticoids function to regulate ion and water balance of the body. The hormone aldosterone stimulates the reabsorption of water and sodium ions in the kidney, which results in increased blood pressure and volume.

Hypersecretion of glucocorticoids can cause a condition known as Cushing’s disease, characterized by a shifting of fat storage areas of the body. This can cause the accumulation of adipose tissue in the face and neck, and excessive glucose in the blood. Hyposecretion of the corticosteroids can cause Addison’s disease, which may result in bronzing of the skin, hypoglycemia, and low electrolyte levels in the blood.


Hormonal Interactions in the Regulation of Plant Development

Plants exhibit a unique developmental flexibility to ever-changing environmental conditions. To achieve their profound adaptability, plants are able to maintain permanent stem cell populations and form new organs during the entire plant life cycle. Signaling substances, called plant hormones, such as auxin, cytokinin, abscisic acid, brassinosteroid, ethylene, gibberellin, jasmonic acid, and strigolactone, govern and coordinate these developmental processes. Physiological and genetic studies have dissected the molecular components of signal perception and transduction of the individual hormonal pathways. However, over recent years it has become evident that hormones do not act only in a linear pathway. Hormonal pathways are interconnected by a complex network of interactions and feedback circuits that determines the final outcome of the individual hormone actions. This raises questions about the molecular mechanisms underlying hormonal cross talk and about how these hormonal networks are established, maintained, and modulated throughout plant development.


Contents

Chronic stress and a lack of coping resources available or used by an individual can often lead to the development of psychological issues such as delusions, [7] depression and anxiety (see below for further information). [8] This is particularly true regarding chronic stressors. These are stressors that may not be as intense as an acute stressor like a natural disaster or a major accident, but they persist over longer periods of time. These types of stressors tend to have a more negative effect on health because they are sustained and thus require the body's physiological response to occur daily. [9]

This depletes the body's energy more quickly and usually occurs over long periods of time, especially when these microstressors cannot be avoided (i.e. stress of living in a dangerous neighborhood). See allostatic load for further discussion of the biological process by which chronic stress may affect the body. For example, studies have found that caregivers, particularly those of dementia patients, have higher levels of depression and slightly worse physical health than non-caregivers. [9]

When humans are under chronic stress, permanent changes in their physiological, emotional, and behavioral responses may occur. [10] Chronic stress can include events such as caring for a spouse with dementia, or may result from brief focal events that have long term effects, such as experiencing a sexual assault. Studies have also shown that psychological stress may directly contribute to the disproportionately high rates of coronary heart disease morbidity and mortality and its etiologic risk factors. Specifically, acute and chronic stress have been shown to raise serum lipids and are associated with clinical coronary events. [11]

However, it is possible for individuals to exhibit hardiness—a term referring to the ability to be both chronically stressed and healthy. [12] Even though psychological stress is often connected with illness or disease, most healthy individuals can still remain disease-free after being confronted with chronic stressful events. This suggests that there are individual differences in vulnerability to the potential pathogenic effects of stress individual differences in vulnerability arise due to both genetic and psychological factors. In addition, the age at which the stress is experienced can dictate its effect on health. Research suggests chronic stress at a young age can have lifelong effects on the biological, psychological, and behavioral responses to stress later in life. [13]

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". [14] The word 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 '30s, biological and psychological circles occasionally used the term to refer to a mental strain or to 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. [15] But ". stress as an explanation of lived experience is absent from both lay and expert life narratives before the 1930s". [16] Physiological stress represents a wide range of physical responses that occur as a direct effect of a stressor causing an upset in the homeostasis of the body. Upon immediate disruption of either psychological or physical equilibrium the body responds by stimulating the nervous, endocrine, and immune systems. The reaction of these systems causes a number of physical changes that have both short- and long-term effects on the body. [ citation needed ]

The Holmes and Rahe stress scale was developed as a method of assessing the risk of disease from life changes. [17] The scale lists both positive and negative changes that elicit stress. These include things such as a major holiday or marriage, or death of a spouse and firing from a job.

Homeostasis is a concept central to the idea of stress. [18] In biology, most biochemical processes strive to maintain equilibrium (homeostasis), 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 of constant flux moving about a homeostatic point that is that organism's optimal condition for living. [19] Factors causing an organism's condition to diverge too far from homeostasis can be experienced as stress. A life-threatening situation such as a major physical trauma or prolonged starvation can greatly disrupt homeostasis. On the other hand, an organism's attempt at restoring conditions back to or near homeostasis, often consuming energy and natural resources, can also be interpreted as stress. [20]

The ambiguity in defining this phenomenon was first recognized by Hans Selye (1907–1982) in 1926. In 1951 a commentator loosely summarized Selye's view of stress as something that ". in addition to being itself, was also the cause of itself, and the result of itself". [21] [22]

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". Neuroscientists such as 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". [23] Indeed, in 1995 Toates already defined stress as a "chronic state that arises only when defense mechanisms are either being chronically stretched or are actually failing," [24] while according to Ursin (1988) stress results from an inconsistency between expected events ("set value") and perceived events ("actual value") that cannot be resolved satisfactorily, [25] which also puts stress into the broader context of cognitive-consistency theory. [26]

Stress can have many profound effects on the human biological systems. [27] Biology primarily attempts to explain major concepts of stress using a stimulus-response paradigm, broadly comparable to 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 one should interpret these mechanisms 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.

The central nervous system works closely with the body's endocrine system to regulate these mechanisms. 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 there follows a brief biological background of neuroanatomy and neurochemistry and how they relate to stress. [ citation needed ]

Stress, either severe, acute stress or chronic low-grade stress may induce abnormalities in three principal regulatory systems in the body: serotonin systems, catecholamine systems, and the hypothalamic-pituitary-adrenocortical axis. Aggressive behavior has also been associated with abnormalities in these systems. [28]

The brain endocrine interactions are relevant in the translation of stress into physiological and psychological changes. The autonomic nervous system (ANS), as mentioned above, plays an important role in translating stress into a response. The ANS responds reflexively to both physical stressors (for example baroreception), and to higher level inputs from the brain. [29]

The ANS is composed of the parasympathetic nervous system and sympathetic nervous system, two branches that are both tonically active with opposing activities. The ANS directly innervates tissue through the postganglionic nerves, which is controlled by preganglionic neurons originating in the intermediolateral cell column. The ANS receives inputs from the medulla, hypothalamus, limbic system, prefrontal cortex, midbrain and monoamine nuclei. [30]

The activity of the sympathetic nervous system drives what is called the "fight or flight" response. The fight or flight response to emergency or stress involves mydriasis, increased heart rate and force contraction, vasoconstriction, bronchodilation, glycogenolysis, gluconeogenesis, lipolysis, sweating, decreased motility of the digestive system, secretion of the epinephrine and cortisol from the adrenal medulla, and relaxation of the bladder wall. The parasympathetic nervous response, "rest and digest", involves return to maintaining homeostasis, and involves miosis, bronchoconstriction, increased activity of the digestive system, and contraction of the bladder walls. [29] Complex relationships between protective and vulnerability factors on the effect of childhood home stress on psychological illness, cardiovascular illness and adaption have been observed. [31] ANS related mechanisms are thought to contribute to increased risk of cardiovascular disease after major stressful events. [32]

The HPA axis is a neuroendocrine system that mediates a stress response. Neurons in the hypothalamus, particularly the paraventricular nucleus, release vasopressin and corticotropin releasing hormone, which travel through the hypophysial portal vessel where they travel to and bind to the corticotropin-releasing hormone receptor on the anterior pituitary gland. Multiple CRH peptides have been identified, and receptors have been identified on multiple areas of the brain, including the amygdala. CRH is the main regulatory molecule of the release of ACTH. [33]

The secretion of ACTH into systemic circulation allows it to bind to and activate Melanocortin receptor, where it stimulates the release of steroid hormones. Steroid hormones bind to glucocorticoid receptors in the brain, providing negative feedback by reducing ACTH release. Some evidence supports a second long term feedback that is non-sensitive to cortisol secretion. The PVN of the hypothalamus receives inputs from the nucleus of the solitary tract, and lamina terminalis. Through these inputs, it receives and can respond to changes in blood. [33]

The PVN innervation from the brain stem nuclei, particularly the noradrenergic nuclei stimulate CRH release. Other regions of the hypothalamus both directly and indirectly inhibit HPA axis activity. Hypothalamic neurons involved in regulating energy balance also influence HPA axis activity through the release of neurotransmitters such as neuropeptide Y, which stimulates HPA axis activity. Generally, the amygdala stimulates, and the prefrontal cortex and hippocampus attenuate, HPA axis activity however, complex relationships do exist between the regions. [33]

The immune system may be heavily influenced by stress. The sympathetic nervous system innervates various immunological structures, such as bone marrow and the spleen, allowing for it to regulate immune function. The adrenergic substances released by the sympathetic nervous system can also bind to and influence various immunological cells, further providing a connection between the systems. The HPA axis ultimately results in the release of cortisol, which generally has immunosuppressive effects. However, the effect of stress on the immune system is disputed, and various models have been proposed in an attempt to account for both the supposedly "immunodeficiency" linked diseases and diseases involving hyper activation of the immune system. One model proposed to account for this suggests a push towards an imbalance of cellular immunity(Th1) and humoral immunity(Th2). The proposed imbalance involved hyperactivity of the Th2 system leading to some forms of immune hypersensitivity, while also increasing risk of some illnesses associated with decreased immune system function, such as infection and cancer. [6]

Chronic stress is a term sometimes used to differentiate it from acute stress. Definitions differ, and may be along the lines of continual activation of the stress response, [34] stress that causes an allostatic shift in bodily functions, [4] or just as "prolonged stress". [35] 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. [36] While responses to acute stressors typically do not impose a health burden on young, healthy individuals, chronic stress in older or unhealthy individuals may have long-term effects that are detrimental to health. [37]

Immunological Edit

Acute time-limited stressors, or stressors that lasted less than two hours, results in an up regulation of natural immunity and down regulation of specific immunity. This type of stress saw in increase in granulocytes, natural killer cells, IgA, Interleukin 6, and an increase in cell cytotoxicity. Brief naturalistic stressors elicit a shift from Th1(cellular) to Th2(humoral) immunity, while decreased T-cell proliferation, and natural killer cell cytotoxicity. Stressful event sequences did not elicit a consistent immune response however, some observations such as decreased T-Cell proliferation and cytotoxicity, increase or decrease in natural killer cell cytotoxicity, and an increase in mitogen PHA. Chronic stress elicited a shift toward Th2 immunity, as well as decreased interleukin 2, T cell proliferation, and antibody response to the influenza vaccine. Distant stressors did not consistently elicit a change in immune function. [6]

Infectious Edit

Some studies have observed increased risk of upper respiratory tract infection during chronic life stress. In patients with HIV, increased life stress and cortisol was associated with poorer progression of HIV. [34]

Chronic disease Edit

A link has been suggested between chronic stress and cardiovascular disease. [34] Stress appears to play a role in hypertension, and may further predispose people to other conditions associated with hypertension. [38] Stress may also precipitate a more serious, or relapse into abuse of alcohol. [4] Stress may also contribute to aging and chronic diseases in aging, such as depression and metabolic disorders. [39]

The immune system also plays a role in stress and the early stages of wound healing. It is responsible for preparing the tissue for repair and promoting recruitment of certain cells to the wound area. [36] 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. [40]

Development Edit

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. [41]

More generally, prenatal life, infancy, childhood, and adolescence are critical periods in which the vulnerability to stressors is particularly high. [42] [43]

Psychopathology Edit

Chronic stress is seen to affect the 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, although this can increase storage of flashbulb memories it decreases long-term potentiation (LTP). [44] [45] The hippocampus is important in the brain for storing certain kinds of memories and damage to the hippocampus can cause trouble in storing new memories but old memories, memories stored before the damage, are not lost. [46] Also high cortisol levels can be tied to the deterioration of the hippocampus and decline of memory that many older adults start to experience with age. [45] These mechanisms and processes may therefore contribute to age-related disease, or originate risk for earlier-onset disorders. For instance, extreme stress (e.g. trauma) is a requisite factor to produce stress-related disorders such as post-traumatic stress disorder. [5]

Chronic stress also shifts learning, forming a preference for habit based learning, and decreased task flexibility and spatial working memory, probably through alterations of the dopaminergic systems. [30] Stress may also increase reward associated with food, leading to weight gain and further changes in eating habits. [47] Stress may contribute to various disorders, such as fibromyalgia, [48] chronic fatigue syndrome, [49] depression, [50] and functional somatic syndromes. [51]

Eustress Edit

Selye published in year 1975 a model dividing stress into eustress and distress. [52] 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. [53]

Coping Edit

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, [54] 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.

A way to control stress is first dealing with what is causing the stress if it is something the individual has control over. Other methods to control stress and reduce it can be: to not procrastinate and leave tasks for the last minute, do things you like, exercise, do breathing routines, go out with friends, and take a break. Having support from a loved one also helps a lot in reducing stress. [45]

One study showed that the power of having support from a loved one, or just having social support, lowered stress in individual subjects. Painful shocks were applied to married women's ankles. In some trials women were able to hold their husband's hand, in other trials they held a stranger's hand, and then held no one's hand. When the women were holding their husband's hand, the response was reduced in many brain areas. When holding the stranger's hand the response was reduced a little, but not as much as when they were holding their husband's hand. Social support helps reduce stress and even more so if the support is from a loved one. [45]

Cognitive appraisal Edit

Lazarus [55] 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. [56]

Health risk factors Edit

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, [57] 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, [58][59] poor attachment histories, [60]sexual abuse) [61] 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.

General adaptation syndrome Edit

Physiologists define stress as how the body reacts to a stressor - a stimulus, real or imagined, that causes stress. Acute stressors affect an organism in the short term chronic stressors over the longer term. The general adaptation syndrome (GAS), developed by Hans Selye, is a profile of how organisms respond to stress GAS is characterized by three phases: a nonspecific mobilization phase, which promotes sympathetic nervous system activity a resistance phase, during which the organism makes efforts to cope with the threat and an exhaustion phase, which occurs if the organism fails to overcome the threat and depletes its physiological resources. [62]

Stage 1 Edit

Alarm is the first stage, which is divided into two phases: the shock phase and the antishock phase. [63]

  • Shock phase: During this phase, the body can endure changes such as hypovolemia, 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 and sympathetic nervous system activate the production of catecholamines including adrenaline, engaging the popularly-known fight-or-flight response. Adrenaline temporarily provides 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).

Stage 2 Edit

Resistance is the second stage. During this stage, increased secretion of glucocorticoids intensifies the body's systemic response. Glucocorticoids can increase the concentration of glucose, fat, and amino acid in blood. In high doses, one glucocorticoid, cortisol, begins to act similarly to a mineralocorticoid (aldosterone) 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. The body attempts to respond to stressful stimuli, but after prolonged activation, the body's chemical resources will be gradually depleted, leading to the final stage.

Stage 3 Edit

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 amino acid 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 in decompensation.

The result can manifest itself in obvious illnesses, such as general trouble with the digestive system (e.g. occult bleeding, melena, constipation/obstipation), diabetes, or even cardiovascular problems (angina pectoris), along with clinical depression and other mental illnesses. [ citation needed ]

The current usage of the word stress arose out of Hans 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. [64]

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. [64] He also coined the term stressor to refer to the causative event or stimulus, as opposed to the resulting state of stress.

Selye was in contact with the tobacco industry from 1958 and they were undeclared allies in litigation and the promotion of the concept of stress, clouding the link between smoking and cancer, and portraying smoking as a "diversion", or in Selye's concept a "deviation", from environmental stress. [65]

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. [64]

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 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. [66] 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. [14] [64]

The American Psychological Association's 2015 Stress In America Study [67] found that nationwide stress is on the rise and that the three leading sources of stress were "money", "family responsibility", and "work".


Nils Wiedemann and Nikolaus Pfanner
Vol. 86, 2017

Abstract

Mitochondria are essential organelles with numerous functions in cellular metabolism and homeostasis. Most of the >1,000 different mitochondrial proteins are synthesized as precursors in the cytosol and are imported into mitochondria by five transport . Read More

Figure 1: Overview of the five major protein import pathways of mitochondria. Presequence-carrying preproteins are imported by the translocase of the outer mitochondrial membrane (TOM) and the presequ.

Figure 2: The presequence pathway into the mitochondrial inner membrane (IM) and matrix. The translocase of the outer membrane (TOM) consists of three receptor proteins, the channel-forming protein To.

Figure 3: Role of the oxidase assembly (OXA) translocase in protein sorting. Proteins synthesized by mitochondrial ribosomes are exported into the inner membrane (IM) by the OXA translocase the ribos.

Figure 4: Carrier pathway into the inner membrane. The precursors of the hydrophobic metabolite carriers are synthesized without a cleavable presequence. The precursors are bound to cytosolic chaperon.

Figure 5: Mitochondrial intermembrane space import and assembly (MIA) machinery. Many intermembrane space (IMS) proteins contain characteristic cysteine motifs. The precursors are kept in a reduced an.

Figure 6: Biogenesis of β-barrel proteins of the outer mitochondrial membrane. The precursors of β-barrel proteins are initially imported by the translocase of the outer membrane (TOM), bind to small .

Figure 7: The dual role of mitochondrial distribution and morphology protein 10 (Mdm10) in protein assembly and organelle contact sites. Mdm10 associates with the sorting and assembly machinery (SAM) .

Figure 8: Multiple import pathways for integral α-helical proteins of the mitochondrial outer membrane. The precursors of proteins with an N-terminal signal anchor sequence are typically inserted into.

Figure 9: The mitochondrial contact site and cristae organizing system (MICOS) interacts with protein translocases. MICOS consists of two core subunits, Mic10 and Mic60. Mic10 forms large oligomers th.


Contents

CRH is produced by parvocellular neuroendocrine cells within the paraventricular nucleus of the hypothalamus and is released at the median eminence from neurosecretory terminals of these neurons into the primary capillary plexus of the hypothalamo-hypophyseal portal system. The portal system carries the CRH to the anterior lobe of the pituitary, where it stimulates corticotropes to secrete adrenocorticotropic hormone (ACTH) and other biologically-active substances (β-endorphin). ACTH stimulates the synthesis of cortisol, glucocorticoids, mineralocorticoids and DHEA. [7]

In the short term, CRH can suppress appetite, increase subjective feelings of anxiety, and perform other functions like boosting attention. Although the distal action of CRH is immunosuppression via the action of cortisol, CRH itself can actually heighten inflammation, a process being investigated in multiple sclerosis research. [8]

The CRH-1 receptor antagonist pexacerfont is currently under investigation for the treatment of generalized anxiety disorder. [9] Another CRH-1 antagonist antalarmin has been researched in animal studies for the treatment of anxiety, depression and other conditions, but no human trials with this compound have been carried out.

Also, abnormally high levels of CRH have been found in the cerebrospinal fluid of people that have committed suicide. [10]

Recent research has linked the activation of the CRH1 receptor with the euphoric feelings that accompany alcohol consumption. A CRH1 receptor antagonist developed by Pfizer, CP-154,526 is under investigation for the potential treatment of alcoholism. [11] [12]

Alpha-helical CRH-(9–41) acts as a CRH antagonist. [13]

CRH is also synthesized by the placenta and seems to determine the duration of pregnancy. [14]

Levels rise towards the end of pregnancy just before birth and current theory suggests three roles of CRH in parturition: [15]

  • Increases levels of dehydroepiandrosterone (DHEA) directly by action on the fetal adrenal gland, and indirectly via the mother's pituitary gland. DHEA has a role in preparing for and stimulating cervical contractions.
  • Increases prostaglandin availability in uteroplacental tissues. Prostaglandins activate cervical contractions.
  • Prior to parturition it may have a role inhibiting contractions, through increasing cAMP levels in the myometrium.

In culture, trophoblast CRH is inhibited by progesterone, which remains high throughout pregnancy. Its release is stimulated by glucocorticoids and catecholamines, which increase prior to parturition lifting this progesterone block. [16]

The 41-amino acid sequence of CRH was first discovered in sheep by Vale et al. in 1981. [17] Its full sequence is:

The rat and human peptides are identical and differ from the ovine sequence only by 7 amino acids. [18]

In mammals, studies suggest that CRH has no significant thyrotropic effect. However, in representatives of all non-mammalian vertebrates, it has been found that, in addition to its corticotropic function, CRH has a potent thyrotropic function, acting with TRH to control the thyroid axis (TRH has been found to be less potent than CRH in some species). [19] [20]

Corticotropin-releasing hormone has been shown to interact with its receptors corticotropin-releasing hormone receptor 1 (CRFR1) and corticotropin-releasing hormone 2 (CRFR2) in order to induce its effects. [21] [22] [23] Injection of CRF into the rodent paraventricular nucleus of the hypothalamus (PVN) can increase CRFR1 expression, with increased expression leading to depression-like behaviors. [24] Sex differences have also been observed with respect to both CRF and the receptors that it interacts with. CRFR1 has been shown to exist at higher levels in the female nucleus accumbens, olfactory tubercle, and rostral anteroventral periventricular nucleus (AVPV) when compared to males, while male voles show increased levels of CRFR2 in the bed nucleus of the stria terminalis compared to females. [25]


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Self-regulation of the autonomic nervous system (ANS) can essentially be broken down into two opposing functions: it goes up or it goes down!

In a car, we can press the gas pedal to access more energy, or the brake pedal to slow down or stop. Similarly, the ANS has two parts, or branches: the sympathetic nervous system (SNS), which makes us go up into greater arousal, and the parasympathetic nervous system (PNS), which helps us come down into calmer, less aroused states.

Upregulation means there’s more firing of nerve cells (neurons) along a nerve pathway. So, upregulation of the SNS refers to when this “going up” branch of the nervous system is more active. This “pressing of the gas pedal” increases the amount of energy available in the body. This is why the SNS is often referred to as the “fight-or-flight” nervous system, although it can also upregulate in pleasant situations requiring more energy.

Its opposite, and the focus of this article, is downregulation. Sympathetic downregulation brings down the charge along the pathways of the SNS. At the same time, the PNS upregulates, which helps the SNS downregulate. (We will examine the important exception to this general rule in a future article.)

Both upregulation and downregulation of the SNS are biological processes that we can feel and experience happening within us. Recently, a woman I work with in therapy was able to describe the involuntary muscular tensions, unpleasant pangs, and fluttering sensations of her anxiety (upregulation). She also described the wonderful (downregulation) sensations of her body finally letting go into blissful sleep when she settles down in bed at night.

As most of us can intuit, SNS upregulation can feel terrible when it’s a response to something stressful happening. However, SNS upregulation can also feel great when it’s in response to something fun or exciting: our team scoring a touchdown, or dancing when our favorite song comes on. In contrast, SNS downregulation almost always feels soothing, calming, or relaxing.

I am focusing on SNS downregulation because it’s incompatible with states of anxiety, rage, or stress. Additionally, SNS downregulation keeps the SNS in check, so that it doesn’t “overshoot” and produce too much stress to effectively cope with a problem.

So, then, how do we encourage SNS downregulation? How do we help the body settle down into a state in which it can rest, digest, and repair? For that matter, how do we know when we’re in a downregulated state?

Well, here’s the catch. Downregulating the stress response is an acquired capacity. It’s like a muscle: you have to build it over time in order for it to be strong.

Although infants are born with the capacity for stress response (fussing, crying, etc.), their parasympathetic pathways, which help downregulate the SNS stress response, are not online at birth. This means babies can go up, but they can’t come down on their own. (They will go into a “freeze” state if ignored long enough this looks calm, but it really isn’t.) The baby’s nervous system develops the ability to calm down through thousands and thousands of supportive, soothing interactions with caregivers. At first, the caregiver is essentially functioning as the child’s parasympathetic nervous system. The development of this “braking system” continues throughout childhood, through continued positive interactions that meet the child’s needs.

There are many situations in which a child may not receive enough soothing in order to learn to downregulate sufficiently. These situations are not always the fault of the parents. Perhaps the child’s mother had a lot of her own unmanaged anxiety, was depressed, and/or experienced posttraumatic stress. Or maybe the family lived in poverty, with constant stressors impacting everyone’s sense of safety. Perhaps someone in the family passed away or suffered a major illness, rendering them unavailable for care. Maybe the child grew up in wartime or, unbeknownst to their parents, was frequently bullied at school.

Great things happen when we are parasympathetically dominant. Our breath is full, slow, and deep. The digestive system works well. The body can focus on repair, including reduction of inflammation, tissue repair, and hormone production. Subjectively, people feel fully present and alive. Many report feeling a pleasant softness and warmth, perhaps even throughout their bodies.

It’s important to point out that disconnecting from stress is not the same as resolving (downregulating) it. Alcohol and drugs, eating disorders, exercise or sexual compulsion, or even “zoning out” on the internet may make the chronically stuck upregulation of the SNS seem to go away for a time. However, as the people I work with in the therapy room could tell you, it’s not the same as sinking into a lovely, full-body sense of calm and relaxation.

Great things happen when we are parasympathetically dominant. Our breath is full, slow, and deep. The digestive system works well. The body can focus on repair, including reduction of inflammation, tissue repair, and hormone production. Subjectively, people feel fully present and alive. Many report feeling a pleasant softness and warmth, perhaps even throughout their bodies. When the SNS is on “standby” and the PNS is more active, people have a “buffer” for stress. They have energy to get through their day, but they can stay calm and present in challenging situations.

One of my first tasks in therapy is to assess and support the person’s ability to downregulate their stress responses. After they are provoked by something, how quickly and smoothly does their system deactivate? Are they still bothered by a small aversive event hours or days afterward?

Here’s a vital point often overlooked by therapists who haven’t had sufficient training in this area: In therapy, it is essential to make sure the person has the ability to downregulate the stress response before going into highly stressful material. In other words, you should never go into material that’s overwhelming, because overwhelming inherently means it’s bigger than your capacity to deal with it. So instead of the issue resolving, more symptoms arise. The way around this is to first support the capacity for downregulation. Then, only after this “braking system” is on board, take the difficult material a small bit at a time.

If someone doesn’t have a strong enough ability to come out of the stress response, how can they develop it?

  • Therapy: Working with downregulation of the stress response can be tricky, as it involves the deepest survival energies of the body. It is advisable to work with a therapist who has extensive training in this area. Remember, SNS downregulation was originally designed to come online under the guidance of another person (usually a parent) whose nervous system is well-developed.
  • Relaxation: Some people benefit from seeking activities or situations that cause the relaxation response and then deliberately spending time “feeling into” the resulting good sensations in their body. However, in relaxation states, some people experience a rebound in tension, stress, or anxiety. This is called “relaxation-induced anxiety” (RIA) or, in severe cases, “relaxation-induced panic.” In my experience, people with RIA are well served by working with a trained practitioner.
  • Physical exercise: Exercise is often helpful, as it tends to burn off excess SNS charge and encourage the production of endorphins. Exercise promotes good mood, self-esteem, and a sense of accomplishment.
  • Meditation: There are many forms of meditation, some of which specifically aim to produce downregulated states. However, in my experience, meditation can be unhelpful for some people who have a lot of traumatic response stored in their nervous systems. In these cases, their nervous systems simply won’t cooperate, and those around them may not have the awareness or tools to work with this issue.
  • Resonance: Simply put, resonance is the feeling you get from being around another person or other living being. I usually explain it by asking people to think of how they feel when they place their open palm onto the rib cage of a calm, happy dog. That feeling of warmth, relaxation, and well-being is a downregulatory feeling obtained via resonance with the dog’s nervous system. Of course, when others around us are tense, our bodies tend to pick up on that and become tense too. Thus, being around stressed, anxious, or angry people is usually the opposite of what’s needed to develop SNS downregulation.

In summary, the ability to go within and really settle oneself is developed during infancy and childhood. This capacity to downregulate stress states is important in maintaining health, relationships, and happiness. Those whose life circumstances didn’t permit development of this capacity during childhood can still develop it through awareness and work with a skilled professional.


Adrenal medulla hormones - adrenaline and noradrenaline

Two non-steroid hormones produced by the adrenal gland are adrenaline (also called epinephrine) and noradrenaline (also called norepinephrine).

Adrenaline is often called the “stress hormone” because it is the major hormone secreted in response to stress.

The adrenal medulla consists of modified neurons of the sympathetic nervous system. The production of adrenaline and noradrenaline is under the control of the hypothalamus via this direct connection with the sympathetic nervous system.

The hormones - adrenaline and noradrenaline also serve as excitatory neurotransmitters in the sympathetic nervous system.

The adrenal medulla secretes a mixture of 85 percent adrenaline and 15 percent noradrenaline.

Adrenaline and noradrenaline act to increase heart rate and blood pressure, and cause vasodilation (widening) of blood vessels in the heart and respiratory system.

These hormones also stimulate the liver to break down stored glycogen and release glucose into the blood. When the body is “at rest,” these two hormones sufficiently stimulate cardiovascular function to maintain adequate blood pressure without additional input by the sympathetic nervous system.

Vudeo: Human endocrine system: adrenal glands - epinephrine(adrenaline) and aldosterone


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A timeline for social stress

Socially interacting individuals perceive, generate, and integrate various relevant sensory stimuli during an interaction. For male A. carolinensis that includes visual stimuli such as eyespots and stereotyped behavior. However, even before social interactions occur(Fig. 1), the neuroendocrine status of an individual (stage 1), perhaps influenced by previous interactions(stage 4), can influence the rate and probability of the behavioral responses(Summers et al., 2005b). Tonic neuroendocrine status sets the stage for behavioral tone (stage 1), which is primarily inhibitory regulation of aggressive behavior. High serotonergic activity in reactive submissive subordinate males, and those that will become so appears to inhibit aggression. On the other hand, in putatively proactive(Koolhaas et al., 1999) and aggressive dominant males, tonically low 5-HT release lowers the threshold,making aggression much more rapid and likely. Neuroendocrine tone prior to aggressive interaction may be subsequently influenced by motivational factors(stage 2), including perception of a combatant and his sign stimuli, which corresponds to changes in dopaminergic activity in specific brain nuclei. Brief presentation of a simulated opponent is effective in evoking rapid changes in neuroendocrine activity. While sympathetically mediated plasma catecholamine levels were no different from increases elicited by environmental disturbance, social challenge caused distinct changes in accumbal and amygdalar DA and 5-HT levels(Watt et al., 2006). Changes in the amygdala are associated with general social threat presence. In concert with amygdalar activity, the level of perceived social threat, individual variation in threat level assessment, and motivation to convey aggressiveness,all affect monoamine levels in the nucleus accumbens. This suggests that perception of a non-displaying opponent is sufficient both for recognition of social context and for inducing rapid activity changes in key forebrain limbic nuclei to initiate appropriate behavioral responses. The latency to aggressive behavior, attack and darkening of the eyespot sign stimuli are most rapid in those that become dominant. However, regardless of level of aggressive behavioral expression and individual social status, once agonistic interactions begin, stress related elevation in serotonergic activity in aggression neurocircuitry and glucocorticoids in plasma occurs rapidly. For a short period, aggressive behavior is elevated in both dominant and subordinate animals, despite high serotonergic and glucocorticoid activity (stage 3). However, the stress response of dominant males to this aggressive interaction is relatively short lived, and serotonergic activity along with glucocorticoid concentrations return to normal. For subordinate males, chronically elevated glucocorticoid (Greenberg et al.,1984) and serotonergic activity (stage 4) limits aggressive behavior while they are in contact with the dominant male, and again if they are reintroduced to the same dominant male. Presumably, these chronically elevated stress chemicals may be reflected in the elevated serotonergic activity measured before aggressive interaction (stage 1). However,subordinate males actually are more aggressive in a second aggressive bout when the dominant male that he is fighting is unknown to him(Forster et al., 2005). Whether elevated glucocorticoids plays a role in enhanced aggression towards an unknown opponent remains to be tested. Previous interactions are known to influence aggressive responses, even if it simply involves watching aggression between other individuals (Oliveira et al., 2001 Oliveira et al.,1998). In addition, bullied individuals react more aggressively toward a different smaller opponent(Øverli et al.,2004).


Watch the video: Ένζυμα - βιολογικοί καταλύτες (May 2022).


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