Alterations in emotional and associative learning i. However, recent evidence with optogenetics approaches indicates that PVN projections to the CeA are activated during retrieval of long-term fear memories.
In contrast, retrieval of short-term memories is mostly dependent on PFC inputs to the BLA, indicating a time-dependent shift in fear memories circuits Do-Monte et al. Specifically, dorsal PAG is related to unconditioned threats exposure and ventral PAG is activated in conditioned threats, each one with distinct behavioral outputs.
Another important limbic structure for stress processing is the hippocampal formation McEwen et al. The hippocampal inhibitory control over the HPA axis acts in a negative feedback manner inhibiting it Jacobson and Sapolsky, ; Herman et al. However, the CA1 and subiculum monosynaptic glutamatergic efferents to PL and IL can become functionally disrupted after intense psychological stress Zheng and Zhang, Therefore, in the presence of psychological stressors, if the activity of the amygdala and HIPPO becomes more prevalent, the stress system can switch to a bottom-up control Arnsten, On top of that, prolonged psychological stress decreases glutamatergic projection to interneurons in BLA, leading to loss of BLA inhibition by the PFC and finally, to the hyperexcitability of BLA, which is responsible for behavioral abnormalities related to stress Wei et al.
At this point, among several hypothalamic nuclei that are directly involved in regulating HPA axis and autonomic responses to stressors, the PVN stands out as the principal integrator of stress signals Herman et al. Many of the above circuitry and brain areas responsible for physical and psychological stressors may sound exclusively related to brainstem and forebrain, respectively. However, some structures are also engaged with different modalities of stressor Figure 2.
The best-characterized reward circuit in the brain is made up of dopaminergic neurons in the VTA that project to the NAc, a subdivision of the ventral striatum Bath et al.
The primary brain reward centers are inter-connected in complex ways in the brain reward circuitry, but mostly VTA and NAc regulates limbic areas mentioned above Heshmati and Russo, The dopaminergic tonus of VTA is fundamental to the recognition of rewards or punishment in the environment Russo and Nestler, On the other hand, the optogenetic stimulation of VTA dopaminergic neurons drives to a conditioned place preference Tsai et al.
However, VTA is composed by different neuronal subpopulations, which participate in distinct circuits that encode different motivational signature Lammel et al. Indeed, dopaminergic neurons that innervate the mPFC show reduced firing after social defeat chronic stress Chaudhury et al. Dopaminergic neurons in VTA exhibit two patterns of spontaneous firing activity: a slow-frequency, single-spike firing and a burst firing, effectively regulating the activity of neurons in dopaminergic target areas and encoding reward-related signals Grace et al.
This mechanism of encoding and engaging specific networks makes sense since the behavioral response to a rewarding approach vs. Accordingly, associating this fined-tuned VTA regulation to the stress processing, it has been proposed that a specific ventral VTA pathway is related to painful physical stress. Several findings showed that dopaminergic cells that specifically project to the mPFC regulate the process of noxious stimuli Abercrombie et al.
But it is important to mention that although dopamine has a central role in processing physical stressors, in this scenario, the NAc detains the central role in regulating the reward system Grace et al. Therefore, we can see that while mesocortical pathways encode physical processing, the NAc may represent an important hub in processing psychological stress.
Not only the PFC activity corresponds to an integrative hot point of limbic and reward circuitry, but also its contribution to the inhibition of the HPA axis by PFC top-down control is crucial.
The CeA, previously mentioned as a central hub in fear response is also considered as a key node for stress integration Ulrich-Lai and Herman, The NTS can be activated during conditioning paradigms, suggesting that this pathway also plays a role in the integration of anticipatory stress Pezzone et al.
It is important to highlight that different modalities of stressors that activate the PVN also activate the LC-Norepinephrine LC-NE system, such as restraint, shock notably unpredictable , audiogenic stress, autonomic and immunological challenges and also social stress Wood and Valentino, The LC is a compact pontine nucleus adjacent to the fourth ventricle and houses the majority of the NE-expressing neurons in the brain and innervates the entire neuraxis Swanson and Hartman, Recent techniques, such as chemogenetics, optogenetics, combined with traditional retrograde tracing, which enable selective manipulation of LC-NE system in rodents, determined the pivotal role of the LC-NE, for example, for stress-induced anxiety-like behavior McCall et al.
Interestingly, Corticotrophin Release Hormone CRH , which initially was discovered and defined as the hormone that initiates the cascade that ultimately leads to glucocorticoids release, seems to stand out as the molecule that coordinates the cross-talk between the two systems Valentino and Van Bockstaele, Different structures that coordinate autonomic and limbic processing such as CeA Van Bockstaele et al.
This communication between HPA and LC-NE axis determines the structural basis for emotional arousal, facilitates cognition and promote flexible behavioral responses to stress Cole and Koob, ; Valentino and Van Bockstaele, , since CRH release in the LC during stress facilitates shifting of attention between diverse stimuli Snyder et al. Therefore, this crosstalk enables organisms to tailor different strategies to coping with constant changing environmental challenges.
Each pre-ganglionic fiber connects with many post-ganglionic neurons located in one or several pre-spinal ganglia or sympathetic paravertebral nuclei Boron and Boulpaep, Although, there are many efferent pathways of the ANS, only two neurons are necessary to transmit impulses between the CNS to the effector tissue Mccorry, Other pre-ganglionic neurons, which end at the spinal cord, do not make synapses with a post-ganglionic neuron.
For instance, they make synapses directly with chromaffin cells in the adrenal medulla Mccorry, ; Boron and Boulpaep, Thus, these two components increase the capacity of the sympathetic division in influencing body visceral responses Boron and Boulpaep, The sympathetic system activation leads to activation of signaling pathways that evoke changes in blood vessels, glands, visceral organs and smooth muscles Tank and Lee Wong, Pre-ganglionic parasympathetic neurons originate from craniosacral vertebral segments brainstem and sacral spinal cord synapse with post-ganglionic neurons in the terminal nodes located more peripherally, and usually on the wall of the target organs.
Post-parasympathetic ganglionic neurons stimulate the muscarinic and nicotinic receptors present on the membrane of the target cells by releasing acetylcholine Boron and Boulpaep, The effect caused by any of these substances, acetylcholine, norepinephrine and epinephrine, depends on the biochemical properties of the cells and on the receptor distribution in a determined tissue Mccorry, Although, these sympathetic and parasympathetic systems act independently from each other Antunes-Rodrigues et al.
E and NE interact with adrenergic receptors present in cell membranes of smooth muscles and in numerous organs, as well as in neurons widespread in the CNS Mccorry, ; Tank and Lee Wong, These receptors are the G-protein coupled receptors GPCRs , which are homologous to muscarinic receptors, i. Their effects include: maintaining alertness, metabolic actions increased glucose via glycogenolysis and gluconeogenesis, lipolysis, increased oxygen consumption and thermogenesis and cardiovascular actions Aires, The central noradrenergic system, specifically the LC is involved in multiple neurochemical circuits, having connections with neuroanatomical structures involved in the stress response, such as the HIPPO, amygdala and temporal neocortex.
Studies indicate an important role of the LC in response to acute stress Myers et al. However, chronic activation of the LC may have a potential role in the development of pathological behaviors related to stress Southwick et al.
Thus, the release of NE has central actions, coordinates and modulates autonomic, endocrine and neuroendocrine responses, through extensive brain and spinal cord connections, while direct projections from LC to medial parvocellular division of the PVN Cunningham and Sawchenko, allows the modulation of the HPA axis Armario et al. On the other hand, the activity of LC itself may be influenced by CRH through afferent projections from amygdala and brainstem nuclei McCall et al.
When an organism faces a threatening stimulus, whether it is psychological or physical, as explained in the previous sections, many brain areas are activated in a coordinated fashion to recruit a complex structure known as hypothalamus, which is composed by many sub nuclei.
As already discussed, among those nuclei is the PVN, which is responsible for eliciting the activation of the HPA axis, one of the main components of the stress response. The PVN synthesizes three different neurochemical compounds that behave either as neurotransmitters or hormones, depending on where they are acting. These compounds are oxytocin, vasopressin and CRH Vale et al.
ACTH is secreted through the hypophyseal portal system, and acts on the cortex of the adrenal gland, more specifically on the middle layer named fascicullata Vale et al. The main glucocorticoid in humans is cortisol, and its equivalent in rodents is corticosterone de Kloet, Although the HPA axis has an ultradian rhythm Young et al.
There are many evidences indicating that the suprachiasmatic nucleus SCN of the hypothalamus is the generator of the circadian rhythm Welsh et al. This phenomenon is called short and long negative feedback loops, respectively de Kloet et al. Glucocorticoids are steroids and easily trespass cell membranes and since they are released in the bloodstream they can virtually reach any cell in the body. Although peripherally the glucocorticoids act massively in several target-organs, here we focus on their effects on the brain.
Cortisol, or corticosterone in rodents, exerts their effects in the brain by binding to two types of receptors, the glucocorticoid receptor GR and the mineralocorticoid receptor MR; Reul and de Kloet, ; de Kloet et al. These receptors mediate the effects of glucocorticoids in the brain through genomic and non-genomic mechanisms Verkuyl et al.
Such difference is translated to receptor occupancy throughout the day, during the through phase of the circadian cycle, when glucocorticoid levels are low, MRs are occupied whereas the GRs are mostly free. During the peak phase of the circadian cycle, or after high glucocorticoid release due to the stress response, MRs are completely occupied while GRs are partially occupied Kitchener et al. Although glucocorticoids are able to reach all neurons in the brain, they exert effects on those neurons expressing GRs and MRs.
GRs are abundant and widely spread throughout the brain. On the other hand, MRs are expressed in restricted areas of the brain Reul and de Kloet, Moreover, it has also been shown that not only genomic processes are triggered by GR and MR, actually there are studies clearly showing rapid effects of membrane-located MR and GR activation Borski, ; Johnson et al.
Important to mention, it has been demonstrated that GR levels, and consequently HPA axis function, can be modulated by the environment, as well as life experiences acute and chronic stressors , through stable changes in the DNA chromatin, which does not alter DNA sequence, a mechanism known as epigenetics Hunter et al.
Alterations such as methylation and acetylation of histones occur genomewide enhancing or hampering chromatin activity, however DNA methylation can also occur in a gene-specific fashion altering its expression Tsankova et al. In fact, Weaver et al. These authors demonstrated that pups, which received low care licking and grooming the pups from their dams, had higher hippocampal NC3R1 methylation associated with lower GR expression, when compared to those that received high levels of licking and grooming.
Epigenetic modulation of GR expression has also been described in humans as highlighted by Palma-Gudiel et al. In the other hand, pre-clinical data have associated stress-induced epigenetic alterations with vulnerability or resilience to psychiatry-like conditions Covington et al.
Although, the discovery of the interplay between the inflammatory and endocrine systems is dated as a long-time story, it still remains as a hot topic in the field of stress research. At the same period Hans Selye discovered his canonical findings on stress, the prestigious Mayo Clinique developed the substance E Neeck, ; Hillier, ; Lupien, This substance crystalized by Dr. Kendall Mason et al. Most recently, research on the relationship between stress hormones and immune system has unraveled many intricate pathways that also can be explored for their clinical implications.
It has been postulated that besides preparing the body to deal with the environment demands, stress activates the immune system, which engages active defense against physical injury and pathogens. Ultimately, cytokines are produced to promote multiple kinds of inflammatory responses Takahashi et al. But reports stated that stress-enhanced inflammatory activity is present in the absence of infectious pathogens, especially in depressed patients Audet et al.
To address whether stress or its hormones are pro or anti-inflammatory, evidence using rodent models demonstrated that stress itself can be both pro- and anti-inflammatory.
Some authors have proposed that the timing of immune challenges and measurements determines the direction of glucocorticoid actions. Those authors proposed that glucocorticoids initially present anti-inflammatory action, but later on sensitizes the immune response on the recovery phase after stressor; Frank et al.
Stress can directly influence immune signaling in two main ways, by reducing the inhibitory effects of glucocorticoid actions, or by directly stimulating the immune system via HPA axis and SAM Liu et al. But not only the neural components of stress engage the immune system, the immune system also affects the CNS, modulating the HPA axis Berkenbosch et al.
Therefore, acutely, stressful experiences enhanced levels of circulatory pro-inflammatory cytokines Steptoe et al. Some of these inflammatory cytokines are either locally produced by activated microglia Wohleb et al. Interestingly, the sites that have increased pro-inflammatory immune reactivity appear to be related to acute stressor modalities.
Stress mediators operate in a feedback loop after HPA axis activation, and regulate, in a positive or negative way, different brain structures to restore homeostasis de Kloet et al. When the timing of stress response is inappropriate, aberrant HPA axis activity could lead to pathological states Heim et al.
Moreover, stress also differs when it occurs in early-life or adulthood of an individual, which can increase or decrease the possibility of developing brain disorders Lupien et al. In ultradian and circadian cycles, peaks of corticosterone release contribute to regulation of basal metabolic demand and the responsiveness of stress Lightman and Conway-Campbell, The origin of pulsatile corticosterone release in an ultradian and circadian fashion is not fully elucidated, but it has been a general assumption that the hypothalamus modulates this phenomenon, specifically, the hypothalamic SCN has efferent projections to neuroendocrine cells in the PVN that trigger the HPA axis activation Engeland and Arnhold, Acute stress mediators start acting within seconds after the stressor detection and provide quick responses to an appropriated strategy, involving modulation of limbic-cortical circuits Bains et al.
These effects of corticosterone in the PVN occur mainly via non-genomic GR activity and endocannabinoid signaling Di et al. Interestingly, firing frequency of BLA neurons remains at high levels even after corticosterone washout, mainly modulated by GR and cannabinoid receptor 1 Karst et al. In cortical structures, such as the PFC, acute stress situation increases GR-dependent glutamate release Musazzi et al. By contrast, neurons in the BLA and NAc increase dendritic density, increase excitatory tone and decrease inhibitory tone in this context Vyas et al.
It is interesting to note that when chronic stress is experienced early in life, its effects on the brain last longer than when it occurs during adulthood Lupien et al. At this point, in our evolutionary history, stress could be implied in a maladaptive performance in a large proportion of the population, considering the large number of comorbidities that occur from dysfunction of the stress system de Kloet et al.
The HPA axis dysregulation and prolonged exposure to glucocorticoids reduce the ability of neurons to resist insults, increasing the risk for injury by other toxic events Lupien et al.
Moreover, new researches have called attention to adversities in early life, which are greatly associated with higher vulnerability to disorders later in life, causing a long-term impact in the circuitry responsible for cognitive and emotional function Gold et al.
In this sense, both basic and clinical researches have advanced in recent years but much remains to be understood about the subject. In general, animal models have provided a comprehensive view of the stress effects on the brain, abundantly on the limbic structures Hariri and Holmes, The amygdala is a highly conserved brain structure that is fundamental to detect potential danger Janak and Tye, , while HIPPO provides support to encoding environmental information associated with the stressor Herman et al.
The identification of these highly evolutionary conserved networks that are affected by stress, allowed important discoveries in clinical research Hariri and Holmes, Increasing data highlight that highly debilitating stress comorbidities such as depression, anxiety disorders, PTSD and epilepsy share pathogenic mechanisms with stress dysfunction and between each other.
These mechanisms are probably deeply connected and the structural and functional change caused by one disease triggers the other, despite these it is still not clear on the relationship between them Gold et al. Considering this, we presented in this review a short glimpse of how stress is related to these CNS pathologies.
For further review, we suggest to look into the literature cited here. A significant percentage of patients with Major Depression MD have increased concentrations of cortisol in plasma, urine and cerebrospinal fluid, exaggerated cortisol response after ACTH hormone stimulation and hyperplasia of the pituitary and adrenal glands Gold et al. Chronic stressors in early life result in permanent epigenetic, endocrine, neural, immune and inflammatory changes, constituting a relevant risk factor for several neuropsychiatric diseases in adult life Xiong and Zhang, ; Zhang et al.
In epilepsy, stress can influence in multiple ways, often as seizure-precipitating but also increased the risk of epilepsy development van Campen et al. However, studies indicate that infancy coincides with a period referred as hyporesponsive period to stress Stress Hyporesponsive Period—SHRP , which is supposed to be a period that is necessary for the proper development of the brain after birth Sapolsky and Meaney, ; de Kloet et al.
It corresponds with a period of low peripheral concentration of glucocorticoids, in which a physiological response to mild stress increased glucocorticoids and adrenaline, increased cardiovascular circulation, immune system modifications does not occur. There is no consensus when exactly this period starts or how long it lasts, but it is suggested that it could last from around the 2nd to 12th postnatal day in rodents Sapolsky and Meaney, and up to 5 years in humans Gunnar and Donzella, ; Curley et al.
Interestingly, psychological Sapolsky and Meaney, and multimodal stressors Godoy et al. The effects of stress during early life ELS on the brain have been deeply studied for review see Lupien et al.
More recently it has been demonstrated that ELS led to an early emergence of timed developmental suppression of fear behavior that correlates to an early maturation Bath et al. Depression-anxiety comorbidity is strongly associated with impairment in health, as well as in cognitive and emotional functions Kroenke et al. Similarly, chronic treatment with corticosterone not only generates depressive-like symptoms but also induces amygdala hypertrophy and increases anxiogenic behavioral responses Mitra and Sapolsky, In humans, individual differences in amygdala reactivity to threat-related facial expressions predict vulnerability to stress, such as subjects with hyperactivation of the amygdala are more likely to experience depression and anxiety symptoms Yang et al.
Also, hyperactivation of LC-NE is related to neuropsychiatric disorders such as PTSD and MD, the activation of this system out of proper context may lead to hyperarousal, loss of concentration, restlessness and impaired focused attention, which are characteristic symptoms of stress-related psychiatric disorders Southwick et al.
However, some clinical investigations reported low levels of cortisol in PTSD patients, while individuals with anxiety disorders or depression show an increase of cortisol response Daskalakis et al. However, there are studies also showing no differences Baker et al. Because this topic remains controversial in the literature, more insights such as those presented in Zoladz and Diamond are recommended. Actually, exposure to severe stressors such as urban violence, sexual abuse, combat in war, disasters and many others, is believed to be associated to development of PTSD, leading individuals to present physiological and behavioral alterations including nightmares, hypervigilance, flashbacks of the trauma and sleep disturbances DSM-V, Zoladz and Diamond, ; Yehuda et al.
Although a positive correlation has been reported between the severity of the trauma and PTSD symptomatology in veteran soldiers Snow et al. It has also been reported that the type of stressor seems to play a bigger role than its severity Kessler et al.
Interestingly, not everybody develops PTSD after trauma exposure, which suggests that other factors despite the trauma severity and type , such as socioeconomic profile, psychiatry disorder history, substance abuse, immune system, genetics and epigenetics play a role on the susceptibility for PTSD. Actually, there are evidences showing that the interplay between environment and genetics and epigenetics are risk factors for PTSD development Mehta and Binder, ; Wilker and Kolassa, ; DiGangi et al.
In patients with epilepsy, stress is usually reported as one of the major seizure precipitants Frucht et al. In adults, there is a positive correlation between stress and frequency of epileptic seizures Swinkels et al.
Therefore, many evidences indicate that stress is relevant in the phases of epileptogenesis, both in adults and young people. Corticosterone plays a contributory role in the epileptogenic process in animal models of epilepsy Karst et al. Other pathologies affect the peripheral nervous system and many different organs. The CRH circuitry connecting LC-NE and PVN is strategically positioned so it may control autonomic responses to visceral stimuli and may underlie the co-morbidity of pelvic visceral and behavioral symptoms observed in many stress-related disorders Valentino et al.
Although most immediate responses coordinated by SAM axis are important for survival, when levels of circulating catecholamines are maintained elevated for prolonged periods of time, they can lead to different pathologies.
In the past decades identification of neuronal circuits associated to stress, as well as their interaction with mediators over time, was critical not only for understanding physiological stress responses, but also to understand their clinical implications.
Stress-related brain disorders are extremely prevalent, so identification of mechanisms related to stress and consequently the potential development of new pharmacological therapeutic approaches are necessary and urgent.
As an example, pre-clinical studies on psychopathology-related topics are being done with classic GR antagonist RU Arp et al. These compounds are the so-called selective glucocorticoid receptor modulators SGRMs which upon binding to the GR promote a differential conformation of the receptor leading to differential recruitment of corregulators and therefore enhancing or hampering gene expression in a cell-tissue specific manner.
Thus, the same compound can induce agonist- and antagonist-like effects, for instance the SGRMs C acts as an antagonist in neurogenesis related processes such as proliferation and survival of hippocampal neurons, and as an agonist in fear memory retention on the avoidance behavior task Zalachoras et al.
In the other hand the C compound acts as an antagonist in the same task whereas showing agonist effects on plasmatic corticosterone levels Atucha et al. From our own experience the Wistar Audiogenic Rat WAR strain is a genetically selected experimental epilepsy model, which displays after 56 generations of inbreeding, not only seizure-associated behaviors and electrophysiological alterations, but also comorbidities which includes high anxiety, hyperactive HPA axis, adrenal medulla hyperplasia, ectopic beats, high blood pressure, tachychardia and central respiratory alterations Fazan et al.
Further experiments are therefore needed in order to evaluate the pharmacological profile of new anti-epileptic, anxiolytic or even anti-depressive drugs, using as a model of comorbidities of the WAR strain. In the clinical scenario a final comment can be done, when referring to the additional complexity associated, for example, to the presence of comorbid neurological and neuropsychiatric conditions, such as, for example, the epilepsies, autism and mood disorders, recognizing that we are talking about network disorders Kanner et al.
In the particular case of depression, anxiety and epilepsy, Kanner and Nogueira et al. Therefore stressors, which work as triggers, such as those cited in the current review, are common to all the situations.
On the other hand, Rayner highlights that complex cognitive networks associated to depression interact so strongly with epilepsy related networks, in a way that the difficulties with diagnosis and treatment increase, as soon as we recognize that those networks share common structures and mechanisms.
One way to overcome this, in order to make relevant and reliable contributions in this field, is the construction of algorhythms from computational neuroscience modeling, where actual data, either from basic science or from human clinical settings are used to generate predictions with translational value.
In that context, recently Spiga et al. In brief, these authors showed in a rat model, that although the steroidogenic regulatory network architecture is sufficient to respond to both small and large ACTH perturbations, coupling the regulatory network with the immune system would explain dissociated dynamics between ACTH and glucocorticoids observed when inflammatory stress is present.
We are able to adapt to the dynamic and challenging environment we live in, as well as to unexpected life events we face every now and then. Examples are endless and, most of the time, we can overcome these events.
We are able to do so because the existence of quite complex networks, which integrate body and brain, in order to enhance performance, promote adaptation and ultimately survival, the stress system. A diversity of brain areas integrates sensorial, physiological and emotional signs.
When different brain networks interpret these signs as a threat real or potential , a series of responses follow, increasing performance to deal with the situation and retain that information to better cope with similar situations in the future, characterizing the stress response.
The downside of the stress system is that sometimes it is not able to overcome the environmental, physiological or emotional demand. The aim of this review article was to bring comprehensive basic concepts about the stress system such as history of stress research, neuroanatomy, major effectors of the stress response, time domains of stress and the clinical implication of malfunction might have over the susceptibility to the development of increasingly-common brapdin disorders.
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Abercrombie, E. Differential effect of stress on in vivo dopamine release in striatum, nucleus accumbens, and medial frontal cortex.
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Search Search for:. The Centre for Studies on Human Stress CSHS is dedicated to improving the physical and mental health of Canadians by empowering individuals with scientifically grounded information on the effects of stress on the brain and body.
Search here:. History of stress. History of stress The term stress was borrowed from the field of physics by one of the fathers of stress research Hans Selye.
The Great Debate Selye pioneered the field of stress research and provided convincing arguments that stress impacted health.
Stage 1 : Alarm reaction This is the immediate reaction to a stressor. Did you know? Hans Selye pioneered the field of stress research and provided arguments that stress impacted health.
As noted, stress is difficult to define because it is so different for each of us. A good example is afforded by observing passengers on a steep roller coaster ride. Some are hunched down in the back seats, eyes shut, jaws clenched and white knuckled with an iron grip on the retaining bar.
But up front are the wide-eyed thrill seekers, yelling and relishing each steep plunge who race to get on the very next ride. And in between you may find a few with an air of nonchalance that borders on boredom.
So, was the roller coaster ride stressful? The roller coaster analogy is useful in explaining why the same stressor can differ so much for each of us. What distinguished the passengers in the back from those up front was the sense of control they had over the event.
While neither group had any more or less control their perceptions and expectations were quite different. As the stress level increases from low to moderate, so does performance eustress. At the optimal level the peak of the curve , performance has reached its peak. Stress is everywhere and, as shown in [link] , it has been on the rise over the last several years. Each of us is acquainted with stress—some are more familiar than others.
Nearly half of U. Stress is an experience that evokes a variety of responses, including those that are physiological e. The scientific study of how stress and other psychological factors impact health falls within the realm of health psychology , a subfield of psychology devoted to understanding the importance of psychological influences on health, illness, and how people respond when they become ill Taylor, Health psychology emerged as a discipline in the s, a time during which there was increasing awareness of the role behavioral and lifestyle factors play in the development of illnesses and diseases Straub, In addition to studying the connection between stress and illness, health psychologists investigate issues such as why people make certain lifestyle choices e.
Health psychologists also design and investigate the effectiveness of interventions aimed at changing unhealthy behaviors. Perhaps one of the more fundamental tasks of health psychologists is to identify which groups of people are especially at risk for negative health outcomes, based on psychological or behavioral factors.
For example, measuring differences in stress levels among demographic groups and how these levels change over time can help identify populations who may have an increased risk for illness or disease. All three surveys demonstrated higher stress in women than in men.
Unemployed individuals reported high levels of stress in all three surveys, as did those with less education and income; retired persons reported the lowest stress levels. However, from to the greatest increase in stress levels occurred among men, Whites, people aged 45—64, college graduates, and those with full-time employment. One interpretation of these findings is that concerns surrounding the — economic downturn e.
Across categories of sex, age, race, education level, employment status, and income, stress levels generally show a marked increase over this quarter-century time span. As previously stated, scientific interest in stress goes back nearly a century.
One of the early pioneers in the study of stress was Walter Cannon , an eminent American physiologist at Harvard Medical School [link]. Imagine that you are hiking in the beautiful mountains of Colorado on a warm and sunny spring day. At one point during your hike, a large, frightening-looking black bear appears from behind a stand of trees and sits about 50 yards from you.
The bear notices you, sits up, and begins to lumber in your direction. Prompted by a deluge of epinephrine adrenaline and norepinephrine noradrenaline from your adrenal glands, your pupils begin to dilate. Your heart starts to pound and speeds up, you begin to breathe heavily and perspire, you get butterflies in your stomach, and your muscles become tense, preparing you to take some kind of direct action.
Cannon proposed that this reaction, which he called the fight-or-flight response , occurs when a person experiences very strong emotions—especially those associated with a perceived threat Cannon, During the fight-or-flight response, the body is rapidly aroused by activation of both the sympathetic nervous system and the endocrine system [link].
This arousal helps prepare the person to either fight or flee from a perceived threat. According to Cannon, the fight-or-flight response is a built-in mechanism that assists in maintaining homeostasis—an internal environment in which physiological variables such as blood pressure, respiration, digestion, and temperature are stabilized at levels optimal for survival.
Thus, Cannon viewed the fight-or-flight response as adaptive because it enables us to adjust internally and externally to changes in our surroundings, which is helpful in species survival. Another important early contributor to the stress field was Hans Selye , mentioned earlier. As a young assistant in the biochemistry department at McGill University in the s, Selye was engaged in research involving sex hormones in rats. Although he was unable to find an answer for what he was initially researching, he incidentally discovered that when exposed to prolonged negative stimulation stressors —such as extreme cold, surgical injury, excessive muscular exercise, and shock—the rats showed signs of adrenal enlargement, thymus and lymph node shrinkage, and stomach ulceration.
Selye realized that these responses were triggered by a coordinated series of physiological reactions that unfold over time during continued exposure to a stressor. These physiological reactions were nonspecific, which means that regardless of the type of stressor, the same pattern of reactions would occur.
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