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Can stress and arousal be independent?


I'm trying to figure out if it's possible to have a stress response without being initially, or simultaneously aroused. I'm defining stress to be physiological stress (ie. release of cortisol) and arousal to be activation of the sympathetic nervous system.

Every example I can think of, these two are not independent. In the case of "fight-or-flight," one initially activates the sympathetic nervous system, which is then followed by the release of cortisol. Or in individuals with major depressive disorder, their sympathetic nervous systems are constantly activated while cortisol is being secreted.

So, is it possible to experience cortisol release without activation of the sympathetic nervous system?


Stress response has 2 main components:

  1. Quick response, within minutes, is by the Sympathomedullary Pathway (SAM): hypothalamus > sympathetic nervous system > release of adrenaline and noradrenaline from the adrenal medulla > stimulation of the heart, dilation of the muscle arteries, constriction of the gut and skin arteries, glcogenolysis (the breakdown of glycogen into glucose) > more glucose available as a fuel
  2. Delayed response, within hours, is by the The Hypothalamic Pituitary-Adrenal (HPA) System: hypothalamus > pituitary gland > ACTH > release of cortisol from the adrenal cortex > gluconeogenesis (formation of glucose in the body from other substances) > more glucose available as a fuel

Cortisol secretion from the adrenal cortex can be stimulated by things other than stress, for example, hypoglycemia, but hypoglycemia will simultaneously activate the sympathetic nervous system, which will trigger the release of adrenaline (Neuroendocrine Response to Hypoglycemia).

Some cortisol is also secreted along with aldosterone in response to hyperkalemia or hyponatremia (Vivo.colostate.edu), for example in SIADH (A Case of Transient Hypercortisolism Simultaneously Occurring With the Syndrome of Inappropriate Antidiuretic Hormone Secretion Induced by Olanzapine).

Cortisol can be also increased without stimulation of the sympathetic system in Cushing syndrome due to a pituitary adenoma or, rarely, other tumors that secrete ACTH or in adrenal adenoma, which secretes cortisol.


Immune system. Relationship to anxiety disorders

The demonstration that behavioral states and CNS processes are associated with immune function suggests that there may be a relationship between anxiety and the immune system. Stress and immunity have been studied extensively, but there have been relatively few studies of anxiety and immunity. Many of the neurobiologic processes associated with stress and with depression have been observed in anxiety and are known to influence the immune system. A review of the immune response to stress and of immune alterations in depression has been presented in an effort to provide further understanding of the biology of anxiety. It appears that a variety of factors such as age sex nature, intensity, and chronicity of a stressful life events and psychologic response to life stress need to be considered in the investigation of behavior and immunity. The biologic effects of stress on immunity are multifaceted, including complex neuroendocrine and neurotransmitter interactions. Further investigation is required of anxiety and immunity in clearly delineated and diagnosed anxiety states and disorders. Such studies may help to elucidate the pathophysiology of anxiety disorders.


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.



Are You Too Stressed to Be Productive? Or Not Stressed Enough?

If you’re like me, you often ask yourself how you can get more work done in a day. How can you best boost your productivity? I always assumed that if I could just reduce any stress I was facing, my productivity would rise. But my intuition was, in fact, wrong. It’s true that stress can be a health risk, and that we’re often encouraged to avoid it if we want to live happy, productive, and long lives. But research suggests that some stress can actually be beneficial to performance.

Take a look at the picture below. According to what is known as “The Yerkes-Dodson law,” performance increases with physiological or mental arousal (stress) but only up to a point. When the level of stress becomes too high, performance decreases.

There’s more: The shape of the curve varies based on the complexity and familiarity of the task. Different tasks require different levels of arousal for optimal performance, research has found. For example, difficult or unfamiliar tasks require lower levels of arousal to facilitate concentration by contrast, you may better perform tasks demanding stamina or persistence with higher levels of arousal to induce and increase motivation.

Given this relationship between stress and performance, it’s probably beneficial to understand how much stress you are currently experiencing at work. If you are curious, take the following test (which is adapted from the commonly used Perceived Stress Scale, created by Sheldon Cohen, Tom Kamarck, and Robin Mermelstein).

Higher scores, as you might guess, correspond to higher levels of stress. Based on my use of this test in executive education classrooms and in research conducted with other groups, scores around 13 are considered average. Usually, scores in this range indicate that your attention and interest are at the proper level, allowing you to be productive at work. Referring to the Yerkes-Dodson law, such scores generally correspond to an optimal level of arousal and thus performance.

When Stress Helps You Get More Done

But if your score is much higher or much lower, you’re likely experiencing stress in a way that is detrimental to productivity. In particular, scores of 20 or more are generally considered to indicate an unproductive level of stress. But even scores that indicate low levels of stress—commonly, scores of 4 or lower–could be problematic since they signal an insufficient level of arousal to keep you engaged in your work. If this is the case, try to find healthy ways of raising your stress by taking on more challenging tasks or responsibilities. Increasing stress may feel counterintuitive, but remember that, according to the research, increasing arousal also corresponds to increasing attention and interest (up to a point).

For comparison, here are some average scores from research conducted using this scale:

If your score approaches or exceeds 20, here are some strategies that may help you reduce stress to a more productive level:

Increase your control. One simple solution to lowering stress is to find more ways to increase your control over the work you do. People tend to believe that high-level positions bring a lot of stress, but research suggests just the opposite: Leaders with higher levels of responsibility experience lower stress levels than those with less on their shoulders. This is because leaders have more control over their activities. Independent of where you sit in the organizational hierarchy, you may have ways to increase your sense of control—namely, by focusing on aspects of your work where you can make choices (for example, choosing one project over another or simply choosing the order in which you answer e-mails).

Find more opportunities to be authentic. Evidence suggests that people often experience feelings of inauthenticity at work. That is, they conform to the opinions of colleagues rather than voicing their own, and they go with others’ flow rather than setting their own agenda. This, my research suggests, has important implications for your stress level and performance. When people behave in inauthentic ways, they experience higher levels of anxiety than when they are simply themselves. So, try to find ways to express who you are at work, such as offering to share your unique talents or decorating your office to reflect who you are.

This article also appears in:

HBR Guide to Being More Productive

Use rituals. Basketball superstar Michael Jordan wore his North Carolina shorts underneath his Chicago Bulls shorts at every game Curtis Martin of the New York Jets reads Psalm 91 before every game and Wade Boggs, as third baseman for the Boston Red Sox, ate chicken before each game and took batting practice at exactly 5:17 p.m., fielded exactly 117 ground balls, and ran sprints at precisely 7:17 p.m. These rituals may sound strange, but they can actually improve performance.

In one recent experiment, people asked to hit a golf ball into a hole received either a so-called “lucky” golf ball or an ordinary golf ball. In another experiment, participants performing a motor dexterity task (placing 36 small balls in 36 holes by tilting the plastic cube containing them) were either asked to simply start the game or heard the researcher say they would cross their fingers for them. The superstitious rituals enhanced people’s confidence in their abilities, motivated greater effort — and improved subsequent performance.

Similarly, research in sports psychology demonstrates the performance benefits of pre-performance routines, from improving attention and execution to increasing emotional stability and confidence. And recently, my colleagues and I have found that when people engage in rituals before undertaking high-stakes tasks, they feel less anxious and stressed about the task and end up performing better as a result.

A moderate amount of stress may put you in the right mindset to tackle your work. But if you are feeling overwhelmed, I hope you’ll try out some of these strategies to not only improve your productivity but also to increase your happiness.


Stress management

These recent discoveries about the effects of stress on health shouldn’t leave you worrying. We now understand much more about effective strategies for reducing stress responses. Such beneficial strategies include:

  • Maintaining a healthy social support network
  • Engaging in regular physical exercise
  • Getting an adequate amount of sleep each night

These approaches have important benefits for physical and mental health, and form critical building blocks for a healthy lifestyle. If you would like additional support or if you are experiencing extreme or chronic stress, a licensed psychologist can help you identify the challenges and stressors that affect your daily life and find ways to help you best cope for improving your overall physical and mental well-being.

APA gratefully acknowledges the assistance of William Shaw, PhD Susan Labott-Smith, PhD, ABPP Matthew M. Burg, PhD Camelia Hostinar, PhD Nicholas Alen, BA Miranda A.L. van Tilburg, PhD Gary G. Berntson, PhD Steven M. Tovian, PhD, ABPP, FAClinP, FAClinHP and Malina Spirito, PsyD, MEd in developing this article.

The full text of articles from APA Help Center may be reproduced and distributed for noncommercial purposes with credit given to the American Psychological Association. Any electronic reproductions must link to the original article on the APA Help Center. Any exceptions to this, including excerpting, paraphrasing or reproduction in a commercial work, must be presented in writing to the APA. Images from the APA Help Center may not be reproduced


Methodological Considerations for TL and TA Measurement

With a growing research interest in telomere biology, a consensus in laboratory measurements seems critical with high precision and accuracy. Currently, the TL and TA are measured in many different laboratories utilizing different assays (e.g., telomere restriction fragment, length analysis by Southern blot analysis, quantitative PCR, and Telomerase Repeat Amplification Protocol) (Epel et al., 2010 Lin J. et al., 2019). Application of different approaches makes it challenging to compare results from different studies.

Based on tissue type and collection methods (e.g., blood including plasma, serum and peripheral blood mononuclear cells and saliva samples, including swabs and buccal cells), several specimen types have been used for TL and TA measurement (Lin J. et al., 2019). Each specimen offers advantages and challenges and, due to cell type differences, it might influence TL and TA outcomes. For instance, quantitative-PCR provides the advantage of being able to use smaller amounts of DNA, thereby making it amenable to epidemiology studies involving large numbers of people. An alternative method uses fluorescent probes to quantify not only mean TL, but also chromosome-specific TL. Of note, all these novel techniques for TA measurement are currently at the proof of concept stage, and only a number of those have been applied in studies involving clinical tissues or body fluid samples. When incorporating TL and TA into a research study, it is important to thoroughly evaluate the research question, population, sample type, timing of the analysis, and available resources in order to select optimal TL and TA measurement method.

To our knowledge, no study has evaluated TA and TL in elite athletes within the sport context, such as competition (prior, during and after). In future studies, measuring TA and TL biomarkers in this population may require extra attention in methodology with a rigorous design to accommodate specificity and characteristics of this population.


Factors in Determining Optimal Stress for a Given Task

In reality, optimal stress and optimal performance depends on four different factors: skill level, personality, trait anxiety, and task complexity (as discussed above).

Skill Level

Your skill level directly influences how well you perform on any given task. That is why it is extremely imperative to train a task so that it is well-learned. Once a task is well-learned, your mind will respond to stress and high-pressure situations a lot better than if you are a novice to the task. This goes for anything—from a hostage rescue situation to shooting to delivering a speech. In addition, in high-pressure situations, we are less able to think on our feet and methodically, which is why it is extremely important to be able to fall back on well-rehearsed responses.

Personality

Your personality will also affect how well you perform in high-pressure situations. Some scientists believe that extroverts naturally perform better than introverts in high-pressure situations, given all other things equal. People who are introverts on the other hand, perform better than extroverts in environments with less stimuli and ample preparation. It is useful to note that the vast majority of people are not classified as either introverts/extroverts most of the population are actually ambiverts—people who possess traits of both introverts and extroverts.

Trait Anxiety

Trait anxiety is also known as limiting beliefs. People who are self-confident and believe in their abilities are able to stay focused and concentrate on tasks better. People who are not confident in their abilities will be distracted by their limiting beliefs and self-doubt in high-pressure situations.

Task Complexity

Task complexity is, of course, the complexity of the given task. It is the level of attention and the amount of effort asserted in order to successfully complete the task. Again, simple activities can be performed successfully with high stress (or arousal) whereas most complex and unfamiliar tasks require a certain level of calmness stress in order to perform successfully.


Socioeconomic determinants of health: Stress and the biology of inequality

It is well established that health depends on socioeconomic circumstances, but the biology of this relation is not well described. Psychosocial factors operating throughout the life course, beginning in early life, influence a variety of biological variables. Research with non-human primates shows the effects of dominance hierarchy on biology, and similar metabolic differentials are evident in a hierarchy of white collar civil servants. The neuroendocrine “fight or flight” response produces physiological and metabolic alterations which parallel those observed with lower socioeconomic status. The biological effects of the psychosocial environment could explain health inequalities between relatively affluent groups.


References

Joels, M., Pu, Z. W., Wiegert, O., Oitzl, M. S. & Krugers, H. J. Learning under stress: how does it work? Trends Cogn. Sci. 10, 152–158 (2006).

Schwabe, L., Joëls, M., Roozendaal, B., Wolf, O. T. & Oitzl, M. S. Stress effects on memory: an update and integration. Neurosci. Biobehav. Rev. 36, 1740–1749 (2012).

Pitman, R. K. et al. Biological studies of post-traumatic stress disorder. Nat. Rev. Neurosci. 13, 769–787 (2012).

Joëls, M., Fernandez, G. & Roozendaal, B. Stress and emotional memory: a matter of timing. Trends Cogn. Sci. 15, 280–288 (2011).

Arnsten, A. F. T. Stress signalling pathways that impair prefrontal cortex structure and function. Nat. Rev. Neurosci. 10, 410–422 (2009).

Sandi, C. & Haller, J. Stress and the social brain: behavioural effects and neurobiological mechanisms. Nat. Rev. Neurosci. 16, 290–304 (2015).

de Kloet, E. R., Joels, M. & Holsboer, F. Stress and the brain: from adaptation to disease. Nat. Rev. Neurosci. 6, 463–475 (2005).

Folkman, S., Lazarus, R. S., Dunkel-Schetter, C., DeLongis, A. & Gruen, R. J. Dynamics of a stressful encounter: cognitive appraisal, coping, and encounter outcomes. J. Pers. Soc. Psychol. 50, 992–1003 (1986).

Lazarus, R. S . Emotion and Adaptation xiii 557 (Oxford Univ. Press, 1991).

Joëls, M. & Baram, T. Z. The neuro-symphony of stress. Nat. Rev. Neurosci. 10, 459–466 (2009).

Katsuki, H., Izumi, Y. & Zorumski, C. F. Noradrenergic regulation of synaptic plasticity in the hippocampal CA1 region. J. Neurophysiol. 77, 3013–3020 (1997).

DeKloet, E. R., Reul, J. & Sutanto, W. Corticosteroids and the brain. J. Steroid Biochem. Mol. Biol. 37, 387–394 (1990).

Chao, H. M., Choo, P. H. & McEwen, B. S. Glucocorticoid and mineralocorticoid receptor mRNA expression in rat brain. Neuroendocrinology 50, 365–371 (1989).

Groeneweg, F. L., Karst, H., de Kloet, E. R. & Joëls, M. Rapid non-genomic effects of corticosteroids and their role in the central stress response. J. Endocrinol. 209, 153–167 (2011).

Karst, H., Berger, S., Erdmann, G., Schutz, G. & Joels, M. Metaplasticity of amygdalar responses to the stress hormone corticosterone. Proc. Natl Acad. Sci. USA 107, 14449–14454 (2010).

Karst, H. et al. Mineralocorticoid receptors are indispensable for nongenomic modulation of hippocampal glutamate transmission by corticosterone. Proc. Natl Acad. Sci. USA 102, 19204–19207 (2005).

Joëls, M., Sarabdjitsingh, R. A. & Karst, H. Unraveling the time domains of corticosteroid hormone influences on brain activity: Rapid, slow, and chronic modes. Pharmacol. Rev. 64, 901–938 (2012).

Schwabe, L. & Wolf, O. Timing matters: temporal dynamics of stress effects on memory retrieval. Cogn. Affect. Behav. Neurosci. 14, 1041–1048 (2014).

Schönfeld, P., Ackermann, K. & Schwabe, L. Remembering under stress: different roles of autonomic arousal and glucocorticoids in memory retrieval. Psychoneuroendocrinology 39, 249–256 (2014).

Smeets, T., Giesbrecht, T., Jelicic, M. & Merckelbach, H. Context-dependent enhancement of declarative memory performance following acute psychosocial stress. Biol. Psychol. 76, 116–123 (2007).

Zoladz, P. R. et al. Pre-learning stress differentially affects long-term memory for emotional words, depending on temporal proximity to the learning experience. Physiol. Behav. 103, 467–476 (2011).

Domes, G., Heinrichs, M., Reichwald, U. & Hautzinger, M. Hypothalamic-pituitary-adrenal axis reactivity to psychological stress and memory in middle-aged women: High responders exhibit enhanced declarative memory performance. Psychoneuroendocrinology 27, 843–853 (2002).

Schwabe, L., Bohringer, A., Chatterjee, M. & Schachinger, H. Effects of pre-learning stress on memory for neutral, positive and negative words: different roles of cortisol and autonomic arousal. Neurobiol. Learn. Mem. 90, 44–53 (2008).

Payne, J. et al. The impact of stress on neutral and emotional aspects of episodic memory. Memory 14, 1–16 (2006).

Schwabe, L. & Wolf, O. T. Learning under stress impairs memory formation. Neurobiol. Learn. Mem. 93, 183–188 (2010).

Smeets, T., Otgaar, H., Candel, I. & Wolf, O. T. True or false? Memory is differentially affected by stress-induced cortisol elevations and sympathetic activity at consolidation and retrieval. Psychoneuroendocrinology 33, 1378–1386 (2008).

Elzinga, B. M., Bakker, A. & Bremner, J. D. Stress-induced cortisol elevations are associated with impaired delayed, but not immediate recall. Psychiatry Res. 134, 211–223 (2005).

Andreano, J. M. & Cahill, L. Glucocorticoid release and memory consolidation in men and women. Psychol. Sci. 17, 466–470 (2006).

Rasch, B. et al. A genetic variation of the noradrenergic system is related to differential amygdala activation during encoding of emotional memories. Proc. Natl Acad. Sci. USA 106, 19191–19196 (2009).

Vukojevic, V. et al. Epigenetic modification of the glucocorticoid receptor gene is linked to traumatic memory and post-traumatic stress disorder risk in genocide survivors. J. Neurosci. 34, 10274–10284 (2014).

Schwabe, L., Bohbot, V. D. & Wolf, O. T. Prenatal stress changes learning strategies in adulthood. Hippocampus 22, 2136–2143 (2012).

McIntyre, C. K., Hatfield, T. & McGaugh, J. L. Amygdala norepinephrine levels after training predict inhibitory avoidance retention performance in rats. Eur. J. Neurosci. 16, 1223–1226 (2002).

Buchanan, T. W. & Lovallo, W. R. Enhanced memory for emotional material following stress-level cortisol treatment in humans. Psychoneuroendocrinology 26, 307–317 (2001).

Cahill, L., Prins, B., Weber, M. & McGaugh, J. L. [beta]-adrenergic activation and memory for emotional events. Nature 371, 702–704 (1994).

Hermans, E. J., Henckens, MJAG, Joëls, M. & Fernández, G. Dynamic adaptation of large-scale brain networks in response to acute stressors. Trends Neurosci. 37, 304–314 (2014).

Hermans, E. J. et al. Stress-related noradrenergic activity prompts large-scale neural network reconfiguration. Science 334, 1151–1153 (2011).

Strelzyk, F. et al. Tune it down to live it up? Rapid, nongenomic effects of cortisol on the human brain. J. Neurosci. 32, 616–625 (2012).

Henckens, M. J., Hermans, E. J., Pu, Z., Joëls, M. & Fernández, G. Stressed memories: how acute stress affects memory formation in humans. J. Neurosci. 29, 10111–10119 (2009).

Weymar, M., Schwabe, L., Löw, A. & Hamm, A. O. Stress sensitizes the brain: increased processing of unpleasant pictures after exposure to acute stress. J. Cogn. Neurosci. 24, 1511–1518 (2011).

Strange, B. A. & Dolan, R. J. Β-adrenergic modulation of emotional memory-evoked human amygdala and hippocampal responses. Proc. Natl Acad. Sci. USA 101, 11454–11458 (2004).

van Stegeren, A. H., Wolf, O. T., Everaerd, W., Rombouts, S. A. R. B. in Progress in Brain Research (eds Ronald E., De Kloet M. S. O. & Eric V. ) Vol. 167, 263–268 (Elsevier, 2007).

van Stegeren, A. H., Roozendaal, B., Kindt, M., Wolf, O. T. & Joels, M. Interacting noradrenergic and corticosteroid systems shift human brain activation patterns during encoding. Neurobiol. Learn. Mem. 93, 56–65 (2010).

de Quervain, D. J. F., Roozendaal, B., Nitsch, R. M., McGaugh, J. L. & Hock, C. Acute cortisone administration impairs retrieval of long-term declarative memory in humans. Nat. Neurosci. 3, 313–314 (2000).

Wiegert, O., Joëls, M. & Krugers, H. Timing is essential for rapid effects of corticosterone on synaptic potentiation in the mouse hippocampus. Learn. Mem. 13, 110–113 (2006).

Henckens, M. J. et al. Dynamically changing effects of corticosteroids on human hippocampal and prefrontal processing. Hum. Brain Mapp. 33, 2885–2897 (2012).

Henckens, M., van Wingen, G. A., Joels, M. & Fernandez, G. Time-dependent effects of corticosteroids on human amygdala processing. J. Neurosci. 30, 12725–12732 (2010).

van Marle, H. J. F., Hermans, E. J., Qin, S. Z. & Fernandez, G. Enhanced resting-state connectivity of amygdala in the immediate aftermath of acute psychological stress. Neuroimage 53, 348–354 (2010).

Cahill, L. & Alkire, M. T. Epinephrine enhancement of human memory consolidation: Interaction with arousal at encoding. Neurobiol. Learn. Mem. 79, 194–198 (2003).

Cahill, L., Gorski, L. & Le, K. Enhanced human memory consolidation with post-learning stress: Interaction with the degree of arousal at encoding. Learn. Mem. 10, 270–274 (2003).

Beckner, V. E., Tucker, D. M., Delville, Y. & Mohr, D. C. Stress facilitates consolidation of verbal memory for a film but does not affect retrieval. Behav. Neurosci. 120, 518–527 (2006).

Roozendaal, B. & McGaugh, J. L. Amygdaloid nuclei lesions differentially affect glucocorticoid-induced memory enhancement in an inhibitory avoidance task. Neurobiol. Learn. Mem. 65, 1–8 (1996).

Roozendaal, B., Okuda, S., De Quervain, D. J. F. & McGaligh, J. L. Glucocorticoids interact with emotion-induced noradrenergic activation in influencing different memory functions. Neuroscience 138, 901–910 (2006).

Roozendaal, B., Okuda, S., Van der Zee, E. A. & McGaugh, J. L. Glucocorticoid enhancement of memory requires arousal-induced noradrenergic activation in the basolateral amygdala. Proc. Natl Acad. Sci. USA 103, 6741–6746 (2006).

Barsegyan, A., Mackenzie, S. M., Kurose, B. D., McGaugh, J. L. & Roozendaal, B. Glucocorticoids in the prefrontal cortex enhance memory consolidation and impair working memory by a common neural mechanism. Proc. Natl Acad. Sci. USA 107, 16655–16660 (2010).

McGaugh, J. L., Cahill, L. & Roozendaal, B. Involvement of the amygdala in memory storage: Interaction with other brain systems. Proc. Natl Acad. Sci. USA 93, 13508–13514 (1996).

de Quervain, D. J. F., Roozendaal, B. & McGaugh, J. L. Stress and glucocorticoids impair retrieval of long-term spatial memory. Nature 394, 787–790 (1998).

Quaedflieg, C. W., Schwabe, L., Meyer, T. & Smeets, T. Time dependent effects of stress prior to encoding on event-related potentials and 24 h delayed retrieval. Psychoneuroendocrinology 38, 3057–3069 (2013).

Buchanan, T. W., Tranel, D. & Adolphs, R. Impaired memory retrieval correlates with individual differences in cortisol response but not autonomic response. Learn. Mem. 13, 382–387 (2006).

Quesada, A. A., Wiemers, U. S., Schoofs, D. & Wolf, O. T. Psychosocial stress exposure impairs memory retrieval in children. Psychoneuroendocrinology 37, 125–136 (2012).

Hupbach, A. & Fieman, R. Moderate stress enhances immediate and delayed retrieval of educationally relevant material in healthy young men. Behav. Neurosci. 126, 819–825 (2012).

Schwabe, L. et al. Stress effects on declarative memory retrieval are blocked by a β-adrenoceptor antagonist in humans. Psychoneuroendocrinology 34, 446–454 (2009).

Kuhlmann, S., Piel, M. & Wolf, O. T. Impaired memory retrieval after psychosocial stress in healthy young men. J. Neurosci. 25, 2977–2982 (2005).

Schwabe, L. & Wolf, O. T. The context counts: congruent learning and testing environments prevent memory retrieval impairment following stress. Cogn. Affect. Behav. Neurosci. 9, 229–236 (2009).

Tollenaar, M. S., Elzinga, B. M., Spinhoven, P. & Everaerd, W. Immediate and prolonged effects of cortisol, but not propranolol, on memory retrieval in healthy young men. Neurobiol. Learn. Mem. 91, 23–31 (2009).

Roozendaal, B., Griffith, Q. K., Buranday, J., de Quervain, DJ-F & McGaugh, J. L. The hippocampus mediates glucocorticoid-induced impairment of spatial memory retrieval: dependence on the basolateral amygdala. Proc. Natl Acad. Sci. USA 100, 1328–1333 (2003).

De Quervain, D. J. F. et al. Glucocorticoid-induced impairment of declarative memory retrieval is associated with reduced blood flow in the medial temporal lobe. Eur. J. Neurosci. 17, 1296–1302 (2003).

de Quervain, D. J., Aerni, A. & Roozendaal, B. Preventive effect of beta-adrenoceptor blockade on glucocorticoid-induced memory retrieval deficits. Am. J. Psychiatry 164, 967–969 (2007).

Dudai, Y. The restless engram: consolidations never end. Annu. Rev. Neurosci. 35, 227–247 (2012).

Nader, K., Schafe, G. E. & Le Doux, J. E. Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval. Nature 406, 722–726 (2000).

Nader, K. & Hardt, O. A single standard for memory: the case for reconsolidation. Nat. Rev. Neurosci. 10, 224–234 (2009).

Schwabe, L., Nader, K. & Pruessner, J. C. Reconsolidation of human memory: brain mechanisms and clinical relevance. Biol. Psychiatry 76, 274–280 (2014).

Schacter, D. L. & Loftus, E. F. Memory and law: what can cognitive neuroscience contribute? Nat. Neurosci. 16, 119–123 (2013).

Sandrini, M., Censor, N., Mishoe, J. & Cohen, L. Causal role of prefrontal cortex in strengthening of episodic memories through reconsolidation. Curr. Biol. 23, 2181–2184 (2013).

Cai, W.-H., Blundell, J., Han, J., Greene, R. W. & Powell, C. M. Postreactivation glucocorticoids impair recall of established fear memory. J. Neurosci. 26, 9560–9566 (2006).

Wang, X.-Y., Zhao, M., Ghitza, U. E., Li, Y.-Q. & Lu, L. Stress impairs reconsolidation of drug memory via glucocorticoid receptors in the basolateral amygdala. J. Neurosci. 28, 5602–5610 (2008).

Bos, M. G., Schuijer, J., Lodestijn, F., Beckers, T. & Kindt, M. Stress enhances reconsolidation of declarative memory. Psychoneuroendocrinology 46, 102–113 (2014).

Coccoz, V., Maldonado, H. & Delorenzi, A. The enhancement of reconsolidation with a naturalistic mild stressor improves the expression of a declarative memory in humans. Neuroscience 185, 61–72 (2011).

Schwabe, L. & Wolf, O. T. Stress impairs the reconsolidation of autobiographical memories. Neurobiol. Learn. Mem. 94, 153–157 (2010).

Loftus, E. F. & Palmer, J. C. Reconstruction of automobile destruction: an example of the interaction between language and memory. J. Verbal Learning Verbal Behav. 13, 585–589 (1974).

Hoscheidt, S. M., LaBar, K. S., Ryan, L., Jacobs, W. J. & Nadel, L. Encoding negative events under stress: High subjective arousal is related to accurate emotional memory despite misinformation exposure. Neurobiol. Learn. Mem. 112, 237–247 (2014).

Schmidt, P.-I., Rosga, K., Schatto, C., Breidenstein, A. & Schwabe, L. Stress reduces the incorporation of misinformation into an established memory. Learn. Mem. 21, 744–747 (2014).

Wingard, J. C. & Packard, M. G. The amygdala and emotional modulation of competition between cognitive and habit memory. Behav. Brain Res. 193, 126–131 (2008).

Poldrack, R. A. & Packard, M. G. Competition among multiple memory systems: Converging evidence from animal and human brain studies. Neuropsychologia 41, 245–251 (2003).

Schwabe, L. & Wolf, O. T. Stress and multiple memory systems: from ‘thinking’ to ‘doing’. Trends Cogn. Sci. 17, 60–68 (2013).

Schwabe, L., Wolf, O. T. & Oitzl, M. S. Memory formation under stress: quantity and quality. Neurosci. Biobehav. Rev. 34, 584–591 (2010).

Packard, M. G. & Teather, L. A. Amygdala modulation of multiple memory systems: hippocampus and caudate-putamen. Neurobiol. Learn. Mem. 69, 163–203 (1998).

Packard, M. G. & Wingard, J. C. Amygdala and ‘emotional’ modulation of the relative use of multiple memory systems. Neurobiol. Learn. Mem. 82, 243–252 (2004).

Schwabe, L., Schachinger, H., de Kloet, E. R. & Oitzl, M. S. Corticosteroids operate as a switch between memory systems. J. Cogn. Neurosci. 22, 1362–1372 (2010).

Vogel, S., Fernández, G., Joëls, M. & Schwabe, L. Cognitive adaptation under stress: a case for the mineralocorticoid receptor. Trends Cogn. Sci. 20, 192–203 (2016).

Elliott, A. E. & Packard, M. G. Intra-amygdala anxiogenic drug infusion prior to retrieval biases rats towards the use of habit memory. Neurobiol. Learn. Mem. 90, 616–623 (2008).

Schwabe, L. et al. Stress modulates the use of spatial versus stimulus-response learning strategies in humans. Learn. Mem. 14, 109–116 (2007).

Schwabe, L. & Wolf, O. T. Stress increases behavioural resistance to extinction. Psychoneuroendocrinology 36, 1287–1293 (2011).

Schwabe, L. & Wolf, O. T. Stress modulates the engagement of multiple memory systems in classification learning. J. Neurosci. 32, 11042–11049 (2012).

Vogel, S. et al. Blocking the mineralocorticoid receptor in humans prevents the stress-induced enhancement of centromedial amygdala connectivity with the dorsal striatum. Neuropsychopharmacology 40, 947–956 (2015).

Schwabe, L., Tegenthoff, M., Höffken, O. & Wolf, O. T. Mineralocorticoid receptor blockade prevents stress-induced modulation of multiple memory systems in the human brain. Biol. Psychiatry 74, 801–808 (2013).

Balleine, B. W. & Dickinson, A. The role of incentive learning in instrumental outcome revaluation by sensory-specific satiety. Anim. Learn. Behav. 26, 46–59 (1998).

Schwabe, L., Tegenthoff, M., Höffken, O. & Wolf, O. T. Concurrent glucocorticoid and noradrenergic activity shifts instrumental behaviour from goal-directed to habitual control. J. Neurosci. 30, 8190–8196 (2010).

Schwabe, L., Höffken, O., Tegenthoff, M. & Wolf, O. T. Preventing the stress-induced shift from goal-directed to habit action with a β-adrenergic antagonist. J. Neurosci. 31, 17317–17325 (2011).

Schwabe, L., Tegenthoff, M., Höffken, O. & Wolf, O. T. Simultaneous glucocorticoid and noradrenergic activity disrupts the neural basis of goal-directed action in the human brain. J. Neurosci. 32, 10146–10155 (2012).

Seehagen, S., Schneider, S., Rudolph, J., Ernst, S. & Zmyj, N. Stress impairs cognitive flexibility in infants. Proc. Natl Acad. Sci. USA 112, 12882–12886 (2015).

Braun, S. & Hauber, W. Acute stressor effects on goal-directed action in rats. Learn. Mem. 20, 700–709 (2013).

Vanaelst, B. et al. Prevalence of negative life events and chronic adversities in european pre- and primary-school children: Results from the idefics study. Arch. Public Health 70, 26 (2012).

Valizadeh, L., Farnam, A. & Rahkar Farshi, M. Investigation of stress symptoms among primary school children. J. Caring Sci. 1, 25–30 (2012).

Joëls, M. Corticosteroid effects in the brain: U-shape it. Trends Pharmacol. Sci. 27, 244–250 (2006).

Smith, A., Brice, C., Collins, A., McNamara, R. & Matthews, V. . Scale of Occupational Stress: A Further Analysis of the Impact of Demographic Factors and Type of Job. HSE, (2000).

Thorne, K. J., Andrews, J. J. W. & Nordstokke, D. Relations among children's coping strategies and anxiety: the mediating role of coping efficacy. J. Gen. Psychol. 140, 204–223 (2013).

McGaugh, J. L. Making lasting memories: remembering the significant. Proc. Natl Acad. Sci. USA 110 Suppl 2, 10402–10407 (2013).

Ochsner, K. N. Are affective events richly recollected or simply familiar? The experience and process of recognizing feelings past. J. Exp. Psychol. Gen. 129, 242–261 (2000).

Godden, D. R. & Baddeley, A. D. Context-dependent memory in two natural environments: On land and underwater. Br. J. Psychol. 66, 325–331 (1975).

Pacak, K. et al. Heterogeneous neurochemical responses to different stressors: a test of Selye’s doctrine of nonspecificity. Am. J. Physiol. Regul. Integr. Comp. Physiol. 275, R1247–R1255 (1998).

Schwabe, L., Dalm, S., Schachinger, H. & Oitzl, M. S. Chronic stress modulates the use of spatial and stimulus-response learning strategies in mice and man. Neurobiol. Learn. Mem. 90, 495–503 (2008).


EMOTIONAL EATING

Chronic stress is often accompanied by anxiety, depression, anger, apathy, and alienation 87 . Threatening and cognitively meaningful stimuli activate the emotional nervous system which, in part, determines behavioral output (e.g., fight-or-flight). Stress-induced elevations of GC secretion can intensify emotions and motivation 88 . Given the rewarding properties of food, it is hypothesized that hyperpalatable foods may serve as 𠇌omfort food” that acts as a form of self-medication to dispel unwanted distress. Individuals in negative affective states have been shown to favor the consumption of hedonically rewarding foods high in sugar and/or fat, whereas intake during happy states favor less palatable dried fruits 89 . Following laboratory exposure to ego threats, people exhibiting high negative affect or greater cortisol reactivity ate more food of high-sugar and high-fat content 28 . Similarly, in naturalistic settings, people with high cortisol reactivity report greater snacking in response to daily stressors 90 .


CANLI et al. (2000)

AIM:
To demonstrate that images causing high arousal levels will be remembered better than those that are less emotive. To investigate whether the amygdala is sensitive to varying degrees of emotional intensity to external stimuli and find what level of intensity affects the memory of the stimuli.
• Is the amygdala sensitive to varying degrees of individually experienced emotional intensity?
• What degree of emotional intensity affects the role of the amygdala in enhancing memory of emotional stimuli.

BACKGROUND:
There are two types of medical scans: structural – take detailed pictures of the brain structure functional – show the location of activity in the brain. The study used an fMRI machine (functional magnetic resonance imaging) which detects changes in blood flow in the brain to illustrate how the brain works during different tasks. The individual is placed in a scanner which sends a magnetic field and affects the spinning of the hydrogen molecules in the brain and enables the scan to create a detailed picture of the brain. The amygdala has been shown to have an association with the processing of emotion and storing of memory.
LeBar & Phelps (1998) suggested that emotional arousal aids the process of memory consolidation and therefore emotional experiences are memorized better.
Canli et al (1999) found strong amygdala activation to resulted in improved memorization for the causing stimuli. He wanted to replicate his study with repeated measures design rather than independent to make sure that the initial results were not due to chance.

RESEARCH METHOD:
Participants were required to lay in an fMRI scanner, which is a big and heavy apparatus, therefore the study was conducted in a laboratory and was a laboratory experiment.

EXPERIMENTAL DESIGN:
This was a repeated measure design experiment as the participants were unexpectedly asked to repeat the procedure again three weeks after.

VARIABLES:
The independent variable can be considered the level of arousal of each picture shown to the participants.
The dependent variable was the effect that this arousal level had on the memory of each picture which reflected on the ability of the participants to recognize the images at a 3 week follow up.

SAMPLE:
Participants were recruited by means of volunteer sampling and consisted of 10 healthy, right-handed women. Women were chosen specifically as it was believed that they would be more likely to show physiological reaction to stimuli.

PROCEDURE:
Informed consent was collected from the participants and they were informed about the aim of the experiment.
While the participants laid in a 1.5 Tesla fMRI scanner, they were shown 96 pictures with various valence ratings from the International Affective Picture System, projected over their head and mirrored for convenient viewing. The picture order was randomized and each picture was viewed for 2.88 seconds, with an interval of 12.96 seconds between two pictures in during which a fixed crossed was projected. The participants had to view the pictures the entire time they were projected and when the cross appeared, they had to rate the emotional arousal the picture triggered in them by pressing one out of four buttons with their right hand the buttons ranged from 0 to 3 with 0 being ‘not emotionally intense at all’ and 3 ‘extremely emotionally intense’.
While the participants were laying in the scanner, the fMRI machine collected information about the activity in the brain during the picture viewing.
After 3 weeks, the participants were asked to return to the laboratory, where they had to undergo an unexpected task. It consisted of them viewing the same 96 pictures plus 48 additional foils and asked to judge if the pictures were wforgottenotte, familiar or remembered

RESULTS:
There was an appropriate correlation between the subjective valance rating of the pictures and the valence of the pictures, with correlational coefficients of -0.66 and 0.68. Additionally, amygdala activation was also found to correlate with the emotional intensity reported by the participants – the more emotionality intense the picture was, the higher the amygdala activity of the participants while viewing it – perceived arousal is associated with amygdala activation.
At the follow-up, the emotionally intense pictures were remembered significantly better. Pictures rated 0 to 2 had a homogenous distribution of forgotten, familiar or remembered labels while pictures rated with 3 were more likely to be labeled as ‘remembered’. For pictures rated a 3, the amygdala activation could almost always predict correctly the label the participants would give it at follow up.

CONCLUSION:
There is an association with the perceived emotional intensity of stimuli and the memory of it – the higher valance a picture has, the more likely it is to be remembered. High levels of arousal can produce more vivid memories. The amygdala has been found sensitive to emotional intensity, predominantly the left amygdala’s activity during information encoding being an indicator for the formation of the memory.