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Fear is high only if the observed risk and seriousness both are high and is low if one or the other of the seen risk or seriousness is low.<ref>{{cite doi|10.1093/sf/61.4.1033}}</ref>
Fear is high only if the observed risk and seriousness both are high and is low if one or the other of the seen risk or seriousness is low.<ref>{{cite doi|10.1093/sf/61.4.1033}}</ref>


===Fear in the amygdala===
===Neurocircuit of fear in mammals===
The brain structure that is the center of most neurobiological events associated with fear is the [[amygdala]], located behind the pituitary gland. The role of the amygdala in fear is best understood as part of a circuitry of fear learning.<ref name=Olsson/> It is essential for proper adaptation to stress and specific modulation of emotional learning memory. In the presence of a threatening stimulus, the amygdala generates the secretion of hormones that influence fear and aggression.<ref>Best, Ben (2004). [http://www.benbest.com/science/anatmind/anatmd9.html The Amygdala and the Emotions]. benbest.com</ref> Once response to the stimulus in the form of fear or aggression commences, the amygdala may elicit the release of hormones into the body to put the person into a state of alertness, in which they are ready to move, run, fight, etc. This defensive response is generally referred to in physiology as the [[fight-or-flight response]] regulated by the hypothalamus.<ref>Gleitman, Henry; Fridlund, Alan J. and Reisberg, Daniel (2004). ''Psychology'' (6 ed.). W. W. Norton & Company. ISBN 0-393-97767-6.</ref> Once the person is in safe mode, meaning that there are no longer any potential threats surrounding them, the amygdala will send this information to the medial [[prefrontal cortex]] (mPFC) where it is stored for similar future situations. The storing of memory in the mPFC is known as [[memory consolidation]].<ref name=Travis/>
The brain structure that is the center of most neurobiological events associated with fear is the [[amygdala]], located behind the pituitary gland. The amygdala is part of a circuitry of fear learning.<ref name=Olsson/> It is essential for proper adaptation to stress and specific modulation of emotional learning memory. In the presence of a threatening stimulus, the amygdala generates the secretion of hormones that influence fear and aggression.<ref>Best, Ben (2004). [http://www.benbest.com/science/anatmind/anatmd9.html The Amygdala and the Emotions]. benbest.com</ref> Once response to the stimulus in the form of fear or aggression commences, the amygdala may elicit the release of hormones into the body to put the person into a state of alertness, in which they are ready to move, run, fight, etc. This defensive response is generally referred to in physiology as the [[fight-or-flight response]] regulated by the hypothalamus, part of the [[limbic system]].<ref>Gleitman, Henry; Fridlund, Alan J. and Reisberg, Daniel (2004). ''Psychology'' (6 ed.). W. W. Norton & Company. ISBN 0-393-97767-6.</ref> Once the person is in safe mode, meaning that there are no longer any potential threats surrounding them, the amygdala will send this information to the medial [[prefrontal cortex]] (mPFC) where it is stored for similar future situations, which is known as [[memory consolidation]].<ref name=Travis/>
Some of the hormones involved during the state of fight-or-flight include epinephrine and norepinephrine and cortisol. Epinephrine regulates heart rate and metabolism as well as dilating blood vessels and air passages. [[Norepinephrine]] increases heart rate, blood flow to skeletal muscles and the release of glucose from energy stores.<ref>von Bohlen und Halbach, O; Dermietzel, R (2006). ''Neurotransmitters and neuromodulators: handbook of receptors and biological effects''. Wiley-VCH. p. 125. ISBN 978-3-527-31307-5.</ref> [[Cortisol]] increases blood sugar and helps with metabolism.<ref>Hoehn K, Marieb EN (2010). ''Human Anatomy & Physiology''. San Francisco: Benjamin Cummings. ISBN 0-321-60261-7.</ref>
Some of the hormones involved during the state of fight-or-flight include adrenaline, epinephrine, norepinephrine and cortisol. Epinephrine regulates heart rate and metabolism as well as dilating blood vessels and air passages. [[Norepinephrine]] increases heart rate, blood flow to skeletal muscles and the release of glucose from energy stores.<ref>von Bohlen und Halbach, O; Dermietzel, R (2006). ''Neurotransmitters and neuromodulators: handbook of receptors and biological effects''. Wiley-VCH. p. 125. ISBN 978-3-527-31307-5.</ref> [[Cortisol]] increases blood sugar, demarginalizes neutrophilic leukocytes,increases calcium and much more.<ref>Hoehn K, Marieb EN (2010). ''Human Anatomy & Physiology''. San Francisco: Benjamin Cummings. ISBN 0-321-60261-7.</ref>


After a situation which incites fear occurs, the amygdala and [[hippocampus]] record the event through synaptic [[neuroplasticity|plasticity]].<ref>{{cite pmid|16208455}}</ref> The stimulation to the hippocampus will cause the individual to remember many details surrounding the situation.<ref>Schacter, Daniel L.; Gilbert, Daniel T. and Wegner, Daniel M. (2011) ''Psychology Study Guide'', Worth Publishers, ISBN 1429206152.</ref> Plasticity and memory formation in the amygdala are generated by activation of the neurons in the region. Experimental data supports the notion that synaptic plasiticity of the neurons leading to the lateral amygdala occurs with fear conditioning.<ref>{{cite pmid|14514027}}</ref> In some cases, this forms permanent fear responses such as [[post-traumatic stress disorder]] (PTSD) or a [[phobia]].<ref>American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders: DSM-IV. Washington, DC. ISBN 0-89042-061-0.</ref> MRI and fMRI scans have shown that the amygdala in individuals diagnosed with such disorders including [[bipolar disorder|bipolar]] or [[panic disorder]] is larger and wired for a higher level of fear.<ref>{{cite pmid|12619902}}</ref>
After a situation which incites fear occurs, the amygdala and [[hippocampus]] record the event through synaptic [[neuroplasticity|plasticity]].<ref>{{cite pmid|16208455}}</ref> The stimulation to the hippocampus will cause the individual to remember many details surrounding the situation.<ref>Schacter, Daniel L.; Gilbert, Daniel T. and Wegner, Daniel M. (2011) ''Psychology Study Guide'', Worth Publishers, ISBN 1429206152.</ref> Plasticity and memory formation in the amygdala are generated by activation of the neurons in the region. Experimental data supports the notion that synaptic plasticity of the neurons leading to the lateral amygdala occurs with fear conditioning.<ref>{{cite pmid|14514027}}</ref> In some cases, this forms permanent fear responses such as [[post-traumatic stress disorder]] (PTSD) or a [[phobia]].<ref>American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders: DSM-IV. Washington, DC. ISBN 0-89042-061-0.</ref> MRI and fMRI scans have shown that the amygdala in individuals diagnosed with such disorders including [[bipolar disorder|bipolar]] or [[panic disorder]] is larger and wired for a higher level of fear.<ref>{{cite pmid|12619902}}</ref>


A treatment for fear conditioning and phobias via the amygdala is the use of [[glucocorticoid]]s.<ref>{{cite doi|10.1073/pnas.1103410108}}</ref> In one study, glucocorticoid receptors in the central nucleus of the amygdala were disrupted in order to better understand the mechanisms of fear and fear conditioning. The glucocorticoid receptors were inhibited using lentiviral vectors containing Cre-recombinase injected into mice. Results of this study showed that disruption of the glucocorticoid receptors prevented conditioned fear behavior. The mice were subjected to auditory cues which caused them to freeze normally. However, a reduction of freezing was observed in the mice that had inhibited glucocorticoid receptors.<ref>{{cite pmid|18695245}}</ref>
A treatment for fear conditioning and phobias via the amygdala is the use of [[glucocorticoid]]s.<ref>{{cite doi|10.1073/pnas.1103410108}}</ref> In one study, glucocorticoid receptors in the central nucleus of the amygdala were disrupted in order to better understand the mechanisms of fear and fear conditioning. The glucocorticoid receptors were inhibited using lentiviral vectors containing Cre-recombinase injected into mice. Results showed that disruption of the glucocorticoid receptors prevented conditioned fear behavior. The mice were subjected to auditory cues which caused them to freeze normally. However, a reduction of freezing was observed in the mice that had inhibited glucocorticoid receptors.<ref>{{cite pmid|18695245}}</ref>


==Diagnosing fear==
==Diagnosing fear==
Fear is distinguished from the related emotional state of [[anxiety]], which typically occurs without any certain or immediate external threat. [[Panic]] occurs when one is intimidated of a certain thing that reminds them of their fear, and experiencing an alarm response.
Fear is distinguished from the related emotional state of [[anxiety]], which typically occurs without any certain or immediate external threat. [[Panic]] occurs when one is intimidated of a certain thing that reminds them of their fear, and experiencing an alarm response.


There are many physiological changes in the body associated with fear, which can be summarized as the "fight or flight" response. An innate response for coping with danger, it works by accelerating the heart rate, dilating the blood vessels, and increasing muscle tension and breathing rate. As the name suggests, this primitive mechanism helps an organism survive by either running away or fighting off the danger. After the series of physiological changes, only then does the consciousness realize an emotion of fear.<ref>{{cite web|last=Edmundson|first=Laurel Duphiney|title=The Neurobiology of Fear|url=http://serendip.brynmawr.edu/bb/neuro/neuro00/web2/Edmundson.html|publisher=Serendip|accessdate=9 April 2012}}</ref>
There are many physiological changes in the body associated with fear, summarized as the [[fight-or-flight response]]. An inborn response for coping with danger, it works by accelerating the breathing rate ([[hyperventilation]]), heart rate, constriction of the peripheral blood vessels leading to blushing and vasodilation of the central vessels (pooling) , increasing muscle tension including the muscles attached to each hair follicle to contract and causing "goose bumps" aka [[piloerection]](making a cold person warmer or a frightened animal look more impressive), increased blood glucose ([[hyperglycemia]]), increased serum calcium, increase in neutrophilic leukocytes, sleep disturbance and "butterflies in the stomach" ([[dyspepsia]]). As the name suggests, this primitive mechanism helps an organism survive by either running away or fighting the danger.<ref>{{cite web|last=Edmundson|first=Laurel Duphiney|title=The Neurobiology of Fear|url=http://serendip.brynmawr.edu/bb/neuro/neuro00/web2/Edmundson.html|publisher=Serendip|accessdate=9 April 2012}}</ref>With the series of physiological changes, the consciousness realize an emotion of fear.

==Fear [[pheromones]] and why fear is contagious==

In threatening situations all living organisms emit odorant substances, initially called alarm substances, which are chemical signals now called alarm [[pheromones]] ("Schreckstoff" in German). This is to defend themselves and at the same time to inform members of the same species of danger. For example, stressed rats release odorant cues, that cause other rats to move away from the source of the signal. Alarm pheromones are synthesized, emitted and perceived by all living organisms studied to date with the possible exception of viruses and prions: i.e. bacteria, prokaryotes, plants, plankton, parasites, insects, aquatic organisms, birds, reptiles, and mammals including humans.

Alarm pheromones were first described in 1968 in ants <ref>Moser JC, Brownlee RC, Silverstein R. Alarm pheromones of the ant atta texana. J Insect Physiol. 1968 Apr;14(4):529-35.</ref> and earthworms <ref>Ressler RH, Cialdini RB, Ghoca ML, Kleist SM. Alarm pheromone in the earthworm Lumbricus terrestris. Science. 1968 Aug 9;161(3841):597-9.</ref>, and 4 years later also in mammals, both mice and rats <ref> Rottman SJ, Snowdon CT. Demonstration and analysis of an alarm pheromone in mice. J Comp Physiol Psychol. 1972 Dec;81(3):483-90.</ref>. Over the next two decades identification and characterization of these pheromones proceeded in all manner of microbes bacteria, fungi, plankton , insects and sea animals, including fish, but it was not until 1990, that more insight into mammalian alarm pheromones was gleaned. By using the “forced swimming test” in rats as a model of fear induction the first mammalian "alarm susbstance" was found .<ref>Abel EL, Bilitzke PJ. A possible alarm substance in the forced swimming test. Physiol Behav. 1990 Aug;48(2):233-9.</ref>
Shortly thereafter this alarm substance was shown to fulfill criteria for pheromones (well-defined behavioral effect, species specificity, minimal influence of experience and control for nonspecific arousal). Activity testing with alarm pheromone and their preference/avoidance for odors from cylinders containing the pheromone showed it has very low volatility.<ref>Abel EL. Alarm substance emitted by rats in the forced-swim test is a low volatile pheromone. Physiol Behav. 1991 Oct;50(4):723-7.</ref>

Pheromone production was subsequently found to be associated with or mediated by the [[pituitary gland]].<ref> Abel EL. The pituitary mediates production or release of an alarm chemosignal in rats. Horm Behav. 1994 Jun;28(2):139-45. </ref>
In 1994 a connection between alarm chemosignals in the mouse and their [[immune system]] was noted. <ref>Cocke R, Moynihan JA, Cohen N, Grota LJ, Ader R. Exposure to conspecific alarm chemosignals alters immune responses in [[BALB/c mice]]. Brain Behav Immun. 1993 Mar;7(1):36-46.</ref>

Severe pain or distress induces inflammatory cytokines in the brain and alarm pheromones: In 2011 real time [[RT-PCR]] analysis of rat brain tissues indicated that shocking the footpad of a rat increased their production of pro-inflammatory [[cytokines]] in deep brain structures, namely [[IL-1β]] , [[hnCRH]] and [[c-fos]] mRNA expressions in the [[paraventricular nucleus]] and the bed nucleus of the [[stria terminalis]], and increased stress hormone levels in plasma ([[corticosterone]]). <ref>Arakawa H, Arakawa K, Blandino P Jr, Deak T. The role of neuroinflammation in the release of aversive odor cues from footshock-stressed rats: Implications for the neural mechanism of alarm pheromones. Psychoneuroendocrinology. 2011 May;36(4):557-68.</ref>

A few years later a link between alarm pheromone levels and [[pain perception]] was discovered in honeybees: They became less responsive to pain after they had been stimulated with a chemical component of a bee alarm pheromone (isopentyl acetate)<ref>Núñez J, Almeida L, Balderrama N, Giurfa M. Alarm pheromone induces stress analgesia via an opioid system in the honeybee. Physiol Behav. 1997 Dec 31;63(1):75-80.</ref> The experiment also showed that the bee’s fear induced pain tolerance was mediated by an endorphine.

In 2004 it was demonstrated that rats’ alarm pheromones had different effects on the “recipient “rat (the rat perceiving the pheromone) depending which body region they were released from: Pheromone production from the face modified the behavior in the recipient rat, e.g. caused sniffing or movement, versus pheromone secreted from the rat's anal area induced autonomic nervous system stress responses, like increase in core body temperature.<ref>Kiyokawa Y, Kikusui T, Takeuchi Y, Mori Y. Alarm pheromones with different functions are released from different regions of the body surface of male rats. Chem Senses. 2004 Jan;29(1):35-40.</ref> Further experiments showed that when a rat perceived alarm pheromones it increased its defensive and risk assessment behavior.<ref>Kiyokawa Y, Shimozuru M, Kikusui T, Takeuchi Y, Mori Y. Alarm pheromone increases defensive and risk assessment behaviors in male rats. Physiol Behav. 2006 Feb 28;87(2):383-7. </ref> and its acoustic [[startle reflex]] was enhanced.

The [[neurocircuit]] for alarm pheromone perception in rats was shown to be related to hypothalamus, brainstem, and amygdaloid nuclei, all of which are evolutionary ancient structures deeply inside or in the case of the brainstem underneath the brain away from the cortex, and involved in the stress-response, as is the case in humans, <ref>Kiyokawa Y, Kikusui T, Takeuchi Y, Mori Y. Mapping the neural circuit activated by alarm pheromone perception by c-Fos immunohistochemistry. Brain Res. 2005 May 10;1043(1-2):145-54.</ref>

To evaluate the degree to which anxiolytics could alleviate anxiety in mammals, the change in the acoustic startle reflex of rats with alarm pheromone-induced anxiety (ie reduction of defensiveness) has been used experimentally. Pretreatment of rats with one of five [[anxiolytic|anxiolytics]] used in clinical medicine was able to reduce their anxiety: namely [[midazolam]], [[phenelzine]] (a nonselective monoamine oxidase (MAO) inhibitor), [[propranolol]], a nonselective [[β-adrenergic receptor antagonist]], [[clonidine]], an α2-adrenergic receptor agonist or [[CP-154,526]], a [[corticotropin-releasing factor subtype 1 receptor]] (CRF1) antagonist,).<ref>Inagaki H, Kiyokawa Y, Takeuchi Y, Mori Y. The alarm pheromone in male rats as a unique anxiety model: psychopharmacological evidence using anxiolytics. Pharmacol Biochem Behav. 2010 Feb;94(4):575-9.</ref>

It has been proposed that fear pheromones evolved as molecules of [[keystone]] significance. In ecological communities they may determine species compositions as well as affect rates of energy and material exchange. Thus they generate “structure” in trophic webs and play critical roles in maintaining natural systems.<ref>Ferrer RP, Zimmer RK. Community ecology and the evolution of molecules of keystone significance. Biol Bull. 2012 Oct;223(2):167-77.</ref>

Evidence of chemosensory alarm signals in humans has emerged slowly: Although alarm pheromones have not been physically isolated and their chemical structure has not been identified in man so far, there is evidence for their presence.
When human sweat was examined, chemosensory anxiety signals were found to prime the recipients defensive behavior prior to conscious attention on the startle reflex level.<ref>Prehn A, Ohrt A, Sojka B, Ferstl R, Pause BM. Chemosensory anxiety signals augment the startle reflex in humans. Neurosci Lett. 2006 Feb 13;394(2):127-30.</ref>

Researchers collected alarm induced sweat and exercise induced sweat from "donors" extracted it, pooled it and presented it to 16 unrelated "detector" subjects undergoing functional [[MRI]]. While stress induced sweat from males produced a comparably strong emotional response in both female and male detectors, female stress sweat produced a markedly stronger arousal in female detectors than male detectors. Statistical tests pinpointed this gender-specificity to the right amygdala (strongest in the superficial nuclei). When comparing the [[olfactory bulb]] responses to the corresponding stimuli, no significant differences between male and female detectors were observed. Imaging results complement behavioral evidence regarding the question whether gender differences in response to alarm chemosignals are initiated at the perceptual level versus the emotional level: Since no significant differences in the olfactory bulb, the primary processing site for chemosensory signals in mammal, were found, it is believed that the specific response to female fear signals is based on processing the meaning, rather than strength of chemosensory cues from each gender. <ref>Radulescu AR, Mujica-Parodi LR. Human gender differences in the perception of conspecific alarm chemosensory cues. PLoS One. 2013 Jul 24;8(7):e68485.</ref>
Alleviation of an acute stress/fear response because an [[affiliative conspecific ]]is present is called [[social buffering]].

"Social buffering" can mitigate the conditioned fear responses of [[conspecifics]]: Honeybees exposed to a colony environment influenced by high levels of predation threat did not show increased aggression and aggressive-like gene expression patterns in individual bees, but decreased aggression. That they did not habituate to threats is suggested by the fact that the disturbed colonies also decreased their foraging. <ref>Rittschof CC, Robinson GE. Manipulation of colony environment modulates honey bee aggression and brain gene expression. Genes Brain Behav. 2013 Nov;12(8):802-11. doi: 10.1111/gbb.12087. </ref> In male rats it has been shown that olfactory signals are responsible in mediating the social buffering. <ref>Takahashi Y, Kiyokawa Y, Kodama Y, Arata S, Takeuchi Y, Mori Y. Olfactory signals mediate social buffering of conditioned fear responses in male rats. Behav Brain Res. 2013 Mar 1;240:46-51.</ref>

[[Androstadienone]] is a steroidal, endogenous odorant or pheromone found in human sweat, axillary hair and plasma. Volunteers were given an approach–avoidance task: Upon seeing either an angry or a happy cartoon face on a computer screen they pushed away or pulled toward them a joystick as fast as possible, once during exposure to androstadienone, masked with clove oil scent, and once to placebo/ clove oil exposure only. Androstadienone sped up participants’ reaction, especially when reacting to angry faces. The faster responses have been interpreted as anandrostadienone-related activation of the fear system.<ref>:Frey MC, Weyers P, Pauli P, Mühlberger A. Androstadienone in motor reactions of men and women toward angry faces. Percept Mot Skills. 2012 Jun;114(3):807-25.</ref> A potential mechanism of action is that androstadienone alters the emotional face processing. Androstadienone is known to influences activity of the [[fusiform gyrus]] relevant for face recognition.

Defective development of the olfactory bulb and thus odor discrimination impairs detection of pheromones and pheromone related behavior, like aggressive behavior and mating in male rats: The enzyme [[ERK5 MAP kinase]] has been implicated in regulating the development of the main olfactory bulb and odor discrimination; it is highly expressed in developing rat brains, but absent in most regions of adult rat brains. Expression of [[ERK5]] during mouse development is critical for pheromone response and associated animal behavior in adult mice. Conditional deletion of the gene which encodes ERK5 in mouse neural stem cells impairs several pheromone-mediated behaviors, including aggression and mating in male mice. These behavior impairments were not caused by a reduction in the level of testosterone, by physical immobility, by heightened fear or anxiety, or by depression. Using mouse urine as a natural pheromone-containing solution, it has been shown that the impairment was associated with defective detection of related pheromones, and with changes in their inborn preference for pheromones related to sexual and reproductive activities. <ref>Zou J, Storm DR, Xia Z. Conditional deletion of ERK5 MAP kinase in the nervous system impairs pheromone information processing and pheromone-evoked behaviors. PLoS One. 2013 Oct 9;8(10):e76901. doi: 10.1371/journal.pone.0076901.</ref>


==Fears in culture==
==Fears in culture==

Revision as of 07:18, 22 January 2014

A scared child shows fear in an uncertain environment.

Fear is an emotion induced by a perceived threat which causes entities to quickly pull far away from it and usually hide. It is a basic survival mechanism occurring in response to a specific stimulus which is perceived as a risk of significant loss of health, wealth, status, power, security or of anything held valuable. In short, fear is a motivating force arising from the ability to recognize danger leading to an urge to confront it or flee from it (also known as the fight-or-flight response) but in extreme cases of fear (horror and terror) a freeze or paralysis response is possible.

Some psychologists such as John B. Watson, Robert Plutchik, and Paul Ekman have suggested that there is only a small set of basic or innate emotions and that fear is one of them. This hypothesized set includes such emotions as joy, sadness, fright, dread, horror, panic, anxiety, acute stress reaction and anger. Fear should be distinguished from the emotion anxiety, which typically occurs without any certain or immediate external threat.

Fear is frequently related to the specific behaviors of escape and avoidance, whereas anxiety is the result of threats which are perceived to be uncontrollable or unavoidable.[1] It is worth noting that fear almost always relates to future events, such as worsening of a situation, or continuation of a situation that is unacceptable. Fear can also be an instant reaction to something presently happening. All people have an instinctual response to potential danger, which is in fact important to the survival of all species. The reactions elicited from fear are seen through advantages in evolution.[2] Fear can be a manipulating and controlling factor in an individual's life.[3]

Common fears

According to surveys, some of the most common fears are of demons and ghosts, the existence of evil powers, cockroaches, spiders, snakes, heights, water, enclosed spaces, tunnels, bridges, needles, social rejection, failure, examinations and public speaking. In a test of what people fear the most, Bill Tancer analyzed the most frequent online search queries that involved the phrase, "fear of...". This follows the assumption that people tend to seek information on the issues that concern them the most. His top ten list of fears consisted of flying, heights, clowns, intimacy, death, rejection, people, snakes, failure, and driving.[4]

Though most arachnids are harmless, a person with arachnophobia may still panic or feel uneasy around one. Sometimes, even an object resembling a spider can trigger a panic attack in an arachnophobic individual. The above cartoon is a depiction of the nursery rhyme "Little Miss Muffet", in which the title character is "frightened away" by a spider.

One of the most common fears in humans is the fear of public speaking. People may be comfortable speaking inside a room but when it becomes public speaking, fear enters in the form of suspicion over whether the words uttered are correct or incorrect because there are many to judge them. Another common fear can be of pain, or of someone damaging a person. Fear of pain in a plausible situation brings flinching, or cringing.

In a 2005 Gallup poll (U.S.A.), a national sample of adolescents between the ages of 13 and 15 were asked what they feared the most. The question was open ended and participants were able to say whatever they wanted. The top ten fears were, in order: terrorist attacks, spiders, death, being a failure, war, criminal or gang violence, being alone, the future, and nuclear war.[5]

Fear of death

Psychologists have addressed the hypothesis that fear of death motivates religious commitment, and that it may be alleviated by assurances about an afterlife. Empirical research on this topic has been equivocal.[citation needed] According to Kahoe and Dunn, people who are most firm in their faith and attend religious services weekly are the least afraid of dying. A survey of people in various Christian denominations showed a negative correlation between fear of death and religious concern.[6]

In another study, data from a sample of white, Christian men and women were used to test the hypothesis that traditional, church-centered religiousness and de-institutionalized spiritual seeking are distinct ways of approaching fear of death in old age. Both religiousness and spirituality were related to positive psychosocial functioning, but only church-centered religiousness protected subjects against the fear of death.[7]

Shelly Kagan examines the philosophical background of whether fear of death makes sense (not about the actual kind of emotional reaction). In this context he states in one of his lectures, that there are certain conditions to fear in general to make sense:[8]

  • fear requires something bad, as the object of fear and
  • there's got to be a nonnegligible chance of the bad state of affairs happening, to their mind

Fear of the unknown

Many people are scared of the "unknown." The unknown can branch out to many areas such as the hereafter, the next ten years, or even tomorrow. Many people are too scared to take the path they want to, because of what may lie ahead. Fear of the unknown is one of the reasons that people do not make an effort to enhance their scholarly education. However, if they do, most people would rather teach things they've been taught than go and do research on something new. They perceive this as a risk that may cause them fear and stress.[3] This can lead to habits such as procrastination.

People usually fear uncertainty. Parents tell their children not to talk to strangers in order to protect them. However, some research suggests we should not fear strangers but be mindful of the risks that they could pose on children.[9]

Fear of survival

According to Irfan Jamil, coadjutor bishop of Lahore, as the world constantly changes, the greatest fear is the fear of survival. The social, economical, spiritual, political and educational circumstances in life make survival difficult in regard to such pressures that can come out of it.[10]

Unpredictability

The fear and stress of living in a constantly-unpredictable environment can cause a number of anxiety disorders and other psychological problems.

Causes

People develop specific fears as a result of learning. This has been studied in psychology as fear conditioning, beginning with John B. Watson's Little Albert experiment in 1920, which was inspired after observing a child with an irrational fear of dogs. In this study, an 11-month-old boy was conditioned to fear a white rat in the laboratory. The fear became generalized to include other white, furry objects, such as a rabbit, dog, and even a ball of cotton.

In the real world, fear can be acquired by a frightening traumatic accident. For example, if a child falls into a well and struggles to get out, he or she may develop a fear of wells, heights (acrophobia), enclosed spaces (claustrophobia), or water (aquaphobia). There are studies looking at areas of the brain that are affected in relation to fear. When looking at these areas (such as the amygdala), it was proposed that a person learns to fear regardless of whether they themselves have experienced trauma, or if they have observed the fear in others. In a study completed by Andreas Olsson, Katherine I. Nearing and Elizabeth A. Phelps the amygdala were affected both when subjects observed someone else being submitted to an aversive event, knowing that the same treatment awaited themselves, and when subjects were subsequently placed in a fear-provoking situation.[11] This suggests that fear can develop in both conditions, not just simply from personal history.

The creation of fear is affected by cultural influences and historical experience, especially during childhood or after serious accident happened. For example, in the early 20th century, many Americans feared polio, a disease that cripples the body part it affects, leaving that body part immobilized for the rest of one's life. There are also consistent cross-cultural differences in how people respond to fear. Display rules affect how likely people are to show the facial expression of fear and other emotions.

Although fear is learned, the capacity to fear is part of human nature. Many studies have found that certain fears (e.g. animals, heights) are much more common than others (e.g. flowers, clouds). These fears are also easier to induce in the laboratory. This phenomenon is known as preparedness. Because early humans that were quick to fear dangerous situations were more likely to survive and reproduce, preparedness is theorized to be a genetic effect that is the result of natural selection.

From an evolutionary psychology perspective, different fears may be different adaptations that have been useful in our evolutionary past. They may have developed during different time periods. Some fears, such as fear of heights, may be common to all mammals and developed during the mesozoic period. Other fears, such as fear of snakes, may be common to all simians and developed during the cenozoic time period. Still others, such as fear of mice and insects, may be unique to humans and developed during the paleolithic and neolithic time periods (when mice and insects become important carriers of infectious diseases and harmful for crops and stored foods).[12]

Fear is high only if the observed risk and seriousness both are high and is low if one or the other of the seen risk or seriousness is low.[13]

Neurocircuit of fear in mammals

The brain structure that is the center of most neurobiological events associated with fear is the amygdala, located behind the pituitary gland. The amygdala is part of a circuitry of fear learning.[2] It is essential for proper adaptation to stress and specific modulation of emotional learning memory. In the presence of a threatening stimulus, the amygdala generates the secretion of hormones that influence fear and aggression.[14] Once response to the stimulus in the form of fear or aggression commences, the amygdala may elicit the release of hormones into the body to put the person into a state of alertness, in which they are ready to move, run, fight, etc. This defensive response is generally referred to in physiology as the fight-or-flight response regulated by the hypothalamus, part of the limbic system.[15] Once the person is in safe mode, meaning that there are no longer any potential threats surrounding them, the amygdala will send this information to the medial prefrontal cortex (mPFC) where it is stored for similar future situations, which is known as memory consolidation.[16]

Some of the hormones involved during the state of fight-or-flight include adrenaline, epinephrine, norepinephrine and cortisol. Epinephrine regulates heart rate and metabolism as well as dilating blood vessels and air passages. Norepinephrine increases heart rate, blood flow to skeletal muscles and the release of glucose from energy stores.[17] Cortisol increases blood sugar, demarginalizes neutrophilic leukocytes,increases calcium and much more.[18]

After a situation which incites fear occurs, the amygdala and hippocampus record the event through synaptic plasticity.[19] The stimulation to the hippocampus will cause the individual to remember many details surrounding the situation.[20] Plasticity and memory formation in the amygdala are generated by activation of the neurons in the region. Experimental data supports the notion that synaptic plasticity of the neurons leading to the lateral amygdala occurs with fear conditioning.[21] In some cases, this forms permanent fear responses such as post-traumatic stress disorder (PTSD) or a phobia.[22] MRI and fMRI scans have shown that the amygdala in individuals diagnosed with such disorders including bipolar or panic disorder is larger and wired for a higher level of fear.[23]

A treatment for fear conditioning and phobias via the amygdala is the use of glucocorticoids.[24] In one study, glucocorticoid receptors in the central nucleus of the amygdala were disrupted in order to better understand the mechanisms of fear and fear conditioning. The glucocorticoid receptors were inhibited using lentiviral vectors containing Cre-recombinase injected into mice. Results showed that disruption of the glucocorticoid receptors prevented conditioned fear behavior. The mice were subjected to auditory cues which caused them to freeze normally. However, a reduction of freezing was observed in the mice that had inhibited glucocorticoid receptors.[25]

Diagnosing fear

Fear is distinguished from the related emotional state of anxiety, which typically occurs without any certain or immediate external threat. Panic occurs when one is intimidated of a certain thing that reminds them of their fear, and experiencing an alarm response.

There are many physiological changes in the body associated with fear, summarized as the fight-or-flight response. An inborn response for coping with danger, it works by accelerating the breathing rate (hyperventilation), heart rate, constriction of the peripheral blood vessels leading to blushing and vasodilation of the central vessels (pooling) , increasing muscle tension including the muscles attached to each hair follicle to contract and causing "goose bumps" aka piloerection(making a cold person warmer or a frightened animal look more impressive), increased blood glucose (hyperglycemia), increased serum calcium, increase in neutrophilic leukocytes, sleep disturbance and "butterflies in the stomach" (dyspepsia). As the name suggests, this primitive mechanism helps an organism survive by either running away or fighting the danger.[26]With the series of physiological changes, the consciousness realize an emotion of fear.

Fear pheromones and why fear is contagious

In threatening situations all living organisms emit odorant substances, initially called alarm substances, which are chemical signals now called alarm pheromones ("Schreckstoff" in German). This is to defend themselves and at the same time to inform members of the same species of danger. For example, stressed rats release odorant cues, that cause other rats to move away from the source of the signal. Alarm pheromones are synthesized, emitted and perceived by all living organisms studied to date with the possible exception of viruses and prions: i.e. bacteria, prokaryotes, plants, plankton, parasites, insects, aquatic organisms, birds, reptiles, and mammals including humans.

Alarm pheromones were first described in 1968 in ants [27] and earthworms [28], and 4 years later also in mammals, both mice and rats [29]. Over the next two decades identification and characterization of these pheromones proceeded in all manner of microbes bacteria, fungi, plankton , insects and sea animals, including fish, but it was not until 1990, that more insight into mammalian alarm pheromones was gleaned. By using the “forced swimming test” in rats as a model of fear induction the first mammalian "alarm susbstance" was found .[30]

Shortly thereafter this alarm substance was shown to fulfill criteria for pheromones (well-defined behavioral effect, species specificity, minimal influence of experience and control for nonspecific arousal). Activity testing with alarm pheromone and their preference/avoidance for odors from cylinders containing the pheromone showed it has very low volatility.[31]

Pheromone production was subsequently found to be associated with or mediated by the pituitary gland.[32] In 1994 a connection between alarm chemosignals in the mouse and their immune system was noted. [33]

Severe pain or distress induces inflammatory cytokines in the brain and alarm pheromones: In 2011 real time RT-PCR analysis of rat brain tissues indicated that shocking the footpad of a rat increased their production of pro-inflammatory cytokines in deep brain structures, namely IL-1β , hnCRH and c-fos mRNA expressions in the paraventricular nucleus and the bed nucleus of the stria terminalis, and increased stress hormone levels in plasma (corticosterone). [34]

A few years later a link between alarm pheromone levels and pain perception was discovered in honeybees: They became less responsive to pain after they had been stimulated with a chemical component of a bee alarm pheromone (isopentyl acetate)[35] The experiment also showed that the bee’s fear induced pain tolerance was mediated by an endorphine.

In 2004 it was demonstrated that rats’ alarm pheromones had different effects on the “recipient “rat (the rat perceiving the pheromone) depending which body region they were released from: Pheromone production from the face modified the behavior in the recipient rat, e.g. caused sniffing or movement, versus pheromone secreted from the rat's anal area induced autonomic nervous system stress responses, like increase in core body temperature.[36] Further experiments showed that when a rat perceived alarm pheromones it increased its defensive and risk assessment behavior.[37] and its acoustic startle reflex was enhanced.

The neurocircuit for alarm pheromone perception in rats was shown to be related to hypothalamus, brainstem, and amygdaloid nuclei, all of which are evolutionary ancient structures deeply inside or in the case of the brainstem underneath the brain away from the cortex, and involved in the stress-response, as is the case in humans, [38]

To evaluate the degree to which anxiolytics could alleviate anxiety in mammals, the change in the acoustic startle reflex of rats with alarm pheromone-induced anxiety (ie reduction of defensiveness) has been used experimentally. Pretreatment of rats with one of five anxiolytics used in clinical medicine was able to reduce their anxiety: namely midazolam, phenelzine (a nonselective monoamine oxidase (MAO) inhibitor), propranolol, a nonselective β-adrenergic receptor antagonist, clonidine, an α2-adrenergic receptor agonist or CP-154,526, a corticotropin-releasing factor subtype 1 receptor (CRF1) antagonist,).[39]

It has been proposed that fear pheromones evolved as molecules of keystone significance. In ecological communities they may determine species compositions as well as affect rates of energy and material exchange. Thus they generate “structure” in trophic webs and play critical roles in maintaining natural systems.[40]

Evidence of chemosensory alarm signals in humans has emerged slowly: Although alarm pheromones have not been physically isolated and their chemical structure has not been identified in man so far, there is evidence for their presence. When human sweat was examined, chemosensory anxiety signals were found to prime the recipients defensive behavior prior to conscious attention on the startle reflex level.[41]

Researchers collected alarm induced sweat and exercise induced sweat from "donors" extracted it, pooled it and presented it to 16 unrelated "detector" subjects undergoing functional MRI. While stress induced sweat from males produced a comparably strong emotional response in both female and male detectors, female stress sweat produced a markedly stronger arousal in female detectors than male detectors. Statistical tests pinpointed this gender-specificity to the right amygdala (strongest in the superficial nuclei). When comparing the olfactory bulb responses to the corresponding stimuli, no significant differences between male and female detectors were observed. Imaging results complement behavioral evidence regarding the question whether gender differences in response to alarm chemosignals are initiated at the perceptual level versus the emotional level: Since no significant differences in the olfactory bulb, the primary processing site for chemosensory signals in mammal, were found, it is believed that the specific response to female fear signals is based on processing the meaning, rather than strength of chemosensory cues from each gender. [42] Alleviation of an acute stress/fear response because an affiliative conspecific is present is called social buffering.

"Social buffering" can mitigate the conditioned fear responses of conspecifics: Honeybees exposed to a colony environment influenced by high levels of predation threat did not show increased aggression and aggressive-like gene expression patterns in individual bees, but decreased aggression. That they did not habituate to threats is suggested by the fact that the disturbed colonies also decreased their foraging. [43] In male rats it has been shown that olfactory signals are responsible in mediating the social buffering. [44]

Androstadienone is a steroidal, endogenous odorant or pheromone found in human sweat, axillary hair and plasma. Volunteers were given an approach–avoidance task: Upon seeing either an angry or a happy cartoon face on a computer screen they pushed away or pulled toward them a joystick as fast as possible, once during exposure to androstadienone, masked with clove oil scent, and once to placebo/ clove oil exposure only. Androstadienone sped up participants’ reaction, especially when reacting to angry faces. The faster responses have been interpreted as anandrostadienone-related activation of the fear system.[45] A potential mechanism of action is that androstadienone alters the emotional face processing. Androstadienone is known to influences activity of the fusiform gyrus relevant for face recognition.

Defective development of the olfactory bulb and thus odor discrimination impairs detection of pheromones and pheromone related behavior, like aggressive behavior and mating in male rats: The enzyme ERK5 MAP kinase has been implicated in regulating the development of the main olfactory bulb and odor discrimination; it is highly expressed in developing rat brains, but absent in most regions of adult rat brains. Expression of ERK5 during mouse development is critical for pheromone response and associated animal behavior in adult mice. Conditional deletion of the gene which encodes ERK5 in mouse neural stem cells impairs several pheromone-mediated behaviors, including aggression and mating in male mice. These behavior impairments were not caused by a reduction in the level of testosterone, by physical immobility, by heightened fear or anxiety, or by depression. Using mouse urine as a natural pheromone-containing solution, it has been shown that the impairment was associated with defective detection of related pheromones, and with changes in their inborn preference for pheromones related to sexual and reproductive activities. [46]


Fears in culture

Painting by Guido Reni c. 1611

Death

The fear of the end and its existence is in other words the fear of death. The fear of death ritualized the lives of our ancestors. These rituals were designed to reduce that fear; they helped collect the cultural ideas that we now have in the present. These rituals also helped preserve the cultural ideas. The results and methods of human existence had been changing at the same time that social formation was changing. One can say that the formation of communities happened because people lived in fear. The result of this fear forced people to unite to fight dangers together rather than fight alone.

Religion

Religions are filled with different fears that humans have had throughout many centuries. The fears aren't just metaphysical (including the problems of life and death) but are also moral. Death is seen as a boundary to another world. That world would always be different depending on how each individual lived their lives. The origins of this intangible fear are not found in the present world. In a sense we can assume that fear was a big influence on things such as morality.

There is another fear in the Bible that has a different meaning. It says to fear God. This is not a fear as in being afraid of God. Fear is used to express a Filial or a slavish passion. In good men, the fear of God is holy awe or reverence of God and his laws, which springs from a just view and real love of the divine character, leading the subject of it to hate and shun every thing that can offend such a holy being and inclining them to aim at perfect obedience.

Fear is often used as a tool by religious leaders to manipulate people. At the Salem witch trials, many innocent women were burnt alive through irrational fear instilled in them by the religious leaders of the community.

Manipulation

M. Korstanje argues that the fear may be politically and culturally manipulated to dissuade citizenry about the implementation of market-oriented policies, otherwise would be widely rejected. In contexts of disasters, nation-states manage the fear not only to provide their citizens with an explanation about the event or blaming some minorities, but also to adjust their previous beliefs. The manipulation of fear is done by means of symbolic instruments as terror movies and the administration ideologies that lead to nationalism. After a disaster, the fear is re-channeled in a climate of euphoria based on patriotism. The fear and evilness are inextricably intertwined.[47]

Mirroring fears

Our fears are portrayed through sources such as books and movies. For example, many horror movies and books include characters who fear the antagonist of the plot. Fear is also found in mythological folklore and folklore superstitions. One of the important characteristics of historical and mythical heroes across the cultures is to be fearless in the face of big and often lethal enemies.

Neurology

Pathogens can suppress amygdala activity. Rats infected with the toxoplasmosis parasite become less fearful of cats, sometimes even seeking out their urine-marked areas. This behavior often leads to them being eaten by cats. The parasite then reproduces within the body of the cat. There is evidence that the parasite concentrates itself in the amygdala of infected rats.[48] In a separate experiment, rats with lesions in the amygdala did not express fear or anxiety towards unwanted stimuli. These rats pulled on levers supplying food that sometimes sent out electrical shocks. While they learned to avoid pressing on them, they did not distance themselves from these shock-inducing levers.[49]

Several brain structures other than the amygdala have also been observed to be activated when individuals are presented with fearful vs. neutral faces, namely the occipitocerebellar regions including the fusiform gyrus and the inferior parietal / superior temporal gyri.[50] Interestingly, fearful eyes, brows and mouth seem to separately reproduce these brain responses.[50] Scientist from Zurich studies show that the hormone oxytocin related to stress and sex reduces activity in your brain fear center.[51]

Process of fear:

  • The thalamus collects sensory data from the senses
  • Sensory cortex receives data from thalamus and interprets it
  • Sensory cortex organizes information for dissemination to hypothalamus (fight or flight), amygdala (fear), hippocampus (memory)

Overcoming fear

Neuroscientists and psychologists are making breakthroughs in helping people overcome fear. Because fear is more complex than just forgetting or deleting memories, an active and successful approach involves a person repeatedly confronting their fears. By confronting their fears— in a safe manner— a person can suppress the fear-triggering memory or stimulus. Known as ‘exposure therapy’, this practice can help cure up to 90% of people, with specific phobias.[16]

See also

3

References

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  49. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1016/S0140-6736(05)62234-9, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1016/S0140-6736(05)62234-9 instead.
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Further reading

Rasheeal Dixon |Year 2012 How to overcome fear, and start living fearless http://amzn.com/1475122047