Fear

For other uses, see Fear (disambiguation).
"Scared" and "Terror" redirect here. For other uses, see Scared (disambiguation) and Terror (disambiguation).
A scared child shows fear in an uncertain environment.

Fear is a feeling induced by perceived danger or threat that occurs in certain types of organisms, which causes a change in metabolic and organ functions and ultimately a change in behavior, such as fleeing, hiding, or freezing from perceived traumatic events. Fear in human beings may occur in response to a specific stimulus occurring in the present, or in anticipation or expectation of a future threat perceived as a risk to body or life. The fear response arises from the perception of danger leading to confrontation with or escape from/avoiding the threat (also known as the fight-or-flight response), which in extreme cases of fear (horror and terror) can be a freeze response or paralysis.

In humans and animals, fear is modulated by the process of cognition and learning. Thus fear is judged as rational or appropriate and irrational or inappropriate. An irrational fear is called a phobia.

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 acute stress reaction, anger, angst, anxiety, fright, horror, joy, panic, and sadness. Fear is closely related to, but should be distinguished from, the emotion anxiety, which occurs as the result of threats that are perceived to be uncontrollable or unavoidable.[1] The fear response serves survival by generating appropriate behavioral responses, so it has been preserved throughout evolution.[2]

Signs and symptoms

Many physiological changes in the body are 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", or more clinically, piloerection (making a cold person warmer or a frightened animal look more impressive), sweating, increased blood glucose (hyperglycemia), increased serum calcium, increase in white blood cells called neutrophilic leukocytes, alertness leading to sleep disturbance and "butterflies in the stomach" (dyspepsia). This primitive mechanism may help an organism survive by either running away or fighting the danger.[3] With the series of physiological changes, the consciousness realizes an emotion of fear.

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.

Fear can be learned by experiencing or watching 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.[4] This suggests that fear can develop in both conditions, not just simply from personal history.

Fear is affected by cultural and historical context. 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 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 many fears are 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).[5]

Fear is high only if the observed risk and seriousness both are high, and is low, if risk or seriousness is low.[6]

Top 10 types in the U.S.

In a 2005 Gallup poll (U.S.), a national sample of adolescents between the ages of 13 and 17 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.[7]

In an estimate of what people fear the most, book author Bill Tancer analyzed the most frequent online queries that involved the phrase, "fear of..." following the assumption that people tend to seek information on the issues that concern them the most. His top ten list of fears published 2008 consisted of flying, heights, clowns, intimacy, death, rejection, people, snakes, failure, and driving.[8]

Common phobias

See also: Phobia

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.[9][10][11]

Fear of death

Death anxiety is multidimensional; it covers "fears related to one's own death, the death of others, fear of the unknown after death, fear of obliteration, and fear of the dying process, which includes fear of a slow death and a painful death".[12]

The Yale philosopher Shelly Kagan examined fear of death in a 2007 Yale open course[13] by examining the following questions: Is fear of death a reasonable appropriate response? What conditions are required and what are appropriate conditions for feeling fear of death? What is meant by fear, and how much fear is appropriate? According to Kagan for fear in general to make sense, three conditions should be met: the object of fear needs to be "something bad", there needs to be a non-negligible chance that the bad state of affairs will happen, and there needs to be some uncertainty about the bad state of affairs. The amount of fear should be appropriate to the size of "the bad". If the 3 conditions aren't met, fear is an inappropriate emotion. He argues, that death does not meet the first two criteria, even if death is a "deprivation of good things" and even if one believes in a painful afterlife. Because death is certain, it also does not meet the third criterion, but he grants that the unpredictability of when one dies may be cause to a sense of fear.

In a 2003 study of 167 women and 121 men, aged 65–87, low self-efficacy predicted fear of the unknown after death and fear of dying for women and men better than demographics, social support, and physical health. Fear of death was measured by a "Multidimensional Fear of Death Scale" which included the 8 subscales Fear of Dying, Fear of the Dead, Fear of Being Destroyed, Fear for Significant Others, Fear of the Unknown, Fear of Conscious Death, Fear for the Body After Death, and Fear of Premature Death. In hierarchical multiple regression analysis the most potent predictors of death fears were low "spiritual health efficacy", defined as beliefs relating to one's perceived ability to generate spiritually based faith and inner strength, and low "instrumental efficacy", defined as beliefs relating to one's perceived ability to manage activities of daily living.[12]

Psychologists have tested the hypothesis that fear of death motivates religious commitment, and assurances about an afterlife alleviate the fear and empirical research on this topic has been equivocal. Religiosity can be related to fear of death when the afterlife is portrayed as time of punishment. "Intrinsic religiosity", as opposed to mere "formal religious involvement" has been found to be negatively correlated with death anxiety.[12] In a 1976 study people of various Christian denominations those most firm in their faith, attending religious services weekly were the least afraid of dying. The survey found a negative correlation between fear of death and "religious concern".[14]

In a 2006 study of white, Christian men and women the hypothesis was tested that traditional, church-centered religiousness and de-institutionalized spiritual seeking are 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.[15]

Fear of the unknown

Fear of the unknown or irrational fear is caused by negative thinking (worry) which arises from anxiety. Many people are scared of the "unknown". The irrational fear can branch out to many areas such as the hereafter, the next ten years, or even tomorrow. In these cases specialists use False Evidence Appearing Real as a definition. Being scared makes people to anticipate and aggravate of what may lie ahead rather than plan and evaluate. E.g. Continuation of scholarly education, most educators perceive this as a risk that may cause them fear and stress[16] and they would rather teach things they've been taught than go and do research. This can lead to habits such as laziness and procrastination. The ambiguity of a situations that tend to be uncertain and unpredictable can cause anxiety, other psychological and physical problems in some populations; especially those who engage it constantly. E.g. War-ridden or Conflict places, Terrorism, Abuse ...etc. Poor parenting that instills fear can also debilitate children's psyche development or personality. E.g. Parents tell their children not to talk to strangers in order to protect them. In school they would be motivated to not show fear in talking with strangers, but to be assertive and also aware of the risks and the environment that it takes place. Ambiguous and mixed messages like this can affect their self-esteem and self-confidence. Researcher's say talking to strangers isn't something to be thwarted but allowed in a parent's presence if required.[17] Developing a sense of equanimity to handle various situations is often advocated as an antidote to irrational fear and essential skill by a number of ancient philosophies.

Mechanism

Often laboratory studies with rats are conducted to examine the acquisition and extinction of conditioned fear responses.[18] In 2004, researchers conditioned rats (rattus norvegicus) to fear a certain stimulus, through electric shock.[19] The researchers were able to then cause an extinction of this conditioned fear, to a point that no medications or drugs were able to further aid in the extinction process. However the rats did show signs of avoidance learning, not fear, but simply avoiding the area that brought pain to the tests rats. The avoidance learning of rats is seen as a conditioned response, and therefore the behavior can be unconditioned, as supported by the earlier research. Species-specific defense reactions (SSDRs) or avoidance learning in nature is the specific tendency to avoid certain threats or stimuli, it is how animals survive in the wild. Humans and animals both share these species-specific defense reactions, such as the flight, fight, which also include pseudo-aggression, fake or intimidating aggression, freeze response to threats, which is controlled by the sympathetic nervous system. These SSDRs are learned very quickly through social interactions between others of the same species, other species, and interaction with the environment.[20] These acquired sets of reactions or responses are not easily forgotten. The animal that survives is the animal that already knows what to fear and how to avoid this threat. An example in humans is the reaction to the sight of a snake, many jump backwards before cognitively realizing what they are jumping away from, and in some cases it is a stick rather than a snake.

As with many functions of the brain, there are various regions of the brain involved in deciphering fear in humans and other nonhuman species.[21] The amygdala communicates both directions between the prefrontal cortex, hypothalamus, the sensory cortex, the hippocampus, thalamus, septum, and the brainstem. The amygdala plays an important role in SSDR, such as the ventral amygdalofugal, which is essential for associative learning, and SSDRs are learned through interaction with the environment and others of the same species. An emotional response is created only after the signals have been relayed between the different regions of the brain, and activating the sympathetic nervous systems; which controls the flight, fight, freeze, fright, and faint response.[22] Often a damaged amygdala can cause impairment in the recognition of fear (like the human case of patient S.M.).[23] This impairment can cause different species to lack the sensation of fear, and often can become overly confident, confronting larger peers, or walking up to predatory creatures.

Robert C. Bolles (1970), a researcher at University of Washington, wanted to understand species-specific defense reactions and avoidance learning among animals, but found that the theories of avoidance learning and the tools that were used to measure this tendency were out of touch with the natural world.[24] He theorized the species-specific defense reaction (SSDR).[25] There are three forms of SSDRs: flight, fight (pseudo-aggression), or freeze. Even domesticated animals have SSDRs, and in those moments it is seen that animals revert to atavistic standards and become "wild" again. Dr. Bolles states that responses are often dependent on the reinforcement of a safety signal, and not the aversive conditioned stimuli. This safety signal can be a source of feedback or even stimulus change. Intrinsic feedback or information coming from within, muscle twitches, increased heart rate, is seen to be more important in SSRDs than extrinsic feedback, stimuli that comes from the external environment. Dr. Bolles found that most creatures have some intrinsic set of fears, to help assure survival of the species. Rats will run away from any shocking event, and pigeons will flap their wings harder when threatened, the wing flapping in pigeons and the scattered running of rats are considered a species-specific defense reaction or behavior. Bolles believed that SSDR are conditioned through pavlovian conditioning, and not operant conditioning; SSDR arise from the association between the environmental stimuli and adverse events.[26] Michael S. Fanselow conducted an experiment, to test some specific defense reactions, he observed that rats in two different shock situations responded differently, based on instinct or defensive topography, rather than contextual information.[27]

Species specific defense responses are created out of fear, and are essential for survival.[28] Rats that lack the gene stathmin show no avoidance learning, or a lack of fear, and will often walk directly up to cats and be eaten.[29] Animals use these SSDR to continue living, to help increase their chance of fitness, by surviving long enough to procreate. Humans and animals alike have created fear to know what should avoided, and this fear can be learned through association with others in the community, or learned through personal experience with a creature, species, or situations that should be avoided. SSDRs are an evolutionary adaptation that has been seen in many species throughout the world including rats, chimpanzees, prairie dogs, and even humans, an adaptation created to help individual creatures survive in a hostile world.

Fear learning changes across the lifetime due to natural developmental changes in the brain.[30][31] This includes changes in the prefrontal cortex and the amygdala.[32]

Neurocircuit 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.[33] 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.[34] 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.[35]

Some of the hormones involved during the state of fight-or-flight include epinephrine, which regulates heart rate and metabolism as well as dilating blood vessels and air passages, norepinephrine increasing heart rate, blood flow to skeletal muscles and the release of glucose from energy stores.[36] and cortisol which increases blood sugar, increases circulating neutrophilic leukocytes, calcium amongst other things.[37]

After a situation which incites fear occurs, the amygdala and hippocampus record the event through synaptic plasticity.[38] The stimulation to the hippocampus will cause the individual to remember many details surrounding the situation.[39] 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.[40] In some cases, this forms permanent fear responses such as post-traumatic stress disorder (PTSD) or a phobia.[41] 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.[42]

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.[43] 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.[44]

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.[45] Interestingly, fearful eyes, brows and mouth seem to separately reproduce these brain responses.[45] Scientist from Zurich studies show that the hormone oxytocin related to stress and sex reduces activity in your brain fear center.[46]

Pheromones and why fear can be contagious

In threatening situations insects, aquatic organisms, birds, reptiles, and mammals 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 and leads to observable behavior change like freezing, defensive behavior, or dispersion depending on circumstances and species. For example, stressed rats release odorant cues that cause other rats to move away from the source of the signal. Pheromones are synthesized, emitted and perceived by all living organisms studied to date, with the exception of viruses and prions: i.e. in bacteria, prokaryotes, plants, plankton, parasites, insects, invertebrates and vertebrates (aquatic organisms, birds, reptiles, and mammals).

After the discovery of pheromones in 1959, alarm pheromones were first described in 1968 in ants[47] and earthworms,[48] and 4 years later also found in mammals, both mice and rats.[49] Over the next two decades identification and characterization of these pheromones proceeded in all manner of insects and sea animals, including fish, but it was not until 1990 that more insight into mammalian alarm pheromones was gleaned.

Early on, in 1985, a link between odors released by stressed rats and pain perception was discovered: unstressed rats exposed to these odors developed opioid-mediated analgesia.[50] In 1997, researchers found bees became less responsive to pain after they had been stimulated with isoamyl acetate, a chemical smelling of banana, and a component of bee alarm pheromone.[51] The experiment also showed that the bees' fear-induced pain tolerance was mediated by an endorphine.

By using the forced swimming test in rats as a model of fear-induction, the first mammalian "alarm substance" was found.[52]

In 1991, 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. Rat activity testing with alarm pheromone and their preference/avoidance for odors from cylinders containing the pheromone showed, that the pheromone had very low volatility.[53]

In 1993 a connection between alarm chemosignals in mice and their immune response was found.[54]

Pheromone production in mice was found to be associated with or mediated by the pituitary gland in 1994.[55]

It was not until 2011 that a link between severe pain, neuroinflammation and alarm pheromones release in rats was found: real time RT-PCR analysis of rat brain tissues indicated that shocking the footpad of a rat increased its production of proinflammatory cytokines in deep brain structures, namely of IL-1β, heteronuclear Corticotropin-releasing hormone and c-fos mRNA expressions in both the paraventricular nucleus and the bed nucleus of the stria terminalis, and it increased stress hormone levels in plasma (corticosterone).[56]

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 behavior in the recipient rat, e.g. caused sniffing or movement, whereas pheromone secreted from the rat's anal area induced autonomic nervous system stress responses, like an increase in core body temperature.[57] Further experiments showed that when a rat perceived alarm pheromones, it increased its defensive and risk assessment behavior.[58] and its acoustic startle reflex was enhanced.

The neurocircuit for how rats perceive alarm pheromones was shown to be related to hypothalamus, brainstem, and amygdala, all of which are evolutionary ancient structures deep inside or in the case of the brainstem underneath the brain away from the cortex, and involved in the fight-or-flight response, as is the case in humans.[59]

Alarm pheromone-induced anxiety in rats has been used to evaluate the degree to which anxiolytics can alleviate anxiety in humans. For this the change in the acoustic startle reflex of rats with alarm pheromone-induced anxiety (i.e. reduction of defensiveness) has been measured. 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 beta blocker, clonidine, an alpha 2 adrenergic agonist or CP-154,526, a corticotropin-releasing hormone antagonist.[60]

Faulty development of odor discrimination impairs the perception of pheromones and pheromone-related behavior, like aggressive behavior and mating in male rats: The enzyme Mitogen-activated protein kinase 7 (MAPK7) has been implicated in regulating the development of the olfactory bulb and odor discrimination and it is highly expressed in developing rat brains, but absent in most regions of adult rat brains. conditional deletion of the MAPK7gene 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.[61]

Lastly, alleviation of an acute fear response because a friendly peer (or in biological language: an affiliative conspecific) tends and befriends is called "social buffering". The term is in analogy to the 1985 "buffering" hypothesis in psychology, where social support has been proven to mitigate the negative health effects of alarm pheromone mediated distress.[62] The role of a "social pheromone" is suggested by the recent discovery that olfactory signals are responsible in mediating the "social buffering" in male rats.[63] "Social buffering" was also observed to mitigate the conditioned fear responses of honeybees. A bee colony exposed to an environment of high threat of predation did not show increased aggression and aggressive-like gene expression patterns in individual bees, but decreased aggression. That the bees did not simply habituate to threats is suggested by the fact that the disturbed colonies also decreased their foraging.[64]

Biologists have proposed in 2012 that fear pheromones evolved as molecules of "keystone significance", a term coined in analogy to keystone species. Pheromones may determine species compositions, and affect rates of energy and material exchange in an ecological community. Thus pheromones generate structure in a trophic web and play critical roles in maintaining natural systems.[65]

Fear pheromones in humans

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. Androstadienone, for example, a steroidal, endogenous odorant, is a pheromone candidate found in human sweat, axillary hair and plasma. The closely related compound androstenone is involved in communicating dominance, aggression or competition; sex hormone influences on androstenone perception in humans showed high testosterone level related to heightened androstenone sensitivity in men, a high testosterone level related to unhappiness in response to androstenone in men, and a high estradiol level related to disliking of androstenone in women.[66]

A German study from 2006 showed when anxiety-induced versus exercise-induced human sweat from a dozen people was pooled and offered to seven study participants, of five able to olfactorily distinguish exercise-induced sweat from room air, three could also distinguish exercise-induced sweat from anxiety induced sweat. The acoustic startle reflex response to a sound when sensing anxiety sweat was larger than when sensing exercise-induced sweat, as measured by electromyograph analysis of the orbital muscle, which is responsible for the eyeblink component. This showed for the first time that fear chemosignals can modulate the startle reflex in humans without emotional mediation; fear chemosignals primed the recipient's "defensive behavior" prior to the subjects' conscious attention on the acoustic startle reflex level.[67]

In analogy to the social buffering of rats and honeybees in response to chemosignals, induction of empathy by "smelling anxiety" of another person has been found in humans.[68]

A study from 2013 provided brain imaging evidence that human responses to fear chemosignals may be gender-specific. Researchers collected alarm-induced sweat and exercise-induced sweat from donors extracted it, pooled it and presented it to 16 unrelated people undergoing functional brain MRI. While stress-induced sweat from males produced a comparably strong emotional response in both females and males, stress-induced sweat from females produced a markedly stronger arousal in women than in men. Statistical tests pinpointed this gender-specificity to the right amygdala and strongest in the superficial nuclei. Since no significant differences were found in the olfactory bulb, the response to female fear-induced signals is likely based on processing the meaning, i.e. on the emotional level, rather than the strength of chemosensory cues from each gender, i.e. the perceptual level.[69]

An approach-avoidance task was set up where volunteers seeing either an angry or a happy cartoon face on a computer screen pushed away or pulled toward them a joystick as fast as possible. Volunteers smelling anandrostadienone, masked with clove oil scent responded faster, especially to angry faces, than those smelling clove oil only, which was interpreted as anandrostadienone-related activation of the fear system.[70] A potential mechanism of action is, that androstadienone alters the "emotional face processing". Androstadienone is known to influence activity of the fusiform gyrus which is relevant for face recognition.

Management

Pharmaceutical

A drug treatment for fear conditioning and phobias via the amygdala is the use of glucocorticoids.[71] 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.[72]

Psychology

Cognitive behavioral therapy has been successful in helping people overcome fear. Because fear is more complex than just forgetting or deleting memories, an active and successful approach involves people 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.[35]

Society and 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. This assumption, however, flies in the face of concepts such as Moral Absolutism and Moral Universalism – which would hold that our morals are rooted in either the divine or natural laws of the universe, and would not be generated by any human feeling, thought or emotion.

See also: fear of God

Manipulation

Fear may be politically and culturally manipulated to persuade citizenry of ideas which would otherwise be widely rejected or dissuade citizenry from ideas which would otherwise be wildly supported. 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.[73]

Mirroring fears

Fear is found in mythology and folklore, and portrayed in books and movies. The Story of the Youth Who Went Forth to Learn What Fear Was is a German fairy tale dealing with the topic of not knowing fear. For example, many stories include characters who fear the antagonist of the plot. One of the important characteristics of historical and mythical heroes across cultures is to be fearless in the face of big and often lethal enemies.

Inability to experience

People who have damage to the amygdala, such as from Urbach–Wiethe disease, are unable to experience fear. This is not debilitating, but a lack of fear can allow someone to get into a dangerous situation they otherwise would have avoided.[74]

See also

References

  1. ↑ Öhman, A. (2000). "Fear and anxiety: Evolutionary, cognitive, and clinical perspectives". In M. Lewis & J. M. Haviland-Jones (Eds.). Handbook of emotions. pp. 573–593. New York: The Guilford Press.
  2. 1 2 Olsson, A.; Phelps, E. A. (2007). "Social learning of fear". Nature Neuroscience. 10 (9): 1095–1102. doi:10.1038/nn1968. PMID 17726475.
  3. ↑ Edmundson, Laurel Duphiney. "The Neurobiology of Fear". Serendip. Retrieved 9 April 2012.
  4. ↑ Olsson, A.; Nearing, K. I.; Phelps, E. A. (2006). "Learning fears by observing others: The neural systems of social fear transmission". Social Cognitive and Affective Neuroscience. 2 (1): 3–11. doi:10.1093/scan/nsm005. PMC 2555428Freely accessible. PMID 18985115.
  5. ↑ Bracha, H. (2006). "Human brain evolution and the "Neuroevolutionary Time-depth Principle:" Implications for the Reclassification of fear-circuitry-related traits in DSM-V and for studying resilience to warzone-related posttraumatic stress disorder". Progress in Neuro-Psychopharmacology and Biological Psychiatry. 30 (5): 827–853. doi:10.1016/j.pnpbp.2006.01.008. PMID 16563589.
  6. ↑ Warr, M.; Stafford, M. (1983). "Fear of Victimization: A Look at the Proximate Causes". Social Forces. 61 (4): 1033–1043. doi:10.1093/sf/61.4.1033.
  7. ↑ Gallup Poll: What Frightens America's Youth, gallup.com (29 March 2005).
  8. ↑ Tancer, B. (September 2, 2008). Click: What millions of people are doing online and why it matters. Hyperion. ISBN 1401323049.
  9. ↑ Welch, Ashley (October 15, 2015). "Things Americans fear most". CBS News.
  10. ↑ Ingraham, Christopher (October 30, 2014). "America's top fears: Public speaking, heights and bugs". The Washington Post.
  11. ↑ Brewer, Geoffrey (March 19, 2001). "Snakes Top List of American's Fears". Gallup.
  12. 1 2 3 Fry, PS (September 2003). "Perceived self-efficacy domains as predictors of fear of the unknown and fear of dying among older adults.". Psychol Aging. 18 (3): 474–86. doi:10.1037/0882-7974.18.3.474. PMID 14518809.
  13. ↑ Lecture 22: Fear of Death in PHIL 176: Death Yale Open Course 2007
  14. ↑ Kahoe, R. D., & Dunn, R. F.; Dunn (1976). "The fear of death and religious attitudes and behavior". Journal for the Scientific Study of Religion. 14 (4): 379–382. doi:10.2307/1384409. JSTOR 1384409.
  15. ↑ Wink, P. (2006). "Who is afraid of death? Religiousness, spirituality, and death anxiety in late adulthood". Journal of Religion, Spirituality & Aging. 18 (2): 93–110. doi:10.1300/J496v18n02_08.
  16. ↑ Burton, L.D. (2011). "Fear". Journal of Research on Christian Education. 20 (2): 113–116. doi:10.1080/10656219.2011.592801.
  17. ↑ Fox, E.R. (1987). "Fear of the unknown". Western Journal of Medicine. 7 (3): 22–25. doi:10.1108/17578043200800026.
  18. ↑ Morgan, Maria; LeDoux, Joseph (1995). "Differential Contribution of Dorsal and Ventral Medial Prefrontal". Behavioral Neuroscience. 109 (4): 681–688. doi:10.1037/0735-7044.109.4.681. PMID 7576212.
  19. ↑ Cammarota, Martín; Bevilaqua, Lia R. M., Kerr, Daniel, Medina, Jorge, H., Izquierdo, Iván (Feb 1, 2003). "Inhibition of mRNA and Protein Synthesis in the CA1 Region of the Dorsal Hippocampus Blocks Reinstallment of an Extinguished Conditioned Fear Response". Journal of Neuroscience. 23 (3): 737–741. PMID 12574401.
  20. ↑ Davis, Stephen (2008). 21st Century Psychology: A Reference Handbook, Vol. 1. Thousand Oaks, California: SAGE Publication, Inc. pp. 282–286. ISBN 978-1-4129-4968-2.
  21. ↑ Robert, Patrick. "The Amygdala and Its Allies". 2002. The Brain. Retrieved 2 October 2013.
  22. ↑ Bracha, H.S. (Sep 9, 2004). "Freeze, flight, fight, fright, faint: adaptationist perspectives on the acute stress response spectrum". National Library of Medicine Institutes of Health. 9 (9): 679–685. PMID 15337864.
  23. ↑ Adolphs, Ralph; Gosselin, F., Buchanan, T. W., Tranel, D. Schyns, P., Damasio, A.; Buchanan, Tony W.; Tranel, Daniel; Schyns, Philippe; Damasio, Antonio R. (Jan 6, 2005). "A Mechanism for Impaired Fear Recognition After Amygdala Damage". Nature. 433 (7021): 68–72. Bibcode:2005Natur.433...68A. doi:10.1038/nature03086. PMID 15635411.
  24. ↑ Bolles, Robert (1970). "Species-Specific Defense Reactions and Avoidance Learning". Psychological Review. 77 (1): 32–48. doi:10.1037/h0028589.
  25. ↑ Crawford, Mary; Masterson (1982). "Species-Specific Defense Reactions and Avoidance Learning". The Pavolovian Journal of Biological Science. 17 (5): 204–214. doi:10.1007/BF03001275 (inactive 2015-12-13).
  26. ↑ Kiein, Stephen (2002). Boilogical Influences on Learning. Mississippi State University: McGraw-Hill Higher Education.
  27. ↑ Fanselow, Michael (1986). "Associative vs topographical accounts of the immediate shock-freezing deficit in rats: Implications for the response selection rules governing species-specific defensive reactions". Learning and Motivation. 17 (1): 16–39. doi:10.1016/0023-9690(86)90018-4.
  28. ↑ Crawford, M; Masterson (Oct 1982). "F. A". Pavlov Journal of Biological Sciences. 17 (4): 201–2143.
  29. ↑ Brocke, B.; Lesch, K. P.; Armbruster, D.; Moser, D. A.; Müller, A.; Strobel, A.; Kirschbaum, C. (2010). "Stathmin, a gene regulating neural plasticity, affects fear and anxiety processing in humans". The American Journal of Genetic BioNeuropsychiatry. 153B (1): 243–251. doi:10.1002/ajmg.b.30989. PMID 19526456.
  30. ↑ Kim, Jee Hyun; Ganella, Despina E (2015-02-01). "A Review of Preclinical Studies to Understand Fear During Adolescence". Australian Psychologist. 50 (1): 25–31. doi:10.1111/ap.12066. ISSN 1742-9544.
  31. ↑ Kim, Jee Hyun; Richardson, Rick. "New Findings on Extinction of Conditioned Fear Early in Development: Theoretical and Clinical Implications". Biological Psychiatry. 67 (4): 297–303. doi:10.1016/j.biopsych.2009.09.003.
  32. ↑ Li, Stella; Kim, Jee Hyun; Richardson, Rick. "Differential involvement of the medial prefrontal cortex in the expression of learned fear across development.". Behavioral Neuroscience. 126 (2): 217–225. doi:10.1037/a0027151.
  33. ↑ Best, Ben (2004). The Amygdala and the Emotions. benbest.com
  34. ↑ Gleitman, Henry; Fridlund, Alan J. and Reisberg, Daniel (2004). Psychology (6 ed.). W. W. Norton & Company. ISBN 0-393-97767-6.
  35. 1 2 Travis, John (2004). "Fear not: Scientists are learning how people can unlearn fear". Science News. 165 (3): 42–44. doi:10.2307/4014925. JSTOR 4014925.
  36. ↑ 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.
  37. ↑ Hoehn K, Marieb EN (2010). Human Anatomy & Physiology. San Francisco: Benjamin Cummings. ISBN 0-321-60261-7.
  38. ↑ Amunts, K.; Kedo, O.; Kindler, M.; Pieperhoff, P.; Mohlberg, H.; Shah, N. J.; Habel, U.; Schneider, F.; Zilles, K. (2005). "Cytoarchitectonic mapping of the human amygdala, hippocampal region and entorhinal cortex: Intersubject variability and probability maps". Anatomy and Embryology. 210 (5–6): 343–352. doi:10.1007/s00429-005-0025-5. PMID 16208455.
  39. ↑ Schacter, Daniel L.; Gilbert, Daniel T. and Wegner, Daniel M. (2011) Psychology Study Guide, Worth Publishers, ISBN 1429206152.
  40. ↑ Ledoux, J. (2003). "The emotional brain, fear, and the amygdala". Cellular and molecular neurobiology. 23 (4–5): 727–738. doi:10.1023/A:1025048802629. PMID 14514027.
  41. ↑ American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders: DSM-IV. Washington, DC. ISBN 0-89042-061-0.
  42. ↑ Cheng, D. T.; Knight, D. C.; Smith, C. N.; Stein, E. A.; Helmstetter, F. J. (2003). "Functional MRI of human amygdala activity during Pavlovian fear conditioning: Stimulus processing versus response expression". Behavioral neuroscience. 117 (1): 3–10. doi:10.1037/0735-7044.117.1.3. PMID 12619902.
  43. ↑ Berdoy, M.; Webster, J. P.; MacDonald, D. W. (2000). "Fatal attraction in rats infected with Toxoplasma gondii". Proceedings of the Royal Society B: Biological Sciences. 267 (1452): 1591–1594. doi:10.1098/rspb.2000.1182. PMC 1690701Freely accessible. PMID 11007336.
  44. ↑ Larkin, M. (1997). "Amygdala differentiates fear response". The Lancet. 350 (9073): 268–268. doi:10.1016/S0140-6736(05)62234-9.
  45. 1 2 Radua, J.; Phillips, M. L.; Russell, T.; Lawrence, N.; Marshall, N.; Kalidindi, S.; El-Hage, W.; McDonald, C.; Giampietro, V.; Brammer, M. J.; David, A. S.; Surguladze, S. A. (2010). "Neural response to specific components of fearful faces in healthy and schizophrenic adults". NeuroImage. 49 (1): 939–946. doi:10.1016/j.neuroimage.2009.08.030. PMID 19699306.
  46. ↑ Fear not." Ski Mar.-Apr. 2009: 15. Gale Canada In Context. Web. 29 Sep. 2011
  47. ↑ Moser, JC; Brownlee, RC; Silverstein, R (Apr 1968). "Alarm pheromones of the ant atta texana". J Insect Physiol. 14 (4): 529–35. doi:10.1016/0022-1910(68)90068-1. PMID 5649232.
  48. ↑ Ressler, RH; Cialdini, RB; Ghoca, ML; Kleist, SM (1968). "Alarm pheromone in the earthworm Lumbricus terrestris". Science. 161 (3841): 597–9. Bibcode:1968Sci...161..597R. doi:10.1126/science.161.3841.597. PMID 5663305.
  49. ↑ Rottman, SJ; Snowdon, CT (Dec 1972). "Demonstration and analysis of an alarm pheromone in mice". J Comp Physiol Psychol. 81 (3): 483–90. doi:10.1037/h0033703. PMID 4649187.
  50. ↑ Fanselow, MS (1985). "Odors released by stressed rats produce opioid analgesia in unstressed rats". Behav. Neurosci. 1985 (99): 589–592. PMID 3843728.
  51. ↑ Núñez J (1997). "Alarm pheromone induces stress analgesia via an opioid system in the honeybee". Physiol Behav. 63 (1): 75–80. doi:10.1016/s0031-9384(97)00391-0. PMID 9402618.
  52. ↑ Abel, EL; Bilitzke, PJ (Aug 1990). "A possible alarm substance in the forced swimming test". Physiol Behav. 48 (2): 233–9. doi:10.1016/0031-9384(90)90306-o. PMID 2255725.
  53. ↑ Abel, EL (Oct 1991). "Alarm substance emitted by rats in the forced-swim test is a low volatile pheromone". Physiol Behav. 50 (4): 723–7. doi:10.1016/0031-9384(91)90009-d. PMID 1775546.
  54. ↑ Cocke, R; Moynihan, JA; Cohen, N; Grota, LJ; Ader, R (Mar 1993). "Exposure to conspecific alarm chemosignals alters immune responses in BALB/c mice". Brain Behav Immun. 7 (1): 36–46. doi:10.1006/brbi.1993.1004. PMID 8471798.
  55. ↑ Abel, EL (Jun 1994). "The pituitary mediates production or release of an alarm chemosignal in rats". Horm Behav. 28 (2): 139–45. doi:10.1006/hbeh.1994.1011. PMID 7927280.
  56. ↑ Arakawa H (2011). "The role of neuroinflammation in the release of aversive odor cues from footshock-stressed rats: Implications for the neural mechanism of alarm pheromones". Psychoneuroendocrinology. 36 (4): 557–68. doi:10.1016/j.psyneuen.2010.09.001. PMID 20888127.
  57. ↑ Kiyokawa Y (2004). "Alarm pheromones with different functions are released from different regions of the body surface of male rats". Chem Senses. 29 (1): 35–40. doi:10.1093/chemse/bjh004. PMID 14752038.
  58. ↑ Kiyokawa Y (2006). "Alarm pheromone increases defensive and risk assessment behaviors in male rats". Physiol Behav. 87 (2): 383–7. doi:10.1016/j.physbeh.2005.11.003. PMID 16337975.
  59. ↑ Kiyokawa Y (2005). "Mapping the neural circuit activated by alarm pheromone perception by c-Fos immunohistochemistry". Brain Res. 1043 (1–2): 145–54. doi:10.1016/j.brainres.2005.02.061. PMID 15862528.
  60. ↑ Inagaki H (2010). "The alarm pheromone in male rats as a unique anxiety model: psychopharmacological evidence using anxiolytics". Pharmacol Biochem Behav. 94 (4): 575–9. doi:10.1016/j.pbb.2009.11.013. PMID 19969015.
  61. ↑ Zou J (2013). "Conditional deletion of ERK5 MAP kinase in the nervous system impairs pheromone information processing and pheromone-evoked behaviors". PLOS ONE. 8 (10): e76901. Bibcode:2013PLoSO...876901Z. doi:10.1371/journal.pone.0076901. PMC 3793934Freely accessible. PMID 24130808.
  62. ↑ Cohen, Sheldon; Wills, Thomas A. (1985). "Stress, social support, and the buffering hypothesis". Psychological Bulletin. 98 (2): 310–57. doi:10.1037/0033-2909.98.2.310. PMID 3901065.
  63. ↑ 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.
  64. ↑ Rittschof CC; Robinson GE (2013). "Manipulation of colony environment modulates honey bee aggression and brain gene expression". Genes Brain Behav. 12 (8): 802–11. doi:10.1111/gbb.12087. PMC 3863782Freely accessible. PMID 24034579.
  65. ↑ Ferrer RP; Zimmer RK (2012). "Community ecology and the evolution of molecules of keystone significance". Biol Bull. 223 (2): 167–77. PMID 23111129.
  66. ↑ Lübke KT; Pause BM (2014). "Sex-hormone dependent perception of androstenone suggests its involvement in communicating competition and aggression". Physiol Behav. 123: 136–41. doi:10.1016/j.physbeh.2013.10.016. PMID 24184511.
  67. ↑ Prehn, A; Ohrt, A; Sojka, B; Ferstl, R; Pause, BM (2006). "Chemosensory anxiety signals augment the startle reflex in humans". Neurosci Lett. 394 (2): 127–30. doi:10.1016/j.neulet.2005.10.012. PMID 16257486.
  68. ↑ Prehn-Kristensen, A.; Wiesner, C.; Bergmann, T.O.; Wolff, S.; Jansen, O.; Mehdorn, H.M.; et al. (2009). "Induction of empathy by the smell of anxiety". PLoS ONE. 4 (6): e5987. Bibcode:2009PLoSO...4.5987P. doi:10.1371/journal.pone.0005987.
  69. ↑ Radulescu, AR; Mujica-Parodi, LR (Jul 2013). "Human gender differences in the perception of conspecific alarm chemosensory cues". PLOS ONE. 8 (7): e68485. Bibcode:2013PLoSO...868485R. doi:10.1371/journal.pone.0068485.
  70. ↑ Frey MC (2012). "Androstadienone in motor reactions of men and women toward angry faces". Percept Mot Skills. 114 (3): 807–25. doi:10.2466/07.16.22.28.PMS.114.3.807-825. PMID 22913022.
  71. ↑ Sandi, C. (2011). "Healing anxiety disorders with glucocorticoids". Proceedings of the National Academy of Sciences. 108 (16): 6343–6344. Bibcode:2011PNAS..108.6343S. doi:10.1073/pnas.1103410108.
  72. ↑ Kolber, B. J.; Roberts, M. S.; Howell, M. P.; Wozniak, D. F.; Sands, M. S.; Muglia, L. J. (2008). "Central amygdala glucocorticoid receptor action promotes fear-associated CRH activation and conditioning". Proceedings of the National Academy of Sciences. 105 (33): 12004–12009. Bibcode:2008PNAS..10512004K. doi:10.1073/pnas.0803216105. PMC 2575312Freely accessible. PMID 18695245.
  73. ↑ Korstanje, M. E. (2011). "Reconnecting with poverty: New challenges of disaster management". International Journal of Disaster Resilience in the Built Environment. 2 (2): 165–177. doi:10.1108/17595901111149150.
  74. ↑ "World With No Fear". 2015-01-16. Retrieved 2015-01-27.

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