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. The fear response serves survival by generating appropriate behavioral responses, so it has been preserved throughout evolution.
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. With the series of physiological changes, the consciousness realizes an emotion of fear.
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. 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 can lead to paralysis. 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).
Fear is high only if the observed risk and seriousness both are high, and is low, if risk or seriousness is low.
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, failure, war, criminal or gang violence, being alone, the future, and nuclear war.
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.
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.
Fear of death
The Yale philosopher Shelly Kagan examined fear of death in a 2007 Yale open course 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.
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. 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”.
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.
Fear of the unknown
Often laboratory studies with rats are conducted to examine the acquisition and extinction of conditioned fear responses. In 2004, researchers conditioned rats (rattus norvegicus) to fear a certain stimulus, through electric shock. 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. 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. 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. Often a damaged amygdala can cause impairment in the recognition of fear (like the human case of patient S.M.). 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. He theorized the species-specific defense reaction (SSDR). 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. 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.
Species specific defense responses are created out of fear, and are essential for survival. 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. 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. This includes changes in the prefrontal cortex and the amygdala.
Neurocircuit in mammals
- 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)
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. 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. 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. 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.
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, and cortisol which increases blood sugar, increases circulating neutrophilic leukocytes, calcium amongst other things.
After a situation which incites fear occurs, the amygdala and hippocampus record the event through synaptic plasticity. The stimulation to the hippocampus will cause the individual to remember many details surrounding the situation. 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. In some cases, this forms permanent fear responses such as posttraumatic stress disorder (PTSD) or a phobia. 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.
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. 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.
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 occipito cerebellar regions including the fusiform gyrus and the inferior parietal / superior temporal gyrus. Interestingly, fearful eyes, brows and mouth seem to separately reproduce these brain responses. Scientist from Zurich studies show that the hormone oxytocin related to stress and sex reduces activity in your brain’s fear center.
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 and earthworms, and 4 years later also found in mammals, both mice and rats. 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. 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. 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.
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.
In 1993 a connection between alarm chemosignals in mice and their immune response was found.
Pheromone production in mice was found to be associated with or mediated by the pituitary gland in 1994.
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).
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. Further experiments showed that when a rat perceived alarm pheromones, it increased its defensive and risk assessment behavior. 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.
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.
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 MAPK7 gene 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.
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. 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. “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.
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.
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.
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.
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.
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.
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. 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.
A drug treatment for fear conditioning and phobias via the amygdala is the use of glucocorticoids. 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.
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.
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