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Anxiety
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Symptoms
The cognitive effects of anxiety may include thoughts about suspected dangers, such as fear of dying: "You may ... fear that the chest pains are a deadly heart attack or that the shooting pains in your head are the result of a tumor or an aneurysm. You feel an intense fear when you think of dying, or you may think of it more often than normal, or can't get it out of your mind."
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Symptoms
The physiological symptoms of anxiety may include:
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Types
There are various types of anxiety. Existential anxiety can occur when a person faces angst, an existential crisis, or nihilistic feelings. People can also face mathematical anxiety, somatic anxiety, stage fright, or test anxiety. Social anxiety refers to a fear of rejection and negative evaluation (being judged) by other people.
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Types
The philosopher Søren Kierkegaard, in The Concept of Anxiety (1844), described anxiety or dread associated with the "dizziness of freedom" and suggested the possibility for positive resolution of anxiety through the self-conscious exercise of responsibility and choosing. In Art and Artist (1932), the psychologist Otto Rank wrote that the psychological trauma of birth was the pre-eminent human symbol of existential anxiety and encompasses the creative person's simultaneous fear of – and desire for – separation, individuation, and differentiation.
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Types
The theologian Paul Tillich characterized existential anxiety as "the state in which a being is aware of its possible nonbeing" and he listed three categories for the nonbeing and resulting anxiety: ontic (fate and death), moral (guilt and condemnation), and spiritual (emptiness and meaninglessness). According to Tillich, the last of these three types of existential anxiety, i.e. spiritual anxiety, is predominant in modern times while the others were predominant in earlier periods. Tillich argues that this anxiety can be accepted as part of the human condition or it can be resisted but with negative consequences. In its pathological form, spiritual anxiety may tend to "drive the person toward the creation of certitude in systems of meaning which are supported by tradition and authority" even though such "undoubted certitude is not built on the rock of reality".
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Types
According to Viktor Frankl, the author of Man's Search for Meaning, when a person is faced with extreme mortal dangers, the most basic of all human wishes is to find a meaning of life to combat the "trauma of nonbeing" as death is near.
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Types
Depending on the source of the threat, psychoanalytic theory distinguishes the following types of anxiety:
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Types
According to Yerkes-Dodson law, an optimal level of arousal is necessary to best complete a task such as an exam, performance, or competitive event. However, when the anxiety or level of arousal exceeds that optimum, the result is a decline in performance.
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Types
Test anxiety is the uneasiness, apprehension, or nervousness felt by students who have a fear of failing an exam. Students who have test anxiety may experience any of the following: the association of grades with personal worth; fear of embarrassment by a teacher; fear of alienation from parents or friends; time pressures; or feeling a loss of control. Sweating, dizziness, headaches, racing heartbeats, nausea, fidgeting, uncontrollable crying or laughing and drumming on a desk are all common. Because test anxiety hinges on fear of negative evaluation, debate exists as to whether test anxiety is itself a unique anxiety disorder or whether it is a specific type of social phobia. The DSM-IV classifies test anxiety as a type of social phobia.
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Types
Research indicates that test anxiety among U.S. high-school and college students has been rising since the late 1950s. Test anxiety remains a challenge for students, regardless of age, and has considerable physiological and psychological impacts. Management of test anxiety focuses on achieving relaxation and developing mechanisms to manage anxiety. The routine practice of slow, Device-Guided Breathing (DGB) is a major component of behavioral treatments for anxiety conditions.
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Types
Performance anxiety and competitive anxiety (competitive trait anxiety, competitive state anxiety) happen when an individual's performance is measured against others. An important distinction between competitive and non-competitive anxiety is that competitive anxiety makes people view their performance as a threat. As a result, they experience a drop in their ordinary ability, whether physical or mental, due to that perceived stress.
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Types
Competitive anxiety is caused by a range of internal factors including high expectations, outside pressure, lack of experience, and external factors like the location of a competition. It commonly occurs in those participating in high pressure activities like sports and debates. Some common symptoms of competitive anxiety include muscle tension, fatigue, weakness, sense of panic, apprehensiveness, and panic attacks.
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Types
There are 4 major theories of how anxiety affects performance: Drive theory, Inverted U theory, Reversal theory, and The Zone of Optimal Functioning theory.
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Types
Drive theory believes that anxiety is positive and performance improves proportionally to the level of anxiety. This theory is not well accepted.
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Types
The Inverted U theory is based on the idea that performance peaks at a moderate stress level. It is called Inverted U theory because the graph that plots performance against anxiety looks like an inverted "U".
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Types
Reversal theory suggests that performance increases in relation to the individual's interpretation of their arousal levels. If they believed their physical arousal level would help them, their performance would increase, if they didn't, their performance would decrease. For example: Athletes were shown to worry more when focusing on results and perfection rather than the effort and growth involved.
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Types
The Zone of Optimal Functioning theory proposes that there is a zone where positive and negative emotions are in a balance which lead to feelings of dissociation and intense concentration, optimizing the individual's performance levels.
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Types
Humans generally require social acceptance and thus sometimes dread the disapproval of others. Apprehension of being judged by others may cause anxiety in social environments.
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Types
Anxiety during social interactions, particularly between strangers, is common among young people. It may persist into adulthood and become social anxiety or social phobia. "Stranger anxiety" in small children is not considered a phobia. In adults, an excessive fear of other people is not a developmentally common stage; it is called social anxiety. According to Cutting, social phobics do not fear the crowd but the fact that they may be judged negatively.
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Types
Social anxiety varies in degree and severity. For some people, it is characterized by experiencing discomfort or awkwardness during physical social contact (e.g. embracing, shaking hands, etc.), while in other cases it can lead to a fear of interacting with unfamiliar people altogether. Those with this condition may restrict their lifestyles to accommodate the anxiety, minimizing social interaction whenever possible. Social anxiety also forms a core aspect of certain personality disorders, including avoidant personality disorder.
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Types
To the extent that a person is fearful of social encounters with unfamiliar others, some people may experience anxiety particularly during interactions with outgroup members, or people who share different group memberships (i.e., by race, ethnicity, class, gender, etc.). Depending on the nature of the antecedent relations, cognitions, and situational factors, intergroup contact may be stressful and lead to feelings of anxiety. This apprehension or fear of contact with outgroup members is often called interracial or intergroup anxiety.
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Types
As is the case with the more generalized forms of social anxiety, intergroup anxiety has behavioral, cognitive, and affective effects. For instance, increases in schematic processing and simplified information processing can occur when anxiety is high. Indeed, such is consistent with related work on attentional bias in implicit memory. Additionally recent research has found that implicit racial evaluations (i.e. automatic prejudiced attitudes) can be amplified during intergroup interaction. Negative experiences have been illustrated in producing not only negative expectations, but also avoidant, or antagonistic, behavior such as hostility. Furthermore, when compared to anxiety levels and cognitive effort (e.g., impression management and self-presentation) in intragroup contexts, levels and depletion of resources may be exacerbated in the intergroup situation.
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Types
Anxiety can be either a short-term "state" or a long-term personality "trait." Trait anxiety reflects a stable tendency across the lifespan of responding with acute, state anxiety in the anticipation of threatening situations (whether they are actually deemed threatening or not). A meta-analysis showed that a high level of neuroticism is a risk factor for development of anxiety symptoms and disorders. Such anxiety may be conscious or unconscious.
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Types
Personality can also be a trait leading to anxiety and depression and their persistence. Through experience, many find it difficult to collect themselves due to their own personal nature.
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Types
Anxiety induced by the need to choose between similar options is increasingly being recognized as a problem for individuals and for organizations. In 2004, Capgemini wrote: "Today we're all faced with greater choice, more competition and less time to consider our options or seek out the right advice."
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Types
In a decision context, unpredictability or uncertainty may trigger emotional responses in anxious individuals that systematically alter decision-making. There are primarily two forms of this anxiety type. The first form refers to a choice in which there are multiple potential outcomes with known or calculable probabilities. The second form refers to the uncertainty and ambiguity related to a decision context in which there are multiple possible outcomes with unknown probabilities.
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Types
Panic disorder may share symptoms of stress and anxiety, but it is actually very different. Panic disorder is an anxiety disorder that occurs without any triggers. According to the U.S. Department of Health and Human Services, this disorder can be distinguished by unexpected and repeated episodes of intense fear. Someone with panic disorder will eventually develop constant fear of another attack and as this progresses it will begin to affect daily functioning and an individual's general quality of life. It is reported by the Cleveland Clinic that panic disorder affects 2 to 3 percent of adult Americans and can begin around the time of the teenage and early adult years. Some symptoms include: difficulty breathing, chest pain, dizziness, trembling or shaking, feeling faint, nausea, fear that you are losing control or are about to die. Even though they have these symptoms during an attack, the main symptom is the persistent fear of having future panic attacks.
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Anxiety disorders
Anxiety disorders are a group of mental disorders characterized by exaggerated feelings of anxiety and fear responses. Anxiety is a worry about future events and fear is a reaction to current events. These feelings may cause physical symptoms, such as a fast heart rate and shakiness. There are a number of anxiety disorders: including generalized anxiety disorder, specific phobia, social anxiety disorder, separation anxiety disorder, agoraphobia, panic disorder, and selective mutism. The disorder differs by what results in the symptoms. People often have more than one anxiety disorder.
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Anxiety disorders
Anxiety disorders are caused by a complex combination of genetic and environmental factors. To be diagnosed, symptoms typically need to be present for at least six months, be more than would be expected for the situation, and decrease a person's ability to function in their daily lives. Other problems that may result in similar symptoms include hyperthyroidism, heart disease, caffeine, alcohol, or cannabis use, and withdrawal from certain drugs, among others.
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Anxiety disorders
Without treatment, anxiety disorders tend to remain. Treatment may include lifestyle changes, counselling, and medications. Counselling is typically with a type of cognitive behavioral therapy. Medications, such as antidepressants or beta blockers, may improve symptoms. A 2023 review found that regular physical activity is effective for reducing anxiety.
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Anxiety disorders
About 12% of people are affected by an anxiety disorder in a given year and between 12–30% are affected at some point in their life. They occur about twice as often in women than they do in men, and generally begin before the age of 25. The most common are specific phobia which affects nearly 12% and social anxiety disorder which affects 10% at some point in their life. They affect those between the ages of 15 and 35 the most and become less common after the age of 55. Rates appear to be higher in the United States and Europe.
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Anxiety disorders
Anxiety can be either a short-term "state" or a long-term "trait." Whereas trait anxiety represents worrying about future events, anxiety disorders are a group of mental disorders characterized by feelings of anxiety and fears.
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Anxiety disorders
In his book Anxious: The Modern Mind in the Age of Anxiety Joseph LeDoux examines four experiences of anxiety through a brain-based lens:
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Co-morbidity
Anxiety disorders often occur with other mental health disorders, particularly major depressive disorder, bipolar disorder, eating disorders, or certain personality disorders. It also commonly occurs with personality traits such as neuroticism. This observed co-occurrence is partly due to genetic and environmental influences shared between these traits and anxiety.
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Co-morbidity
It is common for those with obsessive–compulsive disorder to experience anxiety. Anxiety is also commonly found in those who experience panic disorders, phobic anxiety disorders, severe stress, dissociative disorders, somatoform disorders, and some neurotic disorders. Anxiety has also been linked to the experience of intrusive thoughts. Studies have revealed that individuals who experience high levels of anxiety (also known as clinical anxiety) are highly vulnerable to the experience of intense intrusive thoughts or psychological disorders that are characterised by intrusive thoughts.
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Risk factors
Anxiety disorders are partly genetic, with twin studies suggesting 30-40% genetic influence on individual differences in anxiety. Environmental factors are also important. Twin studies show that individual-specific environments have a large influence on anxiety, whereas shared environmental influences (environments that affect twins in the same way) operate during childhood but decline through adolescence. Specific measured 'environments' that have been associated with anxiety include child abuse, family history of mental health disorders, and poverty. Anxiety is also associated with drug use, including alcohol, caffeine, and benzodiazepines (which are often prescribed to treat anxiety).
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Risk factors
Neural circuitry involving the amygdala (which regulates emotions like anxiety and fear, stimulating the HPA axis and sympathetic nervous system) and hippocampus (which is implicated in emotional memory along with the amygdala) is thought to underlie anxiety. People who have anxiety tend to show high activity in response to emotional stimuli in the amygdala. Some writers believe that excessive anxiety can lead to an overpotentiation of the limbic system (which includes the amygdala and nucleus accumbens), giving increased future anxiety, but this does not appear to have been proven.
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Risk factors
Research upon adolescents who as infants had been highly apprehensive, vigilant, and fearful finds that their nucleus accumbens is more sensitive than that in other people when deciding to make an action that determined whether they received a reward. This suggests a link between circuits responsible for fear and also reward in anxious people. As researchers note, "a sense of 'responsibility', or self-agency, in a context of uncertainty (probabilistic outcomes) drives the neural system underlying appetitive motivation (i.e., nucleus accumbens) more strongly in temperamentally inhibited than noninhibited adolescents".
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Risk factors
The microbes of the gut can connect with the brain to affect anxiety. There are various pathways along which this communication can take place. One is through the major neurotransmitters. The gut microbes such as Bifidobacterium and Bacillus produce the neurotransmitters GABA and dopamine, respectively. The neurotransmitters signal to the nervous system of the gastrointestinal tract, and those signals will be carried to the brain through the vagus nerve or the spinal system. This is demonstrated by the fact that altering the microbiome has shown anxiety- and depression-reducing effects in mice, but not in subjects without vagus nerves.
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Risk factors
Another key pathway is the HPA axis, as mentioned above. The microbes can control the levels of cytokines in the body, and altering cytokine levels creates direct effects on areas of the brain such as the hypothalamus, the area that triggers HPA axis activity. The HPA axis regulates production of cortisol, a hormone that takes part in the body's stress response. When HPA activity spikes, cortisol levels increase, processing and reducing anxiety in stressful situations. These pathways, as well as the specific effects of individual taxa of microbes, are not yet completely clear, but the communication between the gut microbiome and the brain is undeniable, as is the ability of these pathways to alter anxiety levels.
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Risk factors
With this communication comes the potential to treat. Prebiotics and probiotics have been shown to reduce anxiety. For example, experiments in which mice were given fructo- and galacto-oligosaccharide prebiotics and Lactobacillus probiotics have both demonstrated a capability to reduce anxiety. In humans, results are not as concrete, but promising.
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Risk factors
Genetics and family history (e.g. parental anxiety) may put an individual at increased risk of an anxiety disorder, but generally external stimuli will trigger its onset or exacerbation. Estimates of genetic influence on anxiety, based on studies of twins, range from 25 to 40% depending on the specific type and age-group under study. For example, genetic differences account for about 43% of variance in panic disorder and 28% in generalized anxiety disorder. Longitudinal twin studies have shown the moderate stability of anxiety from childhood through to adulthood is mainly influenced by stability in genetic influence. When investigating how anxiety is passed on from parents to children, it is important to account for sharing of genes as well as environments, for example using the intergenerational children-of-twins design.
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Risk factors
Many studies in the past used a candidate gene approach to test whether single genes were associated with anxiety. These investigations were based on hypotheses about how certain known genes influence neurotransmitters (such as serotonin and norepinephrine) and hormones (such as cortisol) that are implicated in anxiety. None of these findings are well replicated, with the possible exception of TMEM132D, COMT and MAO-A. The epigenetic signature of BDNF, a gene that codes for a protein called brain derived neurotrophic factor that is found in the brain, has also been associated with anxiety and specific patterns of neural activity. and a receptor gene for BDNF called NTRK2 was associated with anxiety in a large genome-wide investigation. The reason that most candidate gene findings have not replicated is that anxiety is a complex trait that is influenced by many genomic variants, each of which has a small effect on its own. Increasingly, studies of anxiety are using a hypothesis-free approach to look for parts of the genome that are implicated in anxiety using big enough samples to find associations with variants that have small effects. The largest explorations of the common genetic architecture of anxiety have been facilitated by the UK Biobank, the ANGST consortium and the CRC Fear, Anxiety and Anxiety Disorders.
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Risk factors
Epigenetics of anxiety and stress–related disorders is the field studying the relationship between epigenetic modifications of genes and anxiety and stress-related disorders, including mental health disorders such as generalized anxiety disorder (GAD), post-traumatic stress disorder, obsessive-compulsive disorder (OCD), and more. These changes can lead to transgenerational stress inheritance.
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Risk factors
Epigenetic modifications play a role in the development and heritability of these disorders and related symptoms. For example, regulation of the hypothalamus-pituitary-adrenal axis by glucocorticoids plays a major role in stress response and is known to be epigenetically regulated.
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Risk factors
Many medical conditions can cause anxiety. This includes conditions that affect the ability to breathe, like COPD and asthma, and the difficulty in breathing that often occurs near death. Conditions that cause abdominal pain or chest pain can cause anxiety and may in some cases be a somatization of anxiety; the same is true for some sexual dysfunctions. Conditions that affect the face or the skin can cause social anxiety especially among adolescents, and developmental disabilities often lead to social anxiety for children as well. Life-threatening conditions like cancer also cause anxiety.
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Risk factors
Furthermore, certain organic diseases may present with anxiety or symptoms that mimic anxiety. These disorders include certain endocrine diseases (hypo- and hyperthyroidism, hyperprolactinemia), metabolic disorders (diabetes), deficiency states (low levels of vitamin D, B2, B12, folic acid), gastrointestinal diseases (celiac disease, non-celiac gluten sensitivity, inflammatory bowel disease), heart diseases, blood diseases (anemia), cerebral vascular accidents (transient ischemic attack, stroke), and brain degenerative diseases (Parkinson's disease, dementia, multiple sclerosis, Huntington's disease), among others.
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Risk factors
Several drugs can cause or worsen anxiety, whether in intoxication, withdrawal or as side effect. These include alcohol, tobacco, sedatives (including prescription benzodiazepines), opioids (including prescription pain killers and illicit drugs like heroin), stimulants (such as caffeine, cocaine and amphetamines), hallucinogens, and inhalants.
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Risk factors
While many often report self-medicating anxiety with these substances, improvements in anxiety from drugs are usually short-lived (with worsening of anxiety in the long term, sometimes with acute anxiety as soon as the drug effects wear off) and tend to be exaggerated. Acute exposure to toxic levels of benzene may cause euphoria, anxiety, and irritability lasting up to 2 weeks after the exposure.
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Risk factors
Poor coping skills (e.g., rigidity/inflexible problem solving, denial, avoidance, impulsivity, extreme self-expectation, negative thoughts, affective instability, and inability to focus on problems) are associated with anxiety. Anxiety is also linked and perpetuated by the person's own pessimistic outcome expectancy and how they cope with feedback negativity. Temperament (e.g., neuroticism) and attitudes (e.g. pessimism) have been found to be risk factors for anxiety.
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Risk factors
Cognitive distortions such as overgeneralizing, catastrophizing, mind reading, emotional reasoning, binocular trick, and mental filter can result in anxiety. For example, an overgeneralized belief that something bad "always" happens may lead someone to have excessive fears of even minimally risky situations and to avoid benign social situations due to anticipatory anxiety of embarrassment. In addition, those who have high anxiety can also create future stressful life events. Together, these findings suggest that anxious thoughts can lead to anticipatory anxiety as well as stressful events, which in turn cause more anxiety. Such unhealthy thoughts can be targets for successful treatment with cognitive therapy.
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Risk factors
Psychodynamic theory posits that anxiety is often the result of opposing unconscious wishes or fears that manifest via maladaptive defense mechanisms (such as suppression, repression, anticipation, regression, somatization, passive aggression, dissociation) that develop to adapt to problems with early objects (e.g., caregivers) and empathic failures in childhood. For example, persistent parental discouragement of anger may result in repression/suppression of angry feelings which manifests as gastrointestinal distress (somatization) when provoked by another while the anger remains unconscious and outside the individual's awareness. Such conflicts can be targets for successful treatment with psychodynamic therapy. While psychodynamic therapy tends to explore the underlying roots of anxiety, cognitive behavioral therapy has also been shown to be a successful treatment for anxiety by altering irrational thoughts and unwanted behaviors.
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Risk factors
An evolutionary psychology explanation is that increased anxiety serves the purpose of increased vigilance regarding potential threats in the environment as well as increased tendency to take proactive actions regarding such possible threats. This may cause false positive reactions but an individual with anxiety may also avoid real threats. This may explain why anxious people are less likely to die due to accidents. There is ample empirical evidence that anxiety can have adaptive value. Within a school, timid fish are more likely than bold fish to survive a predator.
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Risk factors
When people are confronted with unpleasant and potentially harmful stimuli such as foul odors or tastes, PET-scans show increased blood flow in the amygdala. In these studies, the participants also reported moderate anxiety. This might indicate that anxiety is a protective mechanism designed to prevent the organism from engaging in potentially harmful behaviors.
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Risk factors
Social risk factors for anxiety include a history of trauma (e.g., physical, sexual or emotional abuse or assault), bullying, early life experiences and parenting factors (e.g., rejection, lack of warmth, high hostility, harsh discipline, high parental negative affect, anxious childrearing, modelling of dysfunctional and drug-abusing behaviour, discouragement of emotions, poor socialization, poor attachment, and child abuse and neglect), cultural factors (e.g., stoic families/cultures, persecuted minorities including those with disabilities), and socioeconomics (e.g., uneducated, unemployed, impoverished although developed countries have higher rates of anxiety disorders than developing countries). A 2019 comprehensive systematic review of over 50 studies showed that food insecurity in the United States is strongly associated with depression, anxiety, and sleep disorders. Food-insecure individuals had an almost 3 fold risk increase of testing positive for anxiety when compared to food-secure individuals.
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Risk factors
Contextual factors that are thought to contribute to anxiety include gender socialization and learning experiences. In particular, learning mastery (the degree to which people perceive their lives to be under their own control) and instrumentality, which includes such traits as self-confidence, self-efficacy, independence, and competitiveness fully mediate the relation between gender and anxiety. That is, though gender differences in anxiety exist, with higher levels of anxiety in women compared to men, gender socialization and learning mastery explain these gender differences.
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Treatment
The first step in the management of a person with anxiety symptoms involves evaluating the possible presence of an underlying medical cause, the recognition of which is essential in order to decide the correct treatment. Anxiety symptoms may mask an organic disease, or appear associated with or as a result of a medical disorder.
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Treatment
Cognitive behavioral therapy (CBT) is effective for anxiety disorders and is a first line treatment. CBT appears to be equally effective when carried out via the internet. While evidence for mental health apps is promising, it is preliminary.
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Treatment
Anxiety often affects relationships, and interpersonal psychotherapy addresses these issues by improving communication and relationship skills.
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Treatment
Psychopharmacological treatment can be used in parallel to CBT or can be used alone. As a general rule, most anxiety disorders respond well to first-line agents. Such drugs, also used as anti-depressants, are the selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors, that work by blocking the reuptake of specific neurotransmitters and resulting in the increase in availability of these neurotransmitters. Additionally, benzodiazepines are often prescribed to individuals with anxiety disorder. Benzodiazepines produce an anxiolytic response by modulating GABA and increasing its receptor binding. A third common treatment involves a category of drug known as serotonin agonists. This category of drug works by initiating a physiological response at 5-HT1A receptor by increasing the action of serotonin at this receptor. Other treatment options include pregabalin, tricyclic antidepressants, and moclobemide, among others.
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Treatment
Anxiety is considered to be a serious psychiatric illness that has an unknown true pervasiveness due to affected individuals not asking for proper treatment or aid, and due to professionals missing the diagnosis.
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Prevention
The above risk factors give natural avenues for prevention. A 2017 review found that psychological or educational interventions have a small yet statistically significant benefit for the prevention of anxiety in varied population types.
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Pathophysiology
Anxiety disorder appears to be a genetically inherited neurochemical dysfunction that may involve autonomic imbalance; decreased GABA-ergic tone; allelic polymorphism of the catechol-O-methyltransferase (COMT) gene; increased adenosine receptor function; increased cortisol.
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Pathophysiology
In the central nervous system (CNS), the major mediators of the symptoms of anxiety disorders appear to be norepinephrine, serotonin, dopamine, and gamma-aminobutyric acid (GABA). Other neurotransmitters and peptides, such as corticotropin-releasing factor, may be involved. Peripherally, the autonomic nervous system, especially the sympathetic nervous system, mediates many of the symptoms. Increased flow in the right parahippocampal region and reduced serotonin type 1A receptor binding in the anterior and posterior cingulate and raphe of patients are the diagnostic factors for prevalence of anxiety disorder.
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Pathophysiology
The amygdala is central to the processing of fear and anxiety, and its function may be disrupted in anxiety disorders. Anxiety processing in the basolateral amygdala has been implicated with expansion of dendritic arborization of the amygdaloid neurons. SK2 potassium channels mediate inhibitory influence on action potentials and reduce arborization.
A. A. Milne
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Alan Alexander Milne (/mɪln/; 18 January 1882 – 31 January 1956) was an English writer best known for his books about the teddy bear Winnie-the-Pooh, as well as for children's poetry. Milne was primarily a playwright before the huge success of Winnie-the-Pooh overshadowed all his previous work. Milne served in both World Wars, as a lieutenant in the Royal Warwickshire Regiment in the First World War and as a captain in the Home Guard in the Second World War.
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Milne was the father of bookseller Christopher Robin Milne, upon whom the character Christopher Robin is based. It was during a visit to London Zoo, where Christopher became enamoured with the tame and amiable bear Winnipeg, that Milne was inspired to write the story of Winnie-the-Pooh for his son. Milne bequeathed the original manuscripts of the Winnie-the-Pooh stories to the Wren Library at Trinity College, Cambridge, his alma mater.
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Early life and military career
Alan Alexander Milne was born in Kilburn, London, to John Vine Milne, who was born in Jamaica, and Sarah Marie Milne (née Heginbotham), on 18 January 1882. He grew up at Henley House School, 6/7 Mortimer Road (now Crescent), Kilburn, a small independent school run by his father. One of his teachers was H. G. Wells, who taught there in 1889–90. Milne attended Westminster School and Trinity College, Cambridge, where he studied on a mathematics scholarship, graduating with a B.A. in Mathematics in 1903. He edited and wrote for Granta, a student magazine. He collaborated with his brother Kenneth and their articles appeared over the initials AKM. Milne's work came to the attention of the leading British humour magazine Punch, where Milne was to become a contributor and later an assistant editor. Considered a talented cricket fielder, Milne played for two amateur teams that were largely composed of British writers: the Allahakbarries and the Authors XI. His teammates included fellow writers J. M. Barrie, Arthur Conan Doyle and P. G. Wodehouse.
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Early life and military career
Milne joined the British Army in World War I and served as an officer in the Royal Warwickshire Regiment. He was commissioned into the 4th Battalion, Royal Warwickshire Regiment, on 1 February 1915 as a second lieutenant (on probation). His commission was confirmed on 20 December 1915. He served on the Somme as a signals officer from July-November 1916, but caught trench fever and was invalided back to England. Having recuperated, he worked as a signals instructor, before being recruited into Military Intelligence to write propaganda articles for MI7 (b) between 1917 and 1918. He was discharged on 14 February 1919, and settled in Mallord Street, Chelsea. He relinquished his commission on 19 February 1920, retaining the rank of lieutenant.
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Early life and military career
After the war, he wrote a denunciation of war titled Peace with Honour (1934), which he retracted somewhat with 1940's War with Honour. During World War II, Milne was one of the most prominent critics of fellow English writer (and Authors XI cricket teammate) P. G. Wodehouse, who was captured at his country home in France by the Nazis and imprisoned for a year. Wodehouse made radio broadcasts about his internment, which were broadcast from Berlin. Although the light-hearted broadcasts made fun of the Germans, Milne accused Wodehouse of committing an act of near treason by cooperating with his country's enemy. Wodehouse got some revenge on his former friend (e.g. in The Mating Season) by creating fatuous parodies of the Christopher Robin poems in some of his later stories, and claiming that Milne "was probably jealous of all other writers.... But I loved his stuff."
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Early life and military career
Milne married Dorothy "Daphne" de Sélincourt (1890–1971) in 1913 and their son Christopher Robin Milne was born in 1920. In 1925, Milne bought a country home, Cotchford Farm, in Hartfield, East Sussex.
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Early life and military career
During World War II, Milne was a captain in the British Home Guard in Hartfield & Forest Row, insisting on being plain "Mr. Milne" to the members of his platoon. He retired to the farm after a stroke and brain surgery in 1952 left him an invalid, and by August 1953, "he seemed very old and disenchanted." Milne died in January 1956, aged 74.
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Literary career
After graduating from Cambridge University in 1903, A. A. Milne contributed humorous verse and whimsical essays to Punch, joining the staff in 1906 and becoming an assistant editor.
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Literary career
During this period he published 18 plays and three novels, including the murder mystery The Red House Mystery (1922). His son was born in August 1920 and in 1924 Milne produced a collection of children's poems, When We Were Very Young, which were illustrated by Punch staff cartoonist E. H. Shepard. A collection of short stories for children A Gallery of Children, and other stories that became part of the Winnie-the-Pooh books, were first published in 1925.
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Literary career
Milne was an early screenwriter for the nascent British film industry, writing four stories filmed in 1920 for the company Minerva Films (founded in 1920 by the actor Leslie Howard and his friend and story editor Adrian Brunel). These were The Bump, starring Aubrey Smith; Twice Two; Five Pound Reward; and Bookworms. Some of these films survive in the archives of the British Film Institute. Milne had met Howard when the actor starred in Milne's play Mr Pim Passes By in London.
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Literary career
Looking back on this period (in 1926), Milne observed that when he told his agent that he was going to write a detective story, he was told that what the country wanted from a "Punch humorist" was a humorous story; when two years later he said he was writing nursery rhymes, his agent and publisher were convinced he should write another detective story; and after another two years, he was being told that writing a detective story would be in the worst of taste given the demand for children's books. He concluded that "the only excuse which I have yet discovered for writing anything is that I want to write it; and I should be as proud to be delivered of a Telephone Directory con amore as I should be ashamed to create a Blank Verse Tragedy at the bidding of others."
A. A. Milne
924
Literary career
Milne is most famous for his two Pooh books about a boy named Christopher Robin after his son, Christopher Robin Milne (1920–1996), and various characters inspired by his son's stuffed animals, most notably the bear named Winnie-the-Pooh. Christopher Robin Milne's stuffed bear, originally named Edward, was renamed Winnie after a Canadian black bear named Winnie (after Winnipeg), which was used as a military mascot in World War I, and left to London Zoo during the war. "The Pooh" comes from a swan the young Milne named "Pooh". E. H. Shepard illustrated the original Pooh books, using his own son's teddy Growler ("a magnificent bear") as the model. The rest of Christopher Robin Milne's toys, Piglet, Eeyore, Kanga, Roo and Tigger, were incorporated into A. A. Milne's stories, and two more characters – Rabbit and Owl – were created by Milne's imagination. Christopher Robin Milne's own toys are now on display in New York where 750,000 people visit them every year. The fictional Hundred Acre Wood of the Pooh stories derives from Five Hundred Acre Wood in Ashdown Forest in East Sussex, South East England, where the Pooh stories were set. Milne lived on the northern edge of the forest at Cotchford Farm, 51°05′24″N 0°06′25″E / 51.090°N 0.107°E / 51.090; 0.107, and took his son walking there. E. H. Shepard drew on the landscapes of Ashdown Forest as inspiration for many of the illustrations he provided for the Pooh books. The adult Christopher Robin commented: "Pooh's Forest and Ashdown Forest are identical." Popular tourist locations at Ashdown Forest include: Galleon's Lap, The Enchanted Place, the Heffalump Trap and Lone Pine, Eeyore's Sad and Gloomy Place, and the wooden Pooh Bridge where Pooh and Piglet invented Poohsticks.
A. A. Milne
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Literary career
Not yet known as Pooh, he made his first appearance in a poem, "Teddy Bear", published in Punch magazine in February 1924 and republished that year in When We Were Very Young. Pooh first appeared in the London Evening News on Christmas Eve, 1925, in a story called "The Wrong Sort of Bees". Winnie-the-Pooh was published in 1926, followed by The House at Pooh Corner in 1928. A second collection of nursery rhymes, Now We Are Six, was published in 1927. All four books were illustrated by E. H. Shepard. Milne also published four plays in this period. He also "gallantly stepped forward" to contribute a quarter of the costs of dramatising P. G. Wodehouse's A Damsel in Distress. The World of Pooh won the Lewis Carroll Shelf Award in 1958.
A. A. Milne
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Literary career
The success of his children's books was to become a source of considerable annoyance to Milne, whose self-avowed aim was to write whatever he pleased and who had, until then, found a ready audience for each change of direction: he had freed pre-war Punch from its ponderous facetiousness; he had made a considerable reputation as a playwright (like his idol J. M. Barrie) on both sides of the Atlantic; he had produced a witty piece of detective writing in The Red House Mystery (although this was severely criticised by Raymond Chandler for the implausibility of its plot in his essay The Simple Art of Murder in the eponymous collection that appeared in 1950). But once Milne had, in his own words, "said goodbye to all that in 70,000 words" (the approximate length of his four principal children's books), he had no intention of producing any reworkings lacking in originality, given that one of the sources of inspiration, his son, was growing older.
A. A. Milne
924
Literary career
Another reason Milne stopped writing children's books, and especially about Winnie-the-Pooh, was that he felt "amazement and disgust" over the immense fame his son was exposed to, and said that "I feel that the legal Christopher Robin has already had more publicity than I want for him. I do not want CR Milne to ever wish that his name were Charles Robert."
A. A. Milne
924
Literary career
In his literary home, Punch, where the When We Were Very Young verses had first appeared, Methuen continued to publish whatever Milne wrote, including the long poem "The Norman Church" and an assembly of articles entitled Year In, Year Out (which Milne likened to a benefit night for the author).
A. A. Milne
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Literary career
In 1930, Milne adapted Kenneth Grahame's novel The Wind in the Willows for the stage as Toad of Toad Hall. The title was an implicit admission that such chapters as Chapter 7, "The Piper at the Gates of Dawn," could not survive translation to the theatre. A special introduction written by Milne is included in some editions of Grahame's novel.
A. A. Milne
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Literary career
Milne and his wife became estranged from their son, who came to resent what he saw as his father's exploitation of his childhood and came to hate the books that had thrust him into the public eye. Christopher's marriage to his first cousin, Lesley de Sélincourt, distanced him still further from his parents – Lesley's father and Christopher's mother had not spoken to each other for 30 years.
A. A. Milne
924
Death and legacy
I suppose that every one of us hopes secretly for immortality; to leave, I mean, a name behind him which will live forever in this world, whatever he may be doing, himself, in the next.
A. A. Milne
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Death and legacy
—A. A. Milne.
A. A. Milne
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Death and legacy
A. A. Milne died at his home in Hartfield, Sussex, on 31 January 1956, nearly two weeks after his 74th birthday. A memorial service took place on 10 February at All Hallows-by-the-Tower church in London.
A. A. Milne
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Death and legacy
The rights to A. A. Milne's Pooh books were left to four beneficiaries: his family, the Royal Literary Fund, Westminster School and the Garrick Club. After Milne's death in 1956, thirteen days after his 74th birthday, his widow sold her rights to the Pooh characters to Stephen Slesinger, whose widow sold the rights after Slesinger's death to the Walt Disney Company, which has made many Pooh cartoon movies, a Disney Channel television show, as well as Pooh-related merchandise. In 2001, the other beneficiaries sold their interest in the estate to the Disney Corporation for $350m. Previously Disney had been paying twice-yearly royalties to these beneficiaries. The estate of E. H. Shepard also received a sum in the deal. The UK copyright on the text of the original Winnie the Pooh books expires on 1 January 2027; at the beginning of the year after the 70th anniversary of the author's death (PMA-70), and has already expired in those countries with a PMA-50 rule. This applies to all of Milne's works except those first published posthumously. The illustrations in the Pooh books will remain under copyright until the same amount of time has passed, after the illustrator's death; in the UK, this will be on 1 January 2047. In the US, copyright will not expire until 95 years after publication for each of Milne's books first published before 1978, but this includes the illustrations.
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Death and legacy
In 2008, a collection of original illustrations featuring Winnie-the-Pooh and his animal friends sold for more than £1.2 million at auction in Sotheby's, London. Forbes magazine ranked Winnie the Pooh the most valuable fictional character in 2002; Winnie the Pooh merchandising products alone had annual sales of more than $5.9 billion. In 2005, Winnie the Pooh generated $6 billion, a figure surpassed only by Mickey Mouse.
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Death and legacy
A memorial plaque in Ashdown Forest, unveiled by Christopher Robin in 1979, commemorates the work of A. A. Milne and Shepard in creating the world of Pooh. The inscription states they "captured the magic of Ashdown Forest, and gave it to the world". Milne once wrote of Ashdown Forest: "In that enchanted place on the top of the forest a little boy and his bear will always be playing."
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Death and legacy
In 2003, Winnie-the-Pooh was ranked number 7 on the BBC's The Big Read poll which determined the UK's "best-loved novels". In 2006, Winnie-the-Pooh received a star on the Hollywood Walk of Fame, marking the 80th birthday of Milne's creation.
A. A. Milne
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Death and legacy
Marking the 90th anniversary of Milne's creation of the character, and the 90th birthday of Queen Elizabeth II, Winnie-the-Pooh Meets the Queen (2016) sees Pooh meet the Queen at Buckingham Palace. The illustrated and audio adventure is narrated by the actor Jim Broadbent. Also in 2016, a new character, a Penguin, was unveiled in The Best Bear in All the World, which was inspired by a long-lost photograph of Milne and his son Christopher with a toy penguin.
A. A. Milne
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Death and legacy
An exhibition entitled Winnie-the-Pooh: Exploring a Classic appeared at the Victoria and Albert Museum in London from 9 December 2017 to 8 April 2018.
A. A. Milne
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Death and legacy
The composer Harold Fraser-Simson, a near neighbour, produced six books of Milne songs between 1924 and 1932. The poems have been parodied many times, including with the books When We Were Rather Older and Now We Are Sixty. The 1963 film The King's Breakfast was based on Milne's poem of the same name.
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Death and legacy
Milne has been portrayed in television and film. Domhnall Gleeson plays him in Goodbye Christopher Robin, a 2017 biographical drama film. In the 2018 fantasy film Christopher Robin, an extension of the Disney Winnie the Pooh franchise, Tristan Sturrock plays Milne, and filming took place at Ashdown Forest.
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Death and legacy
An elementary school in Houston, Texas, operated by the Houston Independent School District (HISD), is named after Milne. The school, A. A. Milne Elementary School in Brays Oaks, opened in 1991.
A. A. Milne
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Archive
The original manuscripts for Winnie-the-Pooh and The House at Pooh Corner are archived at Trinity College Library, Cambridge.
A. A. Milne
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Archive
The bulk of A. A. Milne's papers are housed at the Harry Ransom Center at the University of Texas at Austin. The collection, established at the centre in 1964, consists of manuscript drafts and fragments for over 150 of Milne's works, as well as correspondence, legal documents, genealogical records, and some personal effects. The library division holds several books formerly belonging to Milne and his wife Dorothy. The center also has small collections of correspondence from Christopher Robin Milne and Milne's frequent illustrator E. H. Shepard.
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Religious views
Milne did not speak out much on the subject of religion, although he used religious terms to explain his decision, while remaining a pacifist, to join the British Home Guard. He wrote: "In fighting Hitler we are truly fighting the Devil, the Anti-Christ ... Hitler was a crusader against God."
A. A. Milne
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Religious views
His best known comment on the subject was recalled on his death:
A. A. Milne
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Religious views
The Old Testament is responsible for more atheism, agnosticism, disbelief – call it what you will – than any book ever written; it has emptied more churches than all the counter-attractions of cinema, motor bicycle and golf course.