Fear and Anxiety: The Science of Mental Health: Fear and Anxiety Vol 10

The biology of fear- and anxiety-related behaviors
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One is through the major neurotransmitters. Another key pathway is the HPA axis, as mentioned above. The HPA axis regulates production of cortisol, a hormone that takes part in the body's stress response. 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.

With this communication comes the potential to treat anxiety. Prebiotics and probiotics have been shown to reduced anxiety. For example, experiments in which mice were given fructo- and galacto-oligosaccharide prebiotics [65] and Lactobacillus probiotics [64] have both demonstrated a capability to reduce anxiety. In humans, results are not as concrete, but promising.

Genetics and family history e. 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. 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.

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. Furthermore, certain organic diseases may present with anxiety or symptoms that mimic anxiety. Several drugs can cause or worsen anxiety, whether in intoxication, withdrawal or from chronic use. These include alcohol , tobacco , cannabis , 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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Acute exposure to toxic levels of benzene may cause euphoria, anxiety, and irritability lasting up to 2 weeks after the exposure. Poor coping skills e. Anxiety is also linked and perpetuated by the person's own pessimistic outcome expectancy and how they cope with feedback negativity. 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.

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In addition, those who have high anxiety can also create future stressful life events. Such unhealthy thoughts can be targets for successful treatment with cognitive therapy. 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.

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. 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 suffering from anxiety may also avoid real threats.

This may explain why anxious people are less likely to die due to accidents. When people are confronted with unpleasant and potentially harmful stimuli such as foul odors or tastes, PET-scans show increased bloodflow in the amygdala. This might indicate that anxiety is a protective mechanism designed to prevent the organism from engaging in potentially harmful behaviors. Social risk factors for anxiety include a history of trauma e. 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, 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.

More specifically, in official online photographs of politicians around the world, women's faces are less prominent than men's. The difference in these images actually tended to be greater in cultures with greater institutional gender equality. 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.

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.

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 dendritic arborization of the amygdaloid neurons. SK2 potassium channels mediate inhibitory influence on action potentials and reduce arborization. Joseph E. LeDoux and Lisa Feldman Barrett have both sought to separate automatic threat responses from additional associated cognitive activity within anxiety. From Wikipedia, the free encyclopedia.

For other uses, see Anxiety disambiguation. Further information: Angst , Existential crisis , and Nihilism. Main articles: Test anxiety , Mathematical anxiety , Stage fright , and Somatic anxiety. Main articles: Stranger anxiety and Social anxiety. Main article: Anxiety disorder. This section does not cite any sources.

Please help improve this section by adding citations to reliable sources.

How to overcome fear and anxiety

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How imagination can help people overcome fear and anxiety

Johns Hopkins University Press. August They applied the concept of defensive distance to both anxiety and fear - and all anxious behavior, independent of defensive distance, is sensitive to anxiolytic drugs, whereas fear behavior is not. This led me, via the requirement to provide a sound teleonomic account of fear and anxiety, to the following simple definitions. Fear is all those behaviors, autonomic and other reactions, that have evolved in response to the evolutionary pressure of removing the animal from danger. Thus, freezing, fighting and fleeing all contribute to defensive avoidance.

Conversely, and essentially opposite to fear, anxiety is all those behaviors, autonomic and other reactions, that have evolved in response to the evolutionary pressure of allowing the animal to approach danger. The fundamentals of an essentially two-dimensional model of defense combining defensive distance with what can be seen as defensive direction, i. But this model was not symmetrical and data continued to accumulate suggesting that it was incomplete. This, coupled with persistent questioning of the details of the theory in relation to human personality by Corr, led to our joint production of the symmetrical 2D model of defense.

This is shown with minor further updating see legend in Figure However, superimposed on these modules is diffuse noradrenergic and serotonergic innervation. The inclusion of these systems on anatomical grounds allows the theory to account with certain assumptions being made about receptor subtypes for the behavioural and therapeutic effects of a variety of drugs here. This antithetical effect of serotonin on the periaqueductal gray accounts for a range of otherwise anomalous effects of serotonergic drugs and also for phenomena such as relaxation-induced panic Graeff, If this paper were simply a history, it should stop at this point.

However, the interest of history is whether we can learn from it. Also, I hope it is clear that this particular history is one of progressive questioning and integration of the available data, producing theories that become progressively more complete, with later theories incorporating earlier ones rather than contradicting them. Issues that currently require obvious attention are as follows:. There are good theoretical reasons for seeing loss as orthogonal to approach and avoidance for example, avoiding loss can produce approach. It is clearly not the basis for distinguishing anxiety from fear.

However, uncertainty is often a factor in generating anxiety does this have some direct relation to, for example, ambiguity aversion? That is, it predisposes both to disorders that are sensitive to anxiolytics and those that are not. Does this involve some system such as the monoamine ones that provide diffuse input to the entire defensive system?

Disentangling the contribution of all its different areas can potentially answer many or all of the previous bullet point questions. How is this related to the fact that the hippocampus has one of the highest concentrations of corticosterone receptors in the brain and is a key structure for the negative feedback control of corticosterone and is involved in post-traumatic stress disorder and depression? There are clearly many more questions to be asked. I hope this paper will help you frame the questions and find their answers.

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Useful information about fear and anxiety and advice on how to overcome it. manage and reduce stress? Our free downloadable pocket guide offers you tips: lirodisa.tk . Anxiety: Current Trends in Theory and Research, Vol II. [10] Emmelkamp, P.M.G. (). “ Behavior. Anxiety is a psychological, physiological, and behavioral state induced in animals Our current knowledge of the biological bases of fear and anxiety is already an important aspect of our modern approach to anxiety and mood disorders. Vol Amsterdam, The Netherlands: Elsevier Science BV; –

To the late Professor Jeffrey Alan Gray who was my undergraduate teacher, unofficial advisor to my PhD and collaborator and co-author for more than 30 years. And to Philip Corr, whose persistent questioning led to the full 2D model and who is teaching me about personality. Blanchard, R. An ethoexperimental analysis of defense, fear and anxiety.

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Experimental studies of conflict.

The Psychology of Fear, Phobia & Anxiety, What Are You Afraid of?

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