Conceptually, according to Pavlov, the regulation of fear is actually a very adaptive phenomenon that helps detect warning signs of an upcoming threat.
If the signal in the environment is followed by an unpleasant, unpleasant or potentially life-threatening signal, it is appropriate for the body to show fear of the signal, especially if this fear helps it avoid the imminent danger.
Contrary to the adaptability of fear regulation, pathological fear and anxiety (by definition) are characterized by behavior that is inconsistent with the true degree of risk - excessive avoidance, excessive levels of subjective fear and anxiety, and cognitive concentration.
In stark contrast to the general sensitivity to fear of formation, most people who experience extreme unhappiness, life-threatening or other traumatic conditions do not eventually develop into anxiety disorders.
Indeed, as many as 95% of people have experienced one or more traumatic events in their lifetime, but only 10-30% of the survivors of the injury develop into anxiety disorders.
Obviously, factors other than the experiment itself can regulate the relationship between trauma and anxiety.
The study actually reveals a number of individual differences that predict (possibly associated with causal) anxiety disorders based on neurological indicators (e.g., related to threats), ranging from personality traits and propensities (e.g., neuroticism, trait anxiety, versus Sensitivity to anxiety). Tonsil reactivity;) genetic markers (e.g., polymorphic affecting the function of serotonin or dopamine systems;
These differences in individual factors may be vulnerable factors and are insufficiently responsive to major negative life events in the quality-stress psychopathology model.
If this quality and stress-based anxiety model should be consistent with the idea that fear is critical to the etiology of these diseases, it is foreseeable that more and more vulnerable people will find differences in sensitivity or Form a tendency to fear. (This type of difference is actually a potential vulnerability mechanism). Research comparing clinical and non-clinical populations supports this view. For example, in a single conditioning process, CS + conditioning in patients with anxiety is stronger than in healthy controls.
Compared with the healthy control group, an increase in the response to CS was sometimes observed in the difference in fear formation in panic disorder patients, which was not related to the outcome (CS-), resulting in deterioration of discrimination training.
Similarly, it has been shown that patients with panic disorder and post-traumatic stress disorder have an extinction of conditional fear compared to normal controls.
No matter how useful such research is, they cannot determine whether the abnormality that causes fear represents the true vulnerability factor (i.e., quality) of the pathology of fear or the diagnostic marker (consequence).
Although fear has played a causal role in the development of anxiety disorders in the context of quality stress, attempts to link known susceptibility factors to dysfunctional and excessive fear training models in non-clinical populations have resulted in more Suspicious results, most studies failed to find a permanent relationship between the two. Nervous or introverted and acquired factors such as fear.
Therefore, this is a paradox: in the basic process of forming fear, people who are at risk of developing one or another anxiety disorder do not behave differently from those who do not have anxiety, even if the adjustment of fear is considered to be the cause of anxiety disorder. The main reason for development. The quality of anxiety - the disease in the stress model.
To be continued https://zen.yandex.ru/profile/editor/id/5d6103cdc31e4900ad8a43b8/5d94bf84ec575b00afa2fb01/edit
