Psychological models While there is not just one explanation for the cause of<unk> , there are certain perspectives researchers use to explain the disorder. The first one is the biological perspective. Past research concluded that there is irregular norepinephrine activity in people who have<unk>  attacks. Current research also supports this perspective as it has been found that those with<unk>  also have a brain circuit that performs improperly. This circuit consists of the amygdala, central gray matter, ventromedial nucleus of the hypothalamus, and the locus ceruleus. There is also a cognitive perspective. Theorists believe that people with<unk>  may experience<unk>  reactions because they mistake their bodily sensations for life-threatening situations. These bodily sensations cause some people to feel as though are out of control which may lead to feelings of<unk> . This misconception of bodily sensations is referred to as anxiety sensitivity, and studies suggest that people who score higher on anxiety sensitivity surveys are fives times more likely to be diagnosed with<unk> .<unk>  has been found to run in families, which suggests that inheritance plays a strong role in determining who will get it. Psychological factors, stressful life events, life transitions, and environment as well as often thinking in a way that exaggerates relatively normal bodily reactions are also believed to play a role in the onset of<unk> . Often the first attacks are triggered by physical illnesses, major stress, or certain medications. People who tend to take on excessive responsibilities may develop a tendency to suffer<unk>  attacks. Post-traumatic stress disorder (PTSD) patients also show a much higher rate of<unk>  than the general population. Prepulse inhibition has been found to be reduced in patients with<unk> . Substance use Substance use disorders are often correlated with<unk>  attacks. In a study, 39% of people with<unk>  had recreationally used substances. Of those who used alcohol, 63% reported that the alcohol use began prior to the onset of<unk> , and 59% of those using illicit substances reported that substance use began first. The study that was conducted documented the<unk> -substance use disorder relationship. Substance use disorder began prior to the onset of<unk>  and substances were used to self-medicate for<unk>  attacks by only a few subjects. In another study, 100 methamphetamine-dependent individuals were analyzed for co-morbid psychiatric disorders; of the 100 individuals, 36% were categorized as having co-morbid psychiatric disorders. Mood and Psychotic disorders were more prevalent than anxiety disorders, which accounted for 7% of the 100 sampled individuals. Smoking Tobacco smoking increases the risk of developing<unk>  with or without agoraphobia and<unk>  attacks; smoking started in adolescence or early adulthood particularly increases this risk of developing<unk> . While the mechanism of how smoking increases<unk>  attacks is not fully understood, a few hypotheses have been derived. Smoking cigarettes may lead to<unk>  attacks by causing changes in respiratory function (e.g. feeling short of breath). These respiratory changes in turn can lead to the formation of<unk>  attacks, as respiratory symptoms are a prominent feature of<unk> . Respiratory abnormalities have been found in children with high levels of anxiety, which suggests that a person with these difficulties may be susceptible to<unk>  attacks, and thus more likely to subsequently develop<unk> . Nicotine, a stimulant, could contribute to<unk>  attacks. However, nicotine withdrawal may also cause significant anxiety which could contribute to<unk>  attacks. It is also possible that<unk>  patients smoke cigarettes as a form of self-medication to lessen anxiety. Nicotine and other psychoactive compounds with antidepressant properties in tobacco smoke which act as monoamine oxidase inhibitors in the brain can alter mood and have a calming effect, depending on dose. Stimulants A number of clinical studies have shown a positive association between caffeine ingestion and<unk>  and/or anxiogenic effects. People who have<unk>  are more sensitive to the anxiety-provoking effects of caffeine. One of the major anxiety-provoking effects of caffeine is an increase in heart rate. Certain cold and flu medications containing decongestants may also contain pseudoephedrine, ephedrine, phenylephrine, naphazoline and oxymetazoline. These may be avoided by the use of decongestants formulated to prevent causing high blood pressure. Alcohol and sedatives About 30% of people with<unk>  use alcohol and 17% use other psychoactive drugs. This is in comparison with 61% (alcohol) and 7.9% (other psychoactive drugs) of the general population who use alcohol and psychoactive drugs, respectively. Utilization of recreational drugs or alcohol generally make symptoms worse. Most stimulant drugs (caffeine, nicotine, cocaine) would be expected to worsen the condition, since they directly increase the symptoms of<unk> , such as heart rate. Deacon and Valentiner (2000) conducted a study that examined co-morbid<unk>  attacks and substance use in a non-clinical sample of young adults who experienced regular<unk>  attacks. The authors found that compared to healthy controls, sedative use was greater for non-clinical participants who experienced<unk>  attacks. These findings are consistent with the suggestion made by Cox, Norton, Dorward, and Fergusson (1989) that<unk>  patients self-medicate if they believe that certain substances will be successful in alleviating their symptoms. If<unk>  patients are indeed self-medicating, there may be a portion of the population with undiagnosed<unk>  who will not seek professional help as a result of their own self-medication. In fact, for some patients<unk>  is only diagnosed after they seek treatment for their self-medication habit. While alcohol initially helps ease<unk>  symptoms, medium- or long-term hazardous alcohol use can cause<unk>  to develop or worsen during alcohol intoxication, especially during alcohol withdrawal syndrome. This effect is not unique to alcohol but can also occur with long-term use of drugs which have a similar mechanism of action to alcohol such as the benzodiazepines which are sometimes prescribed as tranquilizers to people with alcohol problems. The reason chronic alcohol misuse worsens<unk>  is due to distortion of the brain chemistry and function. Approximately 10% of patients will experience notable protracted withdrawal symptoms, which can include<unk> , after discontinuation of benzodiazepines. Protracted withdrawal symptoms tend to resemble those seen during the first couple of months of withdrawal but usually are of a subacute level of severity compared to the symptoms seen during the first 2 or 3 months of withdrawal. It is not known definitively whether such symptoms persisting long after withdrawal are related to true pharmacological withdrawal or whether they are due to structural neuronal damage as a result of chronic use of benzodiazepines or withdrawal. Nevertheless, such symptoms do typically lessen as the months and years go by eventually disappearing altogether. A significant proportion of patients attending mental health services for conditions including anxiety disorders such as<unk>  or social phobia have developed these conditions as a result of recreational alcohol or sedative use. Anxiety may pre-exist alcohol or sedative dependence, which then acts to perpetuate or worsen the underlying anxiety disorder. Someone suffering the toxic effects of recreational alcohol use or chronic sedative use will not benefit from other therapies or medications for underlying psychiatric conditions as they do not address the root cause of the symptoms. Recovery from sedative symptoms may temporarily worsen during alcohol withdrawal or benzodiazepine withdrawal.
Panic disorder
Hyperthyroidism
Depression 
Cardiovascular disease
Late life depression
Hypochondriasis
Blood phobia
Anxiety disorder