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How about brain chemicals? Which ones are affected by anxiety? Firstly, anxiety involves an elevated level of corticoptrophin releasing factor (CRF). This brain chemical causes part of the adrenal gland to release stress hormones called gluccocorticoids. These stress hormones include cortisol and noradrenalin (aka norepindephrine). If CRF is high during anxiety, then the brain is telling the body that danger is in the environment. The result is that the body releases an excess of stress hormones and then you feel stressed-out and afraid?your heart starts pumping fast, your breathing increases, your mind is racing, and you feel kind of scared. This is the body’s normal response to fear; however, the body should also enact fear extinguishing mechanisms. This is where the brain chemical glutamate comes in, one of the brains greatest excitatory chemicals. Research has shown that glutamergic receptor antagonists (drugs that block glutamate binding sites in the brain) are effective in treating anxiety because they help facilitate fear extinction by encouraging a calmer brain. Another chemical that helps calm the brain is known by its acronym GABA. If anxiety leads to an increase in glutamate, then the ratio between glutamate (excitatory) and GABA (inhibitory or calming) is imbalanced. Treatment may involve either decreasing glutamate (through glutamate-inhibitor drugs) or by increasing GABA levels (or both). In any case, an anxious brain needs to be calmed down.

Now back to the amygdala. This brain region, as said before, processes fearful information and coordinates the threat response by integrating information from the senses, environment, and past experience. The amgydala initiates behavioural and autonomic nervous responses by sending this information through projections to motor (movement) areas and brain stem nuclei (sensory nerves). In healthy individuals, the amydgalar response is modulated or controlled by top-down processing mechanisms involving the medial (middle) prefrontal cortex region, the hippocampus, and the anterior cingulate cortex. The hippocampus is involved in memory and the anterior cingulate cortex is involved in emotional regulation and decision making. Top-down mechanisms use stored information from past experiences to help make sense of a situation or a sensation; in this case, the brain uses its past knowledge on anxiety and the given situation to help regulate the anxiety, or in other words, to tell the brain to relax and breathe. Research shows that individuals who experience frequent anxiety attacks or who have been diagnosed with one of the many types of anxiety disorders, respond to threat with increased activity in the amgydala. Research also shows that anxiety-prone people have altered insular function. As mentioned above, the anterior insula is a brain region responsible for environment-emotion evaluation. It might just be that more anxious people have more sensitive and reactive amydalas and misbehaving insulas.

Now perhaps the most important are the neurotransmitters involved in anxiety: the monoamines. More specifically, serotonin and norepinephrine are widely recognized for their roles in mood disorders like anxiety. Another brain chemical, neuropeptides, are also believed to play a role in anxiety. This group includes substance P and neuropeptide Y. Substance P increases during anxiety, prolonging the feeling and increasing the stress response, whereas neuropeptide Y modulates mood and reduces anxiety and stress, meaning that there may be a deficiency of it within the brain of those who experience anxiety attacks. Additionally, the hormones oxytocin and orexin are involved. In a rodent-model study (a study done on rats), oxytocin is shown to act on nuclei (parts of brain cells) in the amygdala, inhibiting or blocking excitatory flow from the amygdala to the autonomic nervous system (the branch of the nervous system that mediates fear response). In other words, oxytocin helps reduce anxiety by decreasing amygdalar reaction to something perceived as stressful or fearful.

Orexin, on the other hand, may be in excess in those prone to anxiety. Orexin is the hormone involved in the “brain reward” pathway, and may lead to excess of the neurotransmitter dopamine?the brain’s greatest stimulating chemical. If dopamine increases, then the brain is on a kind of “high” where everything it perceives is heightened, including fear. This happens because the body naturally converts dopamine to norepinephrine (a major stress hormone) that then converts to adrenaline (major stimulating hormone). Research however, shows that individual differences do exist in neuroendocrine (brain hormone) sensitivity, so different people may experience anxiety because of different abnormalities in their brains. This supports the theory that anxiety attacks have a genetic basis.

This seems like an overwhelming amount of changes that go on in the anxious brain, but there is one more abnormality to explore: the chemical release system, called the HPA axis, which is responsible for the release of the stress hormones during the experience of anxiety. Here is what happens: CRF is released by a brain region called the hypothalamus, which then tells another brain region called the pituitary gland (situated just under the hypothalamus) to release adrenocorticotropin-releasing hormone (ACTH) which tells the adrenal gland to release glucocorticoids?the stress hormones. When an anxiety attack is experienced, however, and the individual is prone to anxiety (maybe because of their genetics), this system is hyperactive, meaning that it is working in overdrive, pumping out too many stress hormones and leading to heightened anxiety. What this system lacks in highly-anxious people are a strong pair of “brakes”. The negative feedback mechanism that tells the brain to work in reverse (lower anxiety and production of stress hormones) is not functioning that well. In result, anxious people have elevated CRF levels and an altered HPA axis: stress hormones are taking over! In normal, non-anxious prone individuals, gluccocorticoids should bind to receptors on the hypothalamus and pituitary gland, telling them to stop releasing any more CRF and ACTH. This is the body`s normal, natural way of lowering anxiety and bringing back a balance.

Obviously, something goes wrong in the brain during an anxiety attack. Given the diversity within the human population in terms of individual genes (called genotypes), what exactly is going wrong in the brains of those who experience anxiety may not always be the same between people. For example, perhaps one person gets anxious because they have insufficient serotonin, which may occur for multiple of reasons (i.e. not enough serotonin receptors, binding insufficiency, or low serotonin levels). But maybe another person has perfectly normal serotonin levels, but has a hyperactive HPA system or a more reactive amygdala. The reasons for an anxiety attack are many, but perhaps the most interesting is their onset. How do anxiety attacks occur? Numerous research studies done on rats have tested anxiety and fear, and most theorize that anxiety attacks arise because of the way an individual’s genes and their environment interact.

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