Physiologically speaking is anxiety and adrenaline the same?

Question

I am wondering from a physiological perspective what is anxiety. From my experience anxiety feels like muscle tension and lots of suppressed energy. For what I know the only thing that can make the body feel like that is adrenaline. So I am wondering if the two are the same or if anxiety is caused by different hormone. However what doesn't seem right about my hypothesis is anger increases adrenaline, but I don't think anger feel like anxiety for the general population. It would be helpful if someone could clarify me what causes the physiology of anxiety.

Answer 1

Not quite the same, although there is some overlap.

What's colloquially known as an "adrenaline rush" (e.g. what you'd experience in a roller coaster or more generally in a fight-or-flight situation) is the result of the body's fast reaction system to stress, sometimes called the sympathetic-adrenal-medullary (SAM) axis. SAM activation causes the adrenal medulla to release epinephrine (adrenaline) and norepinephrine (noradrenaline);.

On the other hand, sustained/chronic stress (eventually) activates the slower stress-response axis, known as the hypothalamo-pituitary-adrenocortical (HPA) axis. In humans, HPA activation releases cortisol from the zona fasciculata of the adrenal cortex. (The adrenal cortex is the outer layer of the adrenal gland, while the adrenal medulla is the inner area of the gland.) One of the actions of cortisol is to contain the activation of the SAM axis. (Textbook of Anxiety Disorders, 2nd ed., p. 571 citing the highly influential paper of Munck et al.) Cortisol has its own negative-feedback loop.

So, in a panic attack you'd experience mostly SAM activation, or at least this will be the dominant effect. On the other hand, anxiety generally refers to a broader class of reactions to stress, including long-term ones. E.g., [older] people with generalized anxiety disorder (GAD) may experience elevated cortisol, and this is reduced by SSRI medication. Other anxiety-related disorders such as PTSD have a much more complicated picture; cortisol levels are not terribly useful in distinguishing PTSD patients from controls. Recent research suggests however that a dysfunctional cortisol feedback loop may be present in PTSD; administration of cortisol after a potentially traumatic event seems to reduce later symptoms.

What I said above is a pretty simplified picture, in which I completely glossed over the complex pathways of stress-mediation in the brain, which actually make studying/treating anxiety disorders much less trivial.