In this article we’re going to explore some of the biological definitions and processes involved in understanding anxiety and stress in the human body. Analysing why we’re programmed in this way from and evolutionary perspective to how we’re responding in today’s environment.
This article is the first in a three-part series that seeks to understand stress and anxiety from a biological perspective, then cognitive and finally behavioural.
Biological responses to anxiety and stress:
The GABA hypothesis argued that anxiety develops because of a dysfunction in neurones that normally produce gamma aminobutyric acid (GABA) automatically once a high arousal level has been reached in the central nervous system. GABA is usually released once arousal reaches a certain level. It then binds with GABA receptors on excited neurones which underpin the experience of anxiety. This process causes inhibitions, reduced arousal, and a decrease in experienced anxiety. Treatment with drugs such as diazepam (valium) reduces anxiety because these drugs bind to the GABA neuroreceptors resulting in a reduction in the experience of anxiety. There is evidence to suggest these drugs reduce the effects of anxiety but these are usually lost after long term use or as soon as medication ceases. Viewing the GABA hypothesis and psychopharmacology in isolation ignores situational and behavioural implications as to why the body is reacting in this way.
Anxiety and stress are closely related; it is unusual to feel chronically anxious without also feeling simultaneously stressed
The hypothalamic-pituitary-adrenal cortex axis in the brain is highly sensitive to environmental change, this pathway stimulates the release of one of many steroids corticosteroids (glucocorticoids such as cortisone, hydrocortisone and corticosterone) through the interaction with the adrenal cortex that is directly involved within studies of stress. This release of steroids facilitates the conversion of stored fat and protein into usable forms of energy and suppress the body’s immune system. These are reactionary systems enabled for short-term low dose usage, but long-term suppression of the immune system will leave the body vulnerable to infection. Controlled by how individuals perceive and evaluate complex environmental stimuli, if these circumstances are threatening or arousing, then messages will be sent to the hypothalamus via the many pathways interconnecting it with the forebrain, and the hypothalamic-pituitary-adrenal axis will be activated. Therefore chronic stress will involve a parallel activation of the adrenal cortex.
A state of stress exists when there is a discrepancy between the perceived demands on an organism and its perceived ability to cope
The automated nervous system (ANS) is an automatic, self-regulating system that within situations of possible threat prepares the body for action and movement; in this moment the ANS provides high levels of sympatheticactivity to help cope with the potential demands, one of the glands controlled by the ANS is the adrenal medulla which releases adrenaline and noradrenaline. Increasing heart-rate, sweat gland activity and blood supply to muscles. The combined activation of the pituitary-adrenal axis and the sympathetic branch of the ANS produces a pattern of peripheral physiological arousal; peripheral arousal is critical to behavioural activity.
An individuals perception of said ‘threat’ is a varying factor but the ANS has not yet evolve to add context into the equation. With the increased speed of e-mail communication, people are potentially handling a higher volume of information than they can cognitively manage. Therefore if these perceived threats are encountered at work; an angry phone call or disagreement with a colleague, the individual may attempt to suppress this unwanted energy as they have no other option but to experience a fight or flight stress response.