Anxiety and depression are common conditions in modern times. With events such as the current Covid-19 crisis exacerbating stress, anxiety and depression in many people due to the worry, uncertainty, isolation and social distancing. Therefore, it is a crucial time to focus on mental health and support cognitive wellness.

Anxiety and depression are considered separate conditions however, they are not mutually exclusive with stress and anxiety considered a major trigger for the onset of depression. Comorbid depression and anxiety disorders occur in up to 25% of general practice patients. About 85% of patients with depression have significant anxiety, and 90% of patients with anxiety disorder have depression.1 This blog looks at the differences (and similarities) between the two considered mechanisms which trigger onset and highlights interventions to help support mood and cognitive and mental health.

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What is anxiety?

Anxiety is a normal reaction to stress and can be beneficial in some situations. It can alert us to dangers and help us prepare and pay attention. Anxiety disorders differ from normal feelings of nervousness or anxiousness and involve excessive fear or anxiety, they are the most common form of mental health disorders, affecting nearly 30% of adults in their lifetime.

What is depression?

Depression is among the most common and costly of all psychiatric disorders. Nearly one in four women and one in six men experience depression during their lifetime, and up to 65% of individuals have recurrent episodes of the disorder. The WHO characterises depression by; persistent sadness and a lack of interest or pleasure in previously rewarding or enjoyable activities. It can also disturb sleep, appetite and concentration.

Anxiety, grief and fear are all normal emotions which are designed to help us protect ourselves, so in what circumstances do these normal emotions lead to anxiety disorders and/or depression?

Theories of pathogenesis2

Most contemporary theories for depression concur that stress can initiate cognitive and possibly biological processes that increase the risk of the disorder. Major stressful life events are one of the best predictors of the onset of depression. Indeed, certain life events, such as those involving social rejection, confer a 21.6% increase in risk for onset of major depressive disorder.2 However although these theories are generally well accepted little has been investigated about the physiological processes that are influenced by stress and that, in concert with cognitive and affective processes, may lead to depression.

Research now has demonstrated that stressful events or ongoing psychological stress increases inflammatory components of the immune system, leading to increases in long term chronic inflammation. This is thought to be a major driver of depression. Increases in inflammation can in turn elicit profound changes in behaviour, which include the initiation of anxiety and depressive symptoms such as sad mood, anhedonia, fatigue, psychomotor retardation, and social-behavioural withdrawal.

In particular social stressors involving conflict, threat, isolation, and rejection have been shown to increase inflammatory markers including IL-6, TNFα and CRP.

A common method of inducing stress in humans is by the Trier Social Stress Test (TSST). Participants in this paradigm are asked to prepare and give an impromptu speech and to perform difficult mental arithmetic in front of a nonresponsive, socially rejecting panel of raters. It was found that:

Stress-related appraisals and reactions appear to modulate inflammation responding to acute social stress Individuals who report experiencing more fear to the TSST have been found to exhibit greater increases in the proinflammatory marker A third study reported that a public speaking tasks (similar to the TSST) induced feelings of anxiety, depression, and anger; greater increases in anxiety and anger were, in turn, independently related to greater increases in circulating IL-6 (an inflammatory marker) Greater difficulty in maintaining a positive cognitive–affective state during the TSST was associated with greater increases in circulating IL-1β and that increases in circulating IL-1β in turn predicted increases in depressive symptoms over the following year. One thing that has become clear over the last few years is that individuals can be exposed to the same type of stressful life events which can trigger high levels of inflammation in some but less in others. People who have an increased inflammatory response are then more likely to develop anxiety disorders and depression. The main factor that determines the initiation of inflammation is the perception of stress. People who perceive stress as helpful or do not consider the same situation as a negative stressful event have a reduced inflammatory response in comparison to those who feel the event is negatively stressful. In one study, perceived stress was inversely related to self‐esteem and positively associated with work‐related stress and depression, respectively.3 Therefore, interventions which aid a healthy perception of stress are useful preventative factors