Skip to content
Skip to main content

About this free course

Download this course

Share this free course

Understanding depression and anxiety
Understanding depression and anxiety

Start this free course now. Just create an account and sign in. Enrol and complete the course for a free statement of participation or digital badge if available.


A major aim of this course was to shed some light on the aetiology of depression and anxiety. At the end of it you should have some idea of the complexity of this enterprise. We have focused on one of the best-studied and hence best-understood contributors to psychopathology – stress. This has biological, social and psychological significance, and its operation can be studied and understood at all these levels.

The clear message you should take away is that interaction between these levels is enormously important in aetiology. Biological factors, such as dysregulation of the HPA axis and its consequences, possible abnormalities in brain neurotransmitter systems, the effects of stress on the developing brain at different ages, and the kinds of genes that an individual carries, appear to play an important part in the development and maintenance of emotional disorders such as depression and anxiety. However, these biological factors cannot be divorced from factors that are thought of as psychosocial, such as abuse in childhood, or stressful events and how we perceive them. This is very evident from the most recent developments in genetics, which show how, via epigenetic processes, experiences are translated into the activity (or expression) of genes, which then modify the workings of the brain in ways that affect mood.

Research into epigenetic influences on mental health and ill-health is burgeoning and is likely to make a very significant contribution to our understanding of aetiology in the years to come. If so, it should also help clarify how existing treatments, both pharmacological and psychotherapeutic, for emotional disorders work, or suggest new approaches that would work more effectively.

The HPA axis is overactive in those with depression and anxiety, suggesting a role for chronic stress. Elevated levels of glucocorticoids such as cortisol and corticosterone, resulting from chronic stress, have toxic effects in some areas of the brain and promote neurogenesis in others.

The monoamine hypothesis of mood disorders has been influential in trying to explain the causes of depression. However the picture is now more complex and the view of a simple chemical imbalance as a cause of depression is outdated.

Hypotheses such as the neurotrophic hypothesis and the network hypothesis have been developed to try to account for the complex effects of antidepressant treatments on the brain.

The life-cycle model of stress links brain development with stress effects over the lifetime.

The cognitive approach concentrates on particular ways of thinking and how these cause and sustain depression.

Genetic and other vulnerabilities (also called predispositions or diatheses) can interact with environmental factors, which include psychosocial stressors such as stressful life events and early life stress (including child abuse) to cause emotional disorders such as depression.

Epigenetic processes add another layer of complexity to the interaction between genes and environment. There is increasingly evidence of the importance of epigenetic processes in the aetiology of mood disorders.