Depression is ranked as the leading cause of disability by the World Health Organisation and has a complex aetiology with environmental factors often playing a significant role. These may include adverse life events, inadequate parenting and insufficient social support all of which are regarded as common causes in the risk of developing depression. However, the impact of such environmental factors is also heavily influenced by genetic predisposition (Kendler & Halberstadt 2013).

In the mid-eighties, it was widely accepted that depressive disorders cannot occur in children as it conflicted with psychoanalytic theory, which held dominance at the time. Empirical based methods of observation more recently invalidated this concept. It is now estimated that depression effects on average 1-2% of children, with this figure growing during adolescence and further increasing in adulthood.

There is also a significant degree of overlap with other childhood disorders or comorbid conditions. Many of which are shown to increase risk of depression, such as ODD and conduct disorder. Conduct disorder is considered to have an equal weighting to early childhood depression in predicting major depression in later life with an approximate 50% correlation.

As children enter adolescence, they become more socially aware, egotistic, self-reflective and introspective. They develop abstract modes of thinking, metacognition and overthinking arise during this time too which all can play a part in reinforcing a depressive cognitive bias.

 

During teenage years, the prevalence of depression is twice as common in girls as boys. This can be attributed to several key differences. Girls tend to be more vulnerable to psychological stressful scenarios and are by nature more emotive than boys. The hormonal shift, which can occur rather abruptly and cause concentrations of certain hormones in the blood to skyrocket, has been proven to cause a profoundly negative impact upon mood in some. Such that depression can be triggered by this regardless of social or environmental factors, with Androgen and Oestrogen being the hormones responsible in such observations (Angold et al 1999). Occurrence of a girl’s first period can also have a strong impact on her psychological wellbeing and catapult her into adulthood rather unexpectedly. As a result, girls often enter into more mature social circles and can experience adverse social scenarios and stresses which they lack the experience and emotional maturity to handle. Depression is commonly attributed to these rapid physiological changes and corresponding social shifts.

There is strong evidence indicating genetic influence for depression, with twin studies showing 30-50% heritability. Life events are common triggers of depressive disorder, for example the death of a loved one, romantic adversity or school bullying. Although what constitutes an adverse life event and its severity of impact is relative to the individual.

Children born to mothers who experienced depression during pregnancy have a higher risk of depression and those born to mothers who have PPD have a greater disposition to emotional and behavioural problems, both of which are attributed to a combination of genetic and environmental factors, which display alterations in amygdala function in brain scans (Rifkin-Graboi et al 2013).

On a neurological level, activity in the ventral striatum appears to be lower in those suffering from depression and those at risk of depression compared to low risk test subjects.

The neurological basis of depression is not well understood as limited success with pharmacological intervention shows. Tricyclics used for adult depression appear to be ineffective for children and adolescents. These work by increasing levels of norepinephrine and serotonin but elicit no difference in response compared to placebo for treatment of children and adolescents (Hazell & Mirzaie 2013). Selective serotonin reuptake inhibitors such as Fluoxetine and Escitalopram prove to be effective and are routinely administered for treating children and teenagers although they only possess a 60% efficacy rate, only 10% above placebo. Why one group of antidepressants is effective whilst the other not remains to be better understood.

 

Anhedonia, a core symptom of depressive disorders has been frequently linked with aberrations in the reward processing domains of the brain. This has been investigated in numerous studies which have generated results of varying corroboration. The most consistent finding between these studies which can be reliably replicated shows that brains of depressed individuals exhibit attenuated responses to reward in the ventral striatum and hyper response to punishment in the amygdala (Ng et al 2018).

 

There is a highly complex aetiology triggering depression. Genetic, biological factors and environmental factors seem to heavily influence the emergence and progression. Many contributing factors remain questionable as often a life event is required to trigger the depressive episode, but the severity of impact is not easy to predict.

 

Meta-analysis of Reward Processing in Major Depressive Disorder Reveals Distinct Abnormalities within the Reward Circuit (2018). Tommy H. Ng, Lauren B. Alloy, David V. Smith. bioRxiv 332981; doi: https://doi.org/10.1101/332981

The Making and Breaking of Affectional Bonds. I. Aetiology and Psychopathology in the Light of Attachment Theory. An expanded version of the Fiftieth Maudsley Lecture, delivered before the Royal College of Psychiatrists, 19 November 1976. By JOHN BOWLBY

The road not taken: life experiences in monozygotic twin pairs discordant for major depression (2013). Kendler, K.S. & Halberstadt, L.J. Molecular Psychiatry (2013) 18, 975—984.

Pubertal changes in hormone levels and depression in girls. (1999) Angold A, Costello E.J., Erkanli A., Worthman C.M. Psychol Med. 1999 Sep;29(5):1043-53.

Tricyclic drugs for depression in children and adolescents (2013). Hazell, P. & Mirzaie, M. Cochrane Database of Systematic Reviews 2013, Issue 6. Art. No.: CD002317. DOI: 10.1002/14651858.CD002317.pub2.

Prenatal Maternal Depression Associates with Microstructure of Right Amygdala in Neonates at Birth (2013). Anne Rifkin-Graboi, Jordan Bai, Helen Chen, Waseem Bak’r Hameed, Lit Wee Sim, Mya Thway Tint, Birit Leutscher-Broekman, Yap-Seng Chong, Peter D. Gluckman, Marielle V. Fortier, Michael J. Meaney, and Anqi Qiu. Biological Psychiatry, Volume 74, Issue 11 (December 1, 2013)