The Etiology of Depression




The age of the first depression onset has both clinical and etiological implications. Childhood depression has a mixture of causes: children with genetically familial early-onset recurrent depression; children exposed to influential psychosocial adversity, and criminality who continue to experience social maladjustment. Adolescent-onset depressions are noteworthy for several factors. Within significant cultural shifts in recent decades, adolescents' encounters with stressful experiences contribute to depressive experiences. After females deliver an infant, there is an intense drop in thyroid hormone level, which decrease serotonin neurotransmission as thyroid hormones control the release of dopamine and serotonin neurotransmitters, leading a majority of women to experience mild “blues”, and between 10 and 20 percent of new mothers experience clinical depression lasting anywhere from several weeks to a year. Despite biological and hormonal etiological factors of postpartum depression, social stressors, family composition, levels of social support, and especially poorer economic circumstances all contribute to the risk of developing postpartum depression.
Timing and Course
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Biological Factors
One-third of major depression risks in adults are derived from genetic differences. The risk of developing major depression is 3 times more for those who have first-degree relatives with depression. In addition, genetic polymorphism affects the ability to respond to stress, linking to the risk of depression. Deficits in the central serotonin system (5-HT), include impaired uptake function of serotonin transporter and serotonin receptor binding leading to a decrease in the release of hormones that regulate our emotion and aggression, resulting in dysfunctional emotionality in response to stress. Specifically, studies have shown that having a short allele of serotonin transporter decreases the transcriptional efficiency of serotonin, decreasing the efficiency of binding toward serotonin receptors. Last but not least, the genetic contribution to depression not only has an internal impact on depressogenic processes but also gene-environment-related interaction. For example, genetic factors impact a depressed person’s parenting style, indirectly determining the dominant role of depression in children.
Genetic vulnerability
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Neuroendocrine Functioning
The neuroendocrine system and brain response correlate to dysregulation of the body’s response to stress, contributing to the arousal of depression. After activating cortisol function, cortisol resolves through an inhibitory feedback process in the HPA axis. Yet, abnormal HPA leads to failure to normalize cortisol, and high cortisol level results in the death of cells in the hippocampus, damaging the connection between neurons, so neurotransmitters fail to regulate emotion, linking to a higher risk of depression.
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Immune System Processes

Research has shown a strong correlation between coronary heart disease and depression. Chronic stress activates the immune system and leads to inflammation. Chronic inflammation results in symptoms of depression and heart disease. Cytokines are signaling molecules to fight pathogens and direct white blood cells toward infections. Downstream products of this process, including C-reactive protein (CRP), a molecule produced by the liver in response to IL-6, are used as an index of the inflammatory response. Chronic stress is associated with increased levels of both CRP and depression. Chronic stressors may prime the immune system to make an inflammation response to stress. Due to dysregulation of the HPA response, the immune system may not return to baseline, triggering depression symptoms such as sickness behaviors.

Stressful Environment
Acute negative life event
80% of depressed cases were preceded by major negative life events. The severity of the impact of the acute life event depends on its subjective meaning to the patients. For example, one person might become depressed under extreme deprivation, but another become depressed because of personal exaggeration of the acute invention. For the immigrant and refugee population, life events of loss and isolation have a significant impact on the psychological functioning of individuals, leading to high rates of depression.
Chronically stressful life circumstances.
A vital feature of Exposure to long-term stressful circumstances (such as: Racial discrimination, Low socioeconomic status, Immigration status )is the bidirectional effect of depression and chronic conditions on each other. For example, poverty or unemployment in the case of immigrants triggers depression, but depression deters individuals’ ability to change their circumstances. Another feature is the co-occurring of chronic stress. For example, single mothers experience a higher rate of depression than married mothers due to experiencing divorce, low socioeconomic position, and poverty at once, in which chronic stress is co-occurring with each other.
The extensive environment is also a source of chronic stress, such as trash, high level of noise, crime, etc. Last but not least, parents are challenged by children’s medical illness, developmental disabilities, and the stress associated with those result in depression. Adolescent mothers are also exposed to a high risk of depression due to the compounding of a co-occurring chronic stressor such as low income, reduced social support, and relationship difficulties.
Adversity in childhood
Children's exposure to adversity (sexual/physical/emotional abuse, bullies, parental drinking, and maltreatment) links to the development of depression. Compared to sexual and physical abuse, emotional abuse is most related to depression. Parental mental illness, violence, and parental divorce were predictive of the recurrence of depression. The extensive environment plus parental lack of care contribute to dysfunctional cognition that increases the risk of depression, Those are just collective trend, but more biological proof are needed

Psychological Vulnerabilities
Cognitive vulnerability
According to Beck and cognitive style models, those who interpret events with absolutely self-critical and helplessness have a higher risk of depression. Poor parent-child communication characterized by criticism and confirmation has a major impact on individuals' self-disproves. The individuals view minor experiences as acute negative life events, seeing everything as a reflection of one’s lack of worth. Such a view can trigger symptoms of dysphoria and futility.
Interpersonal vulnerability.
Depression is associated with impairment in interpersonal functioning, which overall has difficulties in close relationships. Specifically, depression is uniquely associated with marital dissatisfaction. For example, an endurance of Intimate partner violence affects the victim’s trust in others, levels of isolation, and coping styles, leading to 47% of depression among them. Also, poor marital relationships lead to distrust, excessive reassurance-seeking, and insecurities that can further develop into depression.
Personality vulnerability
Neuroticism, defined by negative emotionality and high reactivity to stress, is a vital predictor of depression, which is the genetically transmitted trait that exposes an individual to respond to stressors with anxiety, tension, and anger. Another strong personality that is more likely to develop into depression is a ruminative response style, showing behaviors such as rumination, self-focus, and overanalysis of issues. The sustainable negative and high-tense moods have a higher risk of developing depression.