A unifying framework for depression: Bridging the major biological and psychosocial theories through stress

Abstract

A unifying framework for depression: Bridging the major biological and psychosocial theories through stress AbstractSeveral mechanisms for the development of depression have been proposed, and a comparative examination reveals considerable overlap. is paper begins by summarizing the conclusions drawn in the literature on the major biological theories: HPA-axis hyperactivity, the monoamine theory, the cytokine hypothesis/ macrophage theory, and structural changes to relevant brain regions and neurons. It then discusses the role of psychosocial stress as a bridge between the pathophysiology of depression and its predominantly psychosocial risk factors, touching upon theories o ered in psychology and in population health. is paper further proposes a unifying framework which integrates the major theories. e multiple systems involved, and the directional complexity among them, likely help to explain the wide-ranging symptoms associated with depression, and the wide variety of comorbid medical conditions. ey may also contribute to challenges in treatment, the diversity in symptoms and treatment outcomes among individuals, and the high rates of symptom persistence and relapse. e apparent bi-directionality of associations may suggest the existence of positive-feedback loops which aggravate symptoms; however, further bench research is required to con rm such phenomena. A better understanding of these interweaving associations is warranted. Additionally, given the signi cant in uence of socioeconomic and psychosocial factors on the aetiology of depression, population-level interventions that address the social determinants of health are required. Current individual-level pharmacologic approaches are designed to treat pathophysiology once it is underway, and current individual-level non-pharmacologic interventions (such as talk therapy) are designed to moderate the relationship between psychosocial stress and pathophysiology. In contrast, a key strategy for primary prevention lies in population-level interventions that address the predominantly social causes of one of depression's most notable risk factors: chronic psychosocial stress.

Epigenetic mechanisms underlying the role of brain-derived neurotrophic factor in depression and response to antidepressants

“…Epidemiological studies have clearly shown that chronic psychological stressors are critical contributors to the development of depression in humans (Björkqvist, 2001;Meltzer et al, 2011;Roy and Campbell, 2013;Taylor et al, 2011). Such repeated exposure to a social stressor can be mimicked in rodents by using a modified version of the resident-intruder procedure called social defeat, which generates persistent emotional stress (Tidey and Miczek, 1997).…”

Myopic Misery: Maternal Depression, Child Investments, and the Neurobiological Poverty Trap

“…Since there is also a strong causal association between chronic stress and depression (Hammen, 2005), the obvious pathway runs from poverty to stress, and then to risk of depression. Roy and Campbell (2013) provide an introduction to the biology of the poverty-stress-depression feedback mechanism.…”

Chronic and treatment-resistant depression

“…Other structures in the limbic system (e.g. the hypothalamus, amygdala and hippocampus) have also been associated with depression (Drevets, 2000;Roy & Campbell, 2013).…”

“…Reduced hippocampal volume has consistently been linked to depression and is thought be a consequence of recurrent episodes of depression (Videbech & Ravnkilde, 2004). The importance of the hippocampus in understanding the pathophysiology of depression is also supported by the presence of the monoaminergic and glutamatergic systems in the hippocampus, which are networks of neurons involved in antidepressant action and response (see 1.6.5.1 Neurotransmitter and antidepressant models of depression) (Roy & Campbell, 2013). It is not clear whether structural alterations in depression are a state effect, which are reversible, or if they predate the onset of depression and worsen over time (Palazidou, 2012).…”

“…The HPA axis is made up of the hypothalamus, the anterior pituitary and adrenal cortex (Roy & Campbell, 2013). In response to stress, the HPA axis facilitates the release of several hormones, namely corticotrophin releasing hormone and adrenocorticotrophic hormone.…”