Welcome to day two of our depressive disorders theme. Today we are going to go one level deeper and overview some epidemiology and discover suggested models for the development of depression. The focus for this section will be particularly on major depressive disorder (MDD) and persistent depressive disorder (PDD).
Today's Content Level: Intermediate; Advanced
Epidemiology
•Prevalence = proportion of individuals who have a condition at a particular period of time
•Incidence = proportion or rate of individuals who newly develop a condition during a period of time
Major depressive disorder (MDD) 1
•Prevalence: 12-month prevalence = 10.4%. Lifetime prevalence = 20.6%. Meaning about 10% of the population at a given time has MDD.
•Gender: For every 2 woman with MDD there is 1 man with the disorder.
•Can occur at any age.
•Recurrent major depressive episodes occur in 85% of those with single major depressive episode.
•Higher risk of suicide than the non-depressed general population. 21:1 for males. 27:1 for females.
•Mortality risk in patients with MDD is 2x the general population. This factors in suicide, higher rates of substance use, as well as MDD being correlated to other medical issues (see below).
Persistent depressive disorder (PDD)
•Prevalence: Lifetime prevalence = 3-6%.
•Can occur at any age but most commonly early onset with a chronic course.
Pathogenesis
•Due to the clinical and etiological variability of major depressive disorder, it has been difficult to determine its pathophysiology. Attempts have been made to determine its genetic risks and it's neurobiological deficits, however it has been difficult to find consistent or conclusive answers. In addition, these biological investigations would be incomplete without addressing the other psychological or social factors that also play a critical role in depressive disorders. We will discuss a few highlights from various schools of thought to include genetic, neural, and psychosocial theories.
Genetics 2
•Not surprisingly there has been no identification of a single candidate gene that causes depression. The consensus is that it is likely polygenic (multiple genes) with interaction between genetics and environmental/social factors.
•MDD has been associated with genes for glucocorticoid receptor, monoamine oxidase, and genes responsible for regulation of metabolism.
•Monoamines include norepinephrine, dopamine, serotonin, and histamine. Norepinephrine and serotonin are the two neurotransmitters most implicated in the pathophysiology of depression.
•Genetic variations in genes for growth factors, pro inflammatory cytokines (chemical messengers), and regulation of hormonal pathways in the brain (such as the hypothalamic–pituitary–adrenal axis) have all been studied and found to be associated with MDD.
•Approximately 5-10 % of people evaluated for depression have previously undetected thyroid dysfunction as reflected by an elevated thyroid stimulating hormone (TSH).
Neural Systems 3
•Studies have been performed to determine the neural basis for depression. In its most simple form we have tried to figure out "where in the brain is depression located?". Just like the above section this is obviously very complicated and multiple brain regions are implicated in depression.
•Neuroimaging, neuropsychiatric testing, and brain stimulations have shown structural and functional abnormalities in the following areas:
Subcortical systems (emotion and reward processing).
Medial prefrontal and anterior cingulate cortical regions (emotion processing and regulation).
Lateral prefrontal cortical systems (cognitive control of emotions).
Remember that the current knowledge indicates that the pathophysiology of depression may be distributed across many brain regions and circuits.
Biopsychosocial 4
•Life events & environmental stress: stressful life events often precede first episode of mood disorders (less correlated to subsequent episodes suggesting long-lasting changes may alter neural systems). Most compelling data for childhood trauma, losing a parent before age 11, loss of a spouse, and unemployment.
•Interpersonal relationships: individuals without close interpersonal relationships (single, divorced, separated) are at elevated risk for depression.
•Psychodynamic theories: proposed theories are varied and complex but at the core it involves depression being linked to real or imagined loss and "introjection" becomes a defense mechanism where feelings of anger are directed in-ward at the self.
•Cognitive theory: theory that depression results from specific "cognitive distortions" that are present in people susceptible to depression. These distortions lead to 1) negative views about the self, 2) views the world/environment as hostile, and 3) has altered expectations about the future of suffering and failure.
•Learned helplessness: theory that depressed people have become conditioned that outcomes are independent of responses and this leads to decreased self-esteem and depressed mood.
•Biological factors: aside from the previously discussed genetic and neurobiological factors there are additional biological factors that are habit-based that play a role in depression. Lack of exercise, poor diet, sleep disturbance, and substance use can lead to or worsen depression.
Comorbidities
•Depressive disorders are highly co-morbid with other psychiatric disorders as well as general medical conditions.
•Psychiatric: Alcohol use disorder, anxiety disorders (generalized anxiety disorder, panic disorder, & social anxiety disorder), and OCD.
•Medical: diabetes, cardiac disease, obesity, and more.
Conclusion
I hope today's lesson provided a nice overview about the "who" and the "why" of depressive disorders. In our next session we will cover clinical pearls of depressive disorders to include the clinical interview of depressed patients.
Resources for this post include:
I highly recommend adding both of these to your psych library.
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