Major Depressive Disorder Investigated Disease Process
Major depressive disorder (MDD) is one of the most common mental illnesses, affecting
more than 16 million American adults annually. (mhanational.org, n.d.) In 2017, an estimated 11
million U.S. adults aged 18 or older had at least one major depressive episode with severe
impairment. This number represented 4.5% of all U.S. adults. (nimh.nih.gov, n.d.) Depression is
the leading cause of disability worldwide and is a major contributor to suicide deaths. The
widely accepted definition of major depression is a period of at least two weeks when a person
experiences a depressed mood or loss of interest or pleasure in daily activities and has a majority
of symptoms, such as problems with sleep, eating, energy, concentration, or self-worth. It is
caused by biological, psychological, and social causes of distress that alter brain functions.
Although several studies have been conducted to explain the pathophysiology of MDD,
the results are not conclusive. Currently, there only exists diverse theories on the topic
established on the measurement of indirect markers, post-mortem analysis, and neuro-imaging
procedures. The theories analyze the neural circuitry of depression, stress response circuits in the
body, effects of the interaction of genes and the environment, the relationship between
inflammation and depression, neuropeptides, hormones, and implications of the circadian rhythm
in depression (Fekadu, Shibeshi, & Engldawork, 2016). Most of these studies, however, agree
that depression affects several brain functions and responses in different ways.
Under neural circuitry, abnormalities are observed in the brain region responsible for
mood, reward response, and executive functions. These changes are indicated by a reduction in
the grey matter volume and glial density present in the prefrontal complex and the hippocampus.
The decreased hippocampal function is believed to impede the hypothalamic-pituitary-adrenal
(HPA) axis and potentially result in hypercortisolemia, which is seen in depression. Also, the
mesolimbic dopamine system causes depression as the nucleus accumbens (NAc), and the
ventral tegmental area (VTA) halt the reward response to delightful inducements such as food
and drugs resulting in a lack of pleasure in MDD patients.
While analyzing the stress response circuits, it has been observed that chronic stress and
hyperactivity of the HPA axis cause long-lasting hypercortisolemia, which is present in
depression patients. Also, the amygdala, responsible for emotional and stress responses, is
affected in patients with increased levels of corticosteroids. The hippocampus also decreases in
size and sends inhibitory signals to the HPA axis. Moreover, chronic stress affects the expression
of genes modifying antioxidant systems such as catalase, glutathione peroxidase, glutathione
reductase, and superoxide dismutases (SODs).
Standard of Practice
In 2019, the American Psychological Association (APA) published a new
recommendations for the treatment of MDD. These standards of practice are all evidence-based
and are meant for professionals in psychology and across health care. In the article, they
separated the guidelines for children and adolescents from that of older adults based on the
occurrence rates of the disease in the two groups. For diagnoses, the DSM-5 criteria are the most
recommended where a patient is assessed for five or more symptoms during the same two-week
period (Truschel, 2020) . The symptoms include a depressed mood for the most part of the day,
almost daily, decreased interest in all or almost all daily activities, substantial weight or appetite
loss or gain, reduction of physical movements and thoughts, constant fatigue, frequent feelings of
worthlessness or excessive guilt, indecisiveness and inability to concentrate, and recurrent*
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