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| - | Depression is a commonly occurring form of mental illness that has a global impact on the individual, community and national level. Approximately 350 million people are thought to be affected to date and this number is expected to rise over the coming years <sup>[14]</sup>. The World Health Organization has classified it as the fourth leading cause of disability worldwide <sup>[14]</sup>. A sufferer experiences low mood and aversion to activity that can affect the individual's thoughts, behaviour and feelings and sense of wellbeing. These feelings of severe despair are experienced over an extended period of time and it is common for individuals with depression to simultaneously experience symptoms of anxiety. There are several efficacious and cost effective treatments available to date which range from generic antidepressant drugs to different forms of psychotherapy. Overall, depression is a heterogenous, burdensome disorder that exhibits a highly variable course, an inconsistent response to treatment and an incomplete understanding of the underlying neurobiology. | + | Depression is a commonly occurring form of mental illness that has a global impact on the individual, community and national level. Approximately 350 million people are thought to be affected to date and this number is expected to rise over the coming years. <sup>[16]</sup> The World Health Organization has classified it as the fourth leading cause of disability worldwide. <sup>[15]</sup> A sufferer experiences low mood and aversion to activity that can affect the individual's thoughts, behaviour and feelings and sense of wellbeing. These feelings of severe despair are experienced over an extended period of time and it is common for individuals with depression to simultaneously experience symptoms of anxiety. There are several efficacious and cost effective treatments available to date which range from generic antidepressant drugs to different forms of psychotherapy. |
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| ====== History ====== | ====== History ====== | ||
| - | The Ancient Greeks hypothesized that depression was caused by an imbalance of bodily fluid, or humor. The presence of different humors led to different dominant personalities. As such, an excess of bile resulted in melancholia - characterised by Hippocrates as a distinct disease, consisting of “fears and despondancies, if they last for a long time.” | + | The Ancient Greeks hypothesized that depression was caused by an imbalance of bodily fluid, or humor. The presence of different humors led to different dominant personalities. As such, an excess of bile resulted in melancholia - characterised by Hippocrates as a distinct disease, consisting of “fears and despondancies, if they last for a long time.” <sup>[14]</sup> |
| - | Physicians in the muslim and persian world developed ideas about depression in the Islamic golden age. The 11th century Persian physician Avicenna theorized that depression was a mood disorder in which sufferers become suspicious and develop phobias. Ishaq in Imran (d.908) associated depression with the inflammation of the brain and meninges. | + | Physicians in the muslim and persian world developed ideas about depression in the Islamic golden age. The 11th century Persian physician Avicenna theorized that depression was a mood disorder in which sufferers become suspicious and develop phobias. Ishaq in Imran (d.908) associated depression with the inflammation of the brain and meninges. <sup>[10]</sup> |
| - | Various theories of melancholia flourished in medieval Europe, alongside the theories of Hypocrates, Avicenna and Galen. Acedia, or lethargy, was thought to be linked to be isolation. | + | Various theories of melancholia flourished in medieval Europe, alongside the theories of Hypocrates, Avicenna and Galen. Acedia, or lethargy, was thought to be linked to be isolation. <sup>[14]</sup> |
| - | During the age of enlightenment (18th and 19th century) depression was thought be inheritable and untreatable weakness in temperament. Thus, depressed individuals were locked up in mental institutions and were subject to homelessness and poverty. | + | During the age of enlightenment (18th and 19th century) depression was thought be inheritable and untreatable weakness in temperament. Thus, depressed individuals were locked up in mental institutions and were subject to homelessness and poverty. <sup>[14]</sup> |
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| ====== Types and Symptoms ====== | ====== Types and Symptoms ====== | ||
| - | **Major depressive disorder**: also known as unipolar disorder; severe form of depression. A person with major depressive disorder has had at least one episode of severe depression that lasted almost everyday for at least two weeks. <sup>[1]</sup> | + | **Major depressive disorder**: also known as unipolar disorder; severe form of depression. A person with major depressive disorder has had at least one episode of severe depression that lasted almost everyday for at least two weeks. <sup>[3]</sup> |
| - | During the episode, the individual has felt at least five of the following symptoms: | + | During the episode, the individual has felt at least five of the following symptoms <sup>[1]</sup>: |
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| * feelings of low self-esteem or guilt | * feelings of low self-esteem or guilt | ||
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| - | **Persistent depressive disorder:** previously known as Dysthymic disorder; mild, chronic form of depression<sup>[10]</sup>. A person with persistent depressive disorder has experienced milder symptoms of depression, including: | + | **Persistent depressive disorder:** previously known as Dysthymic disorder <sup>[11]</sup>; mild, chronic form of depression. A person with persistent depressive disorder has experienced milder symptoms of depression, including <sup>[11]</sup>: |
| * increase or decrease in appetite | * increase or decrease in appetite | ||
| * feelings of low self-esteem or guilt | * feelings of low self-esteem or guilt | ||
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| **Cyclothymic disorder**: mild, chronic form of Bipolar disorder. A person with cyclothymic disorder experiences both hypomanic episodes and milder symptoms of major depressive disorder for most days for at least two years, with the symptoms being absent for no more than two months at once during that period <sup>[6]</sup>. | **Cyclothymic disorder**: mild, chronic form of Bipolar disorder. A person with cyclothymic disorder experiences both hypomanic episodes and milder symptoms of major depressive disorder for most days for at least two years, with the symptoms being absent for no more than two months at once during that period <sup>[6]</sup>. | ||
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| ====== Risk Factors ====== | ====== Risk Factors ====== | ||
| - | Almost all community epidemiological studies find that gender, age, and marital status are associated with depression <sup>[11]</sup>. Depression usually presents during the teens, 20s and 30s in both men and women. Women are two times more likely to be diagnosed with depression, but it is still not yet clear whether this is in part due to women being more likely to seek treatment. Individuals who are separated or divorced have significantly higher rates of major depression than the currently married and prevalence of major depression generally goes down with age. | + | Almost all community epidemiological studies find that gender, age, and marital status are associated with depression <sup>[12]</sup>. Depression usually presents during the teens, 20s and 30s in both men and women. Women are two times more likely to be diagnosed with depression, but it is still not yet clear whether this is in part due to women being more likely to seek treatment. Individuals who are separated or divorced have significantly higher rates of major depression than the currently married and prevalence of major depression generally goes down with age. |
| Factors that seem to increase the risk of developing or triggering depression include <sup>[8]</sup>: | Factors that seem to increase the risk of developing or triggering depression include <sup>[8]</sup>: | ||
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| * Certain prescription drugs | * Certain prescription drugs | ||
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| ====== Pathophysiology ====== | ====== Pathophysiology ====== | ||
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| Abnormalities in the cortisol response to stress may underlie depression. The black arrows in Figure 2 show that in response to stress, which is perceived by the brain cortex and the amygdala and transmitted to the hypothalamus, corticotropin-releasing hormone (CRH) is released. This induces the anterior pituitary gland to secrete corticotropin into the bloodstream. Corticotropin stimulates the adrenal cortexes to secrete the glucocorticoid hormone cortisol. The red line in Figure 2 shows that cortisol, in turn, induces feedback inhibition in the hypothalamus and the pituitary, suppressing the production of CRH and corticotropin, respectively. Activation of hippocampal glucocorticoid receptors by cortisol normally leads to feedback inhibition of the HPA axis. In depressed patients this feedback is disrupted thus leading to the hyperactivation of HPA. A molecular basis for the diminished hippocampal response to cortisol is a decreased number of glucocorticoid receptors. The number of receptors is regulated by genes, monoamines and early childhood experiences. Findings in patients with depression that support the hypothalamic–pituitary–cortisol hypothesis include the following: cortisol levels are sometimes increased in severe depression, the size of the anterior pituitary and adrenal cortex is increased, and CRH levels in the cerebrospinal fluid and CRH expression in the limbic brain regions are increased. Furthermore, hippocampal size and the numbers of neurons and glia are decreased, possibly reflecting reduced neurogenesis due to elevated cortisol levels or due to reduced brain-derived neurotrophic factor. <sup>[7]</sup> | Abnormalities in the cortisol response to stress may underlie depression. The black arrows in Figure 2 show that in response to stress, which is perceived by the brain cortex and the amygdala and transmitted to the hypothalamus, corticotropin-releasing hormone (CRH) is released. This induces the anterior pituitary gland to secrete corticotropin into the bloodstream. Corticotropin stimulates the adrenal cortexes to secrete the glucocorticoid hormone cortisol. The red line in Figure 2 shows that cortisol, in turn, induces feedback inhibition in the hypothalamus and the pituitary, suppressing the production of CRH and corticotropin, respectively. Activation of hippocampal glucocorticoid receptors by cortisol normally leads to feedback inhibition of the HPA axis. In depressed patients this feedback is disrupted thus leading to the hyperactivation of HPA. A molecular basis for the diminished hippocampal response to cortisol is a decreased number of glucocorticoid receptors. The number of receptors is regulated by genes, monoamines and early childhood experiences. Findings in patients with depression that support the hypothalamic–pituitary–cortisol hypothesis include the following: cortisol levels are sometimes increased in severe depression, the size of the anterior pituitary and adrenal cortex is increased, and CRH levels in the cerebrospinal fluid and CRH expression in the limbic brain regions are increased. Furthermore, hippocampal size and the numbers of neurons and glia are decreased, possibly reflecting reduced neurogenesis due to elevated cortisol levels or due to reduced brain-derived neurotrophic factor. <sup>[7]</sup> | ||
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| ====== Treatment ====== | ====== Treatment ====== | ||
| - | There are several known, effective treatments for depression that vary from medicinal to psychological in nature. Despite these known methods, fewer than half of those affected in the world receive them. Barriers to effective care include a lack of resources, misdiagnosis, a lack of trained health care providers, and social stigma associated with mental disorders. | + | There are several known, effective treatments for depression that vary from medicinal to psychological in nature. Despite these known methods, fewer than half of those affected in the world receive them. Barriers to effective care include a lack of resources, misdiagnosis, a lack of trained health care providers, and social stigma associated with mental disorders. <sup>[12]</sup> |
| **Antidepressant:** Two of the major classes of drugs used to treat this disorder are Selective Serotonin Reuptake Inhibitors (SSRIs) and Serotonin–norepinephrine reuptake inhibitors (SNRIs). The mechanisms of these drugs are described below. | **Antidepressant:** Two of the major classes of drugs used to treat this disorder are Selective Serotonin Reuptake Inhibitors (SSRIs) and Serotonin–norepinephrine reuptake inhibitors (SNRIs). The mechanisms of these drugs are described below. | ||
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| - | **SSRIs:** As the name suggests, these drugs prevent the reuptake of serotonin. They do this by inhibiting a monoamine transporter protein, SERT [Figure 3], that transports serotonin from the synaptic cleft to the presynaptic neuron. The SSRIs block the reuptake of serotonin, leading to increased concentrations of the neurotransmitter in the synaptic cleft [Figure 3] and, ultimately, to greater postsynaptic neuronal activity. SSRIs are actually a “successor” to SNRIs, as they are “selective” to serotonin, and usually do not affect other hormones in the nervous system. They are by far the most common drugs prescribed. Some examples of SSRIs include: Fluoxetine (Prozac), sertraline (Zoloft), and citalopram (Celexa). Side effects include: Sexual Dysfunction, Sleep Disorders, and headaches if treatment is suddenly stopped <sup>[12]</sup>. | + | **SSRIs:** As the name suggests, these drugs prevent the reuptake of serotonin. They do this by inhibiting a monoamine transporter protein, SERT [Figure 3], that transports serotonin from the synaptic cleft to the presynaptic neuron. The SSRIs block the reuptake of serotonin, leading to increased concentrations of the neurotransmitter in the synaptic cleft [Figure 3] and, ultimately, to greater postsynaptic neuronal activity. SSRIs are actually a “successor” to SNRIs, as they are “selective” to serotonin, and usually do not affect other hormones in the nervous system. They are by far the most common drugs prescribed. Some examples of SSRIs include: Fluoxetine (Prozac), sertraline (Zoloft), and citalopram (Celexa). Side effects include: Sexual Dysfunction, Sleep Disorders, and headaches if treatment is suddenly stopped <sup>[13]</sup>. |
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| - | **SNRIs:** Like SSRIs, SNRIs prevent the reuptake of serotonin by inhibiting the activity of neurotransmitters. Unlike SSRIs, SNRIs also prevent the reuptake of the neurotransmitter Norepinephrine. These can be thought of as the less refined predecessor to SSRIs. Another class of antidepressants, known as tricyclic antidepressant (TCAs), also act in the same way as SNRIs. <sup>[12]</sup> | + | **SNRIs:** Like SSRIs, SNRIs prevent the reuptake of serotonin by inhibiting the activity of neurotransmitters. Unlike SSRIs, SNRIs also prevent the reuptake of the neurotransmitter Norepinephrine. These can be thought of as the less refined predecessor to SSRIs. Another class of antidepressants, known as tricyclic antidepressant (TCAs), also act in the same way as SNRIs. <sup>[13]</sup> |
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| + | ====== Conclusion ====== | ||
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| + | Overall, depression is a heterogenous, burdensome disorder that exhibits a highly variable course, an inconsistent response to treatment and an incomplete understanding of the underlying neurobiology. Its onset is gradual and it can manifest itself not only in psychological symptoms but physical symptoms as well. Future initiatives are focusing on novel treatments that can start to take effect quicker than the 4-5 weeks required for antidepressants. Research is beginning to look at the use of theta-burst stimulation which involves delivering magnetic pulses to the brain. It is a fast acting, simple, non invasive form of treatment. These magnetic pulses stimulate electric current in the brain and the hope is that repeated treatment can capitalize on the brain's neuroplasticity by changing the way in which the brain's neurons fire. However, this is a very new field and much more research needs to be done surrounding the efficacy and safety of this treatment. | ||
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| ====== References ====== | ====== References ====== | ||
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| - | [10] John M. Grohol, Psy.D. (2013). DSM-5 Changes: Depression & Depressive Disorders. Psych Central. | + | [10] Jacquart D. "The Influence of Arabic Medicine in the Medieval West" in Morrison & Rashed 1996, pp. 980 |
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| + | [11] John M. Grohol, Psy.D. (2013). DSM-5 Changes: Depression & Depressive Disorders. Psych Central. | ||
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| + | [12] Kessler, R. C., & Bromet, E. J. (2013). The epidemiology of depression across cultures. Annual Review of Public Health, 34, 119–138. http://doi.org/10.1146/annurev-publhealth-031912-114409 | ||
| - | [11] Kessler, R. C., & Bromet, E. J. (2013). The epidemiology of depression across cultures. Annual Review of Public Health, 34, 119–138. http://doi.org/10.1146/annurev-publhealth-031912-114409 | + | [13] Marken PA, Munro JS. Selecting a Selective Serotonin Reuptake Inhibitor: Clinically Important Distinguishing Features. Primary Care Companion to The Journal of Clinical Psychiatry. 2000;2(6):205-210 |
| - | [12] Marken PA, Munro JS. Selecting a Selective Serotonin Reuptake Inhibitor: Clinically Important Distinguishing Features. Primary Care Companion to The Journal of Clinical Psychiatry. 2000;2(6):205-210. | + | [14] Radden, J (March 2003). "Is this dame melancholy? Equating today's depression and past melancholia". Philosophy, Psychiatry, & Psychology 10 (1): 37–52. doi:10.1353/ppp.2003.0081. |
| - | [13] World Health Organization. (2008). The Global Burden of Disease 2004 update. Retrieved 24 January, 2016, from http://www.who.int/healthinfo/global_burden_disease/GBD_ report_2004update_full.pdf | + | [15] World Health Organization. (2008). The Global Burden of Disease 2004 update. Retrieved 24 January, 2016, from http://www.who.int/healthinfo/global_burden_disease/GBD_ report_2004update_full.pdf |
| - | [14] World Health Organization. (2015). Depression Fact Sheet. Retrieved 24 January, 2016, from http://www.who.int/mediacentre/factsheets/fs369/en/ | + | [16] World Health Organization. (2015). Depression Fact Sheet. Retrieved 24 January, 2016, from http://www.who.int/mediacentre/factsheets/fs369/en/ |
