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The prevalence rates of MAD according to the DSM-IV is approximately 1.3-2% [1]. When evaluating patients with MAD, it is found that these individuals are more likely to have less depressive episodes and be more anxious in comparison to patients with major depression[1]. Individuals diagnosed with major depression have a 3.3 ratio to 8.2 ratio increased likelihood of suffering from a comorbid anxiety disorder [2]. With this being said, 50% of those who meet the criteria of major depression also have anxiety [2]. This can show that those who suffer from depression may raise their chances of developing MAD. When compared to non-diagnosed patients, those diagnosed with MAD have higher rates of family with depression and anxiety, and have major life events or chronic disease[1].

[1] Balestrieri, M., Isola, M., Quartaroli, M., Roncolato, M., & Bellantuono, C. (2010, February

04). Assessing mixed anxiety-depressive disorder. A national primary care survey.

Retrieved November 20, 2020, from

https://www.sciencedirect.com/science/article/pii/S0165178108004071

[2] Hirschfield, R. M. (2001). The Comorbidity of Major Depression and Anxiety Disorders. The

Primary Care Companion to The Journal of Clinical Psychiatry, 03(06), 244-254. doi:10.4088/pcc.v03n0609

Up to 25% of general practice patients are diagnosed with co-morbid anxiety and depression.[1] The comorbidity of these disorders are explained by either shared genetics to both anxiety and depression or from one disorder increasing the likelihood of developing the other.[1] Anxiety and depression may also coincide due to the neurological relationship of hormones, neurotransmitters, and HPA dysregulation. Hormones are your body's chemical messengers, and travel through your bloodstream to help control how certain cells and organs do their work. Their behavior is altered when a person struggles with Mixed Anxiety-Depressive Disorder (MADD), including the corticotropin-releasing hormone (CRH). CRH is involved with regulating the stress response and is dysregulated in MADD, as an increased amount of CRH in cerebrospinal fluid has been reported in both anxiety and depression.[1] However, other neurotransmitters and hormones controlled by your HPA (hypothalamic-pituitary-adrenal axis) are regulated differently in the two disorders.[1] The HPA is a neuroendocrine unit comprised of the hypothalamus, pituitary gland, and adrenal glands, which plays key roles in maintaining homeostasis and the body's response to stress. Cortical areas of the brain such as the OFC (orbito-frontal cortex) demonstrate altered activity patterns in patients with MADD.[2] The OFC is found in the prefrontal cortex of the brain, just above your eye sockets, and shares connections with sensory areas as well as limbic system structures involved in emotion and memory. This area is linked to an overproduction of a neurotransmitter called serotonin in patients with MADD.[2]


 * 1) ^ Jump up to:a b c d John W G, Miller (October 1, 2012). "Depression and anxiety". Medical Journal of Australia: 4 – via JSTOR.


 * 1) ^ Jump up to:a b Möller, Hans-Jürgen; Bandelow, Borwin; Volz, Hans-Peter; Barnikol, Utako Birgit; Seifritz, Erich; Kasper, Siegfried (2016-12). "The relevance of 'mixed anxiety and depression' as a diagnostic category in clinical practice". European Archives of Psychiatry and Clinical Neuroscience. 266 (8): 725–736. doi:10.1007/s00406-016-0684-7. ISSN 0940-1334. PMC 5097109. PMID 27002521 . Check date values in: |date= (help)

Mixed anxiety-depressive disorder causes significant impairments in social functioning.[1] Patients with this comorbidity suffer from more social impairments than those with anxiety or depression alone.[1] Findings have shown that the depressive symptoms of mixed anxiety-depressive disorder have a stronger association with social impairments than anxiety-related symptoms.[1] Similar to patients with anxiety or depression, people with mixed anxiety-depressive disorder may not view social activities or interactions as rewarding.[1] This can lead to withdrawal from others, loneliness, and perceived social disability.[1][2]

1) Saris, I., Aghajani, M., Van der Werff, S., Van der Wee, N., & Penninx, B. (2017, October). Social functioning in patients with depressive and anxiety disorders. Retrieved October 14, 2020, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5601295/

2) Kupferberg, A., Bicks, L., Hasler, G. (2016). Social functioning in major depressive disorder. Neuroscience & Biobehavioral Reviews, 69, 313-332. doi:10.1016/j.neubiorev.2016.07.002

The psychological aspect of Mixed Anxiety-Depressive Disorder or MADD refers to the symptoms and conditions that impact daily living skills and can reduce the health-related quality of life [1]. MADD has been found to be associated with childhood adversity, poor parenting, lifetime traumas, recent life events, high neuroticism, co-morbid substance use disorders, and familial aggregation [1]. It is also associated with higher disability scores and co-morbid physical conditions than having anxiety or depression alone [1]. Some symptoms may include feelings of fear and dread, an exaggerated startle reflex, poor concentration, irritability, and insomnia [2].

[2] “Is Anxiety Psychological or Physical?” Psychology Today, 2016, www.psychologytoday.com/us/blog/hide-and-seek/201608/is-anxiety-psychological-or-physical.

[1] Möller, Hans-Jürgen, et al. “The Relevance of ‘Mixed Anxiety and Depression’ as a Diagnostic Category in Clinical Practice.” European Archives of Psychiatry and Clinical Neuroscience, vol. 266, no. 8, 22 Mar. 2016, pp. 725–736, 10.1007/s00406-016-0684-7.

Mixed Anxiety-Depressive Disorder, also known as MADD or Cothymia, can be thought of as, neurologically, two ends of a spectrum occurring at the same time (Möller et al.). A primary neurotransmitter that is associated with MADD is serotonin, which is also a primary neurotransmitter in both depressive and anxiety disorders (Liu et al.). In the brain, MADD is associated with cortical areas like the orbito-frontal cortex, where serotonin is known to interfere with the inhibitory control functions, or executive functions (Möller et al.). In some studies, it has been shown that Selective Serotonin Reuptake Inhibitors (SSRIs) like Sertraline, Citalopram, and Fluvoxamine, are compellingly effective at treating MADD, as well as Silexan, which targets the serotonin receptor subtype 1A (Möller et al.).

Liu, Y., Zhao, J., & Guo, W. (2018). Emotional Roles of Mono-Aminergic Neurotransmitters in Major Depressive Disorder and Anxiety Disorders. Frontiers in psychology, 9, 2201. https://doi.org/10.3389/fpsyg.2018.02201

Möller, H. J., Bandelow, B., Volz, H. P., Barnikol, U. B., Seifritz, E., & Kasper, S. (2016). The relevance of 'mixed anxiety and depression' as a diagnostic category in clinical practice. European archives of psychiatry and clinical neuroscience, 266(8), 725–736. https://doi.org/10.1007/s00406-016-0684-7