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[[HPA axis|HPA-axis]] abnormalities have been suggested in depression given the association of [[CRHR1]] with depression and the increased frequency of [[Dexamethasone suppression test|dexamethasone test]] non-suppression in people who are depressed. However, this abnormality is not adequate as a diagnosis tool, because its sensitivity is only 44%.<ref>{{cite journal |vauthors=Arana GW, Baldessarini RJ, Ornsteen M |title=The dexamethasone suppression test for diagnosis and prognosis in psychiatry. Commentary and review |journal=Archives of General Psychiatry |volume=42 |issue=12 |pages=1193–204 |date=December 1985 |pmid=3000317 |doi=10.1001/archpsyc.1985.01790350067012}}</ref> These stress-related abnormalities are thought to be the cause of hippocampal volume reductions seen in people who are depressed.<ref>{{cite journal |vauthors=Varghese FP, Brown ES |title=The Hypothalamic-Pituitary-Adrenal Axis in Major Depressive Disorder: A Brief Primer for Primary Care Physicians |journal=Primary Care Companion to the Journal of Clinical Psychiatry |volume=3 |issue=4 |pages=151–55 |date=August 2001 |pmid=15014598 |pmc=181180 |doi=10.4088/pcc.v03n0401 }}</ref> Furthermore, a [[meta-analysis]] yielded decreased dexamethasone suppression, and increased response to psychological stressors.<ref>{{cite journal |vauthors=Lopez-Duran NL, Kovacs M, George CJ |title=Hypothalamic-pituitary-adrenal axis dysregulation in depressed children and adolescents: a meta-analysis |journal=Psychoneuroendocrinology |volume=34 |issue=9 |pages=1272–1283 |year=2009 |pmid=19406581 |pmc=2796553 |doi=10.1016/j.psyneuen.2009.03.016 }}</ref> Further abnormal results have been obscured with the [[cortisol awakening response]], with increased response being associated with depression.<ref>{{cite journal |vauthors=Dedovic K, Ngiam J |title=The cortisol awakening response and major depression: examining the evidence |journal=Neuropsychiatric Disease and Treatment |volume=11 |pages=1181–1189 |year=2015 |pmid=25999722 |pmc=4437603 |doi=10.2147/NDT.S62289 |doi-access=free }}</ref>
There is also a connection between the gut microbiome and the central nervous system, otherwise known as the [[Gut–brain axis|Gut-Brain axis]], which is a two-way communication system between the brain and the gut. Experiments have shown that [[microbiota]] in the gut can play an important role in depression as people with MDD often have gut-brain dysfunction. One analysis showed that those with MDD have different bacteria living in their guts. Bacteria ''[[Bacteroidota|Bacteroidetes]]'' and ''Firmicutes'' were most affected in people with MDD, and they are also impacted in people with Irritable Bowel Syndrome.<ref name=":0">{{cite journal | vauthors = Zhu F, Tu H, Chen T | title = The Microbiota-Gut-Brain Axis in Depression: The Potential Pathophysiological Mechanisms and Microbiota Combined Antidepression Effect | journal = Nutrients | volume = 14 | issue = 10 | pages = 2081 | date = May 2022 | pmid = 35631224 | pmc = 9144102 | doi = 10.3390/nu14102081 | doi-access = free }}</ref> Another study showed that people with IBS have a higher chance of developing depression, which shows the two are connected.<ref>{{cite journal | vauthors = Fond G, Loundou A, Hamdani N, Boukouaci W, Dargel A, Oliveira J, Roger M, Tamouza R, Leboyer M, Boyer L | title = Anxiety and depression comorbidities in irritable bowel syndrome (IBS): a systematic review and meta-analysis | journal = European Archives of Psychiatry and Clinical Neuroscience | volume = 264 | issue = 8 | pages = 651–660 | date = December 2014 | pmid = 24705634 | doi = 10.1007/s00406-014-0502-z }}</ref> There is even evidence suggesting that altering the microbes in the gut can have regulatory effects on developing depression.
Theories unifying [[neuroimaging]] findings have been proposed. The first model proposed is the limbic-cortical model, which involves hyperactivity of the ventral paralimbic regions and hypoactivity of frontal regulatory regions in emotional processing.<ref>{{cite journal |vauthors=Mayberg HS |title=Limbic-cortical dysregulation: a proposed model of depression |journal=The Journal of Neuropsychiatry and Clinical Neurosciences |volume=9 |issue=3 |pages=471–81 |year=1997 |pmid=9276848 |doi=10.1176/jnp.9.3.471}}</ref> Another model, the cortico-striatal model, suggests that abnormalities of the [[prefrontal cortex]] in regulating striatal and subcortical structures result in depression.<ref>{{cite journal |vauthors=Graham J, Salimi-Khorshidi G, Hagan C, Walsh N, Goodyer I, Lennox B, Suckling J |title=Meta-analytic evidence for neuroimaging models of depression: state or trait? |journal=Journal of Affective Disorders |volume=151 |issue=2 |pages=423–431 |year=2013 |pmid=23890584 |doi=10.1016/j.jad.2013.07.002 |doi-access=free }}</ref> Another model proposes hyperactivity of [[Salience network|salience structures]] in identifying negative stimuli, and hypoactivity of cortical regulatory structures resulting in a negative [[emotional bias]] and depression, consistent with emotional bias studies.<ref>{{cite journal |vauthors=Hamilton JP, Etkin A, Furman DJ, Lemus MG, Johnson RF, Gotlib IH |title=Functional neuroimaging of major depressive disorder: a meta-analysis and new integration of base line activation and neural response data |journal=The American Journal of Psychiatry |volume=169 |issue=7 |pages=693–703 |date=July 2012 |pmid=22535198 |doi=10.1176/appi.ajp.2012.11071105 }}</ref>
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The newer field of [[psychoneuroimmunology]], the study between the immune system and the nervous system and emotional state, suggests that cytokines may impact depression.
[[Depression and immune function|Immune system abnormalities]] have been observed, including increased levels of [[cytokines]] -cells produced by immune cells that affect inflammation- involved in generating [[sickness behavior]], creating a pro-inflammatory profile in MDD.<ref>{{cite journal | vauthors = Krishnadas R, Cavanagh J | title = Depression: an inflammatory illness? | journal = Journal of Neurology, Neurosurgery, and Psychiatry | volume = 83 | issue = 5 | pages = 495–502 | date = May 2012 | pmid = 22423117 | doi = 10.1136/jnnp-2011-301779 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Patel A | title = Review: the role of inflammation in depression | journal = Psychiatria Danubina | volume = 25 | issue = Suppl 2 | pages = S216–S223 | date = September 2013 | pmid = 23995180 }}</ref><ref>{{cite journal | vauthors = Dowlati Y, Herrmann N, Swardfager W, Liu H, Sham L, Reim EK, Lanctôt KL | title = A meta-analysis of cytokines in major depression | journal = Biological Psychiatry | volume = 67 | issue = 5 | pages = 446–457 | date = March 2010 | pmid = 20015486 | doi = 10.1016/j.biopsych.2009.09.033 | s2cid = 230209 }}</ref> Some people with depression have increased levels of pro-inflammatory cytokines and some have decreased levels of anti-inflammatory cytokines.<ref>{{cite journal | vauthors = Osimo EF, Pillinger T, Rodriguez IM, Khandaker GM, Pariante CM, Howes OD | title = Inflammatory markers in depression: A meta-analysis of mean differences and variability in 5,166 patients and 5,083 controls | journal = Brain, Behavior, and Immunity | volume = 87 | pages = 901–909 | date = July 2020 | pmid = 32113908 | doi = 10.1016/j.bbi.2020.02.010 | pmc = 7327519 }}</ref> Research suggests that treatments can reduce pro-inflammatory cell production, like the experimental treatment of ketamine with treatment-resistant depression.<ref>{{cite journal | vauthors = Sukhram SD, Yilmaz G, Gu J | title = Antidepressant Effect of Ketamine on Inflammation-Mediated Cytokine Dysregulation in Adults with Treatment-Resistant Depression: Rapid Systematic Review | journal = Oxidative Medicine and Cellular Longevity | volume = 2022 | pages = 1061274 | date = 2022-09-16 | pmid = 36160713 | pmc = 9507757 | doi = 10.1155/2022/1061274 | doi-access = free | editor-first = Ajinkya | editor-last = Sase }}</ref> With this, in MDD, people will more likely have a Th-1 dominant immune profile, which is a pro-inflammatory profile. This suggests that there are components of the immune system affecting the pathology of MDD.
Another way [[Cytokine|cytokines]] can affect depression is in the [[kynurenine pathway]], and when this is overactivated, it can cause depression. This can be due to too much [[Microglia|microglial]] activation and too little [[Astrocyte|astrocytic]] activity. When microglia get activated, they release pro-inflammatory cytokines that cause an increase in the production of [[Cytochrome c oxidase subunit 2|COX<sub>2</sub>]]. This, in turn, causes the production of [[Prostaglandin E2|PGE<sub>2</sub>]], which is a [[prostaglandin]], and this catalyzes the production of [[Indolamines|indolamine]], IDO. IDO causes [[tryptophan]] to get converted into [[kynurenine]] and kynurenine becomes [[quinolinic acid]].<ref>{{cite journal | vauthors = McNally L, Bhagwagar Z, Hannestad J | title = Inflammation, glutamate, and glia in depression: a literature review | journal = CNS Spectrums | volume = 13 | issue = 6 | pages = 501–510 | date = June 2008 | pmid = 18567974 | doi = 10.1017/S1092852900016734 }}</ref> Quinolinic acid is an agonist for [[N-Methyl-D-aspartic acid|NMDA]] receptors, so it activates the pathway. Studies have shown that the post-mortem brains of patients with MDD have higher levels of quinolinic acid than people who did not have MDD. With this, researchers have also seen that the concentration of quinolinic acid correlates to the severity of depressive symptoms.<ref>{{cite journal | vauthors = Hestad K, Alexander J, Rootwelt H, Aaseth JO | title = The Role of Tryptophan Dysmetabolism and Quinolinic Acid in Depressive and Neurodegenerative Diseases | journal = Biomolecules | volume = 12 | issue = 7 | pages = 998 | date = July 2022 | pmid = 35883554 | pmc = 9313172 | doi = 10.3390/biom12070998 | doi-access = free }}</ref><!--
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There is a small amount of evidence that [[sleep deprivation]] may improve depressive symptoms in some individuals,<ref>{{cite journal |vauthors=Ioannou M, Wartenberg C, Greenbrook JT, et al |title=Sleep deprivation as treatment for depression: Systematic review and meta-analysis |journal=Acta Psychiatr Scand |volume=143 |issue=1 |pages=22–35 |date=January 2021 |pmid=33145770 |pmc=7839702 |doi=10.1111/acps.13253 }}</ref> with the effects usually showing up within a day. This effect is usually temporary. Besides sleepiness, this method can cause a side effect of [[mania]] or [[hypomania]].<ref>{{cite journal |vauthors=Giedke H, Schwärzler F |title=Therapeutic use of sleep deprivation in depression |journal=Sleep Medicine Reviews |volume=6 |issue=5 |pages=361–77 |date=October 2002 |pmid=12531127 |doi=10.1053/smrv.2002.0235 }}</ref> There is insufficient evidence for [[Reiki]]<ref>{{cite journal | vauthors = Joyce J, Herbison GP | title = Reiki for depression and anxiety | journal = The Cochrane Database of Systematic Reviews | issue = 4 | pages = CD006833 | date = April 2015 | pmid = 25835541 | doi = 10.1002/14651858.cd006833.pub2 | pmc = 11088458 }}</ref> and [[dance movement therapy]] in depression.<ref>{{cite journal | vauthors = Meekums B, Karkou V, Nelson EA | title = Dance movement therapy for depression | journal = The Cochrane Database of Systematic Reviews | issue = 2 | pages = CD009895 | date = February 2015 | volume = 2016 | pmid = 25695871 | doi = 10.1002/14651858.cd009895.pub2 | pmc = 8928931 | url = http://eprints.whiterose.ac.uk/87222/8/Meekums_et_al-2015-The_Cochrane_Library.pdf }}</ref> [[Medical cannabis|Cannabis]] is specifically not recommended as a treatment.<ref>{{cite journal | vauthors = Black N, Stockings E, Campbell G, et al | title = Cannabinoids for the treatment of mental disorders and symptoms of mental disorders: a systematic review and meta-analysis | journal = The Lancet. Psychiatry | volume = 6 | issue = 12 | pages = 995–1010 | date = December 2019 | pmid = 31672337 | pmc = 6949116 | doi = 10.1016/S2215-0366(19)30401-8 }}</ref>
The [[Human microbiome|microbiome]] of people with major depressive disorder differs from that of healthy people, and [[probiotic]] and [[Synbiotics|synbiotic]] treatment may achieve a modest depressive symptom reduction.<ref>{{cite journal | vauthors = Sanada K, Nakajima S, Kurokawa S, Barceló-Soler A, Ikuse D, Hirata A, Yoshizawa A, Tomizawa Y, Salas-Valero M, Noda Y, Mimura M, Iwanami A, Kishimoto T | title = Gut microbiota and major depressive disorder: A systematic review and meta-analysis | journal = Journal of Affective Disorders | volume = 266 | pages = 1–13 | date = April 2020 | pmid = 32056863 | doi = 10.1016/j.jad.2020.01.102 }}</ref><ref>{{cite journal | vauthors = Alli SR, Gorbovskaya I, Liu JC, Kolla NJ, Brown L, Müller DJ | title = The Gut Microbiome in Depression and Potential Benefit of Prebiotics, Probiotics and Synbiotics: A Systematic Review of Clinical Trials and Observational Studies | journal = International Journal of Molecular Sciences | volume = 23 | issue = 9 | pages = 4494 | date = April 2022 | pmid = 35562885 | pmc = 9101152 | doi = 10.3390/ijms23094494 | doi-access = free }}</ref> With this, [[Fecal microbiota transplant|fecal microbiota transplants]] (FMT) are being researched as add-on therapy treatments for people who do not respond to typical therapies. It has been shown that the patient's depressive symptoms improved, with minor gastrointestinal issues, after a FMT, with improvements in symptoms lasting at least 4 weeks after the transplant.
==Prognosis==
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Major depressive disorder affected approximately 163 million people in 2017 (2% of the global population).<ref name="GBD 2017 prevalence">{{cite journal |author=((GBD 2017 Disease and Injury Incidence and Prevalence Collaborators)) |date=10 November 2018 |title=Global, regional, and national incidence, prevalence, and years lived with disability for 354 diseases and injuries for 195 countries and territories, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017 |journal=Lancet |volume=392 |issue=10159 |pages=1789–1858 |doi=10.1016/S0140-6736(18)32279-7 |pmc=6227754 |pmid=30496104}}</ref> The percentage of people who are affected at one point in their life varies from 7% in Japan to 21% in France. In most countries the number of people who have depression during their lives falls within an 8–18% range. Lifetime rates are higher in the [[developed world]] (15%) compared to the [[developing world]] (11%).<ref name="Kes2013" />
In the United States, 8.4% of adults (21 million individuals) have at least one episode within a year-long period; the probability of having a major depressive episode is higher for females than males (10.5% to 6.2%), and highest for those aged 18 to 25 (17%).<ref name= NIMHMajorDepression>{{cite web |url= https://www.nimh.nih.gov/health/statistics/major-depression |publisher= U.S. [[National Institute of Mental Health]] (NIMH) |date= January 2022 |title= Major depression |archive-url=https://web.archive.org/web/20220809144808/https://www.nimh.nih.gov/health/statistics/major-depression |archive-date= 9 August 2022 |access-date= 14 August 2022}} {{Pd-notice}}</ref> 15% of adolescents, ages 12 to 17, in America are also affected by depression, which is equal to 3.7 million teenagers.
Major depression is about twice as common in women as in men, although it is unclear why this is so, and whether factors unaccounted for are contributing to this.<ref name=Kuehner03>{{cite journal |vauthors=Kuehner C |title=Gender differences in unipolar depression: an update of epidemiological findings and possible explanations |journal=Acta Psychiatrica Scandinavica |volume=108 |issue=3 |pages=163–74 |date=September 2003 |pmid=12890270 |doi=10.1034/j.1600-0447.2003.00204.x |s2cid=19538251 }}</ref> The relative increase in occurrence is related to pubertal development rather than chronological age, reaches adult ratios between the ages of 15 and 18, and appears associated with psychosocial more than hormonal factors.<ref name=Kuehner03 /> In 2019, major depressive disorder was identified (using either the DSM-IV-TR or ICD-10) in the [[Global Burden of Disease Study]] as the fifth most common cause of [[years lived with disability]] and the 18th most common for [[disability-adjusted life years]].<ref>{{citation |author=Institute for Health Metrics and Evaluation |author-link=Institute for Health Metrics and Evaluation |year=2020 |title=Global Burden of Disease 2019 Cause and Risk Summary: Major depressive disorder — Level 4 cause |at=Table 3 |url=https://www.healthdata.org/results/gbd_summaries/2019/major-depressive-disorder-level-4-cause |publisher=University of Washington |place=Seattle, US |access-date=9 July 2022}}</ref><!-- the wording of this sentence is very janky, but this best mimics the source. -->
People are most likely to develop their first depressive episode between the ages of 30 and 40, and there is a second, smaller peak of incidence between ages 50 and 60.<ref>{{cite journal |vauthors=Eaton WW, Anthony JC, Gallo J, et al |title=Natural history of Diagnostic Interview Schedule/DSM-IV major depression. The Baltimore Epidemiologic Catchment Area follow-up |journal=Archives of General Psychiatry |volume=54 |issue=11 |pages=993–99 |date=November 1997 |pmid=9366655 |doi=10.1001/archpsyc.1997.01830230023003 }}</ref> The risk of major depression is increased with neurological conditions such as [[stroke]], [[Parkinson's disease]], or [[multiple sclerosis]], and during the first year after childbirth ([[Postpartum depression
Major depression was the leading cause of [[disease burden]] in North America and other high-income countries, and the fourth-leading cause worldwide as of 2006. In the year 2030, it is predicted to be the second-leading cause of disease burden worldwide after [[HIV]], according to the WHO.<ref>{{cite journal |vauthors=Mathers CD, Loncar D |title=Projections of global mortality and burden of disease from 2002 to 2030 |journal=PLOS Medicine |volume=3 |issue=11 |page=e442 |date=November 2006 |pmid=17132052 |pmc=1664601 |doi=10.1371/journal.pmed.0030442 |doi-access=free }}</ref> Delay or failure in seeking treatment after relapse and the failure of health professionals to provide treatment are two barriers to reducing disability.<ref>{{cite journal |vauthors=Andrews G |title=Reducing the burden of depression |journal=Canadian Journal of Psychiatry |volume=53 |issue=7 |pages=420–27 |date=July 2008 |pmid=18674396 |doi=10.1177/070674370805300703|doi-access=free }}</ref>
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