Editing Estrogen (section)

====Mental health====
Estrogen is considered to play a significant role in women's [[mental health]]. Sudden estrogen withdrawal, fluctuating estrogen, and [[Period of time|periods]] of sustained low estrogen levels correlate with a significant lowering of mood. Clinical recovery from [[postnatal|postpartum]], [[perimenopause]], and [[postmenopause]] depression has been shown to be effective after levels of estrogen were stabilized and/or restored.<ref name="pmid16292022">{{cite journal | vauthors = Douma SL, Husband C, O'Donnell ME, Barwin BN, Woodend AK | title = Estrogen-related mood disorders: reproductive life cycle factors | journal = ANS. Advances in Nursing Science | volume = 28 | issue = 4 | pages = 364–375 | year = 2005 | pmid = 16292022 | doi = 10.1097/00012272-200510000-00008 | s2cid = 9172877 }}</ref><ref name="pmid16388113">{{cite journal | vauthors = Osterlund MK, Witt MR, Gustafsson JA | title = Estrogen action in mood and neurodegenerative disorders: estrogenic compounds with selective properties-the next generation of therapeutics | journal = Endocrine | volume = 28 | issue = 3 | pages = 235–242 | date = December 2005 | pmid = 16388113 | doi = 10.1385/ENDO:28:3:235 | s2cid = 8205014 }}</ref><ref name="pmid17909167">{{cite journal | vauthors = Lasiuk GC, Hegadoren KM | title = The effects of estradiol on central serotonergic systems and its relationship to mood in women | journal = Biological Research for Nursing | volume = 9 | issue = 2 | pages = 147–160 | date = October 2007 | pmid = 17909167 | doi = 10.1177/1099800407305600 | s2cid = 37965502 }}</ref> [[menstrual psychosis|Menstrual exacerbation (including menstrual psychosis)]] is typically triggered by low estrogen levels,<ref>{{cite journal | vauthors = Grigoriadis S, Seeman MV | title = The role of estrogen in schizophrenia: implications for schizophrenia practice guidelines for women | journal = Canadian Journal of Psychiatry | volume = 47 | issue = 5 | pages = 437–442 | date = June 2002 | pmid = 12085678 | doi = 10.1177/070674370204700504 | doi-access = free }}</ref> and is often mistaken for [[premenstrual dysphoric disorder]].<ref>{{cite web |title=PMDD/PMS |url=https://womensmentalhealth.org/specialty-clinics/pms-and-pmdd/ |website=The Massachusetts General Hospital Center for Women's Mental Health |access-date=12 January 2019}}</ref>

Compulsions in male lab mice, such as those in obsessive-compulsive disorder (OCD), may be caused by low estrogen levels. When estrogen levels were raised through the increased activity of the enzyme [[aromatase]] in male lab mice, OCD rituals were dramatically decreased. [[Hypothalamus|Hypothalamic]] protein levels in the gene [[catechol-O-methyl transferase|COMT]] are enhanced by increasing estrogen levels which are believed to return mice that displayed OCD rituals to normal activity. Aromatase deficiency is ultimately suspected which is involved in the synthesis of estrogen in humans and has therapeutic implications in humans having obsessive-compulsive disorder.<ref name="pmid16566897">{{cite journal | vauthors = Hill RA, McInnes KJ, Gong EC, Jones ME, Simpson ER, Boon WC | title = Estrogen deficient male mice develop compulsive behavior | journal = Biological Psychiatry | volume = 61 | issue = 3 | pages = 359–366 | date = February 2007 | pmid = 16566897 | doi = 10.1016/j.biopsych.2006.01.012 | s2cid = 22669945 }}</ref>

Local application of estrogen in the rat hippocampus has been shown to inhibit the re-uptake of [[serotonin]]. Contrarily, local application of estrogen has been shown to block the ability of [[fluvoxamine]] to slow serotonin clearance, suggesting that the same pathways which are involved in SSRI efficacy may also be affected by components of local estrogen signaling pathways.<ref name="pmid22225849">{{cite journal | vauthors = Benmansour S, Weaver RS, Barton AK, Adeniji OS, Frazer A | title = Comparison of the effects of estradiol and progesterone on serotonergic function | journal = Biological Psychiatry | volume = 71 | issue = 7 | pages = 633–641 | date = April 2012 | pmid = 22225849 | pmc = 3307822 | doi = 10.1016/j.biopsych.2011.11.023 }}</ref>