Editing Dehydroepiandrosterone (section)

===Biosynthesis===
DHEA is produced in the [[zona reticularis]] of the [[adrenal cortex]] under the control of [[adrenocorticotropic hormone]] (ACTH) and by the [[gonad]]s under the control of [[gonadotropin-releasing hormone]] (GnRH).<ref name="Erkkola2006">{{cite book | first = Risto | last = Erkkola | name-list-style = vanc |title=The Menopause|url=https://books.google.com/books?id=1AU_NI__fpUC&pg=PA5|year=2006|publisher=Elsevier|isbn=978-0-444-51830-9|pages=5–}}</ref><ref name="KleineRossmanith2016">{{cite book| first1 = Bernhard | last1 = Kleine | first2 = Winfried G. | last2 = Rossmanith | name-list-style = vanc | title=Hormones and the Endocrine System: Textbook of Endocrinology|url=https://books.google.com/books?id=boqRCwAAQBAJ&pg=PA264|date=11 February 2016|publisher=Springer|isbn=978-3-319-15060-4|pages=264–265}}</ref> It is also produced in the brain.<ref name="Pizzorno2013">{{cite book | first = Joseph E. | last = Pizzorno | name-list-style = vanc |title=Textbook of Natural Medicine|url=https://books.google.com/books?id=6cjgo1IixvEC&pg=PA711|year=2013|publisher=Elsevier Health Sciences|isbn=978-1-4377-2333-5|pages=711–}}</ref> DHEA is synthesized from [[cholesterol]] via the [[enzyme]]s [[cholesterol side-chain cleavage enzyme]] (CYP11A1; P450scc) and [[17α-hydroxylase/17,20-lyase]] (CYP17A1), with [[pregnenolone]] and [[17α-hydroxypregnenolone]] as [[metabolic intermediate|intermediate]]s.<ref name="pmid17945481">{{cite journal | vauthors = Rainey WE, Nakamura Y | title = Regulation of the adrenal androgen biosynthesis | journal = The Journal of Steroid Biochemistry and Molecular Biology | volume = 108 | issue = 3–5 | pages = 281–6 | date = February 2008 | pmid = 17945481 | pmc = 2699571 | doi = 10.1016/j.jsbmb.2007.09.015 }}</ref> It is derived mostly from the [[adrenal cortex]], with only about 10% being secreted from the [[gonad]]s.<ref name="Adler2009">{{cite book | first = Robert A. | last = Adler | name-list-style = vanc |title=Osteoporosis: Pathophysiology and Clinical Management|url=https://books.google.com/books?id=eShjlIWB7gEC&pg=PA387|date=14 December 2009|publisher=Springer Science & Business Media|isbn=978-1-934115-19-0|pages=387–}}</ref><ref name="SchillComhaire2006">{{cite book | first1=  Wolf-Bernhard | last1 = Schill | first2 = Frank H. | last2 = Comhaire | first3 = Timothy B. | last3 = Hargreave | name-list-style = vanc |title=Andrology for the Clinician|url=https://books.google.com/books?id=5Ts_AAAAQBAJ&pg=PA243|date=26 August 2006|publisher=Springer Science & Business Media|isbn=978-3-540-33713-3|pages=243–}}</ref><ref name="LinosHeerden2005">{{cite book | first1 = Dimitrios A. | last1 = Linos | first2 = Jon A. | last2 = van Heerden | name-list-style = vanc |title=Adrenal Glands: Diagnostic Aspects and Surgical Therapy|url=https://books.google.com/books?id=r8OLj1LLw3IC&pg=PA161|date=5 December 2005|publisher=Springer Science & Business Media|isbn=978-3-540-26861-1|pages=161–}}</ref> Approximately 50 to 70% of circulating DHEA originates from desulfation of DHEA-S in peripheral tissues.<ref name="Adler2009" /> DHEA-S itself originates almost exclusively from the adrenal cortex, with 95 to 100% being secreted from the adrenal cortex in women.<ref name="Erkkola2006"/><ref name="LinosHeerden2005" />

====Increasing endogenous production====
Regular exercise is known to increase DHEA production in the body.<ref>{{cite journal | vauthors = Filaire E, Duché P, Lac G | title = Effects of amount of training on the saliva concentrations of cortisol, dehydroepiandrosterone and on the dehydroepiandrosterone: cortisol concentration ratio in women over 16 weeks of training | journal = European Journal of Applied Physiology and Occupational Physiology | volume = 78 | issue = 5 | pages = 466–71 | date = October 1998 | pmid = 9809849 | doi = 10.1007/s004210050447 | s2cid = 20583279 }}</ref><ref>{{cite journal | vauthors = Copeland JL, Consitt LA, Tremblay MS | title = Hormonal responses to endurance and resistance exercise in females aged 19-69 years | journal = The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences | volume = 57 | issue = 4 | pages = B158–65 | date = April 2002 | pmid = 11909881 | doi = 10.1093/gerona/57.4.B158 | doi-access = free }}</ref> [[Calorie restriction]] has also been shown to increase DHEA in primates.<ref>{{cite journal | vauthors = Mattison JA, Lane MA, Roth GS, Ingram DK | title = Calorie restriction in rhesus monkeys | journal = Experimental Gerontology | volume = 38 | issue = 1–2 | pages = 35–46 | year = 2003 | pmid = 12543259 | doi = 10.1016/S0531-5565(02)00146-8 | s2cid = 41481691 | url = https://zenodo.org/record/1260075 }}.</ref> Some theorize that the increase in endogenous DHEA brought about by calorie restriction is partially responsible for the longer life expectancy known to be associated with calorie restriction.<ref>{{cite journal | vauthors = Roberts E | title = The importance of being dehydroepiandrosterone sulfate (in the blood of primates): a longer and healthier life? | journal = Biochemical Pharmacology | volume = 57 | issue = 4 | pages = 329–46 | date = February 1999 | pmid = 9933021 | doi = 10.1016/S0006-2952(98)00246-9 }}.</ref>