From Wikipedia, the free encyclopedia
  (Redirected from DHEA)
Jump to: navigation, search
IUPAC name
(3S,8R,9S,10R,13S,14S)-3-hydroxy-10,13-dimethyl-1,2,3,4,7,8,9,11,12,14,15,16-dodecahydrocyclopenta[a]phenanthren-17-one; (1S,2R,5S,10R,11S,15S)-5-Hydroxy-2,15-dimethyltetracyclo[,7.011,15]heptadec-7-en-14-one
Other names
Androstenolone; Prasterone; Androst-5-en-3β-ol-17-one; 3β-Hydroxyandrost-5-en-17-one; 5,6-Didehydroepiandrosterone;[1] Dehydroisoepiandrosterone[2]
3D model (JSmol)
Molar mass 288.424 g/mol
Melting point 148.5
QA14AA07 (WHO)
G03EA03 (WHO) (combination with estrogen)
By mouth, vaginal (insert), intramuscular injection (as prasterone enanthate), injection (as prasterone sodium sulfate)
DHEA: 25 minutes[4]
DHEA-S: 11 hours[4]
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
YesY verify (what is YesYN ?)
Infobox references

Dehydroepiandrosterone (DHEA), also known as androstenolone, is an endogenous steroid hormone.[2][5] It is one of the most abundant circulating steroids in humans,[6] in whom it is produced in the adrenal glands,[7] the gonads, and the brain,[8] where it functions as a metabolic intermediate in the biosynthesis of the androgen and estrogen sex steroids.[5][9] However, DHEA also has a variety of potential biological effects in its own right, binding to an array of nuclear and cell surface receptors,[10] and acting as a neurosteroid and neurotrophin.[11]

Biological function[edit]

As an androgen[edit]

DHEA and other adrenal androgens such as androstenedione, although relatively weak androgens, are responsible for the androgenic effects of adrenarche, such as early pubic and axillary hair growth, adult-type body odor, increased oiliness of hair and skin, and mild acne.[12][13][14] Women with complete androgen insensitivity syndrome (CAIS), who have a non-functional androgen receptor (AR) and are immune to the androgenic effects of DHEA and other androgens, have absent or only sparse/scanty pubic and axillary hair and body hair in general, demonstrating the role of DHEA, testosterone, and other androgens in body hair development at both adrenarche and pubarche.[15][16][17][18]

As a neurosteroid[edit]

As a neurosteroid and neurotrophin, DHEA has important effects in the central nervous system.[19][20][21]

Biological activity[edit]

Hormonal activity[edit]

Androgen receptor[edit]

Although it functions as an endogenous precursor to more potent androgens such as testosterone and DHT, DHEA has been found to possess some degree of androgenic activity in its own right, acting as a low affinity (Ki = 1 μM), weak partial agonist of the androgen receptor (AR). However, its intrinsic activity at the receptor is quite weak, and on account of that, due to competition for binding with full agonists like testosterone, it can actually behave more like an antagonist depending on circulating testosterone and dihydrotestosterone (DHT) levels, and hence, like an antiandrogen. However, its affinity for the receptor is very low, and for that reason, is unlikely to be of much significance under normal circumstances.[22][23]

Estrogen receptors[edit]

In addition to its affinity for the androgen receptor, DHEA has also been found to bind to and activate the ERα and ERβ estrogen receptors with Ki values of 1.1 μM and 0.5 μM, respectively, and EC50 values of >1 μM and 200 nM, respectively. Though it was found to be a partial agonist of the ERα with a maximal efficacy of 30–70%, the concentrations required for this degree of activation make it unlikely that the activity of DHEA at this receptor is physiologically meaningful. Remarkably however, DHEA acts as a full agonist of the ERβ with a maximal response similar to or actually slightly greater than that of estradiol, and its levels in circulation and local tissues in the human body are high enough to activate the receptor to the same degree as that seen with circulating estradiol levels at somewhat higher than their maximal, non-ovulatory concentrations; indeed, when combined with estradiol with both at levels equivalent to those of their physiological concentrations, overall activation of the ERβ was doubled. As such, it has been proposed that DHEA may be an important and potentially major endogenous estrogen in the body.[10][22]

Other nuclear receptors[edit]

DHEA does not bind to or activate the progesterone, glucocorticoid, or mineralocorticoid receptors.[22][24] Other nuclear receptor targets of DHEA besides the androgen and estrogen receptors include the PPARα, PXR, and CAR.[25] However, whereas DHEA is a ligand of the PPARα and PXR in rodents, it is not in humans.[26] In addition to direct interactions, DHEA is thought to regulate a handful of other proteins via indirect, genomic mechanisms, including the enzymes CYP2C11 and 11β-HSD1 – the latter of which is essential for the biosynthesis of the glucocorticoids such as cortisol and has been suggested to be involved in the antiglucocorticoid effects of DHEA – and the carrier protein IGFBP1.[22][27]

Neurosteroid activity[edit]

Neurotransmitter receptors[edit]

DHEA has been found to directly act on several neurotransmitter receptors, including acting as a positive allosteric modulator of the NMDA receptor, as a negative allosteric modulator of the GABAA receptor, and as an agonist of the σ1 receptor.[28][25]

Neurotrophin receptors[edit]

In 2011, the surprising discovery was made that DHEA, as well as DHEA-S, directly bind to and activate the TrkA and p75NTR, receptors of neurotrophins like nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), with high affinity.[25][29] DHEA was subsequently also found to bind to the TrkB and TrkC with high affinity, though it notably activated the TrkC but not the TrkB.[25][30] DHEA and DHEA-S bound to these receptors with affinities that were in the low nanomolar range (around 5 nM), although the affinities were nonetheless approximately two orders of magnitude lower relative to highly potent polypeptide neurotrophins like NGF (0.01–0.1 nM).[25][29][30] In any case, DHEA and DHEA-S both circulate at requisite concentrations to activate these receptors and were thus identified as important endogenous neurotrophic factors.[25][29] They have since been labeled "steroidal microneurotrophins", due to their small-molecule and steroidal nature relative to their polypeptide neurotrophin counterparts.[31] Subsequent research has suggested that DHEA and/or DHEA-S may in fact be phylogenetically ancient "ancestral" ligands of the neurotrophin receptors from early on in the evolution of the nervous system.[25][30] The findings that DHEA binds to and potently activates neurotrophin receptors may explain the positive association between decreased circulating DHEA levels with age and age-related neurodegenerative diseases.[25][29]

Microtubule-associated protein 2[edit]

Similarly to pregnenolone, its synthetic derivative 3β-methoxypregnenolone (MAP-4343), and progesterone, DHEA has been found to bind to microtubule-associated protein 2 (MAP2), specifically the MAP2C subtype (Kd = 27 µM).[25] However, it is unclear whether DHEA increases binding of MAP2 to tubulin like pregnenolone.[25]

Other activity[edit]

G6PDH inhibitor[edit]

DHEA is an uncompetitive inhibitor of G6PDH (Ki = 17 μM; IC50 = 18.7 μM), and is able to lower NADPH levels and reduce NADPH-dependent free radical production.[32][33] It is thought that this action may possibly be responsible for much of the antiinflammatory, antihyperplastic, chemopreventative, antihyperlipidemic, antidiabetic, and antiobesic, as well as certain immunomodulating activities of DHEA (with some experimental evidence to support this notion available).[32][33][34][35] However, it has also been said that inhibition of G6PDH activity by DHEA in vivo has not been observed and that the concentrations required for DHEA to inhibit G6PDH in vitro are very high, thus making the possible contribution of G6PDH inhibition to the effects of DHEA uncertain.[33]


DHEA has been found to competitively inhibit TRPV1.[28]


Comprehensive overview of steroidogenesis, showing DHEA at left among the androgens.[36]


DHEA is produced in the zona reticularis of the adrenal cortex under the control of adrenocorticotropic hormone (ACTH) and by the gonads under the control of gonadotropin-releasing hormone (GnRH).[37][38] It is also produced in the brain.[39] DHEA is synthesized from cholesterol via the enzymes cholesterol side-chain cleavage enzyme (CYP11A1; P450scc) and 17α-hydroxylase/17,20-lyase (CYP17A1), with pregnenolone and 17α-hydroxypregnenolone as intermediates.[40] It is derived mostly from the adrenal cortex, with only about 10% being secreted from the gonads.[41][42][43] Approximately 50 to 70% of circulating DHEA originates from desulfation of DHEA-S in peripheral tissues.[41] DHEA-S itself originates almost exclusively from the adrenal cortex, with 95 to 100% being secreted from the adrenal cortex in women.[37][43]

Increasing endogenous production[edit]

Regular exercise is known to increase DHEA production in the body.[44][45] Calorie restriction has also been shown to increase DHEA in primates.[46] 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.[47] Catalpol and a combination of acetyl-carnitine and propionyl-carnitine on 1:1 ratio also improves endogenous DHEA production and release due to direct cholinergic stimulation of CRH release and an increase of IGF-1 expression respectively.


In the circulation, DHEA is mainly bound to albumin, with a small amount bound to sex hormone-binding globulin (SHBG).[48][49] The small remainder of DHEA not associated with albumin or SHBG is unbound and free in the circulation.[48]

DHEA easily crosses the blood–brain barrier into the central nervous system.[39]


DHEA is transformed into DHEA-S by sulfation at the C3β position via the sulfotransferase enzymes SULT2A1 and to a lesser extent SULT1E1.[40][50][51] This occurs naturally in the adrenal cortex and during first-pass metabolism in the liver and intestines when exogenous DHEA is administered orally.[citation needed] Levels of DHEA-S in circulation are approximately 250 to 300 times those of DHEA.[19] DHEA-S in turn can be converted back into DHEA in peripheral tissues via steroid sulfatase (STS).[52][53]

The terminal half-life of DHEA is short at only 15 to 30 minutes.[54] In contrast, the terminal half-life of DHEA-S is far longer, at 7 to 10 hours.[54] As DHEA-S can be converted back into DHEA, it serves as a circulating reservoir for DHEA, thereby extending the duration of DHEA.[55][19]

Metabolites of DHEA include DHEA-S, 7α-hydroxy-DHEA, 7β-hydroxy-DHEA, 7-keto-DHEA, 7α-hydroxyepiandrosterone, and 7β-hydroxyepiandrosterone, as well as androstenediol and androstenedione.[5]


During pregnancy, DHEA-S is metabolized into the sulfates of 16α-hydroxy-DHEA and 15α-hydroxy-DHEA in the fetal liver as intermediates in the production of the estrogens estriol and estetrol, respectively.


Prior to puberty, DHEA and DHEA-S levels elevate upon differentiation of the zona reticularis of the adrenal cortex.[25] Peak levels of DHEA and DHEA-S are observed around age 20, which is followed by an age-dependent decline throughout life eventually back to prepubertal concentrations.[25] Plasma levels of DHEA in adult men are 10–25 nM, in premenopausal women are 5–30 nM, and in postmenopausal women are 2–20 nM.[25] Conversely, DHEA-S levels are an order of magnitude higher at 1–10 μM.[25] Levels of DHEA and DHEA-S decline to the lower nanomolar and micromolar ranges in men and women aged 60 to 80 years.[25]


As almost all DHEA is derived from the adrenal glands, blood measurements of DHEA-S/DHEA are useful to detect excess adrenal activity as seen in adrenal cancer or hyperplasia, including certain forms of congenital adrenal hyperplasia. Women with polycystic ovary syndrome tend to have elevated levels of DHEA-S.[56]


DHEA, also known as androst-5-en-3β-ol-17-one, is a naturally occurring androstane steroid and a 17-ketosteroid. It is closely related structurally to androstenediol (androst-5-ene-3β,17β-diol), androstenedione (androst-4-ene-3,17-dione), and testosterone (androst-4-en-17β-ol-3-one). DHEA is the 5-dehydro analogue of epiandrosterone (5α-androstan-3β-ol-17-one) and is also known as 5-dehydroepiandrosterone or as δ5-epiandrosterone.


The term "dehydroepiandrosterone" is ambiguous chemically because it does not include the specific positions within epiandrosterone at which hydrogen atoms are missing. DHEA itself is 5,6-didehydroepiandrosterone or 5-dehydroepiandrosterone. A number of naturally occurring isomers also exist and may have similar activities. Some isomers of DHEA are 1-dehydroepiandrosterone (1-androsterone) and 4-dehydroepiandrosterone. These isomers are also technically "DHEA", since they are dehydroepiandrosterones in which hydrogens are removed from the epiandrosterone skeleton.

Dehydroandrosterone (DHA) is the 3α-epimer of DHEA and is also an endogenous androgen.


DHEA was first isolated from human urine in 1934 by Adolf Butenandt and Kurt Tscherning.[57]

See also[edit]


  1. ^ James Devillers (27 April 2009). Endocrine Disruption Modeling. CRC Press. pp. 339–. ISBN 978-1-4200-7636-3. 
  2. ^ a b J. Elks (14 November 2014). The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies. Springer. pp. 641–. ISBN 978-1-4757-2085-3. 
  3. ^ a b Melanie Johns Cupp; Timothy S. Tracy (10 December 2002). Dietary Supplements: Toxicology and Clinical Pharmacology. Springer Science & Business Media. pp. 135–. ISBN 978-1-59259-303-3. 
  4. ^ a b B.J. Oddens; A. Vermeulen (15 November 1996). Androgens and the Aging Male. CRC Press. pp. 5–. ISBN 978-1-85070-763-9. 
  5. ^ a b c Mo Q, Lu SF, Simon NG (April 2006). "Dehydroepiandrosterone and its metabolites: differential effects on androgen receptor trafficking and transcriptional activity". J. Steroid Biochem. Mol. Biol. 99 (1): 50–8. PMID 16524719. doi:10.1016/j.jsbmb.2005.11.011. 
  6. ^ William F Ganong MD, 'Review of Medical Physiology', 22nd Ed, McGraw Hill, 2005, p. 362.
  7. ^ The Merck Index, 13th Edition, 7798
  8. ^ Schulman, Robert A.; Dean, Carolyn (2007). Solve It With Supplements. New York City: Rodale, Inc. p. 100. ISBN 978-1-57954-942-8. DHEA (Dehydroepiandrosterone) is a common hormone produced in the adrenal glands, the gonads, and the brain. 
  9. ^ Thomas Scott (1996). Concise Encyclopedia Biology. Walter de Gruyter. p. 49. ISBN 978-3-11-010661-9. Retrieved 25 May 2012. 
  10. ^ a b Webb SJ, Geoghegan TE, Prough RA, Michael Miller KK (2006). "The biological actions of dehydroepiandrosterone involves multiple receptors". Drug Metabolism Reviews. 38 (1–2): 89–116. PMC 2423429Freely accessible. PMID 16684650. doi:10.1080/03602530600569877. 
  11. ^ Friess E, Schiffelholz T, Steckler T, Steiger A (December 2000). "Dehydroepiandrosterone--a neurosteroid". European Journal of Clinical Investigation. 30 Suppl 3: 46–50. PMID 11281367. doi:10.1046/j.1365-2362.2000.0300s3046.x. 
  12. ^ Ora Hirsch Pescovitz; Erica A. Eugster (2004). Pediatric Endocrinology: Mechanisms, Manifestations, and Management. Lippincott Williams & Wilkins. pp. 362–. ISBN 978-0-7817-4059-3. 
  13. ^ Fima Lifshitz (26 December 2006). Pediatric Endocrinology: Growth, Adrenal, Sexual, Thyroid, Calcium, and Fluid Balance Disorders. CRC Press. pp. 289–. ISBN 978-1-4200-4272-6. 
  14. ^ Sudha Salhan (1 August 2011). Textbook of Gynecology. JP Medical Ltd. pp. 94–. ISBN 978-93-5025-369-4. 
  15. ^ J.P. Lavery; J.S. Sanfilippo (6 December 2012). Pediatric and Adolescent Obstetrics and Gynecology. Springer Science & Business Media. pp. 45–. ISBN 978-1-4612-5064-7. 
  16. ^ Robert L. Nussbaum; Roderick R. McInnes; Huntington F Willard (28 April 2015). Thompson & Thompson Genetics in Medicine. Elsevier Health Sciences. pp. 102–. ISBN 978-0-323-39206-8. 
  17. ^ Marcus E Setchell; C. N. Hudson (4 April 2013). Shaw's Textbook of Operative Gynaecology. Elsevier Health Sciences. pp. 129–. ISBN 81-312-3481-9. 
  18. ^ Bruno Bissonnette; Bernard Dalens (20 July 2006). Syndromes: Rapid Recognition and Perioperative Implications. McGraw Hill Professional. p. 184. ISBN 978-0-07-135455-4. 
  19. ^ a b c Abraham Weizman (1 February 2008). Neuroactive Steroids in Brain Function, Behavior and Neuropsychiatric Disorders: Novel Strategies for Research and Treatment. Springer Science & Business Media. pp. 229–. ISBN 978-1-4020-6854-6. 
  20. ^ Achille G. Gravanis; Synthia H. Mellon (24 June 2011). Hormones in Neurodegeneration, Neuroprotection, and Neurogenesis. John Wiley & Sons. pp. 349–. ISBN 978-3-527-63397-5. 
  21. ^ Sex difference in the human brain, their underpinnings and implications. Elsevier. 3 December 2010. pp. 127–. ISBN 978-0-444-53631-0. 
  22. ^ a b c d Chen F, Knecht K, Birzin E, et al. (November 2005). "Direct agonist/antagonist functions of dehydroepiandrosterone". Endocrinology. 146 (11): 4568–76. PMID 15994348. doi:10.1210/en.2005-0368. 
  23. ^ Gao W, Bohl CE, Dalton JT (September 2005). "Chemistry and structural biology of androgen receptor". Chemical Reviews. 105 (9): 3352–70. PMC 2096617Freely accessible. PMID 16159155. doi:10.1021/cr020456u. 
  24. ^ Lindschau C, Kirsch T, Klinge U, Kolkhof P, Peters I, Fiebeler A (September 2011). "Dehydroepiandrosterone-induced phosphorylation and translocation of FoxO1 depend on the mineralocorticoid receptor". Hypertension. 58 (3): 471–78. PMID 21747041. doi:10.1161/HYPERTENSIONAHA.111.171280. 
  25. ^ a b c d e f g h i j k l m n o Prough RA, Clark BJ, Klinge CM (2016). "Novel mechanisms for DHEA action". J. Mol. Endocrinol. 56 (3): R139–55. PMID 26908835. doi:10.1530/JME-16-0013. 
  26. ^ Ronald Ross Watson (22 July 2011). DHEA in Human Health and Aging. CRC Press. pp. 208–. ISBN 978-1-4398-3884-6. 
  27. ^ Kalimi M, Shafagoj Y, Loria R, Padgett D, Regelson W (February 1994). "Anti-glucocorticoid effects of dehydroepiandrosterone (DHEA)". Molecular and Cellular Biochemistry. 131 (2): 99–104. PMID 8035785. doi:10.1007/BF00925945. 
  28. ^ a b Steven R. King (9 November 2012). Neurosteroids and the Nervous System. Springer Science & Business Media. pp. 15–16. ISBN 978-1-4614-5559-2. 
  29. ^ a b c d Lazaridis I, Charalampopoulos I, Alexaki VI, Avlonitis N, Pediaditakis I, Efstathopoulos P, Calogeropoulou T, Castanas E, Gravanis A (2011). "Neurosteroid dehydroepiandrosterone interacts with nerve growth factor (NGF) receptors, preventing neuronal apoptosis". PLoS Biol. 9 (4): e1001051. PMC 3082517Freely accessible. PMID 21541365. doi:10.1371/journal.pbio.1001051. 
  30. ^ a b c Pediaditakis I, Iliopoulos I, Theologidis I, Delivanoglou N, Margioris AN, Charalampopoulos I, Gravanis A (2015). "Dehydroepiandrosterone: an ancestral ligand of neurotrophin receptors". Endocrinology. 156 (1): 16–23. PMID 25330101. doi:10.1210/en.2014-1596. 
  31. ^ Gravanis A, Calogeropoulou T, Panoutsakopoulou V, Thermos K, Neophytou C, Charalampopoulos I (2012). "Neurosteroids and microneurotrophins signal through NGF receptors to induce prosurvival signaling in neuronal cells". Sci Signal. 5 (246): pt8. PMID 23074265. doi:10.1126/scisignal.2003387. 
  32. ^ a b Schwartz AG, Pashko LL (2004). "Dehydroepiandrosterone, glucose-6-phosphate dehydrogenase, and longevity". Ageing Res. Rev. 3 (2): 171–87. PMID 15177053. doi:10.1016/j.arr.2003.05.001. 
  33. ^ a b c Ciolino HP, MacDonald CJ, Yeh GC (2002). "Inhibition of carcinogen-activating enzymes by 16alpha-fluoro-5-androsten-17-one". Cancer Res. 62 (13): 3685–90. PMID 12097275. 
  34. ^ McCormick DL, Johnson WD, Kozub NM, Rao KV, Lubet RA, Steele VE, Bosland MC (2007). "Chemoprevention of rat prostate carcinogenesis by dietary 16alpha-fluoro-5-androsten-17-one (fluasterone), a minimally androgenic analog of dehydroepiandrosterone". Carcinogenesis. 28 (2): 398–403. PMID 16952912. doi:10.1093/carcin/bgl141. 
  35. ^ Auci D, Kaler L, Subramanian S, Huang Y, Frincke J, Reading C, Offner H (2007). "A new orally bioavailable synthetic androstene inhibits collagen-induced arthritis in the mouse: androstene hormones as regulators of regulatory T cells". Ann. N. Y. Acad. Sci. 1110: 630–40. PMID 17911478. doi:10.1196/annals.1423.066. 
  36. ^ Häggström, Mikael; Richfield, David (2014). "Diagram of the pathways of human steroidogenesis". WikiJournal of Medicine. 1 (1). ISSN 2002-4436. doi:10.15347/wjm/2014.005. 
  37. ^ a b Risto Erkkola (2006). The Menopause. Elsevier. pp. 5–. ISBN 978-0-444-51830-9. 
  38. ^ Bernhard Kleine; Winfried G. Rossmanith (11 February 2016). Hormones and the Endocrine System: Textbook of Endocrinology. Springer. pp. 264–265. ISBN 978-3-319-15060-4. 
  39. ^ a b Joseph E. Pizzorno (2013). Textbook of Natural Medicine. Elsevier Health Sciences. pp. 711–. ISBN 1-4377-2333-0. 
  40. ^ a b Rainey WE, Nakamura Y (February 2008). "Regulation of the adrenal androgen biosynthesis". J. Steroid Biochem. Mol. Biol. 108 (3-5): 281–86. PMC 2699571Freely accessible. PMID 17945481. doi:10.1016/j.jsbmb.2007.09.015. 
  41. ^ a b Robert A. Adler (14 December 2009). Osteoporosis: Pathophysiology and Clinical Management. Springer Science & Business Media. pp. 387–. ISBN 978-1-934115-19-0. 
  42. ^ Wolf-Bernhard Schill; Frank H. Comhaire; Timothy B. Hargreave (26 August 2006). Andrology for the Clinician. Springer Science & Business Media. pp. 243–. ISBN 978-3-540-33713-3. 
  43. ^ a b Dimitrios A. Linos; Jon A. van Heerden (5 December 2005). Adrenal Glands: Diagnostic Aspects and Surgical Therapy. Springer Science & Business Media. pp. 161–. ISBN 978-3-540-26861-1. 
  44. ^ Filaire, E; Duché, P; Lac, G (1998). "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". Eur. J. Appl. Physiol. Occup. Physiol. 78 (5): 466–71. PMID 9809849. doi:10.1007/s004210050447. 
  45. ^ Copeland, J. L.; Consitt, L. A.; Tremblay, M. S. (2002). "Hormonal Responses to Endurance and Resistance Exercise in Females Aged 19–69 Years". J. Gerontol. A. Biol. Sci. Med. Sci. 57 (4): B158–65. doi:10.1093/gerona/57.4.B158. 
  46. ^ Mattison, Julie A.; Lane, Mark A.; Roth, George S.; Ingram, Donald K. (2003). "Calorie restriction in rhesus monkeys". Experimental Gerontology. 38 (1–2): 35–46. PMID 12543259. doi:10.1016/S0531-5565(02)00146-8. .
  47. ^ Roberts, E. (1999). "The importance of dehydroepiandrosterone sulfate in the blood of primates: a longer and healthier life?". Biochemical Pharmacology. 57 (4): 329–46. PMID 9933021. doi:10.1016/S0006-2952(98)00246-9. .
  48. ^ a b Paul M. Coates; M. Coates Paul; Marc Blackman; Marc R. Blackman, Gordon M. Cragg, Mark Levine, Jeffrey D. White, Joel Moss, Mark A. Levine (29 December 2004). Encyclopedia of Dietary Supplements (Print). CRC Press. pp. 169–. ISBN 978-0-8247-5504-1. 
  49. ^ Kenneth L. Becker (2001). Principles and Practice of Endocrinology and Metabolism. Lippincott Williams & Wilkins. pp. 712–. ISBN 978-0-7817-1750-2. 
  50. ^ Mueller JW, Gilligan LC, Idkowiak J, Arlt W, Foster PA (2015). "The Regulation of Steroid Action by Sulfation and Desulfation". Endocr. Rev. 36 (5): 526–63. PMC 4591525Freely accessible. PMID 26213785. doi:10.1210/er.2015-1036. 
  51. ^ Lawrence H Lash (2005). Drug Metabolism and Transport: Molecular Methods and Mechanisms. Springer Science & Business Media. pp. 353–. ISBN 978-1-59259-832-8. 
  52. ^ Robert Morfin (2 September 2003). DHEA and the Brain. CRC Press. pp. 28–. ISBN 978-0-203-30121-0. 
  53. ^ Michał Karasek (2006). Aging and Age-related Diseases: The Basics. Nova Publishers. pp. 66–. ISBN 978-1-59454-426-2. 
  54. ^ a b Bruce Alan White; Susan P. Porterfield (2013). Endocrine and Reproductive Physiology, Mosby Physiology Monograph Series (with Student Consult Online Access),4: Endocrine and Reproductive Physiology. Elsevier Health Sciences. pp. 164–. ISBN 0-323-08704-3. 
  55. ^ Mohammed Y. Kalimi; William Regelson (2000). Dehydroepiandrosterone (DHEA): Biochemical, Physiological and Clinical Aspects. Walter de Gruyter. pp. 41–. ISBN 978-3-11-016111-3. 
  56. ^ Banaszewska B, Spaczyński RZ, Pelesz M, Pawelczyk L (2003). "Incidence of elevated LH/FSH ratioin polycystic ovary syndrome women with normo- and hyperinsulinemia". Annales Academiae Medicae Bialostocensis. 48. 
  57. ^ Schwartz AG, Pashko LL (2001). "Potential therapeutic use of dehydroepiandrosterone and structural analogs". Diabetes Technol. Ther. 3 (2): 221–4. PMID 11478328. doi:10.1089/152091501300209589.