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Table of Contents > Interactions & Depletions > DHEA Print

DHEA



Interactions

DHEA/Drug Interactions:
  • AlprazolamAlprazolam: Alprazolam causes an acute increase in DHEA concentration within seven hours of dosing (55).
  • AmlodipineAmlodipine: Amlodipine may not affect DHEA, but does increase DHEAS in insulin-resistant obese and hypertensive men (56).
  • AnastrozoleAnastrozole: Gynecomastia treatment with aromatase inhibitor anastrozole resulted in a rise in DHEAS (57).
  • Antipsychotic drugsAntipsychotic drugs: In men with mental disorders, receiving antipsychotic drugs, who had been medication-free for at least three months before the study, there were significantly lower serum levels of DHEAS than in controls (58).
  • BenfluorexBenfluorex: Benfluorex has been observed to increase DHEA concentrations (59).
  • Beta-adrenergic antagonistsBeta-adrenergic antagonists: Secretion of DHEAS has been induced in a clinical trial (60).
  • BudesonideBudesonide: Inhaled budesonide decreased serum DHEAS concentrations (61).
  • Calcium channel blockersCalcium channel blockers: Non-significant increases in DHEA and DHEAS levels were observed in clinical trials (62).
  • CanrenoateCanrenoate: Intravenous canrenoate administration increased DHEA levels in young and elderly subjects (63).
  • Conjugated estrogensConjugated estrogens: Conjugated estrogens decreased plasma DHEAS and DHEA in postmenopausal women (64; 65).
  • ContraceptivesContraceptives: Ortho Novum 1/35 and Ovcon 35 significantly decreased serum concentration of DHEAS (66). Other estrogen-containing oral contraceptives have also resulted in decreased DHEAS (67; 68).
  • Cytochrome P450 affecting agentsCytochrome P450 affecting agents: Administration of DHEA to rats results in induction of hepatic microsomal cytochromes P450 1A, P450 3A, and P450 4A (69). In addition, changes in the activities of P450 IIB1, P450 IIC11, and P450 IIIA have occurred (70; 71). This action may impact on the metabolism of a number of drugs. DHEAS, but not DHEA, inhibited the metabolism of triazolam by P450 3A in human liver microsomes (72).
  • DanazolDanazol: Increases in DHEAS with danazol therapy have been reported (73; 74).
  • DexamethasoneDexamethasone: Dexamethasone appears to decrease DHEA concentrations in both healthy and depressed participants (75). Compared with the placebo, dexamethasone reduced DHEAS in women with polycystic ovary syndrome (76).
  • DiltiazemDiltiazem: Diltiazem may increase DHEA and DHEAS levels in obese hypertensive men but not women (77).
  • Ethanol (alcohol)Ethanol (alcohol): Alcohol may increase the effects of DHEA. In premenstrual women, alcohol caused a decrease in DHEA level (78).
  • GefitinibGefitinib: DHEA was significantly lowered compared with pretreatment values in both women and men. DHEAS levels also decreased in women (79).
  • Growth hormoneGrowth hormone: Growth homrone-treated children showed a rise in circulating DHEAS (80). In a separate study, one year of growth hormone treatment resulted in no effect on serum DHEAS levels (81).
  • InsulinInsulin: Insulin has decreased DHEA and DHEAS in healthy populations, apparently by increasing metabolic clearance rate (82; 18).
  • MetforminMetformin: Metformin resulted in a decrease in DHEA in individuals with polycystic ovary syndrome (83).
  • MethylphenidateMethylphenidate: A three month treatment course of methylphenidate increases plasma levels of both DHEA and DHEAS in individuals with attention deficit hyperactivity disorder (84).
  • MetopironeMetopirone: Metopirone may increase plasma DHEA levels in normal and hirsute women (85).
  • NitrendipineNitrendipine: Nitrendipine may increase DHEAS in obese hypertensives (86).
  • Oral hypoglycemic agentsOral hypoglycemic agents: DHEA administration has resulted in some degree of insulin resistance (47) and therefore may decrease the effectiveness of oral hypoglycemic agents.
  • RosiglitazoneRosiglitazone: Decreases in serum DHEAS have been noted (87; 88).
  • VaccinesVaccines: DHEA use has been suggested to result in a decreased rate of developing protective antibody titer after influenza vaccination (89).

DHEA/Herb/Supplement Interactions:
  • Chromium picolinateChromium picolinate: Chromium picolinate supplements increased plasma DHEA in postmenopausal women (90).
  • FiberFiber: Significant inverse correlations have been found between blood levels of DHEAS and dietary fiber intakes (91).
  • FlavonoidsFlavonoids: Dietary flavonoids including kaempferol, quercetin, genistein and daidzein have been found to inhibit sulfonation of DHEA to DHEAS (92). Decreased DHEA has also been noted (93).
  • Polyunsaturated fatty acidsPolyunsaturated fatty acids: A polyunsaturated fatty acid-rich diet did not affect plasma DHEAS in polycystic ovary syndrome patients (94).
  • ProbioticsProbiotics: Consumption of Lactobacillus acidophilus and Bifidobacterium longum do not alter plasma reproductive hormones in premenopausal women (91).
  • Soy proteinSoy protein: Theoretically, there may be an interaction between DHEA and use of herbs or supplements with potential estrogenic effects (i.e. soy proteins, flax). One study found no effect of dietary soy supplementation and DHEAS levels (95). A second noted decreases in DHEA in postmenopausal women and DHEAS in older men (96).
  • Vitamin EVitamin E: Vitamin E (alpha-tocopherol) supplementation did not affect the levels of DHEA in a clinical trial (97). Vitamin E may protect against potential degenerative liver damage associated with DHEA use (anecdotal).
  • YamYam: No significant changes have been observed in serum concentrations of DHEAS with increased yam consumption (98).

DHEA/Food Interactions:
  • AlcoholAlcohol: Alcohol may increase the effects of DHEA. In premenstrual women, alcohol caused a decrease in DHEA level (78).
  • FiberFiber: Significant inverse correlations have been found between blood levels of DHEAS and dietary fiber intakes (91).
  • FlaxFlax: Theoretically, there may be an interaction between DHEA and high intakes of flaxseed due to a potential for estrogenic effects.
  • Polyunsaturated fatty acidsPolyunsaturated fatty acids: A polyunsaturated fatty acid-rich diet did not affect plasma DHEAS in polycystic ovary syndrome patients (94).
  • Soy proteinSoy protein: Theoretically, there may be an interaction between DHEA and use of herbs or supplements with potential estrogenic effects (i.e. soy proteins, flax). One study found no effect of dietary soy supplementation and DHEAS levels (95). A second noted decreases in DHEA in postmenopausal women and DHEAS in older men (96).
  • YamYam: No significant changes have been observed in serum concentrations of DHEAS with increased yam consumption (98).

DHEA/Lab Interactions:
  • ACTHACTH: Treatment with DHEA resulted in increased ACTH responses in women, with no change in men (99).
  • Antibody titersAntibody titers: Mice immunized shortly after oral dosing with DHEAS demonstrated high serum antibody titers (100). In elderly humans given a tetanus vaccination after four days of ingesting DHEAS (100mg daily) there was no change in protective antibody levels as compared to participants receiving placebo (101).
  • Antidiuretic hormoneAntidiuretic hormone: DHEA exhibits a distinct antidiuretic effect in experiments on rats due to inactivation of the processes that lead to destruction of the antidiuretic hormone (102).
  • Beta-endorphinBeta-endorphin: Beta-endorphin levels increased significantly with respect to baseline in elderly men treated with DHEA (103).
  • CortisolCortisol: DHEA administration has resulted in a decrease in plasma cortisol concentrations (104). However, DHEA and DHEAS did not alter prednisolone pharmacokinetics or inhibition of cortisol secretion by prednisolone (105).
  • Fatty acidsFatty acids: 50mg DHEA daily for three months, in patients with X-linked adrenoleukodystrophy, decreased erythrocyte fatty acids: C16:0, C18:0, C20:4omega-6, C22:5omega-6, C18:1omega-9, C20:1omega-9 and C20:3omega-9. In plasma, decreases were found for C18:1omega-9 and increases for C20:1omega-9 (106).
  • GlucagonGlucagon: Fasting glucagons has been shown to decrease with DHEA (50mg daily for three months) (107).
  • Immune cellsImmune cells: DHEA administration has been suggested to increase the number of monocytes, B cells, and natural killer cells (108).
  • InsulinInsulin: 50mg daily DHEA had no effect on serum insulin (109). Decreased insulin has also been observed (107).
  • InterleukinsInterleukins: DHEA has been suggested to increase production of interleukin-2 in vitro (110). DHEA has been suggested to inhibit, or stimulate, production of IL-2 and IL-3 in vitro (111; 112; 113). Low doses of DHEA and DHEAS inhibited the production of IL-6 in vitro (114). Alterations in IL-4 and IFN have also been noted in vitro (115).
  • LipoproteinsLipoproteins: In humans, DHEA use has resulted in a decrease in HDL-cholesterol, LDL-cholesterol, total cholesterol, apoAI, and very low-density lipoproteins (107; 116; 37; 117; 46). An increase in HDL-cholesterol and apoAI levels has also been observed (118). Fifty mg daily DHEA had no effect on total cholesterol, LDL-cholesterol and HDL-cholesterol levels (109).
  • GlucoseGlucose: DHEA administration improved glucose tolerance (OGTT) (119). 50mg daily DHEA had no effect on serum glucose (109). A decrease of blood glucose has been noted in a clinical trial (8).
  • Growth hormoneGrowth hormone: Growth hormone levels increased in elderly men treated with DHEA (103).
  • OsteocalcinOsteocalcin: Serum osteocalcin was significantly increased after treatment with DHEA (26; 120; 121; 122; 22). Decreases have also been noted (7).
  • Platelet aggregationPlatelet aggregation: DHEA has been suggested to inhibit platelet aggregation ex vivo (123).
  • Decreasing tissue plasminogen activator inhibitor 1 and tissue plasminogen activator was observed in healthy humans receiving DHEA (50mg) orally compared to placebo (124).
  • ProlactinProlactin: No effect on prolactin has been observed (125).
  • Serum lipid peroxidationSerum lipid peroxidation: DHEA intake may significantly reduce serum lipid peroxidation (126; 127).
  • Sex hormonesSex hormones: During DHEA supplementation, increases in testosterone/epitestosterone and testosterone/creatinine ratios were observed (128; 129; 130). In other studies, DHEA did not significantly change testosterone levels over a 12-week period (131). 50mg daily DHEA had no effect on testosterone (109). Increases in total testosterone have been noted (132; 16). DHEA, DHEAS, androstenedione, total and free testosterone, DHT, progesterone, 17-hydroxyprogesterone, estrone, estradiol, beta-endorphin levels increased significantly with respect to baseline values, in elderly men. FSH, LH and SHBG levels showed a significant decrease in elderly men and in other populations (7; 103). Six-month oral DHEA supplementation in early and late postmenopausal women led to a progressive increase in estradiol and estrone, while progesterone levels remained constant (133). Maternal serum estradiol levels have increased (125). 50mg daily DHEA had no effect on estradiol (109). In pregnant women with threatened pregnancies, increases in estriol were noted in the majority of patients (134). Total androgen concentrations increased in elderly men and women (16).
  • Thyroid hormoneThyroid hormone: In prediabetic male BHE/cdb rats, DHEA increased metabolic rate and deceased fat stores by altering thyroid hormone status (135). High oral doses of DHEA have been shown to decrease thyroid binding globin concentrations (47).
  • Urinary N-telopeptidesUrinary N-telopeptides: Decreases were noted in one clinical trial after 50-200mg daily use of DHEA in women with anorexia nervosa (22).

Copyright © 2011 Natural Standard (www.naturalstandard.com)


The information in this monograph is intended for informational purposes only, and is meant to help users better understand health concerns. Information is based on review of scientific research data, historical practice patterns, and clinical experience. This information should not be interpreted as specific medical advice. Users should consult with a qualified healthcare provider for specific questions regarding therapies, diagnosis and/or health conditions, prior to making therapeutic decisions.

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