Effects of Dehydroepiandrosterone (DHEA) in Humans

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details. Identifier: NCT00182975
Recruitment Status : Completed
First Posted : September 16, 2005
Last Update Posted : August 25, 2008
Information provided by:
National Institute on Aging (NIA)

September 13, 2005
September 16, 2005
August 25, 2008
September 2002
September 2007   (Final data collection date for primary outcome measure)
body composition (e.g. truncal fat and visceral fat), insulin resistance and serum triglycerides, muscle mass and strength
Same as current
Complete list of historical versions of study NCT00182975 on Archive Site
bone mineral density, arterial-endothelium dependent vasodilatation, sense of well being, RMR (Resting Metabolic Rate), TEF (Thermal Effect of Food)
Same as current
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Effects of Dehydroepiandrosterone (DHEA) in Humans
Is DHEA Replacement Beneficial?
The purpose of this study is to determine whether bringing back the DHEA levels of older persons to the young range produces beneficial effects.

DHEA and DHEA sulfate (DHEAS) plasma concentrations peak at about 20 years of age and decline rapidly and markedly after age 25 yr. DHEA is a PPAR-alpha activator. PPAR-alpha plays major roles in regulating lipid metabolism and controlling inflammation. DHEA also appears to have anabolic effects on muscle and bone. The study is designed to determine the effects of 12 months of DHEA replacement in 65-75 year old women and men on (a) truncal and visceral fat, (b) insulin resistance and serum triglycerides, (c) muscle mass and strength, (d) bone mineral density, (e) chronic inflammation, (f) arterial-endothelium-dependent vasodilation, and (g) sense of well being.

The specific aims of this study are to test the hypotheses that 12 months of DHEA replacement will (a) Result in significant decreases in truncal and visceral fat by shifting metabolism to fat oxidation and increasing energy wastage; (b) Decrease insulin resistance and decrease serum triglycerides; (c) Increase muscle mass and strength, by decreasing catabolic stimuli and increasing anabolic stimuli; (d) Increase bone mineral density by increasing anabolic stimuli and decreasing catabolic stimuli; (e) Reduce chronic inflammation and decrease pro-inflammatory cytokine production by peripheral blood mononuclear cells; (f) Improve arterial endothelium dependent vasodilation; and (g) Improve general sense of well being.

Phase 3
Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: Double
Primary Purpose: Treatment
Drug: DHEA replacement
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*   Includes publications given by the data provider as well as publications identified by Identifier (NCT Number) in Medline.
September 2007
September 2007   (Final data collection date for primary outcome measure)

Inclusion Criteria:

  • 65 to 75 years old
  • Physically healthy
  • Non-smoker
  • On stable medications for at least 6 months
  • Stable body weight for the past year

Exclusion Criteria:

  • Serious active medical problems
  • Hormone therapy
  • Abnormal PSA (prostate specific antigen) in men
Sexes Eligible for Study: All
65 Years to 75 Years   (Older Adult)
Contact information is only displayed when the study is recruiting subjects
United States
R01AG020076 ( U.S. NIH Grant/Contract )
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National Institute on Aging (NIA)
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Principal Investigator: John O. Holloszy, MD Washington University School of Medicine
National Institute on Aging (NIA)
August 2008

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP