Effects of Dehydroepiandrosterone (DHEA) in Humans

This study has been completed.
Sponsor:
Information provided by:
National Institute on Aging (NIA)
ClinicalTrials.gov Identifier:
NCT00182975
First received: September 13, 2005
Last updated: August 21, 2008
Last verified: August 2008

September 13, 2005
August 21, 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 ClinicalTrials.gov 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
Not Provided
Not Provided
 
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.

Interventional
Phase 3
Allocation: Randomized
Endpoint Classification: Safety/Efficacy Study
Intervention Model: Parallel Assignment
Masking: Double-Blind
Primary Purpose: Treatment
Aging
Drug: DHEA replacement
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
142
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
Both
65 Years to 75 Years
Yes
Contact information is only displayed when the study is recruiting subjects
United States
 
NCT00182975
AG0047, R01AG020076
Not Provided
Not Provided
National Institute on Aging (NIA)
Not Provided
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