Effects of Dehydroepiandrosterone (DHEA) in Humans
The purpose of this study is to determine whether bringing back the DHEA levels of older persons to the young range produces beneficial effects.
|Study Design:||Allocation: Randomized
Endpoint Classification: Safety/Efficacy Study
Intervention Model: Parallel Assignment
Primary Purpose: Treatment
|Official Title:||Is DHEA Replacement Beneficial?|
- body composition (e.g. truncal fat and visceral fat), insulin resistance and serum triglycerides, muscle mass and strength
- bone mineral density, arterial-endothelium dependent vasodilatation, sense of well being, RMR (Resting Metabolic Rate), TEF (Thermal Effect of Food)
|Study Start Date:||September 2002|
|Study Completion Date:||September 2007|
|Primary Completion Date:||September 2007 (Final data collection date for primary outcome measure)|
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.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00182975
|United States, Missouri|
|Washington University School of Medicine|
|St. Louis, Missouri, United States, 63131|
|Principal Investigator:||John O. Holloszy, MD||Washington University School of Medicine|