An open label, dose response study to determine the effect of a dietary supplement on dihydrotestosterone, testosterone and estradiol levels in healthy males
Fru Angwafor III1* email and Mark L Anderson2* email
1 Yaounde Teaching Hospital, Head of Urological Service Department, University of Yaounde, Cameroon
2 Director of Research & Development, Triarco Industries, Inc. 400 Hamburg Turnpike, Wayne, NJ, 07418, USA
author email corresponding author email* Contributed equally
Journal of the International Society of Sports Nutrition 2008, 5:12doi:10.1186/1550-2783-5-12
The electronic version of this article is the complete one and can be found online at: Journal of the International Society of Sports Nutrition | Full text | An open label, dose response study to determine the effect of a dietary supplement on dihydrotestosterone, testosterone and estradiol levels in healthy males
Received: 12 May 2008
Accepted: 12 August 2008
Published: 12 August 2008
© 2008 Angwafor and Anderson; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (Creative Commons — Attribution 2.0 Generic
), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Maintaining endogenous testosterone (T) levels as men age may slow the symptoms of sarcopenia, andropause and decline in physical performance. Drugs inhibiting the enzyme 5α-reductase (5AR) produce increased blood levels of T and decreased levels of dihydrotestosterone (DHT). However, symptoms of gynecomastia have been reported due to the aromatase (AER) enzyme converting excess T to estradiol (ES). The carotenoid astaxanthin
(AX) from Haematococcus pluvialis, Saw Palmetto
berry lipid extract (SPLE) from Serenoa repens and the precise combination of these dietary supplements, Alphastat® (Mytosterone(™)), have been reported to have inhibitory effects on both 5AR and AER in-vitro. Concomitant regulation of both enzymes in-vivo would cause DHT and ES blood levels to decrease and T levels to increase. The purpose of this clinical study was to determine if patented Alphastat® (Mytosterone(™)) could produce these effects in a dose dependent manner.
To investigate this clinically, 42 healthy males ages 37 to 70 years were divided into two groups of twenty-one and dosed with either 800 mg/day or 2000 mg/day of Alphastat® (Mytosterone(™)) for fourteen days. Blood samples were collected on days 0, 3, 7 and 14 and assayed for T, DHT and ES. Body weight and blood pressure data were collected prior to blood collection. One-way, repeated measures analysis of variance (ANOVA-RM) was performed at a significance level of alpha = 0.05 to determine differences from baseline within each group. Two-way analysis of variance (ANOVA-2) was performed after baseline subtraction, at a significance level of alpha = 0.05 to determine differences between dose groups. Results are expressed as means ± SEM.
ANOVA-RM showed significant within group increases in serum total T and significant decreases in serum DHT from baseline in both dose groups at a significance level of alpha = 0.05. Significant decreases in serum ES are reported for the 2000 mg/day dose group and not the 800 mg/day dose group. Significant within group effects were confirmed using ANOVA-2 analyses after baseline subtraction. ANOVA-2 analyses also showed no significant difference between dose groups with regard to the increase of T or the decrease of DHT. It did show a significant dose dependant decrease in serum ES levels.
Both dose groups showed significant (p = 0.05) increases in T and decreases in DHT within three days of treatment with Alphastat® (Mytosterone(™)). Between group statistical analysis showed no significant (p = 0.05) difference, indicating the effect was not dose dependent and that 800 mg/per day is equally effective as 2000 mg/day for increasing T and lowering DHT. Blood levels of ES however, decreased significantly (p = 0.05) in the 2000 mg/day dose group but not in the 800 mg/day dose group indicating a dose dependant decrease in E levels.