Scientific Information/Data
Dehydroepiandrosterone (DHEA) is a naturally occurring steroid hormone
precursor synthesized from cholesterol primarily by the adrenal glands,
and it is produced in small amounts in the ovaries, the testes, and the
brain. DHEA production gradually increases in adolescence, typically
peaking between the ages of 20 and 30; then it slowly declines
approximately 2% each year until about age 70, when it slows to 10%-
20% of the amount encountered in a young adult at peak level.*[1-5]
The body’s DHEA level consists of the combined total of DHEA and its
sulfated form DHEA-sulfate (DHEA-S), the most abundant circulating
steroid in humans. They are converted via multiple pathways into
hormones such as testosterone and estrogen as needed. Supplemental
DHEA is aimed at enhancing the DHEA reservoir so that an increased level
is available for conversion to androgens, estrogens, and other hormones
involved in a wide variety of physiological functions.*[1,3-5]
In a randomized, placebo-controlled, crossover trial in men (n = 13) and
women (n = 17) aged 40-70 years, researchers administered a nightly
dose of 50 mg of DHEA to test the hypothesis that a decline in DHEA
contributes to the shift from anabolism to catabolism that is associated
with aging. Within two weeks of DHEA replacement, serum levels of DHEA
and DHEA-S were restored to levels typically found in individuals in their
second decade of life and were sustained throughout the three-month
study period. The levels of the androgens androstenedione, testosterone,
and dihydrotestosterone were doubled in female subjects with only a
slight increase in androstenedione in male subjects. DHEA, at the 50 mg
dose level, induced a 10% increase in bioavailable insulin-like growth
factor (IGF-1), which the authors suggest could result in an improvement
in catabolic processes and physical/psychological well-being over time.*[6]
In a follow-up study led by the same researcher as the study above, a
larger dose (100 mg) of DHEA over a six-month period resulted in the
elevation of circulating DHEA and DHEA-S. In the female subjects, a
biotransformation to androgen levels similar to their younger counterparts
was observed. IGF-1 levels were analyzed in both genders with the male
group showing a higher increase in lean body mass and muscle strength,
suggesting a gender-specific response. Further research is warranted to
explore gender and other potential contributing factors.*[7]
In a randomized trial with healthy subjects (n = 280) aged 60-79 over a
one-year period, subjects were given 50 mg of DHEA daily to re-establish
DHEA levels. Results indicated that replacement therapy normalized a
wide variety of age-related physiological functions and supported wellbeing. The authors suggested a need for further analysis of data.*[8]
A meta-analysis of 25 randomized, double-blind, placebo-controlled
studies in elderly men evaluated the signs and symptoms of low levels
of age-related DHEA and the effect of DHEA supplementation. DHEA
levels were found to be correlated with many representative age-related
phenomena. However, supplementation was found to induce only a small,
albeit significant, effect on body composition that was dependent on
conversion into the bioactive metabolites of androgen or estrogen.*[4]
A recent review explored the role of DHEA as an indirect intermediate
to androgens and estrogens in relation to varying health conditions in
the body and included an overview of the mechanisms of action. The
authors concluded that emerging research continues to confirm that
DHEA supplementation may be beneficial for older individuals or those
with endocrine deficiencies. They suggested that more studies in large
populations are needed to validate immunomodulatory and cardiovascular
benefits, further assess positive effects on lean muscle and fat mass, and
evaluate administration protocols in postmenopausal women.*[3]
Decades of evidence support DHEA supplementation to restore the DHEA
reservoir to peak or near-peak levels in older populations. However,
additional well-designed, large-scale trials are needed to clarify guidelines
for clinical use.*[3,5]
*These statements have not been evaluated by the FDA to treat, prevent, or cure any disease.
References
1. Rutkowski K, Sowa P, Rutkowska-Talipska J, et al. Drugs. 2014
Jul;74(11):1195-207. doi:10.1007/s40265-014-0259-8.
2. Labrie F, Bélanger A, Cusan L, et al. J Clin Endocrinol Metab. 1997;82(8):2396-
2402. doi:10.1210/jcem.82.8.4160.
3. Sahu P, Gidwani B, Dhongade HJ. Steroids. 2020 Jan;153:108507.
doi:10.1016/j.steroids.2019.108507.
4. Corona G, Rastrelli G, Giagulli VA, et al. J Clin Endocrinol Metab. 2013
Sep;98(9):3615-26. doi: 10.1210/jc.2013-1358.
5. Traish AM, Kang HP, Saad F, et al. J Sex Med. 2011 Nov;8(11):2960-82; quiz
2983. doi: 10.1111/j.1743-6109.2011.02523.x.
6. Morales AJ, Nolan JJ, Nelson JC, et al. J Clin Endocrinol Metab. 1994
Jun;78(6):1360-7. doi:10.1210/jcem.78.6.7515387.
7. Morales AJ, Haubrich RH, Hwang JY, et el. Clin Endocrinol (Oxf). 1998
Oct;49(4):421-32. doi:10.1046/j.1365-2265.1998.00507.x.
8. Baulieu EE, Thomas G, Legrain S, et al. Proc Natl Acad Sci U S A. 2000 Apr
11;97(8):4279-4284. doi:10.1073/pnas.97.8.4279.
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