DHEA-S - Male

What Is DHEA-S?

Dehydroepiandrosterone sulfate (DHEA-S) is the most abundant circulating steroid, synthesized in the adrenal cortex from cholesterol. This water-soluble form of DHEA serves as a reservoir for sex hormone production—ultimately fueling testosterone, estrogen, and progesterone synthesis—and supports over 150 anabolic processes in tissues and the brain.

Key Functions of DHEA-S

• Hormone Precursor & Anabolism
  DHEA-S fuels testosterone production, crucial for muscle development, bone strength, and sexual health.
  
• Immune Function
  It counterbalances cortisol-driven immune suppression, bolstering defenses against viruses, bacteria, and parasites.
  
• Bone & Cardiovascular Support
  By enhancing bone health and reducing LDL cholesterol, DHEA-S helps prevent osteoporosis and supports heart health.
  
• Stress Adaptation & Mental Clarity
  It aids recovery from sleep deprivation, overtraining, and mental fatigue—promoting energy, vitality, and cognitive focus.

Clinical Implications of DHEA-S Levels

Low DHEA-S

Suboptimal DHEA-S is often linked to adrenal insufficiency, marked by an elevated cortisol-to-DHEA ratio. Consequences include:

• Insulin Resistance: Hyperinsulinemia can suppress DHEA-S, increasing diabetes risk.
  
• Immune Insufficiency: Lower sIgA production weakens first-line defenses.
  
• Age-Related Conditions: DHEA-S decline correlates with metabolic syndrome, coronary artery disease, osteoporosis, mood disorders, and reduced sex hormone function.

High DHEA-S

Elevated DHEA-S may indicate adrenal hyperplasia or excessive androgen precursor activity, potentially disrupting metabolic balance and hormone feedback loops.

Ideal DHEA-S Ranges

• Standard Range (Men): 85–690 µg/dL
  
• Optimal Functional Range: Top third of standard (approx. 300–690 µg/dL), mirroring levels seen in healthy 30-year-olds to support anti-aging effects.

Factors That Influence DHEA-S

• Supplementation: Exogenous DHEA alters measured levels—always disclose use before testing.
  
• Medications: Agents that elevate cortisol (e.g., corticosteroids) can depress DHEA-S; androgenic drugs may raise it.

Cortisol-to-DHEA-S Ratio

The balance between cortisol and Cortisol : DHEA-S reflects adrenal resilience. A chronically elevated ratio signals prolonged stress, immune suppression, and higher risk of degenerative diseases.

In conclusion, a comprehensive evaluation by a functional medicine telehealth specialist in Florida integrates DHEA-S into a root-cause framework. By pairing evidence-based allopathic treatments with a functional medicine integrative approach—encompassing advanced biomarker profiling, personalized nutrition and lifestyle strategies, and targeted therapeutics—this model transcends symptom management to resolve underlying pathophysiology. Recognizing that true health begins at the cellular level, this strategy builds resilience, preventive care, and longevity. Explore our Longevity Medicine service to further optimize your wellness journey.

Further Reading

• Genazzani, A. R., Stomati, M., Bernardi, F., Pieri, M., Casarosa, E., & Genazzani, A. D. (2004). Long-term low-dose dehydroepiandrosterone replacement therapy in aging men with partial androgen deficiency: Effects on endocrine, neuroendocrine, and symptomatic parameters. Journal of Clinical Endocrinology & Metabolism, 89(6), 2113-2121.
  https://pubmed.ncbi.nlm.nih.gov/15672938/

• El-Sakka, A. I. (2018). Dehydroepiandrosterone and erectile function: A review. Arab Journal of Urology, 16(2), 236-243.
  https://pmc.ncbi.nlm.nih.gov/articles/PMC6119841/

• Reiter, W. J., Pycha, A., Schatzl, G., Pokorny, A., Gruber, D. M., Huber, J. C., & Marberger, M. (1999). Dehydroepiandrosterone in the treatment of erectile dysfunction: A prospective, double-blind, randomized, placebo-controlled study. Urology, 53(3), 590-594.
  https://pubmed.ncbi.nlm.nih.gov/10096389/

• Sun, Y., Wang, Y., Zhang, Y., & Wang, Y. (2002). Treatment of osteoporosis in men using dehydroepiandrosterone sulfate. Zhonghua Nan Ke Xue, 8(2), 134-137.
  https://pubmed.ncbi.nlm.nih.gov/11940375/