5AR is an enzyme that converts testosterone into 5a-DHT, a more potent androgen that binds strongly to androgen receptors. It also influences other conversions, including:

• Androstenedione → androsterone
• Cortisol → allo-tetrahydrocortisol

These pathways impact both reproductive and metabolic systems. When we measure these hormone ratios in urine and blood, we can estimate overall 5AR activity.

Certain hormones regulate 5AR activity:

• DHEA increases 5AR activity
• Progesterone decreases 5AR activity

Tracking these regulators on a 24-hour urine hormone panel can offer helpful context when evaluating enzyme function.

High 5AR activity has been associated with a number of health concerns:

• Obesity and insulin resistance (men and women)
• PCOS and hirsutism (women)
• Benign prostatic hypertrophy (BPH) and male pattern baldness (men)

In these cases, reducing 5AR activity can be beneficial—but moderation is key.

Some natural compounds can help modulate 5AR without the side effects of pharmaceutical drugs:

• Gamma-linolenic acid (GLA)
• DHA and other fatty acids
• Saw Palmetto (Serenoa repens)
• Zinc (especially in combination with vitamin B6)

It’s worth noting that highly concentrated extracts or overuse of inhibitors can lead to over-suppression of 5AR.

Excessive inhibition of 5AR reduces DHT levels and may increase circulating testosterone, which can then be converted into estradiol. This hormonal imbalance can lead to gynecomastia (breast enlargement in men) and other side effects.

Pharmaceutical 5AR inhibitors such as finasteride and dutasteride are prescribed for prostate enlargement, hair loss, and sometimes prostate cancer. However, side effects include:

• Impotence
• Decreased libido
• Reduced ejaculate volume
• Rarely: breast tenderness and allergic reactions

Some reports even suggest a risk of persistent sexual dysfunction or male breast cancer after discontinuation.

DHT is about three times more potent than testosterone at androgen receptors. While excessive DHT can promote prostate growth, it’s not all bad. Research shows that low DHT levels may be linked to poorer prostate cancer survival outcomes.

In fact, one of DHT’s metabolites—3β-Adiol—may play a protective role. This compound activates estrogen receptor beta (ERβ), which has anti-proliferative effects on prostate tissue. By over-inhibiting 5AR, we may reduce the body’s ability to make 3β-Adiol, potentially increasing cancer risk.

Heavy metals like cadmium and arsenic may also inhibit 3β-Adiol production, contributing to prostate cancer risks.

Total levels of DHT or testosterone don’t tell the full story. It’s the ratios that offer clearer insights:

• Testosterone : DHT
• 3β-Adiol : (DHT + 3α-Adiol)

Urine hormone tests and serum profiles can evaluate these ratios. In clinical studies, men with healthier ratios had lower risks of BPH and better cancer prognoses.

We recommend evaluating both urine and serum metabolites to assess 5AR activity and DHT conversion pathways. This is especially relevant for:

• Patients with elevated PSA
• Men with BPH or family history of prostate cancer
• Individuals using 5AR inhibitors
• Women with symptoms of PCOS or elevated testosterone

By offering the Testosterone Metabolites Profile, Meridian Valley Lab supports clinicians in identifying imbalances before they progress into chronic disease.

Practitioners: Use urine and serum metabolites to assess 5AR activity and DHT conversion pathways, especially for patients with elevated PSA, BPH risk, PCOS symptoms, or those currently using 5AR inhibitors. Contact Client Services to request a test kit or discuss the Testosterone Metabolites Profile.

Patients: Ask your licensed provider whether expanded hormone metabolite testing is appropriate for your goals. Meridian Valley Lab provides laboratory services only and cannot advise patients directly.

Call: 855.405.8378 | 206.209.4200

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2. Rittmaster RS. Finasteride. N Engl J Med. 1994;330(2):120–125.
3. Thomas LN, Lazier CB, Gupta R, et al. Differential alterations in 5α-reductase type 1 and type 2 in benign and malignant human prostate. J Clin Endocrinol Metab. 2005;90(12):6265–6272.
4. Mohler JL, Titus MA, Bai S, et al. Activation of the androgen receptor by intratumoral bioconversion of androstanediol to dihydrotestosterone in prostate cancer. Cancer Res. 2011;71(4):1486–1496.
5. Uemura H, Fujinami K, Ishiguro H, et al. Expression of 5 alpha-reductase type 2 in prostate cancer and its relation to tumor progression. J Urol. 2001;166(6):2203–2207.

To request the full reference list, please contact our team or email us at info@meridianvalleylab.com.