Personalized MHT: Androgen Status in Menopausal Transition

For decades, the conversation surrounding menopausal hormone therapy (MHT) has been dominated by the balance of oestrogen and progesterone to combat vasomotor symptoms. However, a critical piece of the metabolic puzzle—androgens—has often been relegated to the sidelines. New research is now shifting the focus, suggesting that the delivery method and the specific progestogen used in MHT can significantly impact a woman’s androgenic profile, which in turn influences cognitive function, libido, and overall systemic health.

The Deep Dive: Why Androgen Status Matters

While oestrogen is the primary target for treating hot flashes and night sweats, androgens (such as testosterone) are fundamental to maintaining muscle mass, bone density, and mental clarity. Many women experience a decline in these hormones during perimenopause, leading to a “functional impairment” that oestrogen alone cannot fix.

The challenge with traditional MHT has been the “collateral damage” caused by certain progestogens, which can suppress endogenous testosterone levels, potentially exacerbating fatigue or loss of libido. This study highlights the unique role of dydrogesterone. Because it is highly selective and biologically similar to natural progesterone, it does not induce the androgenic decline seen with other synthetic options.

Crucially, the study observed a divergence in how the body processes these hormones based on the route of administration. The oral group saw a rise in SHBG—a protein that binds to testosterone. While a rise in SHBG typically reduces the amount of “free” (active) testosterone, the data showed that total testosterone levels remained stable. This suggests that oral oestradiol/dydrogesterone maintains the body’s androgen reservoir without the systemic “crash” associated with less selective therapies.

The Forward Look: Toward Personalized Hormone Management

This research signals a move away from “one-size-fits-all” menopause management and toward a more nuanced, biomarker-driven approach. As clinicians become more aware of the “Androgen Gap,” we can expect the following shifts in practice:

• Routine SHBG Screening: Rather than guessing which MHT will work, providers may begin using SHBG levels at baseline to determine if a patient is a better candidate for oral or transdermal therapy.
• Progestogen Selection: There will likely be a stronger clinical preference for dydrogesterone in patients who report low libido or cognitive “fog,” as its lack of androgen-suppressing activity makes it a superior choice for maintaining systemic vitality.
• Tailored Delivery: For women who need to maintain higher levels of free testosterone (due to low baseline SHBG), transdermal oestradiol may become the gold standard, as it avoids the SHBG-increasing effect of the liver’s first-pass metabolism seen in oral doses.

Ultimately, the goal of MHT is evolving from simple symptom suppression to the holistic preservation of metabolic and sexual health. By protecting the androgenic balance, clinicians can offer a higher quality of life that extends beyond the elimination of hot flashes.