A clear, biology-based explanation of GSM beyond symptom lists and quick fixes.

Genitourinary Syndrome of Menopause (GSM) describes a set of progressive changes affecting the vulva, vagina, urethra, and bladder that commonly emerge during midlife.

Although GSM is a hormone-driven condition, it is not the result of estrogen loss alone. Instead, it reflects coordinated declines in multiple hormonal signals — along with changes in how intimate tissues are maintained, repaired, and supported over time.

Understanding GSM at the tissue level helps explain why symptoms can persist — even when standard treatments are used.

What GSM Includes

Historically, GSM was often referred to as vulvovaginal atrophy, though this term fails to capture the full range of genital and urinary tissue changes now recognized.  These changes typically begin during perimenopause and progress through postmenopause, though the experience varies widely.  GSM may involve one or more of the following experiences:

• Vaginal dryness or reduced lubrication

• Burning, irritation, or friction discomfort

• Tissue thinning or increased fragility

• Loss of elasticity and stretch

• Changes in sensation or arousal response

• Recurrent irritation or infections

• Urinary urgency, frequency, or discomfort

These symptoms reflect changes in tissue structure and function, not just changes in hormone signaling.

Why GSM Develops During Menopause and Midlife

During midlife, several biological systems that support vulvovaginal and urinary tissue gradually shift:

• Hormonal signaling becomes less consistent

• Local steroid conversion within the tissue declines

• Cellular energy production slows

• Structural repair and renewal become less efficient

• Barrier function and hydration retention weaken

• Immune tolerance and microbial stability change

Together, these shifts alter the tissue environment itself.

This is why GSM is best understood as a progressive tissue condition, rather than an acute deficiency that can be corrected by replacing a single hormone.

Why Estrogen Alone Often Isn’t Enough

Estrogen plays an important regulatory role in vaginal and urinary tissue — but it does not directly rebuild tissue structure.  Read more - why vaginal dryness persists in midlife.

Many women using vaginal estrogen still experience:

• Persistent dryness

• Ongoing irritation

• Plateaued improvement

• Fragility with intercourse

• Recurring symptoms over time

This happens because estrogen acts as a signal, not a construction material.

For tissue to function comfortably, it also depends on:

• Functional lipid layers that protect and lubricate

• Healthy cell membranes

• Adequate mitochondrial energy to support turnover

• Antioxidant protection at the local level

• Structural components that maintain elasticity and hydration

When these are compromised, estrogen signaling alone may have limited effect.

→ Read more: Why Estrogen Alone Is Not Enough for Vaginal Tissue

GSM Is a Tissue Environment Condition

Healthy vulvovaginal tissue relies on more than hormone presence. It requires a stable internal environment that supports:

• Hydration retention — the ability to hold moisture, not just apply it

• Elastic matrix integrity — collagen, elastin, and supportive lipids

• Cellular energy availability — to fuel repair and renewal

• Barrier function and immune balance — to reduce irritation

• Microbiome resilience — to support comfort and stability

When these systems lose resilience, GSM symptoms can emerge regardless of estrogen status.

→ Read more: Vaginal Dryness in Midlife: More Than a Hormone Deficiency

Why GSM Is Often Underserved

GSM is frequently:

• Under-recognized

• Minimally explained

• Treated with symptom suppression rather than tissue support

• Framed as an inevitable part of aging

Because conventional care often focuses narrowly on hormone replacement, the deeper biology of tissue maintenance is left unaddressed — even though it plays a central role in long-term comfort and function.

GSM, the Brain, and the Drive–Capacity Gap

GSM primarily describes changes in genital and urinary tissue.
However, many women notice that the impact of GSM extends beyond local symptoms, affecting desire, arousal, motivation, and overall sexual experience.

This disconnect often reflects a growing difference between neural drive and tissue capacity.

In many women, the earliest mismatch appears as reduced neural engagement, with tissue that is still physically capable of response.
In others, and often later in menopause, desire remains present while tissue responsiveness lags.  These patterns can shift or overlap over time.

The drive–capacity gap is our way of referring to this misalignment between neural desire and physical responsiveness.

What Changes in the Brain During Midlife

During midlife, the brain undergoes meaningful shifts in how desire and arousal are generated — changes that are not purely degenerative.

• Dopaminergic signaling becomes more selective, with less automatic initiation and greater reliance on context

• Cortical pattern recognition and integration increase

• Erotic imagination and narrative-based arousal often deepen

• Desire becomes more internally generated and cognitively mediated

In many women, this results in greater erotic intelligence — a clearer sense of preference, boundaries, and turn-on — even as spontaneous or reflexive arousal becomes less prominent.

Importantly, these neural shifts do not always remain synchronized with genital tissue function. Arousal may require different conditions than before, while tissue responsiveness may follow a separate biological trajectory.

When Desire and Capacity Fall Out of Sync

As genital tissue undergoes hormonal and structural change, its ability to respond comfortably to arousal can shift. At the same time, neural desire does not always change in parallel.

In many women, this results in a mismatch:

• The brain remains interested, curious, or engaged

• The tissue responds less reliably — becoming dry, fragile, irritated, or slow to respond

In other cases, the opposite pattern may be present, or both may fluctuate over time.

What’s being disrupted is not desire itself, but the biological capacity to express desire comfortably and coherently.

This lack of synchronization between neural drive and physical responsiveness is what we refer to as the drive–capacity gap.

Why This Gap Is Often Misunderstood — and Under-Addressed

When discomfort, dryness, or pain interfere with arousal, the experience is often labeled as:

• Low libido

• Psychological inhibition

• Relationship dissatisfaction

• Loss of interest

For many women, loss of interest is the lived reality — and that experience is real.

What is often missed is the biological basis of that loss.

During midlife, declining availability of DHEA and related neurosteroids in the brain alters dopaminergic tone, reward sensitivity, and arousal initiation. Desire may not feel “blocked” or suppressed — it may simply fail to arise.

At the same time, genital tissue is undergoing its own hormone-dependent structural changes.

The result is not a psychological conflict, but a loss of coordination between central drive and peripheral capacity.

This is the drive–capacity gap.

Why GSM Alone Doesn’t Explain the Full Experience

GSM describes local tissue changes.
The drive–capacity gap explains how those changes are experienced.

Together, they help clarify why:

• Desire may disappear before tissue ability, or later in the transition erotic intelligence is honed while tissue has lost functional ability. 

• Estrogen can improve tissue markers without restoring sexual confidence

• “Libido treatments” fail when tissue biology isn’t addressed
  

This is not a contradiction, it is a systems-level transition.

Current clinical frameworks divide sexual health into separate categories:

• Desire disorders (treated centrally)

• Genital tissue conditions such as GSM (treated locally)

While both domains are recognized, their interaction is not.

Guidelines do not yet account for the role of declining central neurosteroids, such as DHEA, in shaping desire — nor for how this loss interacts with changing tissue responsiveness.

As a result, care is fragmented:

• Tissue is treated without restoring drive

• Desire is assessed without restoring capacity

• And loss of interest is often misattributed

Because the gap itself is not named, it is not treated as a unified biological problem.

A More Integrated Way to Understand Midlife Sexual Health

Midlife sexual health is not governed by a single system.

It emerges from the interaction between:

• Neural drive (brain, motivation, desire)

• Hormonal signaling (estrogen, androgens, precursors)

• Tissue capacity (hydration, elasticity, resilience, repair)

• Energy availability and vascular support

When these systems move out of alignment, symptoms appear — even if no single system has “failed.”

Recognizing the drive–capacity gap allows for a more accurate, less pathologizing understanding of midlife change.

Educational Note

This content is provided for educational purposes only and is not intended to diagnose, treat, cure, or prevent any medical condition.