Acne in Menopause: Why It Happens, What Is Really Driving It, and How to Treat It Properly

Acne in menopause is one of the most misunderstood skin conditions affecting women today. Many women reach their late 40s or 50s expecting wrinkles, dryness or sensitivity, only to be blindsided by deep, painful breakouts that look and behave nothing like the acne they may have experienced in their teens.

This is not “bad luck skin”. It is not a failure of hygiene. And it is certainly not something that should be treated with teenage acne products.

Acne in menopause is a distinct clinical entity driven by hormonal shifts, inflammatory pathways, barrier dysfunction and metabolic stress. Understanding what is actually happening inside the skin is the difference between endless flare-ups and real, lasting improvement.

What is acne in menopause?

Acne in menopause refers to acne that appears or persists in women during perimenopause and post-menopause, typically from the mid-40s onwards. It may present as:

• persistent acne continuing from adolescence

• new-onset acne appearing for the first time in adult life

• recurrent acne that disappeared for years and then returned

Clinically, menopausal acne tends to be deeper, more inflammatory, slower to heal and far more likely to leave pigmentation or scarring. The skin itself is often drier, more reactive and less resilient than younger skin, which makes conventional acne treatments poorly tolerated and often counterproductive.

Why acne happens in menopause

The primary driver of acne in menopause is not “high testosterone” in the way many people assume. Most menopausal women with acne have blood tests that fall within normal hormonal ranges.

The real issue is relative hyperandrogenism.

Relative hyperandrogenism explained

During menopause, oestrogen levels drop sharply, while androgen levels decline much more slowly. At the same time, levels of sex hormone binding globulin (SHBG) fall. SHBG is the protein that binds and inactivates circulating androgens.

When SHBG drops, more free androgens are available to act on the skin, even if total androgen levels are technically normal.

The result is an androgen-dominant environment at the skin level.

Sebaceous glands respond by increasing oil production, altering sebum composition and triggering inflammatory cascades that lead to acne.

This is why women are often told “your hormones are fine” while their skin is clearly telling a different story.

The sebaceous gland is more than an oil gland

Modern research has confirmed that the sebaceous gland functions as a neuroendocrine and immunologically active organ.

Sebaceous glands are influenced by:

• androgens such as testosterone and DHT

• insulin and insulin-like growth factor-1 (IGF-1)

• stress hormones including corticotropin-releasing hormone (CRH)

• inflammatory cytokines

• vitamin D and retinoid signalling

In menopausal skin, several of these pathways become dysregulated at once.

IGF-1 levels have been shown to correlate with acne severity in adult women. Stress increases CRH, which directly stimulates local androgen production within the skin by increasing enzyme activity that converts DHEA into testosterone.

This means stress is not just an emotional trigger. It directly amplifies acne at a biochemical level.

Acne in menopause is primarily an inflammatory disease

For decades, acne was framed as a bacterial problem. This is now outdated science.

Current evidence shows that inflammation often occurs before clogged pores even form. Cutibacterium acnes does not need to be present in excess to trigger acne. Instead, the issue lies in immune activation and microbiome imbalance.

Key inflammatory mechanisms include:

• activation of toll-like receptor 2 (TLR-2) on keratinocytes and sebocytes

• release of inflammatory cytokines such as IL-8 and IL-12

• chronic low-grade inflammation that persists even between breakouts

Rather than bacterial overgrowth, menopausal acne is associated with the dominance of more inflammatory bacterial strains and the presence of biofilms that make lesions slower to resolve and more resistant to treatment.

This is why over-antibacterial routines often worsen menopausal acne over time.

Skin barrier dysfunction makes everything worse

One of the defining features of menopausal skin is barrier impairment.

Oestrogen plays a critical role in:

• ceramide production

• lipid organisation

• hydration regulation

• barrier repair speed

As oestrogen declines, the skin experiences increased transepidermal water loss, reduced lipid synthesis and slower recovery from inflammation.

In menopausal acne, barrier dysfunction is present not only in active breakouts but also in surrounding “normal-looking” skin. This means the skin is primed for inflammation long before acne becomes visible.

When harsh acne treatments strip lipids and disrupt the acid mantle, inflammation escalates, healing slows and pigmentation risk increases.

It doesn’t work like that. You cannot strip fragile skin into submission and expect it to heal.

The role of insulin resistance and metabolic health

Acne in menopause is often linked to underlying metabolic stress, even in women who appear outwardly healthy.

Insulin resistance and hyperinsulinaemia:

• increase ovarian and adrenal androgen production

• suppress SHBG, increasing free androgen activity

• amplify IGF-1 signalling in the skin

Abdominal obesity, poor sleep, chronic stress and high-glycaemic diets all contribute to this metabolic environment.

Dairy, whey protein supplements and refined carbohydrates have been shown to elevate insulin and IGF-1 levels, which can directly worsen acne severity.

In this context, acne becomes a visible marker of systemic imbalance rather than a purely cosmetic concern.

How acne in menopause presents on the skin

Menopausal acne does not follow a single pattern, which contributes to frequent misdiagnosis.

Common presentations include:

• deep inflammatory papules or nodules, often around the mouth or jaw

• macrocomedones, particularly in smokers or women over 40

• panfacial acne rather than just jawline involvement

• truncal acne affecting the chest, back or shoulders

• persistent redness and pigmentation after lesions resolve

Because menopausal skin is more reactive, post-inflammatory erythema and hyperpigmentation are far more common and longer lasting.

Conditions such as rosacea, steroid-induced acne and gram-negative folliculitis are often mistaken for menopausal acne, highlighting the importance of accurate assessment.

Why traditional acne treatments fail in menopause

Most acne products are designed for young, oily, resilient skin. Menopausal skin is none of those things.

Common reasons treatments fail include:

• excessive use of benzoyl peroxide or alcohol-based products

• aggressive exfoliation that damages the barrier

• prolonged antibiotic use that disrupts the microbiome

• ignoring hormonal and metabolic drivers

Menopausal acne requires a long-term, inflammation-aware strategy rather than a short-term “clear it fast” mindset.

Evidence-based treatment principles for acne in menopause

Effective management of acne in menopause rests on several non-negotiable principles. When these are followed, skin calms, lesions resolve faster and relapse rates reduce significantly.

Support the skin barrier first

Barrier repair is not optional in menopausal acne. Declining oestrogen leads to reduced ceramide synthesis, impaired lipid organisation and increased transepidermal water loss. This creates a pro-inflammatory environment even before acne lesions form.

Restoring skin-identical lipids such as ceramides, cholesterol and essential fatty acids reduces baseline inflammation, improves resilience and dramatically increases tolerance to active treatments. Without barrier support, even well-chosen acne therapies will fail.

Modulate androgen activity at the skin level

Because menopausal acne is driven by relative hyperandrogenism rather than absolute hormone excess, topical modulation of androgen activity at the skin level is a critical and often overlooked strategy.

Roccoco Botanicals Plant Harmonising is formulated specifically for this purpose. It contains botanical actives traditionally used to inhibit the conversion of testosterone to dihydrotestosterone (DHT) and to reduce androgen receptor signalling within the pilosebaceous unit.

By attenuating DHT activity locally in the skin, Plant Harmonising helps:

• reduce androgen-driven sebum stimulation

• calm hormonally mediated inflammation

• support clearer skin without systemic hormone manipulation

This approach is particularly valuable for menopausal women who are not candidates for, or do not wish to use, oral anti-androgen therapy.

Control inflammation, not just oil

Menopausal acne is primarily an inflammatory condition, not an oil problem. Targeting sebum alone ignores the immune activation and cytokine signalling that sustain breakouts.

Anti-inflammatory botanicals, microbiome-supportive formulations and gentle keratolytic activity consistently outperform harsh antibacterial or drying agents in this age group. Reducing inflammation at its source shortens lesion duration, limits post-inflammatory erythema and lowers the risk of pigmentation and scarring.

Use retinoid alternatives intelligently and sparingly

Vitamin A derivatives remain one of the most effective long-term tools for managing acne, but traditional retinoids are often poorly tolerated in menopausal skin due to barrier fragility and heightened inflammatory reactivity.

For this reason, retinol alternatives such as retinaldehyde (retinal) are often a more appropriate choice. Retinal sits one metabolic step closer to retinoic acid than retinol, meaning it requires less enzymatic conversion in the skin to become active. This allows for comparable efficacy at lower concentrations, with a significantly reduced risk of irritation.

Retinal has demonstrated benefits in:

• normalising follicular keratinisation

• reducing inflammatory lesion formation

• supporting collagen synthesis

• improving overall skin texture and tone

When introduced gradually and supported with barrier-repairing formulations, retinal can address acne, photoageing and textural irregularities simultaneously without provoking the excessive dryness, stinging or erythema commonly seen with aggressive retinoid use.

In compromised menopausal skin, overuse of traditional retinoids often escalates inflammation, impairs barrier recovery and prolongs post-inflammatory erythema. A measured approach using gentler vitamin A derivatives respects the biology of menopausal skin and delivers more sustainable results over time.

Acne in menopause is influenced by sleep quality, stress load, insulin signalling, dietary glycaemic load and overall metabolic health. These factors directly affect androgen bioavailability, IGF-1 activity and inflammatory signalling in the skin.

Skincare alone cannot override chronic systemic stress, but when lifestyle factors are addressed alongside targeted topical therapy, outcomes improve significantly.

At the end of the day, menopausal acne responds best when the skin is supported, inflammation is calmed and hormonal signalling is gently rebalanced, not when the skin is stripped, suppressed or overtreated.