“What Causes Acne? The Science Behind Breakouts”

The Myth of the Dirty Pore

For decades, the cultural story around acne blamed poor hygiene, greasy food, and a failure to wash your face properly. This narrative was wrong in almost every detail. Acne is not caused by dirty skin, and aggressive scrubbing or over-washing can actually make it worse by stripping the skin barrier and triggering compensatory sebum production.

What actually causes acne is a chain of events that starts deep inside the hair follicle, driven by genetics, hormones, and systemic biology. Understanding that chain makes it much easier to understand why different treatments work, and why some common skincare habits accomplish nothing.

The Four Pathogenic Factors

1. Excess Sebum Production

Sebum is an oily substance produced by sebaceous glands attached to hair follicles. Its primary job is to moisturize and protect the skin, but when produced in excess, it creates conditions that favor acne development. Sebaceous glands are most active on the face, chest, back, and shoulders, which is exactly where acne most commonly appears.

Sebum production is primarily regulated by androgens, particularly dihydrotestosterone (DHT), which binds to androgen receptors in sebocytes (sebaceous gland cells) and stimulates their activity. This is why androgen surges, during puberty, around menstruation, or in conditions like polycystic ovary syndrome, are so closely associated with acne flares [1].

Insulin and insulin-like growth factor-1 (IGF-1) also stimulate sebaceous gland activity and androgen production. High-glycemic diets and dairy consumption raise IGF-1 levels, which may partly explain why these dietary patterns are associated with worse acne in observational studies [2].

2. Follicular Hyperkeratinization

Normally, skin cells lining the inside of hair follicles shed regularly and are expelled through the pore opening. In acne-prone skin, this process breaks down. Dead keratinocytes (skin cells) accumulate inside the follicle and stick together instead of shedding normally, forming a dense plug called a microcomedone.

The microcomedone is the precursor to all visible acne lesions. It forms before any visible breakout appears, sometimes weeks earlier. A closed comedone (whitehead) forms when the follicular opening remains sealed. An open comedone (blackhead) forms when the opening stays patent and the material inside oxidizes, turning black. Neither type is actually dirty; the black color comes from melanin oxidation, not trapped dirt [3].

What drives abnormal follicular cell shedding is not completely understood, but androgens play a role here too, as does the inflammatory environment in the follicle. Retinoids are the most effective agents at normalizing this process, which is why they are foundational to most acne treatment protocols.

3. Cutibacterium acnes Colonization

Cutibacterium acnes (formerly Propionibacterium acnes) is a normal resident of human skin, particularly in sebum-rich areas. It thrives in the low-oxygen environment of the follicle, using sebum triglycerides as a fuel source. The problem is not simply that the bacteria are present, but that the anaerobic, sebum-rich environment of a plugged follicle allows certain strains to proliferate to a degree that triggers an immune response [4].

Research over the past decade has significantly revised how we understand C. acnes and acne. It is not the case that high bacterial counts uniformly cause acne: the species contains multiple phylotypes, and certain strains appear to be associated with acne pathogenesis while others are associated with healthy skin. Strain composition, not just abundance, influences whether colonization becomes inflammatory [5].

4. Inflammation

Inflammation is not merely a downstream consequence of the first three factors: it is now recognized as an early driver of acne pathogenesis. Studies using dermoscopy and biopsy samples show that inflammatory cells are present in the follicle before visible comedone formation [6].

C. acnes activates toll-like receptors (particularly TLR2) on keratinocytes and immune cells, triggering the release of interleukin-1 alpha (IL-1a), IL-8, and other pro-inflammatory cytokines. Sebaceous lipids also activate inflammatory pathways via PPAR (peroxisome proliferator-activated receptor) signaling. The result is follicular wall rupture, which spills the contents, bacteria, lipids, and keratin debris, into the surrounding dermis and produces the red, painful lesions characteristic of inflammatory acne [7].

Understanding inflammation as an early event, not just a late one, is part of why waiting until visible lesions appear to start treatment is often too late. Preventive use of topicals like retinoids works by interrupting the process before visible lesions form.

Genetic and Hereditary Factors

Genetics plays a substantial role in acne susceptibility. Twin studies estimate heritability at around 80%, meaning genetic factors account for roughly 80% of the variance in acne severity between individuals [8]. The genes involved affect sebaceous gland function, androgen sensitivity, follicular keratinization patterns, and the robustness of the inflammatory response.

Genome-wide association studies have identified multiple loci associated with acne, including variants in genes related to androgen metabolism, inflammation, and skin barrier function. Having a parent or both parents with significant acne history substantially increases an individual’s own risk.

That said, genetics sets a predisposition, not a certainty. Environmental factors, diet, stress, skincare habits, and hormonal health all determine how that predisposition expresses itself.

The Role of the Skin Microbiome

The skin hosts trillions of microorganisms, and research into the skin microbiome has complicated the previously simple story of acne and bacteria. Rather than being a purely pathogenic organism to be eliminated, C. acnes in a healthy microbiome plays a role in producing short-chain fatty acids that maintain a low skin pH and inhibit the growth of more overtly harmful pathogens like Staphylococcus aureus.

Disrupting the microbiome with broad-spectrum antibiotics, a common acne treatment, has consequences beyond killing C. acnes. It reduces overall microbial diversity and can select for resistant strains of multiple species. This is part of the rationale behind using targeted approaches like benzoyl peroxide, which kills bacteria without promoting resistance, or light-based therapies that selectively activate porphyrins within C. acnes [9].

Research into probiotics for acne, both oral and topical, is early-stage but biologically plausible. Some strains of Lactobacillus and Bifidobacterium produce antimicrobial peptides and modulate inflammatory cytokine production in ways that could reduce acne pathogenesis [10].

Internal Triggers and Systemic Drivers

Diet

The connection between diet and acne is stronger than dermatology textbooks acknowledged for most of the 20th century. The strongest evidence involves glycemic load. High-glycemic diets spike insulin and IGF-1, which promote sebum synthesis and increase androgen bioavailability. A randomized controlled trial found that a low-glycemic diet produced significant reductions in acne lesion counts and reductions in serum androgen levels over 12 weeks [11].

Dairy, particularly skimmed milk, has a consistent association with acne in epidemiological studies. This is likely mediated through whey protein’s insulin-stimulating effects and the presence of IGF-1 precursors in milk. Dark chocolate, in contrast, has a more mixed evidence base; small studies have shown effects but methodological limitations make it hard to draw firm conclusions [12].

Stress

Stress reliably worsens acne, and the mechanism is well characterized. Psychological stress activates the hypothalamic-pituitary-adrenal (HPA) axis, increasing cortisol and adrenal androgens (particularly DHEAS). Both amplify sebaceous gland activity. The skin also has its own local stress-response system, producing corticotropin-releasing hormone that directly stimulates sebocytes [13].

Stress also impairs the skin barrier (increasing transepidermal water loss and susceptibility to irritation) and dysregulates immune function in ways that favor inflammatory acne. Sleep deprivation, which activates similar stress pathways, has comparable effects.

Certain Medications and Topical Products

Some medications can induce acneiform eruptions: lithium, corticosteroids, some anticonvulsants, EGFR inhibitors (used in oncology), and anabolic steroids are the most common culprits. Medication-induced acne tends to be monomorphic (all lesions look similar) and distributed atypically (often on the trunk rather than the face).

Comedogenic cosmetic ingredients can worsen acne in susceptible individuals. Heavily occlusive ingredients, certain oils (coconut oil is highly comedogenic for many people), and some hair products that contact the forehead and hairline (“pomade acne”) are worth reviewing if breakouts track with product use.

The Gut-Skin Axis

Emerging research is revealing connections between gut microbiome composition and inflammatory skin conditions including acne. People with acne have measurably different gut microbiome profiles compared to controls, with lower levels of beneficial bacteria like Lactobacillus and Bifidobacterium and higher levels of species associated with systemic inflammation [14].

The proposed mechanisms involve gut barrier integrity, systemic inflammatory tone, and the gut’s role in regulating circulating IGF-1 and androgens. This does not mean probiotic supplementation is a primary acne treatment, but it suggests that gut health is part of the broader picture of what drives breakouts in some individuals.

Why Acne Looks Different at Different Life Stages

Adolescent Acne

Pubertal acne is primarily driven by the androgen surge of puberty, which dramatically increases sebaceous gland size and sebum production. Both sexes are affected, though boys tend to develop more severe acne due to higher androgen levels. The comedonal, mixed, and inflammatory patterns seen in teenage acne reflect the direct impact of rising androgens on follicular biology.

Adult Acne

Adult acne, particularly in women, has a different character. It tends to be inflammatory and cystic along the lower face, often coexisting with dry or combination skin (unlike the oily teen skin typical of adolescent acne). The drivers are more nuanced: cyclic hormonal fluctuations, chronic stress, diet, and subclinical hormonal conditions like PCOS or adrenal hyperactivity often contribute. It responds less well to the same topical protocols that work for teenage acne and often requires addressing the hormonal dimension explicitly [15].

Neonatal and Infantile Acne

Neonatal acne (appearing in the first weeks of life) is common and generally resolves spontaneously. It is thought to be driven by maternal androgen exposure in utero and the infant’s own adrenal androgen production. Infantile acne (appearing after six weeks) is less common and warrants evaluation for any underlying hormonal issues, though most cases are benign and self-resolving.

Related Reading

• Acne Treatment Options: From Topicals to Regenerative Therapies
• Hormonal Acne: Causes, Patterns, and How to Treat It
• Severe Acne Treatment: Options Beyond Accutane
• Red Light Therapy at Home
• Peptide Injections: What They Are and How They Work

References

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