“What Causes Acne? The Science Behind Breakouts”

Acne is caused by four processes inside the hair follicle: androgen-driven excess sebum, skin cells that clump and plug the pore, overgrowth of certain strains of Cutibacterium acnes, and inflammation. Genetics sets how strongly those processes run, with a twin study by Bataille and colleagues (2002) estimating heritability at around 80%, while diet, stress, medications and hormonal conditions such as polycystic ovary syndrome (PCOS) act on the same four steps [8].

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.

Dermatologists call the common form acne vulgaris, and the unit where it starts is the pilosebaceous unit: a hair follicle plus its attached sebaceous gland. Every whitehead, blackhead, papule, pustule, nodule and cyst begins in one of these units, which is why the acne condition overview groups all of them under one diagnosis.

The Four Pathogenic Factors

The four factors below are the standard model of acne pathogenesis used in dermatology. They overlap in time, and each one is the target of a different class of treatment, which is why combination therapy is the norm.

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.

How the four factors compare

Each factor has its own driver and its own set of treatments. The table summarizes the model described above and the drug classes the American Academy of Dermatology guideline discusses for each one [16].

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].

Antibiotic stewardship is now part of mainstream acne care for the same reason. The 2024 American Academy of Dermatology guideline advises pairing topical or oral antibiotics with benzoyl peroxide and limiting how long oral antibiotics are used, so that resistant C. acnes strains are less likely to emerge [16].

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].

Dietary fat itself has a weak evidence base as an acne trigger. Many of the foods blamed for breakouts, such as fries, pizza and pastries, are also high-glycemic, which makes the effect of fat hard to separate. Cooking grease that sits on the skin in a hot kitchen is a different matter, because it can block pores from the outside.

Hormones and Hormonal Conditions

Hormonal acne is not a separate disease: it is the same four-factor process with androgens as the main accelerator. Testosterone is converted to DHT in the skin by the enzyme 5-alpha reductase, and DHT is what drives sebocytes. Flares in the week before a period, after stopping a hormonal contraceptive, or during perimenopause all follow shifts in the balance between androgens and estrogen.

Polycystic ovary syndrome (PCOS) is the hormonal condition most often linked to persistent adult acne in women, usually alongside irregular periods, excess facial or body hair (hirsutism), or scalp hair thinning. Less common causes of high androgens include congenital adrenal hyperplasia and androgen-secreting tumors. Testosterone replacement therapy (TRT) and anabolic steroid use in men can also raise sebum output enough to trigger acne on the chest and back. The hormonal acne treatment guide covers how clinicians treat this pattern.

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.

What Causes Acne on the Chin, Forehead, Back and Chest?

Where acne appears gives a clue to what is driving it, though the pattern is a hint, not a diagnosis. Popular face mapping charts that tie each zone to a specific organ have no research support. The patterns below are the ones dermatologists actually use.

Jawline and chin acne

Deep, tender papules and nodules along the jawline, chin and neck are the classic pattern of hormonal acne in adult women. They often flare in the days before a period and can point to androgen excess, including PCOS. Hormonal treatments such as spironolactone or combined oral contraceptives are commonly considered for this pattern, as described in the guide to hormonal acne causes and patterns.

Forehead and hairline acne

Small closed comedones across the forehead and along the hairline are often linked to hair oils, pomades, hats and helmets. This is a contact pattern: the product or the friction blocks follicles from the outside. Switching to non-comedogenic hair products and keeping them off the skin is the first step.

Back and chest acne

Truncal acne on the back, chest and shoulders follows the distribution of large sebaceous glands. Friction and trapped sweat from backpacks, tight sportswear and equipment straps can add a mechanical component known as acne mechanica. Sudden truncal acne in a man who has started testosterone or anabolic steroids is a common and recognizable pattern.

What Causes Cystic and Severe Acne?

Cystic acne, more precisely nodulocystic acne, forms when inflammation runs deep in the dermis and the follicle wall ruptures below the surface. The same four factors are at work, but the inflammatory response is stronger and the lesions are larger, more painful and more likely to leave scars. A strong family history and high androgen activity are the factors most often seen in people with this form.

The rare severe variants, acne conglobata and acne fulminans, involve interconnected nodules and, in acne fulminans, fever and joint pain. According to the American Academy of Dermatology guideline (Reynolds et al., 2024), oral isotretinoin is strongly recommended for acne that is severe, scarring, causing psychosocial burden, or not responding to standard oral or topical therapy [16]. In the US, isotretinoin is dispensed through iPLEDGE, an FDA-required safety program, because it causes birth defects. The options are compared in detail in treatment for severe acne, and scarring is covered in the post on acne scar treatment.

Conditions That Look Like Acne

Several skin conditions resemble acne vulgaris but have different causes, and they do not respond to the same treatments. Telling them apart is one of the main reasons to see a clinician when acne does not behave as expected.

• Rosacea causes facial redness, flushing and papules, but it has no comedones and is driven by vascular and immune changes rather than follicle plugging.
• Fungal acne (Malassezia folliculitis) produces uniform, itchy bumps on the forehead, chest and back, caused by yeast rather than bacteria, and it can worsen with antibiotics.
• Perioral dermatitis causes small bumps around the mouth and nose, and it is often triggered by topical steroid creams.
• Hidradenitis suppurativa causes deep, recurring nodules in the armpits, groin and under the breasts, and it needs its own treatment plan.
• Steroid acne and drug-induced acneiform eruptions appear as uniform lesions after starting corticosteroids, lithium, EGFR inhibitors or anabolic steroids.

Eczema and psoriasis can coexist with acne and complicate treatment, because many acne topicals irritate an inflamed skin barrier. The eczema condition page covers that overlap.

When to See a Clinician About What Is Causing Your Acne

Over-the-counter benzoyl peroxide, adapalene and salicylic acid are a reasonable first step for mild comedonal or papular acne. It is time for a medical evaluation when acne is nodular or cystic, when it leaves scars or dark marks, when it has not improved after several weeks of consistent over-the-counter care, or when it comes with irregular periods, excess hair growth or sudden onset in adulthood.

Board-certified dermatologists diagnose and treat acne and prescribe retinoids, antibiotics, hormonal therapy and isotretinoin. Primary care physicians treat many mild to moderate cases, and gynecologists and endocrinologists are often involved when PCOS or another hormonal cause is suspected. Integrative and functional medicine practitioners tend to focus on diet, insulin resistance and gut health, areas where the research is supportive but still limited. The acne treatment guide explains how each of these approaches works.

Some clinics also offer procedures that target specific causes, such as blue light or photodynamic therapy for C. acnes, chemical peels for comedones, and red light or low-level laser therapy for inflammation. The 2024 AAD guideline found the evidence for light-based treatments limited, and most of these services are cash pay [16]. The post on red light therapy at home covers what home devices can and cannot do, and the red light therapy guide summarizes the clinic version.

To compare providers, you can browse clinics that offer acne treatment across the US. Listing order on Regenerated.com is not paid ranking, Featured slots are labeled and capped, and Verified means the clinic completed credential checks, not that it paid more. Using the directory is free for patients, and inclusion in the directory is not an endorsement. The guide to Featured, Verified and organic listings explains each label.

Frequently asked questions

What is the main cause of acne?

The main cause of acne is a blocked hair follicle. Androgen hormones such as DHT drive sebaceous glands to make extra sebum, dead skin cells stick together and plug the pore, acne-associated strains of Cutibacterium acnes multiply inside the plug, and the immune system reacts with inflammation. Genetics decides how strongly this chain runs, with twin research estimating heritability near 80%. Diet, stress and medications act on the same steps.

Does dirty skin or poor hygiene cause acne?

Dirty skin does not cause acne. The process starts deep inside the follicle, below the reach of washing, and the dark color of a blackhead comes from oxidized melanin, not dirt. Washing twice a day with a gentle cleanser is enough for most people. Scrubbing hard or washing too often can irritate the skin barrier and make inflammatory acne worse rather than better.

Can food cause acne?

Some foods can make acne worse in some people. The strongest evidence involves high-glycemic diets, which raise insulin and IGF-1; a 12 week randomized trial by Smith and colleagues (2007) found fewer lesions on a low-glycemic diet. Skim milk and whey protein show a consistent association in observational studies. The evidence on chocolate and greasy food is weak, so cutting them out is unlikely to clear acne alone.

What causes acne in adults who never had it as teenagers?

Adult-onset acne is most often driven by hormonal shifts, chronic stress, poor sleep, new skincare or hair products, or medications such as corticosteroids, lithium and testosterone. In women, acne along the jawline with irregular periods or excess hair growth can signal PCOS and is worth a medical evaluation. Adult acne often responds less well to teenage protocols, so a dermatologist may add hormonal therapy such as spironolactone.

Why does acne keep coming back?

Acne keeps coming back because the drivers behind it, such as genetics, androgen sensitivity and sebum output, are still active after the visible spots heal. Microcomedones form weeks before a breakout appears, so stopping treatment once skin looks clear usually allows new lesions to develop. Dermatologists often recommend a topical retinoid for maintenance. Isotretinoin is the one treatment that targets all four causes and can lead to long remissions.

Can stress cause acne breakouts?

Stress can trigger and worsen acne breakouts. Psychological stress activates the HPA axis, raising cortisol and adrenal androgens such as DHEAS, which increase sebum production. Skin cells also release corticotropin-releasing hormone that stimulates sebaceous glands directly, as described by Zouboulis and Bohm (2004). Stress weakens the skin barrier and shifts immune function toward inflammation, and lack of sleep has similar effects on the skin.

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

Sources

1. Deplewski D, Rosenfield RL. “Role of hormones in pilosebaceous unit development.” Endocr Rev. 2000;21(4):363-392. doi:10.1210/edrv.21.4.0404 ↩
2. Melnik BC, John SM, Schmitz G. “Over-stimulation of insulin/IGF-1 signaling by western diet may promote diseases of civilization: lessons learnt from laron syndrome.” Nutr Metab (Lond). 2011;8:41. doi:10.1186/1743-7075-8-41 ↩
3. Kligman AM. “An overview of acne.” J Invest Dermatol. 1974;62(3):268-287. doi:10.1111/1523-1747.ep12676801 ↩
4. Nakatsuji T et al. “Antimicrobials from human skin commensal bacteria protect against Staphylococcus aureus and are deficient in atopic dermatitis.” Sci Transl Med. 2017;9(378):eaah4680. doi:10.1126/scitranslmed.aah4680 ↩
5. Fitz-Gibbon S et al. “Propionibacterium acnes strain populations in the human skin microbiome associated with acne.” J Invest Dermatol. 2013;133(9):2152-2160. doi:10.1038/jid.2013.21 ↩
6. Jeremy AH et al. “Inflammatory events are involved in acne lesion initiation.” J Invest Dermatol. 2003;121(1):20-27. doi:10.1046/j.1523-1747.2003.12321.x ↩
7. Kim J. “Review of the innate immune response in acne vulgaris: activation of Toll-like receptor 2 in acne triggers inflammatory cytokine responses.” Dermatology. 2005;211(3):193-198. doi:10.1159/000087011 ↩
8. Bataille V et al. “The influence of genetics and environmental factors in the pathogenesis of acne: a twin study of acne in women.” J Invest Dermatol. 2002;119(6):1317-1322. doi:10.1046/j.1523-1747.2002.19621.x ↩
9. Kawada A et al. “Acne phototherapy with a high-intensity, enhanced, narrow-band, blue light source: an open study and in vitro investigation.” J Dermatol Sci. 2002;30(2):129-135. doi:10.1016/s0923-1811(02)00068-2 ↩
10. Bowe WP, Patel NB, Logan AC. “Acne vulgaris, probiotics and the gut-brain-skin axis: from anecdote to translational medicine.” Benef Microbes. 2014;5(2):185-199. doi:10.3920/BM2012.0060 ↩
11. Smith RN et al. “The effect of a high-protein, low glycemic-load diet versus a conventional, high glycemic-load diet on biochemical parameters associated with acne vulgaris.” J Am Acad Dermatol. 2007;57(2):247-256. doi:10.1016/j.jaad.2007.01.046 ↩
12. Adebamowo CA et al. “High school dietary dairy intake and teenage acne.” J Am Acad Dermatol. 2005;52(2):207-214. doi:10.1016/j.jaad.2004.08.007 ↩
13. Zouboulis CC, Bohm M. “Neuroendocrine regulation of sebocytes: a pathogenetic link between stress and acne.” Exp Dermatol. 2004;13(Suppl 4):31-35. doi:10.1111/j.1600-0625.2004.00254.x ↩
14. Bowe WP, Logan AC. “Acne vulgaris, probiotics and the gut-brain-skin axis: back to the future?” Gut Pathog. 2011;3(1):1. doi:10.1186/1757-4749-3-1 ↩
15. Dreno B et al. “Acne in women: a real-world study with dermatologist’s evaluation.” Int J Dermatol. 2019;58(3):e37-e38. doi:10.1111/ijd.14176 ↩
16. Reynolds RV, Yeung H, Cheng CE, et al. “Guidelines of care for the management of acne vulgaris.” J Am Acad Dermatol. 2024;90(5):1006.e1-1006.e30. doi:10.1016/j.jaad.2023.12.017 PubMed 38300170 ↩