Acne is a condition of the pilosebaceous unit — a small structure in your skin made up of a hair follicle (a "pore") and an attached oil gland called a sebaceous gland. The oil these glands produce is called sebum.

In a normal pore, sebum travels up to the surface of your skin, dead skin cells shed and flake off, and everything moves along quietly. Acne begins when this smooth process breaks down and the pore gets plugged.

That's also why acne shows up in specific places: the face, chest, back, and shoulders — the parts of the body where sebaceous glands are largest and most numerous. It rarely appears on your palms or shins for the same reason.

Dermatologists describe four biological processes that together produce acne. They interact with each other rather than happening in a strict sequence — often all four are underway at the same time in the same pore.

The earliest stage is a microcomedone — an invisible plug forming deep in the pore. From there:

A comedone becomes either a blackhead (the plug reaches the surface and darkens from oxidation — not dirt) or a whitehead (it stays trapped under the skin). If inflammation kicks in, it becomes a papule (a small red bump), a pustule (with visible pus), or, deeper down, a painful nodule or cyst.

If you rank all the things that influence whether someone gets acne, hormones and genetics dominate the list. Most of the other factors people worry about — diet, stress, skincare — sit far below these two.

Androgens are a group of hormones — including testosterone, DHT, and DHEA-S — that bind to receptors in your oil glands and tell them to grow and produce more sebum. Interestingly, most people with acne have completely normal hormone levels in their blood. The action happens locally, right in the skin.

This is why the timing of acne is so predictable. Oil production starts to rise around age 7 or 8 (during a stage called adrenarche, when the adrenal glands begin producing androgens) and accelerates through puberty, peaking in the late teens and early twenties. One of the most compelling pieces of evidence for how central androgens are: people who genetically lack functional androgen receptors don't develop acne at all.

For women, acne often tracks with the menstrual cycle. Studies show most women with acne notice a flare in the week or so before their period, when estrogen drops and the hormonal balance shifts. Many women also develop what's often called "hormonal acne" along the jawline and lower face (the "U-zone") — often deeper, more inflammatory, and more resistant to over-the-counter products.

Conditions of androgen excess — like polycystic ovary syndrome (PCOS) — frequently cause or worsen acne. Persistent adult acne, especially alongside irregular periods or excess hair growth, is worth mentioning to a doctor because a hormonal evaluation can help clarify what's going on.

The other huge driver — and the one people tend to underestimate — is genetics. A large twin study found that about 81% of the variation in who gets acne is explained by genes. A second, independent study estimated 85%. Having a parent or sibling with acne substantially raises your risk, and family history predicts more severe and more persistent breakouts.

There's no single "acne gene." Many genes contribute — some affecting oil production, some affecting how your follicles behave, some affecting how strongly your immune system responds to inflammation. The practical takeaway: two people with the exact same diet and skincare routine can have wildly different skin, largely because of biology they were born with.

The old idea that acne is an "infection" caused by bad bacteria is outdated. Cutibacterium acnes — the bacterium linked to acne — is actually a normal resident of healthy skin. It helps maintain the skin's protective acidity and crowds out more harmful bacteria. Some strains of C. acnes are even associated with clear skin.

What matters is the balance and type of bacteria, not the mere presence of the bug. Inflamed acne is linked with a less diverse, less healthy microbial community on the skin — an imbalance dermatologists call dysbiosis.

This is part of why oral antibiotics for acne are a mixed bag: they can calm inflammation, but overusing them can disrupt beneficial bacteria and drive antibiotic resistance. It's also why treatments like benzoyl peroxide are so useful — they reduce C. acnes without teaching the bacteria to resist antibiotics.

Beyond hormones and genes, a handful of everyday factors can nudge acne in one direction or the other. None of them cause acne on their own — but they can matter. Here's the current evidence, from strongest to weakest.

Because acne is an inflammatory condition, it can leave lasting changes on the skin even after the active pimple is gone. Understanding the difference between them matters, because they respond to different treatments.

A 2023 review of 37 studies found scars in about 47% of people with acne. The deeper and longer-lasting the inflammation, the higher the risk of scarring — which is why dermatologists urge treating acne earlier rather than "waiting it out."

Acne is most common precisely when androgen-driven oil production is at its peak — the late teens and early twenties. It affects up to 50 million Americans each year, and roughly 85% of people between ages 12 and 24 experience at least mild acne.

Two things worth knowing about that peak:

First, adolescent acne often persists well into the 20s and 30s. Roughly 50% of women experience acne in their 20s, and 30–40% in their 30s.

Second, adult-onset acne — acne that appears for the first time after age 25 — is increasingly recognized, especially in women.

If you're a college student dealing with breakouts, you're squarely in the largest and best-studied group affected by this condition. That doesn't make it less annoying — but it does mean you're not an outlier, and effective, evidence-based treatments have been developed for exactly this stage of life.