Acne starts when a hair follicle gets clogged with oil and dead skin cells, then progresses through a chain reaction involving hormones, bacteria, and your immune system. Nearly 10% of young people worldwide have acne at any given time, and the rate is about 25% higher in young women than young men. Understanding what’s actually happening beneath your skin helps explain why breakouts show up where they do, why they vary in severity, and why certain habits seem to make them worse.
The Four Steps That Create a Pimple
Every pimple begins as a “microcomedone,” a tiny blockage invisible to the naked eye. From there, four overlapping processes turn it into something you can see and feel: excess oil production, a buildup of dead skin cells inside the pore, bacterial overgrowth, and inflammation. These don’t happen in a neat sequence. They feed into each other, which is why acne can escalate quickly and why treating just one factor often isn’t enough.
How Oil Production Gets Out of Control
Your skin’s oil glands (called sebaceous glands) are directly controlled by hormones, especially androgens like testosterone. These glands actually contain the enzymes needed to convert weaker hormones into more potent forms right at the skin’s surface. The locally produced hormones then ramp up oil output. This is why acne typically kicks in during puberty, when androgen levels surge, and why hormonal shifts during menstrual cycles, pregnancy, or polycystic ovary syndrome can trigger breakouts in adults.
Another hormone, insulin-like growth factor 1 (IGF-1), amplifies the process. IGF-1 stimulates the oil glands to produce even more fat-rich sebum. It also interferes with a protein that normally keeps androgen activity in check, essentially removing the brakes on oil production. This IGF-1 connection is one reason diet plays a role in acne, which we’ll get to later.
Dead Skin Cells Seal the Pore Shut
Your pores are lined with skin cells that normally shed and get pushed to the surface by flowing oil. In acne-prone skin, these cells stick together instead of shedding cleanly. They form a plug at the top of the follicle, trapping oil underneath. This process, called follicular hyperkeratinization, creates the initial blockage that every type of acne lesion builds on.
What triggers the sticky buildup isn’t fully understood, but it appears to be driven partly by the same hormones that increase oil production and partly by localized inflammation that changes how skin cells behave. Even before a visible pimple appears, there are already inflammatory signals circulating around the follicle, altering the skin cell turnover process from the inside.
Bacteria Fuel the Fire
A bacterium called Cutibacterium acnes lives naturally on everyone’s skin. It feeds on sebum and thrives in low-oxygen environments, which makes a clogged, oil-filled pore an ideal home. As C. acnes multiplies inside the blocked follicle, it releases enzymes that break down the oil into irritating byproducts called free fatty acids. It also produces enzymes that degrade the structural components of skin tissue, including hyaluronic acid in the surrounding layers, which helps the bacteria spread and deepens the damage.
The real problem isn’t just the bacteria, though. It’s how your immune system responds to them. C. acnes activates your skin’s innate immune sensors, triggering a cascade of inflammatory signaling molecules. These signals recruit white blood cells (particularly neutrophils) to the site, and those immune cells release their own damaging chemicals as they try to fight the infection. The follicle wall can rupture from the combined assault of bacterial enzymes and immune activity, spilling its contents into the surrounding skin and spreading inflammation outward.
Inflammation Starts Earlier Than You Think
One of the more surprising findings in acne research is that inflammation doesn’t just show up once a pimple is red and swollen. Inflammatory signals are present even in skin that looks completely normal, before any visible lesion forms. Blood vessels near the hair follicle deliver immune signaling molecules that influence both the skin cell buildup and the oil production process. By the time you notice a bump, the inflammatory process has been running for days or even weeks.
This early, invisible inflammation helps explain why acne can feel unpredictable. What appears to be a sudden breakout is actually the visible stage of a process that started well before anything showed on the surface.
What Each Type of Lesion Looks Like Inside
The different types of acne reflect how far the clogging and inflammation have progressed:
- Blackheads (open comedones): The pore is clogged with oil and dead skin cells but remains open at the surface. The dark color comes from oxidation when the plug is exposed to air, not from dirt.
- Whiteheads (closed comedones): The same clog, but a thin layer of skin covers the opening, keeping it sealed and giving it a white or flesh-toned appearance.
- Papules: A comedone that has become inflamed, forming a small red or pink bump. No visible pus yet.
- Pustules: An inflamed bump with a white or yellow center filled with pus, surrounded by a red ring. This is the classic “pimple.”
- Nodules: Large, firm, painful bumps that develop deep within the skin when the follicle wall ruptures and inflammation spreads into deeper tissue layers.
- Cysts: Large, pus-filled lesions that form deep under the skin. These carry the highest risk of permanent scarring.
Genetics Set the Stage
If your parents had significant acne, your chances of developing it are high. Twin studies estimate that acne severity is about 85% heritable. Identical twins show a concordance rate of 0.86, meaning if one twin has acne, the other almost certainly does too. Fraternal twins, who share roughly half their genes, have a concordance rate of only 0.42. What you inherit likely includes the size and activity level of your oil glands, how your skin cells shed inside the follicle, and how aggressively your immune system responds to C. acnes.
How Diet Connects to Breakouts
The link between diet and acne runs through insulin and IGF-1. High-glycemic foods (white bread, sugary drinks, processed snacks) cause a sharp spike in blood sugar, which triggers higher insulin and IGF-1 levels. Those hormones, as described earlier, directly stimulate oil production and remove the molecular brakes on androgen activity in the skin.
Dairy has a similar effect. Both whey and casein, the two main proteins in milk, raise serum levels of IGF-1 and insulin. This appears to be true regardless of whether the milk is whole or skim, which is why low-fat dairy doesn’t necessarily help. The effect is most consistently linked to milk and whey protein supplements, with less clear data on cheese and yogurt. Cutting these foods doesn’t cure acne on its own, but for some people it meaningfully reduces the hormonal signals that drive oil overproduction.
Other Common Triggers
Beyond hormones and diet, several external factors can worsen the clogging and inflammation cycle. Friction or pressure on the skin from helmets, tight clothing, or resting your face on your hands can push debris deeper into pores. Certain cosmetics and sunscreens contain oils that mimic the pore-clogging effect of excess sebum (look for “non-comedogenic” on labels). Stress raises cortisol and androgen levels, which circles back to increased oil production. And over-washing or scrubbing your face can damage the skin barrier, paradoxically increasing inflammation and making breakouts worse rather than better.