Keratosis pilaris (KP) is caused by a buildup of keratin, a protective protein your skin naturally produces, that plugs individual hair follicles and creates those small, rough bumps. The process is driven primarily by genetics, but hormones, dry air, and certain medical conditions all play a role in how severe it gets and when it flares. About 40% of adults and up to 50–80% of adolescents have some degree of KP, making it one of the most common skin conditions that exists.
How Keratin Plugs Form
Your skin cells constantly regenerate. Old cells on the surface shed, and new ones push up from below. In people with KP, this process goes wrong at the hair follicle. Instead of shedding normally, dead skin cells clump together with keratin and form a hard plug in the opening of the follicle. That plug is the bump you feel when you run your hand over your skin.
The leading explanation for why this happens points to a defect in how cells lining the hair follicle mature and shed. But a more recent theory, based on close examination of KP bumps under magnification, suggests the problem may actually start with the hair shaft itself. Researchers have found that hairs trapped inside KP bumps are tightly coiled, and they retain that coiled shape even after being extracted from the plug. This raises the possibility that an abnormally curved hair ruptures the follicle wall from the inside, triggering inflammation that then causes the surrounding skin to over-produce keratin as a protective response. In other words, the plug may be a consequence of irritation rather than the primary defect.
The Genetic Component
KP runs in families and follows what appears to be an autosomal dominant inheritance pattern, meaning you only need to inherit the relevant gene variant from one parent to develop it. The gene most closely linked to KP is FLG, which produces a protein called filaggrin. Filaggrin is essential for building a strong, smooth outer layer of skin. When this gene is mutated, the skin barrier doesn’t form properly, leading to both the excess keratin production and the mild inflammation visible around each bump.
That said, filaggrin mutations only explain part of the picture. A study in The American Journal of Pathology found that just 35% of KP patients carried common filaggrin mutations. The remaining 65% had KP without any detectable filaggrin defect, which means other genetic factors are involved that researchers haven’t fully identified yet. This is why KP severity varies so much from person to person, even within the same family.
Hormonal Triggers
Hormones are a major reason KP tends to peak during certain life stages. The condition often first appears or worsens during puberty, when rising androgen levels increase keratin production in hair follicles. This hormonal link also explains why KP is more common in premenopausal women than in postmenopausal women, and why pregnancy can trigger new onset or noticeable worsening. Case studies have documented women developing KP for the first time during pregnancy, with the severity closely tracking hormonal shifts.
Obesity and insulin resistance also appear to play a role, likely because both conditions influence androgen levels and skin cell turnover. KP is more prevalent in people with higher body weight, and it’s formally associated with diabetes mellitus as a co-occurring condition.
Why It Gets Worse in Winter
If your KP flares every cold season, that’s not coincidental. Low humidity and cold air strip moisture from your skin, and since KP bumps are essentially plugs of dry skin around hair follicles, anything that dries your skin out makes them more prominent. Indoor heating compounds the problem by dropping humidity even further.
Hot showers, which many people take more frequently in winter, also worsen KP by stripping the skin’s natural oils. The bumps may fade or flatten in summer when humidity rises and your skin retains more moisture naturally.
Linked Skin Conditions
KP doesn’t usually appear in isolation. It shares a genetic root with two other common skin conditions: eczema (atopic dermatitis) and ichthyosis vulgaris, a condition that causes dry, scaly skin. All three involve loss-of-function mutations in the filaggrin gene, which is why they frequently overlap. If you have eczema, your chances of also having KP are significantly higher than the general population.
In rarer cases, KP can be a feature of genetic syndromes that affect a cell signaling pathway involved in growth and development. Up to 80% of individuals with cardiofaciocutaneous syndrome, a rare genetic condition, develop KP. It’s also common in certain forms of Noonan syndrome. For the vast majority of people with KP, though, it’s a standalone cosmetic concern rather than a sign of a broader syndrome.
Nutritional and Medication Factors
Vitamin A deficiency has long been suspected of contributing to KP, and there is some clinical basis for this. Vitamin A regulates how skin cells grow and shed, so when levels are low, the normal turnover process can stall and keratin accumulates more readily. Poor dietary habits and malnutrition are listed among the factors that can worsen KP symptoms in adults. However, most people with KP in developed countries are not vitamin A deficient, so supplementation alone is unlikely to resolve the condition.
Certain medications can also trigger or worsen KP. Drugs that interfere with a specific cell growth pathway (the same pathway disrupted in the genetic syndromes mentioned above) are the most common culprits. These include some targeted cancer therapies and immunosuppressant medications. If KP appears or worsens shortly after starting a new medication, that timing is worth noting.
KP Variants and Why They Look Different
Not all KP looks the same, and the underlying causes of each variant differ slightly. The most common form produces skin-colored or slightly red bumps on the upper arms, thighs, and cheeks. But a variant called keratosis pilaris rubra involves significantly more redness that extends well beyond the area around each bump. This redness comes from a stronger inflammatory response in the skin, and unlike standard KP, it tends to persist past puberty rather than improving with age.
Other, less common variants can cause darkened spots (post-inflammatory hyperpigmentation, especially in darker skin tones) or mild scarring. The underlying keratin plug is the same in all variants. What differs is how aggressively the surrounding skin reacts to it, which circles back to individual genetic makeup and skin type.
Why Some People Outgrow It
KP often improves naturally with age, which supports the hormonal theory. As androgen levels stabilize after adolescence, keratin production at the follicle tends to slow. Many people notice their KP becoming less prominent in their twenties and thirties. But for others, particularly those with filaggrin mutations or co-existing eczema, the condition can persist throughout adulthood. The genetic defect in skin barrier function doesn’t resolve on its own, even when hormonal triggers ease up.