Seborrheic Dermatitis and Dandruff: Causes and Treatment

Yeasts of the genus Malassezia live on everyone's skin and feed on sebum. They are not a sign of infection or dirt; they are a normal part of the skin microbiome. The problem appears in predisposed people: the yeasts produce lipases that break down sebum triglycerides into fatty acids. Some of these (including oleic acid) are irritating, and the immune system responds with inflammation. The review by Adalsteinsson et al. (2020) describes this mechanism: Malassezia hydrolysis of free fatty acids with activation of the immune system through pattern recognition receptors, the inflammasome, IL-1β and NF-kB, with M. restricta and M. globosa considered the most virulent species.

Why does one person get dandruff and another not, despite a similar number of yeasts? Individual susceptibility comes in here: sebum composition, immune sensitivity, epidermal barrier function and genetic factors. The authors of the same review note that no clear genetic predisposition has been established, although associations with certain HLA alleles and possible links to psoriasis and atopic dermatitis have been described. So the sheer 'amount of yeast' does not explain the disease, and treatment that only reduces their number often produces remission rather than a lasting cure.

Several practical conclusions follow from this mechanism. First, SD is not caused by washing the hair too rarely, although accumulated sebum and scales can worsen symptoms. Second, it is not a food allergy, so strict elimination diets have no justification. Third, because the disease is tied to sebaceous gland activity, flares often occur when skin is more seborrheic (youth, adulthood) and when the body's load increases: stress, lack of sleep, illness, cold and dry air.

Typical dandruff is fine whitish or grey flakes on the scalp and hair with mild itching. In SD the scales are usually greasier, yellowish, sitting on reddened skin; lesions involve the hairline, eyebrows, nasolabial folds, outer ears and the area behind the ears, as well as the breastbone and upper back. Severity changes over time: it usually worsens in autumn and winter and during periods of stress.

Not every scalp flaking is dandruff. Scalp psoriasis causes thicker, silvery, sharply demarcated patches that often extend beyond the hairline; a combination of the two diseases is sometimes called sebopsoriasis. Atopic and contact dermatitis (for example after dyes or shampoos) usually cause stronger itching, oozing or cracking. Scalp ringworm, more common in children, causes patches of hair loss and hairs broken off at the skin. Rosacea may coexist with facial SD. Telling these conditions apart can be difficult, so for lesions that do not respond to treatment after a few weeks it is worth seeing a dermatologist.

What does this mean in practice? First, antifungal drugs really work, and the effect is visible after a few weeks. Second, ketoconazole and ciclopirox do not clearly stand out from each other, so the choice depends on availability, form (shampoo, cream, foam) and tolerance. Third, the evidence concerns mainly short periods, so we do not know well how best to maintain remission, which is why advice on maintenance dosing rests on clinical practice rather than hard data.

The Belgian trial is valuable because it compares two popular shampoo ingredients in severe dandruff and SD. The result supports ketoconazole, especially for reducing relapses, but zinc pyrithione was also effective and is sometimes cheaper and more readily available without a prescription. Other ingredients used in anti-dandruff shampoos, such as selenium sulfide, salicylic acid or coal tar, have a long history of use, though the evidence for their efficacy is less systematically collected (the review by Borda et al., 2019, lists them among commonly used therapies).

The conclusion is twofold. Topical steroids are effective in SD and it is reasonable to reach for them in clearly inflammatory flares, but briefly: reviews stress that the evidence concerns short courses, and chronic use on the face carries a risk of skin thinning, telangiectasia and rebound flares after stopping. That is why they are usually used for a few days to two weeks, after which one moves to antifungal maintenance. Calcineurin inhibitors (tacrolimus, pimecrolimus) are an alternative for the face when steroids are best avoided; in the Cochrane review they were comparable to steroids in the short term but more often caused adverse effects, mainly burning.

Because SD is chronic, the key is not only to treat flares but also to prevent them. Common triggers include psychological stress, lack of sleep, illness, cold and dry air, and reduced immunity. In HIV infection the disease is more frequent and severe, which Adalsteinsson et al. link to immune dysregulation and disruption of the skin microbiota with unchecked Malassezia proliferation. If SD suddenly becomes severe, resistant to treatment or appears with no previous history in an adult, it is worth discussing general causes with a doctor.

To prevent relapses, intermittent maintenance treatment is most often used: an antifungal shampoo once a week or once every two weeks and, for facial SD, an antifungal cream a few times a month in higher-risk periods (autumn, winter). This advice comes from clinical practice; as noted, long-term randomised trials defining the optimal regimen are lacking. Simple habits matter too: gentle cleansing of facial skin, avoiding harsh, alcohol-based cosmetics, and not scrubbing the skin until it is irritated.

Fashionable 'home remedies' and natural cures are similarly uncertain. Reviews list tea tree oil and other plant extracts as alternatives in use, but the quality of evidence is much lower than for antifungals and steroids, and essential oils can cause contact dermatitis. If someone wants to try such a product, it is worth doing so carefully, on a small patch of skin, and without giving up treatment of proven efficacy.

You may come across the claim that seborrheic dermatitis is linked to Parkinson's disease. It is true that SD is common in people with Parkinson's: the review by Rietcheck et al. (2021) states that it develops in more than half of patients with this disease and can be severe and resistant to topical treatment. The authors of the review by Adalsteinsson et al. link this probably to parasympathetic hyperactivity with increased sebum production and to reduced facial mobility, which leads to sebum accumulation.

It is important, however, not to reverse this reasoning. The vast majority of people with dandruff or SD do not have and will not develop Parkinson's disease: SD affects a few percent of the population, and Parkinson's disease is far rarer. Having dandruff is not in itself a reason for worry or for neurological testing. Only when SD appears together with resting tremor, slowness of movement, stiffness or a change in gait should you see a doctor about those neurological symptoms.

Dandruff and seborrheic dermatitis are a well-understood, chronic but easily controlled condition, not a hygiene defect. The best-documented treatment is antifungal: shampoo with ketoconazole, ciclopirox or zinc pyrithione, plus short steroid courses for clear inflammation. Least well understood is how to maintain remission for years, so a maintenance plan is worth tailoring individually and returning to, without guilt, in harder seasons.