top of page
  • Writer's pictureMartin Laurence

Parkinson's and seborrheic dermatitis

Seborrheic dermatitis is a type of skin inflammation caused by overgrowth of Malassezia (Borda 2015). It has long been known to be associated with Parkinson’s disease: about half of Parkinson’s patients eventually develop seborrheic dermatitis (Arsic 2014). The mechanisms underlying this strong association are not known. Three hypotheses have been proposed:

  1. Treatments or behaviors associated with Parkinson’s disease increase availability of skin fats, and these fats “overfeed” Malassezia on the skin.

  2. Parkinson’s patients secrete more skin fats due to autonomic dysfunction, and these fats “overfeed” Malassezia on the skin.

  3. Seborrheic dermatitis is a biomarker of poor immune control of Malassezia, and Malassezia overgrowth in the brain kills dopaminergic neurons, causing Parkinson’s disease.

Seborrheic dermatitis significantly increases the risk of a future Parkinson’s diagnosis—as much as five years in advance (Tanner 2012). Hypothesis (1) can only explain seborrheic dermatitis occurring after Parkinson’s onset. So hypothesis (1) is inconsistent with this observation.

Hypothesis (2) was proposed by Sam Shuster’s group in 1973 (Burton 1973). After studying this link for 17 years, they stated that: “There is no evidence of a neural control of sebaceous function,” abandoning this hypothesis (Cowley 1990). Moreover, though seborrheic dermatitis tends to occur in sebum-rich parts of the skin, sebum amounts within the normal physiological range do not correlate with seborrheic dermatitis symptoms (Burton 1983). Hypothesis (2) is thus inconsistent with these two observations.

Hypothesis (3) has much supporting evidence. Malassezia overgrowth was quickly recognized as a symptom of AIDS: seborrheic dermatitis often appears when helper T cell counts drop below 500 cells per microliter of blood (Borda 2015; Moreno 2019). Even in HIV negative individuals, weak T cell responses against Malassezia are associated with an increased risk of seborrheic dermatitis (Neuber 1996; Lally 2010). Parkinson’s patients have lower helper T cell counts as compared to age-matched controls (Bas 2001, Baba 2005, Stevens 2012, Niwa 2012, Saunders 2012, Kustrimovic 2016). They are also more susceptible to another common fungal infection of the skin, tinea pedis (Aono 2013). This suggests the link between Parkinson’s disease and seborrheic dermatitis is mainly immunological: they both seem to be caused by a weak helper T cell response, especially against fungi.

Because about half of Parkinson’s patients go on to develop seborrheic dermatitis, if Malassezia are in fact causally involved in Parkinson’s disease, then they probably explain at least 50% of cases. This would make them the main cause of Parkinson’s disease.

This post was mainly based on Laurence 2019.

Animated Parkinson’s video:

Seborrheic dermatitis on the face. From Roymishali via Wikipedia (shared under the Creative Commons Attribution-Share Alike 3.0 Unported).

431 views1 comment

Recent Posts

See All

1 comentario

08 may 2022

Thanks for the anti-malassezia efforts. I have battled seborrheic dermatitis and essential tremor for 60 years now. I have read the articles here and at the fungal acne bible. I have a question about feeding malassezia. In ordinary biology an invasive organism will be limited by consuming the available food. If a control agent such as an anti fungal is introduced, then there should be excess food. It would seem then that other agents, shampoos etc, that feed malassezia should be irrelevant. Unless perhaps these other agents are more potent food than the natural skin oils. Am I missing something?

Me gusta
Post: Blog2_Post
bottom of page