The Malassezia theory :
As shown in my previous article (https://morganwlfc.wordpress.com/2015/03/09/dermatology-a-review-of-scientific-litterature-on-the-causes-of-seborrheic-dermatitis-s-d/), there is still a lot of uncertainty around the causes of Seborrheic Dermatitis. However a majority of studies point towards the role of Malassezia. This yeast is lipophilic (its food is lipids). That’s why SD is mainly found in sebaceous gland areas. Indeed sebaceous gland produce sebum, which is rich in lipids (triglycerides).
Malassezia is on everyone’s skin. But for some reason, only some develop the condition. Basically, Malassezia breaks down the triglycerides into free fatty acids. Then the free fatty acids initiate an irritant response with flaking and inflammation (redness) (Dawson Thomas, 2007, Journal of Investigative Dermatology)
This response is seen only in those who suffer from Seborrheic Dermatitis (still Dawson Thomas):
“Role of individual susceptibility
We have shown that a fatty acid metabolite of Malassezia, oleic acid, induces flaking in dandruff-susceptible patients, but not in non-susceptible patients (Ro and Dawson, 2005). This finding provides evidence of role of these fatty acid metabolites in dandruff development and suggests an underlying difference between individuals that predisposes some to the development of dandruff or seborrheic dermatitis. Additionally, immunodeficiency such as acquired immune deficiency syndrome allows excess Malassezia proliferation, resulting in severe D/SD. Physical factors, nutritional disorders, drugs, and neurotransmitter abnormalities are additional aggravating factors. The difference between dandruff-susceptible and non-susceptible individuals remains unclear. Multiple possibilities exist, including innate differences in stratum corneum barrier function, skin permeability, and immune response to free fatty acids or proteins and polysaccharides from Malassezia. Further work will be necessary to fully understand the susceptibility response.”
Degraded by Malassezia
Irritant and desquamative response due to personal predispositions
Table illustrating the Malassezia theory
This theory can explain a lot of things patients have observed. For example, why antifungal treatments are not treating the root cause of SD. Many have noticed that when the antifungal is withdrawn the yeast comes back, and so does SD. Not even mentionning the fact that the yeast can develop a resistance against the topical treatment.
Many SD sufferers have noticed that treatments are not effective in the long term. Even worse, many of these treatments have considerable side effects. We must keep in mind that SD is a chronic disease. The fact that the majority of studies made to test the efficiency of treatments don’t exceed a few weeks is shameful, and is certainly not good enough for SD sufferers. But at least, if this theory is right, the search for the root cause of SD would be dramatically narrowed, as Dawson says “further work would be needed to understand the susceptibility response”. It turns out that I have an hypothesis to further explain the susceptibility response. But before I develop this hypothesis, there is at least one thing that I think isn’t consistent with the Malassezia theory, which I call the “oil paradox”.
Here is the beast, err yeast:
Photomicrographs of different Malassezia species stained by methylene blue. (a) M. furfur; (b) M. globosa; (c) M. restricta; (d) M. slooffiae; and (e) M. sympodialis. Magnification 1000X
(from Rudramurthy SM, Honnavar P, Dogra S, Yegneswaran PP, Handa S, Chakrabarti A. Association of Malassezia species with dandruff. The Indian Journal of Medical Research. 2014;139(3):431-437. )
As you can see there are different species of Malassezia. No one really knows which type is most important in SD, although most studies point towards M. Globosa and M. Restricta. Now let’s focus on the oil paradox.
The oil paradox:
Now that we have seen the Malassezia theory, it’s quite interesting to test if the theory works in practice. SD patients are very open to the idea of trying new treatments, creams etc. They are even more open to natural treatments, as they believe that it can’t do any harm. Many of them have tried putting olive and coconut oil on their skin.
The starting point of those who use these is the following: “my skin was dehydrated and that was the underlying problem » (http://www.curezone.org/forums/am.asp?i=1867304). Indeed, those who suffer from SD often have a very dry skin on lesional areas. So putting an oil, be it olive or coconut oil, may rehydrate the skin. However, if you look at the theory above, you would think putting oil is crazy. Both coconut and olive oil will feed the Malassezia yeast, as they are rich in triglycerides as Elaine Siegfried pointed out :
« While oil application may be risk free, a potential concern arises when considering a possible Malasseziavirulence factor regulated by its metabolic lipid pathways. In vivo, Malassezia digests sebum into saturated and unsaturated fatty acids.1 Only the saturated molecules are essential while the unsaturated fatty acids are a by-product.1 Organic oils (such as olive oil) contain both saturated and unsaturated lipids and may be counterproductive to treat a condition whose etiology is linked to Malassezia. In fact, olive oil is a standard in vitro culture media for Malassezia.7 Saturated fatty acids likely encourage Malassezia overgrowth and excess unsaturated fatty acids may induce inflammation and scaling. As nondigestible oil, mineral oil may provide a triglyceride-free alternative to organic oils.
Based on the evidence currently available, it may be prudent to avoid organic oils, especially olive oil, when treating seborrheic dermatitis or other inflammatory skin diseases triggered by colonizing microflora. »
Siegfried E, Glenn E. Use of Olive Oil for the Treatment of Seborrheic Dermatitis in Children. Arch Pediatr Adolesc Med.2012;166(10):967.
So by applying these oils on the lesions, you are actually likely to make your SD worse. And it did for me, and a good number of people I’ve talked to on forums or Facebook. But what is intriguing is that in some cases, against all odds, applying coconut or olive oil IMPROVED their SD. Look at this Curezone thread on olive oil for example (http://www.curezone.org/forums/am.asp?i=1867304). There is even more evidence on coconut oil.
So here we have a problem. Why are olive oil and coconut oil working for some ? Of course you might argue that the quality of the evidence (testimonials on Facebook or Curezone) is very weak compared to scientific trials. How can we be sure that these people really suffer from SD ? Are they telling the truth ? We have seen false reviews in the past, but I don’t see why someone would post a false review on the effects of olive oil. My opinion is that their claim has to be assessed. If they are right the Malassezia theory would be seriously challenged. From my own experience (very subjective I know) coconut and olive oil help more or less 50 % of people, and worsens the condition for the other half. Does that mean that there are two (or more) subtypes of SD ? I don’t know.
Further research is required to understand why some people improve their SD with these oils.The results might change drastically our knowledge of Seborrheic Dermatitis. On the other hand, the fact that olive and coconut oil worsened the situation in many cases shows that the theory is right in many cases.
This oil paradox shows that there is still a lot of work to be done before we can fully understand how SD works. Meanwhile patients have to find out by themselves which treatment works better for them, if any at all. Actually it’s a shame that this oil paradox weakens the Malassezia theory. Because I think that I have found a very appealing hypothesis to explain how the « susceptibility response » works.
Striking similarities with asthma and my hypothesis:
I do a lot of research on SD, and therefore I spend a lot of time reading forums and talking with fellow sufferers on social media. Many (including me), believe they have identified what can trigger their SD. No scientific proof here, but a lot of observations. If you are new to the condition, this list might help you to identify yours.
– wood burning
– cold weather
– foods : wheat (and other foods containing gluten), milk very frequent. Eggs, peanuts and many others (rare)
– alcohol : beer
– antibiotics: some have noticed that their SD first appeared shortly after taking antibiotics.
This is NOT the cause of SD
I have probably forgotten a few, contributions are very welcome. If you can spot your triggers, avoid them at any cost. Easier said than done I know. For example it might be difficult to avoid the cold weather or a mouldy house. My own experience is that when I remove my own triggers my symptoms are decreasing by more or less 90%.
These triggers are very interesting, and are not really discussed by scientists at the moment, despite the huge body of evidence given by patients.
I argue that triggers can fit into the Malassezia theory. As one can observe, these triggers are very similar to the ones causing asthma. Some asthma researchers believe that :
« The asthma genes are triggered by something in our surrounding environment so that the asthma symptoms emerge in the unfortunate children » (http://sciencenordic.com/new-asthma-susceptibility-gene-identified)
You can read more on the gene-environnement interaction here 😦http://en.wikipedia.org/wiki/Gene%E2%80%93environment_interaction)
Is seborrheic dermatitis influenced by the same pattern ? The idea is definitely appealing. The personal predisposition would be in our genes, and these genes would be activated by our environnement, explaining the flares and remissions. This is consistent both with patients’ reports and the Malassezia theory, but there is a long way to go before anything can be proven scientifically. Moreover the oil paradox has to be explained too. In the meantime if you can identify your own triggers I believe that you can significantly improve your condition.