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Possible Causes of Seborrheic Dermatitis

Book Extract

This article is an extract from: Seborrheic Dermatitis - The Owner's Manual; a book dedicated to understanding seborrheic dermatitis. See the book overview page for more information.

Despite the frequency of seborrheic dermatitis, there is still much controversy in the medical community. The controversy includes the underlying causes of seborrheic dermatitis, it’s medical classification and it’s pathogenesis.

Some classify it as a cutaneous disease, others as a fungal disease, while others simply classify it as an inflammatory disease. However, the controversy and confusion regarding the cause of the disease is even more riddled.

Some possible causes which have been implicated include:

  • Hormones
  • Fungal infection by malassezia
  • Exaggerated response to malassezia
  • An abnormally high rate of cell division
  • Underlying immune system issues

And each of these theories is discussed next.

Hormones and Seborrheic Dermatitis

Even though there are no studies which have been able to make a direct connection between hormones and seborrheic dermatitis, there does seem to be a connection between sebaceous gland activity and presence of the disease.

For example, except for infantile seborrheic dermatitis, it is rare before puberty and most commonly occurs during the stages of life when the sebaceous glands are most active. This includes adolescence (10-19 years) and young adulthood (18-35). And these changes in sebaceous gland activity are typically the result of hormonal changes in the body.

In addition to this, since the disease is more common in men than in women, some researchers hypothesize that the influence of androgens on the pilosebaceous unit may play a significant role in the progression of seborrheic dermatitis.

However, this approach does not appear to fully explain why the hormonally triggered sebaceous gland activity results in the progression specifically of seborrheic dermatitis.

Fungal Infection by Malassezia

This theory was first established by Louis-Charles Malassezia in 1864 and implies that specific lipophilic (feeds on lipids) yeasts are responsible for the progression of seborrheic dermatitis and various other skin conditions.

These yeasts are categorized as Malassezia and are actually found on the normal skin of 75-98% of the healthy adult population. However, since seborrheic dermatitis most commonly occurs on lipid-rich areas of the skin (face, scalp, and trunk), it responds especially well to antifungal treatment.

Recolonization by malassezia leads to disease recurrence, and scientists have indicated Malassezia as the main culprit behind seborrheic dermatitis.

Regardless of these facts, scientists have struggled to observe the specific method in which Malassezia causes seborrheic dermatitis.

When examined under the microscope, no observation of the yeast morphing into its pathogenic (spore-forming) phase has been observed in seborrheic dermatitis. Which is the case with other diseases in which malassezia has been directly implicated as the cause (such as pityriasis versicolor).

Additionally, no clear differences have been observed between the amount of malassezia residing on the skin of healthy subjects and those suffering from seborrheic dermatitis. However, lesion-specific yeast density has been observed, indicating some sort of relationship does exist, but it becomes difficult to understand if the yeast density is the result of seborrheic dermatitis or seborrheic dermatitis is the result of yeast density.

When scientists tried to identify differences between the presence of specific malassezia strains, lots of overlapping evidence surfaced. Some studies have shown that various strains seem to dominate seborrheic dermatitis affected individuals, while other studies demonstrated contradictory evidence.

One of the most common findings is an increased number of Malassezia furfur in seborrheic dermatitis individuals. This, along with the simple fact that when individuals successfully treated with nystatin relapsed after being introduced to a nystatin resistant strain, appears to demonstrate that a definite connection exists and that specific strains may be responsible for the progression of seborrheic dermatitis.

Exaggerated Response to Malassezia

Research in this area is one of the most contradictory. While some researchers demonstrate that seborrheic dermatitis is not due to an altered immune response to the malassezia [1], others attempt to demonstrate that it is.

Research Showing No Altered Immune Response

Research which demonstrated that there is no difference in immune response did so by introducing the Malassezia (malassezia furfur specifically) to the skin of individuals with and without seborrheic dermatitis.

Study funding may play a role
The specific research paper discussed was sponsored by Unilever (the makers of Head and Shoulders).

After the introduction, the skin was closely monitored and the response was analyzed. In the end, researchers could not find any significant differences in the antibody response between healthy individuals and those affected by seborrheic dermatitis.

However, they did note that individuals with seborrheic dermatitis demonstrated characteristics of the adaptive immune system being triggered in seborrheic dermatitis sufferers versus the innate immune system in healthy controls.

Research Showing A Significant Connection

The contradicting research mainly examines the connection between the various associated factors of malassezia and the resulting immune response.

These factors include the oleic acid [2] that malassezia leaves behind and a wide variety of other compounds specific to malassezia strains specifically isolated from seborrheic dermatitis affected skin [3].

Unfortunately, these studies are far too complicated to summarize here, but overall, they demonstrate that there are marked differences in the immune response of seborrheic dermatitis affected individuals.

A major part of this exaggerated immune response seems to stem from a disrupted skin barrier.

High concentrations of Malassezia furfur, even in its non-pathogenic form, have been shown to reduce the protective barrier of the skin and affect the skin’s innate control of inflammation [4].

At the same time, the Malassezia produces the potential irritants discussed above. Thus, researchers hypothesize that the level of an individual’s susceptibility to the combination of barrier disruption and irritation determines the specific outcome.

Less susceptible people experiencing no symptoms, while the more susceptible undergo significant changes in skin barrier function, inflammation, and the myriad of other symptoms commonly seen in seborrheic dermatitis.

In addition to this, when DNA analysis was performed on the lesion skin of 15 sufferers, researchers observed significant differences compared to healthy skin. Most significant of these differences was a marked increase in inflammatory gene expression and suppressed lipid metabolism gene expression (in lesion skin). More specifically, the gene-encoding differences related to lipid biosynthesis (creation of fatty acids) was reduced by nearly 50%.

When all of this is viewed together, it becomes apparent that there are clearly significant differences between healthy and seborrheic dermatitis affected individuals.

Yet, the differences are not as clear-cut as one would hope; instead, it’s an interrelation of a large variety of factors that scientists are still trying to grasp.

Abnormally High Rate of Cell Division

This theory suggests that seborrheic dermatitis and the accompanying yeast activity is only a secondary feature of seborrheic dermatitis which occurs due to an increased rate of cell turnover rate and skin inflammation[5]. Specifically, it was suggested that the increased yeast colonization is the result of excess dead skin (scales) which directly provides additional surface area and nutrients needed for survival.

The evidence used for this argument was that even when malassezia was suppressed with anti-fungal treatment, no effect on dandruff resolution was observed in the subjects studied.

One of the biggest issues with this theory is that most of these findings/discussions were published more than 30 years ago. Since this time, both research methods and antifungal solutions have significantly advanced.

There does not appear to be any recent research which has further supported this theory.

Underlying Immune System Issues

The theory of underlying immune system issues is quite difficult to fully grasp, due to its broad reach and the complicated relationship of immune system function to seborrheic dermatitis.

The origins of this theory stem from the fact that seborrheic dermatitis is significantly more common in immunosuppressed individuals than in the common population. In fact, the difference is quite staggering, with 34% [6] to 83% [7] of immunosuppressed individuals being affected by seborrheic dermatitis compared to with only an estimated 3% of the general population.

For the most part, this has been attributed to weakened cellular immunity, which is one of the main defenses against viral and fungal infections. But, this connection also indicates that, once again seborrheic dermatitis does have a significant fungal and/or viral component and the state of the immune system plays a large role in its progression and development.

Seborrheic dermatitis is not the only disease that has been correlated with immunosuppressed individuals, and various other diseases are also frequent. This list includes:

  • Oral candidiasis
  • Hairy leukoplakia
  • Pruritic papular eruption
  • Herpes simplex

The progression of these has been shown to have a direct relationship to the T-helper cell counts of the specific individual.

In the end though, it is still unclear how seborrheic dermatitis progresses in an individual with an overall competent immune system.

Does the malassezia yeast degrade the cellular immunity of the skin allowing it to colonize and disrupt barrier function or is the malassezia secondary to immune system malfunction? This is a question that has yet to be answered, but overall, it appears that an intimate relationship exists and it is yet to be fully understood.

Additional Factors to Consider

Since the cause of seborrheic dermatitis is it not fully understood, it’s important to understand the limitations of the current understanding.

Who Funds the Research

Many of the research studies appear to be funded by companies that produce antifungal treatments (particularly those studies which compare the effectiveness of various antifungal preparations for treatment).

The issue here is that these companies have specifically chosen to dedicate their time and efforts on proving various antifungal preparations instead of focusing on solving the initial cause. As the focus becomes too narrow, it becomes hard to make any conclusions. It’s like comparing tire patch kits without looking at why the tire may be flat in the first place.

Much of the research on the malassezia yeast has focused on ways to minimize its population. However, there are studies which clearly show that individuals with healthy skin can have similar amounts of malassezia yeast on their skin as those experiencing issues [8, 9]).

Perhaps it would be more beneficial for research to focus on the biological differences in the skin’s composition instead of just the number of malassezia yeasts present; as there does appear to be differences in distribution of not only the specific type of malassezia yeasts, but also the diversity of other common microbes present on the skin [9, 10].

Many Inconclusive Studies

When reviewing the literature, the sheer amount of inconclusive research had made it difficult to sift out the important facts. This is especially true when attempting to pinpoint the underlying cause of seborrheic dermatitis that departs from the common areas of focus.

For example, some studies have explored the possible implication of:

  • Nutritional deficiencies, such as Vitamin E [11], essential fatty acids, vitamins A, E and D, vitamins B1, B2, B6, niacin and biotin, vitamin C selenium, zinc, iron [12]
  • Immunodeficiency syndrome [7]
  • Skin surface pH level [13]
  • Stress and depression [14]
  • Oxidative stress [15]

Unfortunately, many of these studies simply end with the conclusion that further research is needed. Perhaps future exploration of these topics may reveal something that could completely change our perspective on the condition and lead to the discovery of more lasting treatment approaches.

Section Summary

This section covered the most commonly mentioned underlying causes of seborrheic dermatitis. As we have learned, researchers are still struggling to come to a single conclusion.

This confusion extends to the actual classification of seborrheic dermatitis. Is it a fungal infection, an immune system issue, or something entirely different.

Here is a summary of what was discussed:

  1. Hormones appear to play a significant role in triggering the onset of seborrheic dermatitis, mainly through their influence on sebaceous gland activity
  2. Malassezia resides on the skin of individuals with symptoms of seborrheic dermatitis and individuals with healthy skin
  3. Skin most affected by seborrheic dermatitis, appears to have a higher density of malassezia present
  4. Specific strains of malassezia may play a more significant role in seborrheic dermatitis progression then others
  5. Research examining differences in immune response to malassezia is inconclusive and contradictory
  6. The case for an altered immune response is quite strong, especially since the malassezia fungus is present on healthy subjects
  7. Study funding should be considered as this may drive the direction of the research and the current understanding of the condition
  8. Smaller studies have proposed the cause of seborrheic dermatitis may be related to more systemic issues (nutrient deficiencies, stress, lipid oxidation, etc), but conclude that more research is needed

Book Extract

This article is an extract from: Seborrheic Dermatitis - The Owner's Manual; a book dedicated to understanding seborrheic dermatitis. See the book overview page for more information.


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  3. George Gaitanis, Prokopios Magiatis, Konstantina Stathopoulou, Ioannis D Bassukas, Evangelos C Alexopoulos, Aristea Velegraki, Alexios-Leandros Skaltsounis "AhR ligands, malassezin, and indolo[3,2-b]carbazole are selectively produced by Malassezia furfur strains isolated from seborrheic dermatitis." The Journal of investigative dermatology 128.7 (2008): 1620-5. PubMed
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  8. Takashi Sugita, Masako Takashima, Minako Kodama, Ryoji Tsuboi, Akemi Nishikawa "Description of a new yeast species, Malassezia japonica, and its detection in patients with atopic dermatitis and healthy subjects." Journal of clinical microbiology 41.10 (2003): 4695-9. PubMed
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  10. Zhijue Xu, Zongxiu Wang, Chao Yuan, Xiaoping Liu, Fang Yang, Ting Wang, Junling Wang, Kenji Manabe, Ou Qin, Xuemin Wang, Yan Zhang, Menghui Zhang "Dandruff is associated with the conjoined interactions between host and microorganisms." Scientific reports 6 (2016): 24877. PubMed
  11. S Passi, A Morrone, C De Luca, M Picardo, F Ippolito "Blood levels of vitamin E, polyunsaturated fatty acids of phospholipids, lipoperoxides and glutathione peroxidase in patients affected with seborrheic dermatitis." Journal of dermatological science 2.3 (1991): 171-8. PubMed
  12. S Brenner, C Horwitz "Possible nutrient mediators in psoriasis and seborrheic dermatitis. II. Nutrient mediators: essential fatty acids; vitamins A, E and D; vitamins B1, B2, B6, niacin and biotin; vitamin C selenium; zinc; iron." World review of nutrition and dietetics 55 (1988): 165-82. PubMed
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About Michael Anders

After being affected by seborrheic dermatitis, I have made it my goal to gather and organize all the information that has helped me in my journey.

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