Possible Causes of Seborrheic Dermatitis

• Seborrheic dermatitis is a common skin condition with unclear causes.
• Hormones, fungal infections (Malassezia), and immune responses are suspected factors.
• Research is ongoing, with some studies funded by treatment companies, influencing focus.
• Lifestyle factors like stress and nutrition may also play a role.
• Understanding the causes is key to better managing seborrheic dermatitis.

Table of Contents

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Unraveling The Possible Causes Of Seborrheic Dermatitis

Hormonal Influence On Seborrheic Dermatitis

Malassezia Fungal Infection

Exaggerated Immune Response To Malassezia

Abnormally High Rate Of Cell Division

Underlying Immune System Issues

Additional Factors To Consider

Section Summary

Unraveling the Possible Causes of Seborrheic Dermatitis

Seborrheic dermatitis is a frequent skin condition, yet its origins remain debated within the medical community. This ongoing discussion encompasses the fundamental causes, medical classification, and how the condition develops (pathogenesis).

The classification itself is varied – some consider it a skin disease, others a fungal issue, and some an inflammatory condition. However, pinpointing the exact cause is even more complex, with several theories under investigation.

Potential factors implicated in seborrheic dermatitis include:

• Hormonal influences
• Fungal involvement of Malassezia yeast
• An overreaction to Malassezia
• Accelerated skin cell turnover
• Underlying immune system irregularities

Let’s delve into each of these potential causes.

Hormonal Influence on Seborrheic Dermatitis

While direct scientific studies definitively linking hormones to seborrheic dermatitis are lacking, a connection between sebaceous gland activity and the condition’s presence is observed.

Notably, seborrheic dermatitis is uncommon before puberty (excluding infantile cases) and peaks during life stages marked by heightened sebaceous gland activity – adolescence (10-19 years) and young adulthood (18-35). These fluctuations in sebaceous gland activity are often driven by hormonal shifts in the body.

Adding to this, men experience seborrheic dermatitis more frequently than women. Some researchers propose that androgens, male hormones influencing the pilosebaceous unit (hair follicle and sebaceous gland), might contribute to seborrheic dermatitis development.

However, it’s not fully understood why hormonally driven sebaceous gland activity specifically leads to seborrheic dermatitis in some individuals.

Malassezia Fungal Infection

The theory implicating fungi dates back to Louis-Charles Malassezia in 1864. It suggests that specific types of lipophilic yeasts, meaning they thrive on skin oils, are responsible for seborrheic dermatitis and other skin issues.

These yeasts belong to the Malassezia genus and are commonly found on the skin of 75-98% of healthy adults. Seborrheic dermatitis often appears in oil-rich areas like the face, scalp, and trunk, and importantly, it often improves with antifungal treatments.

When Malassezia yeast re-establishes itself after treatment, the condition can return, leading some scientists to consider Malassezia as a primary factor in seborrheic dermatitis.

Despite this evidence, the precise mechanism by which Malassezia triggers seborrheic dermatitis remains unclear.

Microscopic examinations of affected skin don’t typically show Malassezia transitioning into its pathogenic, spore-forming phase, unlike in other Malassezia-related diseases like pityriasis versicolor.

Furthermore, the quantity of Malassezia on the skin doesn’t consistently differ between healthy individuals and those with seborrheic dermatitis. However, a higher density of yeast in lesions has been noted, suggesting a relationship. It’s still debated whether increased yeast density is a cause or consequence of seborrheic dermatitis.

Studies attempting to differentiate specific Malassezia strains have produced mixed results. Some indicate certain strains are more prevalent in individuals with seborrheic dermatitis, while others contradict these findings.

One consistent observation is a higher presence of Malassezia furfur in people with seborrheic dermatitis. The fact that individuals successfully treated with an antifungal relapsed when exposed to a resistant strain supports the idea that specific Malassezia strains may contribute to the condition.

Exaggerated Immune Response to Malassezia

Research into the immune response to Malassezia in seborrheic dermatitis is marked by contradictions. Some studies suggest the condition isn’t due to an altered immune response to Malassezia [1], while others argue the opposite.

Research Suggesting No Altered Immune Response

One study indicating no difference in immune response involved applying Malassezia furfur to the skin of individuals with and without seborrheic dermatitis.

Researchers monitored the skin’s reaction and analyzed antibody responses. They found no significant differences in antibody responses between healthy individuals and those with seborrheic dermatitis.

However, they observed that in seborrheic dermatitis sufferers, the adaptive immune system (a more specific, learned response) appeared to be triggered, whereas the innate immune system (a general, rapid response) was more active in healthy controls.

Research Demonstrating a Significant Immune Connection

Contradictory research focuses on the link between Malassezia-related factors and the resulting immune response.

These factors include oleic acid [2], a byproduct of Malassezia, and other compounds specific to Malassezia strains isolated from seborrheic dermatitis lesions [3].

While these studies are complex, they generally indicate notable differences in the immune response of individuals with seborrheic dermatitis.

A key aspect of this exaggerated immune response seems to be a compromised skin barrier.

Even non-pathogenic forms of Malassezia furfur at high concentrations can weaken the skin’s protective barrier and disrupt its natural inflammation control [4].

Simultaneously, Malassezia produces potential irritants. Researchers propose that an individual’s susceptibility to the combination of barrier disruption and irritation determines the outcome. Less susceptible individuals may remain symptom-free, while more susceptible individuals may develop significant skin barrier dysfunction, inflammation, and other seborrheic dermatitis symptoms.

Furthermore, DNA analysis of lesion skin from 15 sufferers revealed significant differences compared to healthy skin. The most prominent differences were increased expression of inflammatory genes and reduced expression of genes related to lipid metabolism (in lesion skin). Specifically, genes encoding for lipid biosynthesis (fatty acid creation) were nearly halved.

Collectively, these findings suggest clear differences between healthy individuals and those with seborrheic dermatitis. However, the relationship is complex, involving a network of factors that scientists are still working to fully understand.

Abnormally High Rate of Cell Division

This theory proposes that seborrheic dermatitis and associated yeast overgrowth are secondary to an increased rate of skin cell turnover and inflammation [5]. The idea is that excess dead skin cells (scales) provide more surface area and nutrients, promoting yeast colonization.

Evidence for this theory included observations that antifungal treatments, while suppressing Malassezia, didn’t always resolve dandruff in studied subjects.

However, it’s important to note that much of the research supporting this theory is over 30 years old. Since then, research methods and antifungal treatments have advanced considerably. Current research supporting this theory appears to be limited.

Underlying Immune System Issues

The concept of underlying immune system problems as a cause of seborrheic dermatitis is broad and complex, given the intricate role of the immune system.

This theory is supported by the significantly higher prevalence of seborrheic dermatitis in individuals with weakened immune systems (immunosuppressed) compared to the general population. Studies report 34% [] to 83% [6] of immunosuppressed individuals are affected, compared to an estimated 3% of the general population.

This increased susceptibility is largely attributed to weakened cellular immunity, a key defense against fungal and viral infections. This connection reinforces the idea that seborrheic dermatitis has a fungal and potentially viral component, and immune system health plays a significant role in its development.

Seborrheic dermatitis is not the only condition more common in immunosuppressed individuals. Others include oral candidiasis, hairy leukoplakia, pruritic papular eruption, and herpes simplex. The progression of these conditions has been linked to T-helper cell counts, a measure of immune function.

However, it remains unclear how seborrheic dermatitis develops in individuals with generally healthy immune systems.

Is Malassezia yeast capable of weakening skin immunity, allowing it to colonize and disrupt the skin barrier, or is Malassezia overgrowth a consequence of an underlying immune system dysfunction? The precise relationship is still under investigation, but a strong connection undoubtedly exists.

Additional Factors to Consider

Given the incomplete understanding of seborrheic dermatitis causes, it’s crucial to acknowledge the limitations of current research.

Research Funding Bias

A significant portion of research, particularly studies comparing antifungal treatments, appears to be funded by companies that produce these treatments.

The concern is that this funding model may prioritize research on treatment effectiveness over exploring the root causes of seborrheic dermatitis. This narrow focus can limit our overall understanding. It’s analogous to focusing solely on tire patch effectiveness without investigating why tires are going flat in the first place.

Much of the Malassezia research has been directed at minimizing yeast populations. However, studies show that healthy individuals can have similar amounts of Malassezia on their skin as those with seborrheic dermatitis [7, 8]).

A more beneficial research direction might be to investigate biological differences in skin composition, rather than just Malassezia quantity. Differences in the distribution of specific Malassezia types and the diversity of other skin microbes may be significant [8, 9].

Inconclusive and Varied Studies

The sheer volume of inconclusive research in the literature makes it challenging to extract definitive answers, especially regarding less-explored causes of seborrheic dermatitis.

For example, some studies have investigated potential links to:

• Nutritional deficiencies (Vitamin E [], essential fatty acids, vitamins A, E, and D, B vitamins, vitamin C, selenium, zinc, iron [10])
• Immunodeficiency syndromes [6]
• Skin surface pH levels [11]
• Stress and depression [12]
• Oxidative stress [13]

Many of these studies conclude with a need for further research. Future exploration of these areas could potentially revolutionize our understanding of seborrheic dermatitis and lead to more effective, long-term treatments.

Section Summary

This section has explored the most commonly discussed potential causes of seborrheic dermatitis. As highlighted, researchers are still working to reach a definitive consensus.

This uncertainty extends to the very classification of seborrheic dermatitis – is it primarily a fungal issue, an immune system disorder, or something else entirely?

Here’s a summary of the key points: