Over the last decade we have come to learn a lot about the human microbiome, its composition and ways of how they interact with us and we interact with them. Interaction is vast. We, as Homo sapiens, are a true holobiont. We act as a host for our microbiota and, together, form an individual.

The Baas-Becking hypothesis describes the basic principle of microbiology: “Everything is everywhere, but the environment selects.” This principle helps in the understanding that the microbial composition of our skin varies with skin area. The environment is provided largely by skin itself. For instance, it regulates pH. Additionally, skin provides molecules which can be used as a foodstuff by microbes. In areas where we find many active sebaceous glands a large amount of sebum is produced, which can be used by lipophilic microbes. This results in their growth and proliferation. In skin areas with lower production of sebum, these species will not be able to flourish as easily.

In healthy situations, together, we truly are a holobiont. We have a symbiotic relationship where we profit from each other. We provide our microbiota with an environment in which they can flourish and they provide us with means to, for instance, ensure that the barrier function of our skin is upheld. This relationship is much more than just mutually beneficial, it is symbiotic, we indeed need each other. It is an equilibrium, however, this equilibrium is rather vulnerable.

Changes in skin, for instance during puberty, after menopause, or by outside influences like changing of the seasons, sunlight etc. can have a strong impact on our relationship. Increase in sebum, during puberty, is key in the development of acne. Virulent phylotypes of Cutibacterium acnes profit from the increase in sebum production and start to colonize the hair follicle. They start to produce biofilm to provide a protected environment for them to continue their growth. This is followed by the initiation of inflammatory processes which can be severe, finally resulting in the formation of papules and pustules.

The scalp forms a unique habitat for microbes. Cutibacterium and Staphylococcus are the dominating bacterial genera on the scalp. In addition, the scalp inhabits some unique fungal species which cannot be found elsewhere on skin, most importantly Malassezia restricta and Malassezia globosa. Like C. acnes, these lipophilic fungi lack the ability to produce lipids themselves. They rely on the host to provide them with lipids. They produce lipases, which perform the hydrolysis of sebum and ester bonds of triacylglycerols produced by the host, us. The resulting ingredients are partly used by these fungi and ingredients which are of no use to them, like free fatty acids, are excreted. The mono-unsaturated free fatty acids thus produced, e.g. oleic acid, play an important causative role in dandruff. These molecules negatively influence the skin barrier function, allowing for the initiation of, often subclinical, inflammatory processes and hyperkeratinization, where hyperproliferation and altered corneocyte maturation can be observed. This is a key driver of the formation of flakes, i.e. dandruff.

In analogy to Cutibacterium and Staphylococcus, both M. restricta and M. globosa are commensal species. Their presence on our scalp is normal and not a problem, it might well even be beneficial to us. In this context, Cutibacterium acnes was, until recently, considered to be the ‘acne-bacterium’. Killing it, or at least reducing its presence on the skin, was always associated with reducing acne. Current knowledge now shows us that C. acnes is a beneficial and important species to us. Some strains, phylotypes of C. acnes, however, are virulent and play a causative role in acne. Most of the C. acnes strains in our follicles are beneficial to us, though.

At this point in time, such detailed understanding is lacking for M. restricta and M. globosa, unfortunately. Anti-fungal approaches have always been successful in fighting dandruff, albeit not sustainably. Products with anti-fungal activity need to be applied repeatedly. Realizing that both fungal species dominate the fungal community on scalp, they, or at least some of their phylotypes, play a causative role in dandruff.

Despite the fact that we lack the knowledge on the phylotype level of said fungi, the current state of the art is that scalp suffering from dandruff, i.e. dandruff scalp, shows some interesting differences with normal scalp. These differences most probably play a role in the pathological processes taking place in dandruff scalp and drive detrimental processes leading to production of flakes, inflammation and dryness. Comparably to acne, here too it clearly seems to be better to not simply kill microbes, but rather look at the whole microbial composition.

The microbial differences between normal and dandruff scalp are multifaceted. Firstly, a larger fungal load is recognized on dandruff scalp. Where, in the past, scientists saw that as another strong indication of the role of fungi in dandruff, this is now considered to be, at best, one of several microbial aspects of dandruff scalp. Not just the fungal load is increased, also the fungal composition is different from normal scalp. The relative abundance of M. restricta is increased and that of M. globosa is decreased. This can be interpreted in two ways. M. restricta, being the species, which is clearly more present on dandruff scalp, is the fungal species which plays the most important detrimental role in dandruff. Another interpretation is that M. globosa, showing relatively lower abundance on dandruff scalp, might be a beneficial species, which supports scalp health. Knowledge on these important details is currently still lacking, but it looks to be clear that, when wanting to reduce dandruff sustainably, a reduction of fungal load should focus on M. restricta and not on M. globosa.

In analogy with above fungi, dandruff scalp shows a distinctly different bacterial composition compared to normal scalp. In both cases Cutibacterium is the dominant genus, but, on dandruff scalp, a clear relative increase in Staphylococcus is recognized. A similar interpretation as above can be made. Cutibacterium is largely positive and a relative decrease of this genus might play a role in dandruff. Staphylococcus is a genus largely considered to be positive too. In the case of dandruff, this assumption is unjustified. S. epidermidis, for instance, is a species often assumed to be ‘good’, but is considered to be one of the species playing a causative role in dandruff, next to it pathogenic family member, S. aureus. An increase in Staphylococcus, therefore, can largely be seen as an increase of a genus which plays a negative role in the pathological processes in dandruff scalp. Here too, though, a sustainable solution to the microbial imbalance of dandruff scalp seems to be found in reducing Staphylococcus and let Cutibacterium thrive.

In studies performed by us, we saw that a benchmark anti-fungal ingredient, Piroctone Olamine, indeed reduced fungal load, but completely abolished M. globosa. In the same study we saw that the bacterial load was increased with Piroctone Olamine, but the relative abundance of Staphylococcus was increased as well. These results show that this rather unspecific anti-fungal approach does not help in regaining a healthy composition of the scalp microbiome. It merely seems to act on the consequence of the problem and not the problem itself. CutiBiome CLR™ with its multifaceted approach in influencing microbial growth on the scalp, in the same study, showed that fungal load was decreased, but the relative abundance of M. globosa was increased. In addition, CutiBiome CLR™ allowed for growth of Cutibacterium, but, as opposed to Piroctone Olamine, it did not allow for growth of Staphylococcus, thus reducing the relative abundance of Staphylococcus.

These results show that a natural approach based on old wisdom and state-of-the-art science, i.e. CutiBiome CLR™, can be infinitely smarter than even the most well-known and appreciated active ingredient for dandruff.