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“Gorgeous hair is the best revenge.”
Dandruff affects more than 40% of the total adult population, and while hardly life-threatening, it is certainly a condition no one wants. Dandruff treatments have been around for many years, but the specific yeast responsible for dandruff was only accurately identified in 2007. And now, by clarifying the source of the problem, a spate of recent research is making a new generation of more effective antidandruff products possible.
In the U.S., antidandruff products are classified as drugs—they must perform in a clinically substantiated way. Many compounds used to treat dandruff are listed in Table 1, with those officially recognized by the U.S. Food and Drug Administration (FDA) noted. There also are a number of botanicals that claim antidandruff effects, as well as traditional cures such as egg oil in Chinese medicine.
The most obvious consequence of dandruff is the abundance of white flakes in hair and on clothes. But another problem associated with dandruff is red, scaly, itchy, irritated skin that is closely related to seborrheic dermatitis, an inflammatory skin disorder that affects the scalp, face and torso. It targets the sebaceous gland-rich areas of the skin in particular, and that clearly includes the scalp.
There are three key factors influencing the development of dandruff: a specific yeast, abundant sebum and individual susceptibility. The activity of the yeast must be addressed to treat the condition at a fundamental level, and so we must examine it in some detail.
Yeasts are fungi, with more than 1,500 known species. They use organic compounds as a source of energy and do not require sunlight to grow. Yeast has been used for thousands of years, notably giving mankind leavened bread and alcoholic beverages.
The ones of particular interest for understanding and treating dandruff are Malassezia globosa and restricta, especially the globosa. This identification was the result of research by Dawson1 and his team at Procter & Gamble. Yeast is prevalent all over our bodies as a component of normal skin flora. Malassezia are lipid-dependent, and are particularly delighted to be in the scalp where there is a copious supply of sebum to provide necessary nutrition.2 It has been suggested that Malassezia lipid dependency is due to a defect in its synthesis of myristic acid, a precursor of long-chain fatty acids. Sebum is broken down by the lipases excreted by yeast into fatty acids that are used as nutrition, and one particularly troublesome product of the breakdown of triglycerides is oleic acid. As the oleic acid builds up on the scalp, it becomes a primary source of inflammation.
For people with dandruff, skin cells may mature and be shed in two to seven days, compared to a normal scalp where 28 days typically would be required. This increased turnover creates clusters of corneocytes that adhere to each other and make the particles we see. One biological molecule that helps make large dandruff particles is ICAM-1 (Intercellular Adhesion Molecule-1). The structural characteristics of ICAM-1 create protein-binding sites for numerous ligands, and, as a result of these binding characteristics, ICAM-1 has classically been assigned the function of intercellular adhesion.
Zinc here is beneficial in that it can lower the expression of adhesion molecule ICAM-1, reducing the formation of visible dandruff clusters. Thus, the most common active for antidandruff shampoo in the U.S. is zinc pyrithione (ZPT), which is used in P&G’s Head & Shoulders hair care shampoo products, the market leader. Understandably then, the focus of much research has centered on exactly how ZPT works, where the main questions concern how ZPT reduces irritation and the exact mechanism for its action against Malassezia globosa.
The dandruffed scalp always involves inflammation, where interleukin 1α (IL-1α) plays a main role. Elevated levels of IL-1α in the scalp have a positive correlation with the degree of inflammation, and an excess of IL-1α also affects hair growth and hair loss. Zinc has good anti-inflammatory activity, which can inhibit the expression of scalp IL-1α, as well as the capacity of surfactants that induce the expression of IL-1α.