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A Dandruff Whodunit


Most of us brush off dandruff* as a cosmetic problem, spending hundreds of millions of dollars on commercial products to stop the flakes. Dandruff, or seborrheic dermatitis (SD),affects up to 50% of the population and appears linked to fungal/yeast growth that results in itching, inflammation, and even occasional hair loss. Yet a deeper investigation reveals that evidence is inconsistent and the condition has roots in our complex immune system. Severity of symptoms depend on the composition of sebum (body oil), yeasts/fungi, immune/inflammatory response, and individual susceptibility.

While scientists have not made a clear connection between yeast and dandruff, most dandruff shampoos appear to work by suppressing yeast growth. With this approach, are we silencing the warning signs of a deeper imbalance in the body? Do dandruff shampoos and other antifungal treatments reduce healthy populations of yeast along with pathogenic ones? Do certain yeasts provide a symbiotic benefit to our skin and health?

Understanding dandruff as a symptom rather than a cosmetic inconvenience can help us address deficiencies and risks for other conditions such as atopic dermatitis. The latest research reveals exciting clues and patterns that unravel the head-scratching mystery and address our overall skin and immune health.

* ”Dandruff” describes “seborrheic dermatitis” in this report, though dandruff is a general term for the shedding of dead skin cells.

Scanning the scene of the crime

Who are the victims? One survey showed wide ethnic variations, with dandruff highest in African-Americans (81-95%), Caucasians (66-82%) and Chinese (30-42%). In one study, adolescent males with white skin and higher body fat content were more susceptible to dandruff. In a revealing study of older adults, dandruff significantly correlated with the degree of disability and loss of self-sufficiency.

Where does it occur? Dandruff symptoms appear most often on areas with dense sebaceous glands, including the scalp, face and neck, including eyebrows, eyelids, nose, and mouth regions. On the scalp, dandruff affects the stratum corneum, the protective barrier on the scalp that retains moisture and protects from invasion by external irritants and pathogens. Dandruff is also associated with reduced hair shaft size and cuticle damage.

When does it occur? Dandruff symptoms are typically more prominent in winter and spring seasons.

How does it happen? Undesirable flaking occurs as certain outer skin cells called corneocytes are affected by yeast and sloughed off in an inflammatory and immune response. Studies hypothesize that these cells exhibit defects in their protective mechanisms. Strangely, the yeast will clump only on certain corneocytes and create an uneven distribution of affected regions on the scalp.

Suspect #1: Malassezia and fungal imbalance

Malassezia yeast (a form of fungus) has been investigated for decades as a culprit in the dandruff dilemma. Malassezia populations are actually very common on the body, and different species of the yeast are found on different anatomical locations. Interestingly, different species of Malassezia are dominant in different geographic regions. Malassezia globosa and Malassezia restricta are the two most commonly isolated species associated with dandruff. Variations of the yeast have been recently described in moist locations like ear canals and feet. In one study, M. globosa was the only species that increased in growth in response to high temperature and sweat, with high lipase activity.

Diversity of fungus may prove to be as important as gut bacterial flora. In lab studies, pre-treatment with Malassezia protected mice against Salmonella bacteria and tumor growth. In a revealing study of fungal populations, the fungus phylum Ascomycota was associated with healthy scalps but not dandruff-afflicted scalps. This data illuminates the scalp as a diverse community of microorganisms – a mycobiome – that may change to affect the health of the entire body.

Supporting evidence:

Malassezia yeasts may turn pathogenic under specific conditions. These conditions include high temperature, high humidity and internal factors such as the long-term use of corticosteroids and immunosuppressants, chemotherapeutic agents, bone marrow transplantation, AIDS, leukemia and diabetes, which elicit the overgrowth of otherwise harmless Malassezia yeasts.” – Annals of Dermatology, 2011

Malassezia yeast is associated with infantile seborrheic dermatitis (cradle cap), tinea versicolor, blepharitis, and atopic dermatitis. The Malassezia fungal population decreases in childhood but returns at the onset of puberty with increased sebaceous gland and hormone activity. While antifungal dandruff shampoos help control, reduce or clear symptoms, the condition typically continues once treatment is stopped.

The information about Malessezia is rather limited despite its widespread appearance with dandruff. New genetic information reveals that this yeast may be more dangerous than we thought, sharing similar enzymes as the harmful Candida albicans yeast and presenting mating-type genes. In lab studies, Malassezia cultures transformed into hyphae, a growth phase in yeast, after the addition of cholesterol, squalene, or glycine. Hyphal growth, as experienced with both Malassezia and Candida albicans, is associated with penetration of the tissue and infection.

“The potent AhR ligands synthesized by pathogenic Malassezia strains could contribute to tumor promotion by: modification of the UV radiation carcinogenesis, alterations in the salvage/survival of initiated tumor cells, inhibition of cell senescence, interaction with vitamin D metabolism, promotion of immune tolerance and finally pro-carcinogenic modulation of cell cycle progression and apoptosis.” – Medical Hypothesis, 2011

Malassezia produce enzymes called lipases to help them grow, including a phospholipase that releases arachidonic acid. This triggers the production of prostaglandins in tissue which fuels the inflammatory process. Malassezia also produce azelaic acid which depigments the skin when exposed to sunlight.

Recent data shows that Malassezia yeast is capable of producing molecules linked to skin cancer. In fact, basal cell carcinoma in animals reveals populations of Malassezia. Malassezia is associated with dermatitis and ear infections in dogs. Malassezia produce lipase and phospholipase that are believed to be factors in the development of inflammatory symptoms.

Opposing evidence: Some studies have found that Malassezia populations in healthy controls are not different than those with dandruff symptoms. Malassezia populations also appear similar between genders, though men suffer more from dandruff symptoms.

An analysis of the fungal community among dandruff sufferers found a higher incidence of certain other fungi such as Penicillium and Filablasidium floriforme on the scalp. These affected scalps did not have a variety of Cryptococcus species that was evident on healthy scalps. More research is necessary to understand the relationship between healthy skin and diverse fungal populations, as well as potential reactions to fungal overgrowths in dandruff.

Suspect #2: Allergic response

One of the most intriguing aspects of dandruff is its connection to the immune system and the allergic response. New evidence indicates that our adaptive immune system, inflammatory response, and risk of disease is affected by keratinocytes – outermost cells in our skin. Interestingly, atopic and autoimmune diseases have been rising as infectious diseases have been decreasing across the globe.

Supporting evidence: Studies between dandruff and the immune system have been limited, but a few patterns have emerged with related atopic conditions.  The IgE antibody response to Malassezia is very strong with atopic dermatitis, and IgE levels may associate with increased risk of non-melanoma skin cancer. A recent study did not associate Malassezia with severity of atopic dermatitis, but it pointed out that Malassezia may be an allergen and trigger for the condition. With atopic dermatitis, the allergic response may be explained by an autoimmune, cross-reactivity between Malassezia sympodialis and an anti-inflammatory protein thioredoxin. Protein research found similarities between Malassezia and common fungi found on corn, wheat and other food crops. The body can develop allergies to similar proteins, triggering symptoms from exposure to pairs like latex and banana, birch pollen and apple, and dust mites and shrimp.

As with atopic dermatitis, the individual Th2 immune response may be wired to dominate and stimulate the allergy-inflammation cascade. Maternal history of allergic disease can also infect a child’s vulnerability, as shown in cord blood studies on infants of mothers with atopic dermatitis. New studies propose that infants with impaired Th1 immunity through genetic or environmental factors may develop enhanced Th2 cells which increase the risk of allergy.

Probiotics have been studied as promising therapy to decrease the Th2 response and reduce symptoms of allergic disease. Probiotics may suppress allergic contact dermatitis by influencing the immune system in a way that may benefit dandruff sufferers. Lactobacillus acidophilus strain L-92 appeared to increase T cells in the spleen and cervical lymph nodes, as well as Foxp3, IL-10 and TGF-β.

Opposing evidence: In one study, the total IgE count in dandruff subjects was lower than healthy controls, while subjects with atopic dermatitis had much higher levels. In contrast, another study found both higher and lower-than-normal immune responses in dandruff patients as well as high levels of IgG and IgA antibodies. More research is necessary to confirm the exact trigger and mechanism of allergy and autoreactivity in dandruff and other types of dermatitis.

Suspect #3: Inflammation

Inflammation is closely related to the allergy-immune response, particularly through T-helper cells and their by-products such as cytokines of the interleukin (IL) family. Other subtypes like Th 17 and Th22 play important but variable roles in skin inflammation.  Some inflammation is necessary to protect the body from invasion. Yet, when T cells are not controlled, unrestrained inflammatory responses can occur and contribute to fungal infections. Any allergic response also releases histamine that is high in dandruff sufferers. Histamine release may increase the production of IL-17 and Th17 activity in lab studies, creating a vicious cycle of inflammation, invasion, and allergy. Scientists have only just begun to explore the intricate relationships between these cells and skin conditions like dermatitis.

When inflammation occurs, our body fights and manages the damage with antioxidants. For instance, the antioxidant squaleneprotects the skin from oxidative stress with anticancer properties and cholesterol-lowering potential. Interestingly, deep-sea shark liver contains an extremely high concentration of squalene that may explain low incidence of cancer and infectious disease in sharks. Olives are also high in squalene which may explain why the fruit can improve cholesterol and heart disease risk. Squalene oxidizes into squalene hydroperoxide when exposed to sunlight, contributing to skin aging and inflammatory conditions. An unsaturated form of vitamin E, gamma-tocotrienol, was most effective in reducing inflammation related to squalene hydroperoxide.

Supporting evidence: Research links dandruff with increased inflammatory responses due to altered IL activity. Subjects with dandruff showed reduced IL-1α/TP, IFN-γ and NO, and increased IL-1ra/TP, TNF-α/TP, and IL-2/TP. A few isolated case studies showed an outbreak of dandruff in males after they received recombinant interleukin-2 (rIL-2) immunotherapy.

Inflammation may be linked to interactions with Malassezia, as another study found that various species of the yeast differ in how they induce Th2-type IL cytokines. M. globosa appeared to induce IL-5, IL-10, and IL-13 in skin cells, while M. restricta appeared to induce IL-4.

Our unique allergic or autoimmune response may also be programmed to generate excessive inflammation. Atopic dermatitis is associated with a wide range of abnormal IL activity, including IL-25 that promotes both inflammation and reduces the skin barrier function.

Dandruff symptoms have long been treated with anti-inflammatory agents including corticosteroids with marginal success. More recently, calcineurin inhibitors have joined the list of anti-inflammatory treatments by inhibiting T-helper cells. Pimecrolimus has been comparable to ketoconazole in effectiveness, but with more side effects according to one study. Some research concluded that azole-based dandruff treatment works by reducing inflammation.

Suspect #4: Defects in the skin barrier

The skin serves multiple functions, protecting us from invading fungus and bacteria, preventing water loss, and absorbing vital nutrients. Skin permeability determines what is absorbed into the body, dramatically affecting our risk of disease. Similarly, gut permeability is a major factor in autoimmune conditions such as celiac disease, Crohn’s disease, and even Parkinson’s disease. The skin’s barrier primarily resides in the outermost stratum corneum, and it is constantly influenced by the chemistry and activity in underlying skin layers.

Recent studies support the skin’s more complex role in the immune system, including Langerhans cells and Langerin, fatty acid metabolism, and cholesterol balance. The detoxification function of the skin may even play a major role in metabolic syndrome. New perspectives on the sebaceous gland reveal its role as an active neuro-immuno-endocrine organ that utilizes hormones such as estrogens, glucocorticoids, and prolactin.

The skin barrier can be further disrupted by constant irritants in solvents, soaps or airborne toxins. Mechanical damage, UV damage and substances like DMSO and unsaturated fatty acids also increase skin permeability. Calcium flow into damaged skin may be affected by suboptimal magnesium levels and glutamate receptors (NMDA), resulting in aging and skin diseases like dermatitis. Similarly, psychological stress and even electrical fields (EMFs) can elevate intracellular calcium levels and disrupt skin barrier health.

Decreased calcium, increased cytokines, growth factors, and activated hormone receptors (like vitamin D receptors) can enhance barrier formation, while nitric oxide, protease-activated receptor 2 activation, glucocorticoids, and testosterone can inhibit it. New studies show that probiotics can restore the function of the skin barrier by reducing trans-epidermal water loss, vasodilation, edema, and release of TNF-α.

Supporting evidence: Malassezia yeast clumps clusters at certain corneocytes on the scalp, leaving others alone. This inconsistent distribution implies that there may be defects in the skin, including keratinocytes and their final stage as corneocytes.

Mutations in the filaggrin protein are common in 10% of the Western European and North American population and considered a factor in skin barrier defects and increase risk of sensitization, atopic dermatitis, and allergic rhinitis. Research on defects in the skin barrier help link atopic dermatitis with asthma as well as bacterial and viral infections. Scientists propose that a genetic predisposition to skin barrier defects may be exaggerated by allergic sensitization, making it difficult to determine the exact cause.

Our skin may be reflecting the health of our gut lining. New research found that abnormal levels of defensin, part of the intestinal epithelial barrier, were associated with the development of atopic dermatitis later in childhood.

Suspect #5: Fatty acid imbalance affecting the skin barrier

Sebaceous glands produce sebum that is composed primarily of triglycerides, wax esters, free fatty acids and squalene. Sebaceous glands are located all over the body excluding the hands and soles of the feet, and the amount of sebum produced varies based on location. Sebum is thought to provide vital antioxidants, antimicrobial compounds, pheromones, hydration, and hair follicle support. Linoleic acid and α-linolenic acid are the primary fatty acids in the skin that form derivatives like arachidonic acid, γ-linolenic acid, docosahexaenoic acid and eicosapentaenoic acid that help protect us from infection, sunburn, and even skin cancer.

“It has been shown that under conditions of linoleic acid deficiency, linoleic acid is substituted by oleic acid in epidermal acylceramides, which has been associated with an increased transepidermal water loss, perturbations of the intercellular membranes and an altered epidermal homeostasis.” – British Journal of Nutrition, 2009

The triglycerides produced in sebum are the food source for Malassezia. Triglycerides are broken down into fatty acids with the help of enzymes called lipases. A higher ratio of triglycerides to free fatty acids associated with dandruff in both HIV-positive and HIV-negative patients. Omega-3 fatty acids can reduce triglyceride levels, possibly explaining their benefits for heart disease.

During metabolism, Malassezia creates by-products such as oleic acid, a long-chain, monounsaturated omega-9 fatty acid. In a vicious cycle, oleic acid increases the growth of Malassezia and symptoms of dandruff in susceptible individuals. Oleic acid is normally abundant in human fat tissue and sebum, but increased levels can significantly increase the skin permeability, increase calcium in the cells, and allow absorption of substances. Oleic acid can also inhibit many harmful, gram-positive bacteria like Staphylococcus aureus that cause MRSA. Oleic acid is very high in olive, almond, and canola oils and used in many shampoos and soaps – often under the name “sodium salt.” Many products intended for dry or itchy scalps contain oleic acid and may not relieve dandruff sufferers.

Yet, not everyone is equally vulnerable to dandruff and inflammation. Tests showed that applying a solution of oleic acid (and propylene glycol, ethanol, and water) caused flaking in susceptible but not normal subjects. Interestingly, these tests did not increase populations of Malassezia, supporting the theory that dandruff symptoms may be largely due to a malfunctioning skin barrier in certain individuals. These individual differences are affected by genes that control enzymes called desaturases that break down fatty acids, and genetic alterations can drastically affect the skin barrier. Some primary desaturases and their proposed functions were recently described in Dermatoendocrinology:

Supporting evidence: Research links dandruff to higher levels of triglycerides, lower levels of free fatty acids in the skin, and reduced squalenes – naturally occurring antioxidants. Infantile seborrheic dermatitis is also associated with abnormal levels of essential fatty acids, indicating impaired enzyme delta-6-desaturase. The affected infants showed increased blood levels of oleic acid and reduced linoleic acid.

Omega-3 and omega-6 polyunsaturated fatty acids (PUFAs) in sebum help determine skin health, and dietary intake of carbohydratesand fatty acids influence the composition of the sebum. Numerous studies show how topical and systemic application of omega-3 fatty acids can benefit skin health and even reduce the risk of skin cancer. In fact, tests with flaxseed oil supplementation – high in omega-3 fatty acids – led to a decrease in skin sensitivity and improvement in skin barrier health. Blood levels of vitamin E, polyunsaturated fatty acids of phospholipids (PUFA-PL), and erythrocyte glutathione peroxidase (GSH-Px) are lower in individuals with dandruff. Deficient PUFA-PL is accompanied by increased saturated palmitic and stearic acids.

In healthy patients, conjugated linoleic acid (CLA) supplementation improved fatty acid composition, reduced delta-6 desaturase activity,and decreased body fat. Meat and dairy products from grass-fed, cud-chewing animals are highest in CLA. Other studies on atopic dermatitis have presented some favorable results with supplemental gamma-linolenic acid in the form of borage oilflaxseed oil, and evening primrose oil.

Suspect #6: Hormones

Hormones can promote or inhibit fungal growth, as seen with estrogen and Candida albicans, but their relationship with Malassezia needs further study.

Supporting evidence: Estrogens appear to decrease sebum production in the cells, while testosterone and its derivative 5α-DHT appear to increase production and lipid synthesis with the help of peroxisome proliferator-activated receptors (PPARs). Most studies show that men are generally more affected by symptoms than women. Interestingly, men also experience a greater risk of invasive cancers, particularly melanoma of the skin.

Growth hormones enhance sebum secretion, and insulin-like growth factors (IGF-1) increase with growth hormones as well as high-glycemic diets and dairy consumption.

Deficiency of the misnamed hormone vitamin D is also linked to the severity of atopic dermatitis. One study found that the prevalence of dandruff correlated with the number of gloomy days in the area, hinting at the influence of sunlight and corresponding vitamin D and melatonin production. Melatonin is a vital hormone and antioxidant we produce when we experience darkness every night, though this circadian rhythm can be disrupted with artificial lighting. Indeed, it is believed that melatonin plays a major role in Parkinson’s disease and depression, two conditions that are associated with dandruff. Similarly, melatonin inhibited the development of induced atopic dermatitis in mice, reducing IgE levels, and IL-4 and IFN-γ production by activated CD4(+) T cells. New research indicates that melatonin benefits skin health by inhibiting tumor growth fueled by linoleic acid.

Suspect #7: Vitamins, minerals, and metal homeostasis

As nutrients affect inflammation and the immune response, nutritional imbalances can increase vulnerability to pathogenic invasion, infection and symptoms. Multiple papers underline the importance of vitamin E in protecting the skin and reducing inflammation associated with an overgrowth of MalasseziaOther vitamin and mineral deficiencies may also play a role, including essential fatty acids, vitamins A, B1, B2, B6, C, niacin, biotin, selenium, zinc, and iron.

The complex interactions of trace minerals in the body are poorly understood in health research, but they clearly affect metabolism and the immune-inflammation response. Furthermore, metal complexes show intriguing antibacterial and antifungal activity. Copper-zinc ratios appear linked to inflammation, particularly through copper-based enzymes like Cu/Zn superoxide dismutase (SOD1) which detoxifies harmful superoxides. The ratio of copper to zinc helps determine the function of CuZnSOD1, and high levels of zinc can affect both copper and SOD levels. In fact, higher zinc levels were linked to lower copper levels within SOD1. Zinc supplementation has shown promising results in treating Alzheimer’s, possibly by lowering copper levels. Interestingly, high levels of copper were associated with altered vitamin D metabolism and decreased levels of vitamin E in certain liver-related conditions. Another study showed that both vitamins D and E increased blood levels of SOD in atopic dermatitis patients.

Studies are showing that exposure to formaldehyde depletes levels of zinc, copper, and iron in testicular tissue. Certain substances like calcium, phosphorus, and dietary fiber and phytates, and enhancers, such as amino acids, picolinic acid, and prostaglandin E2 can also bind with zinc to decrease accumulation in the body. Another study showed that long-term aluminum exposure reduced the levels of calcium, magnesium, phosphorus, copper, iron, zinc, and other trace minerals in bone. More research is needed to identify environmental sources of mineral disruption that can affect our immune health.

Copper and zinc are not stored in the body, so food sources of these minerals are important. Copper is highest in beef liver, and other sources include clams, oysters, crab, cashews, sunflower seeds, hazelnuts, almonds, peanut butter, lentils, and mushrooms. Zinc is highest in oysters, and other sources include crab, dark turkey, beef, turkey, pork, dark chicken, fruit yogurt, milk, baked beans, cashews, chickpeas (garbanzo beans). Zinc can be depleted with high calcium intake in some cases, particularly when combined with phytic acid in the form of tortillas made with lime.

One of the most complicating factors in studying the effects of metal on the body is the variable distribution of metals in different tissues, organs, bones, and blood, which may or may not correlate with symptoms and disease. We are far from identifying the ideal balance of trace minerals for each individual body, but it is imperative that we pursue this equation to extend wellness and prevent disease where possible.

Supporting evidence: New research indicates that maternal nutrition during pregnancy can dramatically affect a child’s immune health, and high levels of folate and vitamin B-12 in pregnant mothers were associated with risk of atopic dermatitis in their children. The hormone vitamin D in pregnancy plays a major role in forming the immune system of newborns, though more research is necessary to identify patterns and impact of supplementation. Skin health can be negatively impacted by the consumption of alcohol during pregnancy, increasing the risk of atopic dermatitis in infants.

The balance of metallic trace elements in the body are even more intriguing. Recent studies revealed that zinc pyrithione, a popular ingredient in dandruff shampoos, may work by increasing copper levels in the scalp that inhibit Malassezia growth. Interestingly, copper also inhibits histamine. In one study, topical application of zinc-copper reduced IL-1α, IL-2, NO and TNF-α and prevented dermatitis and hypersensitivity in animals. Copper is retained in the skin at very high rates and can permeate the skin to affect blood levels. Zinc also provides antioxidant power. In animal studies of dermatitis, a gel containing copper and zinc improved symptoms.

In an unplanned real-world experiment, trapped Chilean miners experienced relief from symptoms of fungal infections and irritant dermatitis after using socks containing copper oxide particles. Colloidal silver has also been used to treat skin infections, and elastic silver textile helped relieve symptoms in atopic dermatitis patients. Considering the risk of metal toxicity and allergy, we need a better understanding of how metals are absorbed and utilized for health benefits in the body.

Identifying high-risk areas

Fungus or yeast has been identified alongside a range of debilitating conditions in the body. Recent studies propose that dandruff may cause changes in the surface of the eye, tear production, and other signs of dry eye disease. Dandruff as well as acne is strongly associated with hypersecretory meibomian gland dysfunction, though it is not clear if the excess lipid production is due to hyperlipidemia or damming of secretions.

ParasitesThe parasitic and contagious mite Demodex can appear with dandruffas well as damaged areas of the skin susceptible to development into non-melanoma skin cancer. In another study, Demodex increased in students with acne, favoring oily skin and enlarged sebaceous glands. Immune or allergic reactions to Demodex are likely to associate with symptoms.

Bacteria – Interestingly, a study of acne patients showed less growth of Malassezia than controls. Additionally, M. restricta was dominant in acne conditions while M. globosa was more common in controls. This study also hypothesized that overgrowth of bacteria P. acnes may affect populations of Malassezia. Much more research is needed to understand how we are affected by the relationship between fungus and bacteria in the body.

Autoimmune conditions – Risk factors for dandruff include an altered immune system, and most HIV patients are afflicted. Rosacea, acne, blepharitis/meibomian gland dysfunction, atopic dermatitis and psoriasis are some inflammatory autoimmune conditions associated with dandruff. In one study of organ transplant cases, dandruff was also associated with skin cancer. Chronic UV exposure was proposed to suppress immunity and increase risk of dandruff in mountain guides in one interesting study.

Dandruff often occurs with Parkinson’s disease, depression, and treatment with certain drugs like lithium, haloperidol decanoate, buspirone, and chlorpromazine. Preliminary research shows that gastrointestinal dysfunction may also be a risk factor for skin health imbalances. Skin conditions like dermatitis herpetiformis associate with celiac disease and chronic gastritis, revealing strong connections between intestinal disturbances and skin inflammation.

Dandruff crime prevention

Antifungals -Synthetic antifungal shampoos have been used to control but not cure seborrheic dermatitis. Dandruff symptoms typically returnwhen this treatment is discontinued. In one study, ketoconazole (2%) outperformed the other antifungal ingredients as a once-weekly maintenance shampoo. Another study showed effectiveness of sertaconazole. Oral antifungals can also be effective for dandruff but introduce health risks and side effects.

As antifungal shampoo simultaneously reduces symptoms and yeast populations, Malassezia is primarily guilty by association. Yet, it is not clear if long-term reduction of yeast would create additional health risks. For example, new research shows that tiny nanomolar concentrations of zinc pyrithione – a popular dandruff shampoo ingredient – can cause DNA damage. Other imidazole antifungals such as ketoconazole block the production of ergosterol which reduces fungal populations. This activity may pose a health risk because ergosterol converts to vitamin D2 when exposed to UV light. Vitamin D2 is used by the body to support healthy bones, immune functions, brain activity, and also used to prevent cancer.

Natural treatments have not been comprehensively studied, and many antifungal essential oils are harsh on the skin. A promising new direction involves the use of fats to combat fungal, bacterial, and viral growth. Medium-chain fatty acids, high in coconut oil, are toxic to Malassezia. Virgin coconut oil also showed anti-bacterial activity against Staphylococcus aureus which can infect dermatitis sufferers. Yet, it is not evident that natural or synthetic antifungals can improve the health of the skin barrier to cure the condition.

Anti-inflammatories – In past decades, doctors have used topical steroids to control inflammation, but the results are mixed with negative side effects on the adrenal gland and skin. Lithium salts showed greater efficacy (as lithium gluconate 8% ointment) on facial conditions, likely due to anti-inflammatory action. Coal tar and even pine tar have also been used to reduce symptoms, possibly due to a combinatory reduction in sebum, inflammation, and fungus.

Topical calcineurin inhibitors have also been used to inhibit inflammation, but they interfere with the immune response and long-term effects of therapy are not clear. In fact, studies show that inhibiting calcineurin can stimulate tumor growth in skin cells.

Natural anti-inflammatory substances may help relieve symptoms. Interestingly, topical application of epigallocatechin-3-gallate – the primary antioxidant in green tea – also decreased the size and activity of sebaceous glands associated with acne.

Nutritional support: Reducing inflammation in the body through nutritional intervention is a popular approach, though antioxidant therapy alone has not been effective for dandruff. Vitamin D and E supplementation shows the most success in treating atopic dermatitis, but studies on dandruff are limited. Probiotics have also improved symptoms in a range of skin conditions. Notably, researchers in France used oral probiotics to reduce dandruff by 57% in test subjects, improving skin barrier function and reducing populations of Malassezia.

Other promising diets include omega-3 supplementation that influences the fatty acid ratios, improves skin health and inflammation, and reduces risk of allergy in early-life studies. Researchers have not examined how fatty acid consumption can affect sebum composition and dandruff symptoms, but studies of other inflammatory skin conditions are revealing clues. Acne, for examaple, is triggered by high ratios of saturated fats to monounsaturated fats – often a result of high glycemic load diets. Another study linked the consumption of α-linolenic acid, linoleic acid, omega-3 PUFAs, and omega-6 PUFAs to eczema, while consumption of arachidonic acid was linked to lower incidence. In another animal study, a combination of arachidonic acid and omega-3 docosahexaenoic acid (DHA) supplements reduced dermatitis caused by allergens.

UV therapy – With dandruff symptoms increasing over winter and spring months, it is no surprise that UV therapy (narrow-band) helps clear symptoms in severe cases as well as other skin conditions. Yet UV light can also induce DNA damage and risks must be carefully assessed before treatment.

Herbal remedies – A wide range of soothing herbs can help relieve inflammation with dandruff and dermatitis conditions. Aloe, calendula, licorice, and chamomile oil topically improved symptoms. Herbal studies have identified at least thirteen different herbs that inhibited Malassezia (restricta) growth in vitro, including Rhizome Coptidis, Fructus Mume, Radix et Rhizoma Rhei, Herba Houttuyniae, Ginger Pinellia and Dandelion. Lemongrass oil also effectively inhibited Malassezie (furfur). Another study showed that bamboo oil may also inhibit Malassezia.

Home remediesAnecdotal reports claim benefits from natural antifungals including apple cider vinegar, hydrogen peroxide and tea tree oil. While frequent use of soaps are not recommended for atopic dermatitis, daily cleansing of scalp oils provides benefit in dandruff sufferers. Cleansing may reduce sebum that fuels growth of fungus, particularly if the sebum composition promotes excessive yeast activity.

Whodunit or Idunit?

In light of the research, we must approach dandruff, dermatitis, and other skin conditions as signs of underlying imbalance and disease risk that we can influence. The possibility of allergy, chronic inflammation, and compromised immunity beneath dandruff can severely undermine our health. A holistic approach to dandruff therapy that addresses our vulnerability has greater potential for full recovery and long-term wellness:

  • Fight inflammation – Increase anti-inflammatory foods such as fruits and vegetables and avoid fried and sugary foods. Avoid harsh soaps, and cosmetics that may contain irritating ingredients. Consider soothing ingredients in topical treatments such as green tea and aloe. Foods rich in antioxidants like vitamin E, C and A can also reduce oxidative stress in the body, though supplementation has not proven to cure skin disease.
  • Reduce allergen exposure – In many cases, chronic skin conditions are aggravated by allergies to almost anything in products or the environment. Common, unsuspected allergens include nickel, rubber, fragrance, formaldehyde, or irritants such as ingredients in cosmetics, soaps, sunscreens, and deodorants. Identify possible allergens and avoid contact. Probiotics may reduce histamine levels that may be high in dandruff patients.
  • Boost immunity – Daily probiotics and omega-3 supplements appear to benefit skin health by altering the fatty acid composition. Good sleep hygiene can also support the immune system. Many skin conditions have been associated with a deficiency in vitamin D, a hormone produced in sunlight-exposed skin or consumed in certain fish. Some dermatitis patients benefit from gamma-linoleic acid supplementation in the form of borage, flaxseed, or evening primrose oil.

New areas of research in nutrigenomics promise to shed light on the influence of nutrition on genetic behavior, while lipidomics explores the role of fatty acids in disease. We urgently need more information on how different nutrients, probiotics, trace minerals, and fatty acids can influence our inflammation and immune processes. While dandruff and other related conditions have been manageable with antifungal treatments, we risk complications and disease as long as we do not understand the role of our native fungal populations, the inflammation-immune response, and interactions of the skin barrier.


Primary references
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4. Gaitanis G, Magiatis P, Hantschke M, Bassukas ID, Velegraki A. The Malassezia genus in skin and systemic diseases. Clin Microbiol Rev. 2012 Jan;25(1):106-41. doi: 10.1128/ CMR.00021-11. PubMed PMID: 22232373; PubMed Central PMCID: PMC3255962.

5. Del Rosso J and Kim G Seborrheic Dermatitis and Malassezia species: How Are They Related? The Journal of Clinical and Aesthetic Dermatology. 2009 Nov.

6. Osredkar J and Sustar N Copper and Zinc, Biological Role and Significance of Copper/Zinc Imbalance. Clinical Toxicology. 2011 S:3

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3 comments to A Dandruff Whodunit

  • Thank you, and yes this article is still very current considering the slow pace of progress in dandruff research and treatment. I found a recent review article of Malassezia that mentions possible desensitization to Malassezia – a very interesting proposal that might allow for a healthy fungal population without complete eradication and drug resistance. Since at least half of the dandruff population may have an allergy-type response to Malassezia (according to one paper), we may need to focus on dandruff as an immune/allergy issue underlying chronic inflammation. For this condition, I would also recommend identifying and reducing all allergen exposure in the diet/environment to prevent histamine overload, as mentioned in my histamine report.

    Let me know if you find anything more to share on this.

  • Awesome and comprehensive article on the topic of dermatitis/dandruff. I wonder, as this article is three years old, is there any new research to look at? This is possibly the most comprehensive page of info I’ve found, most articles only focus on one of these as THE solution, but all possibilities are examined here.

  • Brandon

    Great, informative article! Thank you! 🙂

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