Complementary and Alternative Approaches I

Introduction

The goals of atopic dermatitis (AD) treatment are to (1) dampen skin inflammation, (2) decrease itch and pain, (3) repair the skin barrier, and (4) restore the microbiome. Conventional treatment of AD is therefore multitiered and includes a combination of emollients, topical antiinflammatory medications, and in more severe cases systemic immunosuppressants and immunomodulators. Conventionally, such immunosuppressants were not target specific and could be poorly tolerated due to their side effect profiles, thus limiting their value in long-term usage. There has not been a safe and efficacious immunosuppressive medication for moderate to severe AD until the recent introduction of dupilumab in 2017. Dupilumab is a monoclonal antibody targeting interleukin-4 (IL4) production approved for use in teens ages 12 to 17 and adults ( ).

While research has made great strides in AD treatment over the last 5 years, a recent survey found that more than half of patients with AD use complementary and alternative medicine (CAM) in addition to their conventional treatments (Darmstadt, 2004). Factors contributing to this staggering number may include treatment resistance or partial response to conventional therapy, safety concerns in infants and children, and the undesirable side effects of long-term topical steroids and systemic agents.

The National Center for Complementary and Alternative Medicine (NCCAM) of the National Insitutes of Health defines CAM as “a group of diverse medical and health care systems, practices, and products that are not presently considered to be part of conventional medicine” ( ). Complementary therapies typically refer to modalities used in tandem with conventional therapies, while alternative therapies are modalities used in place of conventional therapies. We believe that evidence-based CAM modalities may be integrated into conventional treatment plans to improve overall treatment outcomes and/or to limit side effects. For example, certain topical CAM products may reduce topical corticosteroid use and limit skin atrophy and hypopigmentation side effects.

This chapter discusses the existing scientific evidence for CAM in AD, including topical and oral oils, micronutrients, bathing additives, topical endocannabinoids, fabric selection, and cryotherapy. We specifically examine the role of these modalities in augmenting conventional AD treatment. Additional CAM modalities, including acupuncture, acupressure, cupping, herbal supplements, sleep hygiene, and mind-body techniques, will be discussed in Chapter 27 .

Topical natural oils

Natural oils are an attractive treatment modality due to their high free fatty acid (FFA) and triglyceride (TG) content. Long-chain fatty acids, particularly linoleic acid, are components of a healthy skin barrier that are deficient in AD patients ( ). Replacement of these FFAs with topical oils is a potential treatment strategy.

One thing to note is that each topical oil has a unique ratio of FFAs and TGs, which in turn dictates efficacy in AD ( ). For example, oils composed mainly of monounsaturated oleic acid increase skin permeability more than oils containing an even mix of both mono- and polyunsaturated fatty acids. Topical oils also come in various forms and concentrations. When recommending a natural oil to patients, we recommend that patients look for a cold-pressed and/or, virgin natural oil product. Essential oils, which are highly concentrated, and fragranced oils are known triggers of irritant and allergic contact dermatitis and should be avoided in AD patients ( ). A list of topical and oral oils used for AD is summarized in Table 26.1 .

Sunflower seed oil

Sunflower seed oil (SSO) contains linoleic acid, an omega-6 FFA, which is a major fatty acid component of the skin barrier. Linoleic acid exerts positive effects through potent activation of peroxisome proliferator-activated receptor-α (PPAR-α)—a nuclear receptor found in skin cells that plays a role in regulating keratinocyte proliferation, maintaining skin barrier homeostasis, and dampening inflammation ( ). PPAR-α has significantly reduced gene expression in both the skin of lesional and nonlesional AD patients, and its loss likely contributes to the dysregulated inflammatory cascade in AD ( ).

Daily SSO application for 4 weeks has been shown to improve skin erythema and transepidermal water loss (TEWL) in AD patients. Long-term usage is likely needed to maintain its beneficial benefits ( ). Studies in children also suggest that SSO may reduce rates of cutaneous infections. A randomized controlled trial (RCT) of preterm infants in Egypt found that topical application of SSO three times daily significantly reduced rates of invasive nosocomial infections compared with infants who did not receive SSO ( ). Another trial found that topical application of SSO significantly reduced mortality rates in preterm hospitalized infants, likely due to enhanced skin barrier integrity ( ). Given its low cost and efficacy, SSO application has a role in skin barrier repair and can potentially be a lifesaving topical treatment for preterm infants in developing countries.

Sunflower oleodistillate

Sunflower oleodistillate (SOD), a derivative of SSO, is produced through a mineral distillation process resulting in a lipid-rich oil composed largely of oleic and linoleic acids. Compared with naturally occurring SSO, the physical processing of SOD results in a product with a 10-fold higher concentration of phytosterols and vitamins ( ). This phytosterol content confers additional antiinflammatory and barrier-promoting promoting properties ( ). A RCT of 86 pediatric patients with moderate AD found that the addition of 2% SOD to conventional topical corticosteroid therapy led to statistically significant improvements in lichenification, excoriation, and quality of life when compared to once- or twice-daily application of steroids alone ( ). SOD appears to decrease steroid requirements and thus may be a safe alternative in patients who cannot tolerate topical corticosteroids ( ).

Virgin coconut oil

Virgin coconut oil (VCO) is produced by a wet-milling and cold-press process that does not involve heat or chemical processing ( ). VCO contains monolaurin, a medium-chain fatty acid that demonstrates broad-spectrum antibacterial activity against Staphylococcus aureus ( ). Patients with AD are frequently and disproportionately colonized by S. aureus when compared to healthy counterparts. A meta-analysis of 95 observational studies in AD patients reported a pooled prevalence of S. aureus colonization of 70% in lesional skin, 39% in nonlesional skin, and 62% in the nares ( ). A double-blind, controlled trial of 52 patients with AD found that VCO significantly reduced the objective-SCORAD severity index (O-SSI) through its antibacterial activity against S. aureus (based on its culture results) and overall antimicrobial activity as compared to virgin olive oil ( ).

In a RCT of 117 pediatric patients with AD, twice-daily application of VCO for 8 weeks led to significant improvements in SCORAD and TEWL as compared to mineral oil ( ). In preterm very low-birthweight neonates who have an immature stratum corneum, VCO has been used to reduce TEWL eventuating in improved barrier function ( ). The efficacy of VCO is theorized to be due to its superior ability to penetrate the skin and reduce inflammation ( ). Due to its safety and efficacy in both adults and children, VCO is a great alternative daily moisturizer for AD patients or an adjunct to current therapy.

Borage seed oil

Patients with AD are thought to have a reduced rate of conversion from linoleic acid to γ-linolenic acid (GLA), dihomo-γ-linolenic acid, or arachidonic acid as compared with healthy subjects ( ). Thus AD patients are deficient in the barrier-forming FFA GLA. Borage seed oil (BSO), which contains 23% GLA, one of the highest concentrations found in a plant, may be helpful in replenishing barrier GLA ( ). To date, topical BSO has not been studied in AD patients. Sparse investigations of oral BSO supplementation and BSO-containing clothing have had mixed results in improving AD symptomatology and severity ( ). Additional studies are needed to elucidate the role of BSO in AD.

Menthol

Cooling baths have been shown to be beneficial in AD patients ( ), and cooling may be one strategy for combating itching sensations. Menthol is a naturally occurring cyclic terpene alcohol that has a cooling and antipruritic effect when applied to the skin. Menthol’s antipruritic properties are due to its activity on the TRMP8 receptor in C fibers (unmyelinated pain fibers) ( ), direct stimulation of A-delta fibers (myelinated pain fibers) ( ), and selective activation of κ-opioid fibers ( ).

An itch-relieving moisturizing cream containing 3% menthol and ceramides significantly reduced itch in healthy individuals and AD patients; however, 1/60 participants reported stinging sensations ( ). Menthol has also been shown to cause allergic contact dermatitis ( ), and high concentration (40%) products may cause erythema and burning ( ). Moreover, menthol promotes TEWL at a level higher than regular rubbing alcohol, so it should be used with caution in xerotic skin, and should not substitute a proper emollient ( ). Larger RCTs are needed to investigate the positive and negative effects of menthol in AD patients. A 3% menthol is the appropriate concentration to recommend to patients with AD who are interested in menthol products.

Tea-tree oil

Tea-tree oil (TTO) is an essential oil derived from the leaves of the Australian plant Melaleuca alternifolia ( ). TTO contains terpinen-4-ol, a potent antibacterial agent against methicillin-resistant S. aureus (MRSA) and was shown to be as effective as topical mupirocin against S. aureus in vivo ( ). TTO has been studied in acne vulgaris, and topical application was shown to have a statistically significant effect on mean total acne lesions ( ). However, to date, no RCTs have been conducted in AD patients. We suggest avoiding all essential oils, including TTO, in AD patients due to their potential for triggering contact dermatitis ( ).

Olive oil

Despite the perceived safety and benefit of most natural oils in AD, olive oil promotes and exacerbates AD. The negative effects of olive oil are due to its high ratio of short-chain oleic to linoleic acid (7:1), which increases TEWL ( ). Oleic acid also disrupts cutaneous homeostasis through its activation of NMDA cell surface receptors, resulting in delayed barrier repair and epidermal hyperplasia ( ). In a RCT, six drops of oil twice daily for 5 weeks led to a significant reduction in the integrity of stratum corneum and induced mild erythema in participants with and without AD, when compared to SSO. These negative effects of olive oil were more prominent in AD patients when compared to healthy counterparts ( ). A clinical trial of 115 healthy neonates found that olive oil is especially damaging to the immature stratum corneum of infants because it disrupts crucial neonatal lipid organization in the skin ( ). Olive oil and related products should be discouraged in AD patients.