Authors Verm?n M. Verallo-Rowell, Kristine M. Dillague, Bertha S. Syah-Tjundawan, Skin and Cancer Foundation, Pasig, Philippines, and the VMV Skin Research Centre + Clinics, Makati City, Philippines

Posted: 02/17/2009; Dermatitis. 2008;19(6):308-315. ? 2008  American Contact Dermatitis Society

For full article see http://www.medscape.com/viewarticle/586673

Abstract

Background: Atopic dermatitis (AD) skin is dry and readily colonized by Staphylococcus aureus (SA). Coconut and olive oils are traditionally used to moisturize and treat skin infections.
Objective: To compare virgin coconut oil (VCO) and virgin olive oil (VOO) in moisturizing dryness and removing SA from colonized AD skin.
Methods: This was a double-blind controlled trial in two outpatient dermatology clinics with adult AD patients who were diagnosed by history, pattern, evolution, and skin lesions and who were randomized to apply VCO or VOO twice daily at two noninfected sites. SA cultures, photography, and objective-SCORAD severity index (O-SSI) scoring were done at baseline and after 4 weeks.
Results: Twenty-six subjects each received VCO or VOO. Of those on VCO, 20 were positive for SA colonies at baseline versus 12 on VOO. Post intervention, only 1 (5%) VCO subject remained positive versus 6 (50%) of those on VOO. Relative risk for VCO was 0.10, significantly superior to that for VOO (10:1, p = .0028; 95% CI, 0.01-0.73); thus, the number needed to treat was 2.2. For the O-SSI, the difference was not significant at baseline (p = .15) but was significantly different post treatment (p = .004); this was reduced for both oils (p < .005) but was greater with VCO.
Conclusion: VCO and monolaurin's O-SSI reduction and in vitro broad-spectrum activity against SA (given clinical validity here), fungi, and viruses may be useful in the proactive treatment of AD colonization.

Introduction

Atopic Dermatitis (AD) is characterized by dry skin and the frequent isolation ofStaphylococcus aureus (SA) from infected eczema and chronic lesions and as a colonizer of clinically uninfected atopic skin.[1] The prevalence of colonization in normal skin is about 5%; in lesional and nonlesional atopic skin of adults, children, and infants, it is 64 to 100%.[2] Thus, based on a recent systematic review of AD, it is felt that the use of a topical antibiotic for treating SA infection can be effective, but the development of resistance is a concern. Treatment of SA colonization is not as clear-cut. The review further states that antibiotics generally have a minimal therapeutic effect on dermatitis without signs of infection.[3]

A recent review on the mechanisms of disease in AD explored (1) the role of SAcolonization and infection in helping generate the chronic inflammation characteristic of atopic skin and (2) the role of inflammation (from SA and from genetic and environmental causes) that leads to barrier dysfunction that culminates in dry skin. Rather than endorse the more common reactive management of AD, the review recommended early and proactive intervention with antiseptic lotions to reduce SAcolonization.[4]

Few evidence-based data are accepted in modern therapeutics for the widespread traditional practice of using coconut oil (CO) on dry infected skin.[5] In a small trial of patients with xerosis, Agero and Verallo-Rowell found CO comparable to mineral oil in skin moisturization and the absence of irritant effects.[6] No trials have been reported on the topical use of CO specifically for AD, clinically infected or not.

In recent years, the term "virgin" has been used to indicate a health-related value in coconut and olive oils. The virgin status of olive oil is achieved by extracting the oil 24 to 48 hours after harvest and through Good Manufacturing Practice (GMP), including the avoidance of heat, light, and air during processing and storage. These precautions protect heat-sensitive phytochemicals and help prevent the hydrolysis of triglycerides into their component free fatty acids (FFAs), which leads to the rancid smell of spoilage and to skin irritation.[7] The amount of FFAs present is used to define the degree of virginity of the oil, as follows: ordinary, a maximum of 3.3%; fine virgin, a maximum of 1.5%; and virgin, less than 1%. "Extra-virgin olive oil" (EVOO) is a retailing name used to emphasize the fact that the oil is pressed cold immediately after harvest.[8]

Virgin coconut oil (VCO) is also processed on the day of harvest, under similar GMP guidelines.[9] Unlike virgin olive oil (VOO), which has 82% unsaturated fatty acids (FAs), VCO has only 8% unsaturated FAs. The other 92% of the FAs are saturated and chemically stable such that the standard of 0.5% FFA content in VCO is readily achieved as long as the moisture content is kept at the standard of 0.12% or less. Since the nutmeat is exposed to its water at tropical temperatures for 10 months, extra-virgin coconut oil (EVCO) is considered "cold pressed" when the nutmeat is pressed at a temperature that does not exceed 39?C.[10] For the objectives of this study, these differences are minor; hence, the more common terms for these two virgin oils-VCO and VOO-are used in this article.

This 4-week randomized controlled blinded trial compared the effects of VCO and VOO on SA colonization of normal AD skin and on the extent and intensity of objective AD parameters, using the objective SCORing Atopic Dermatitis (SCORAD) severity index (O-SSI)

For methods and results see http://www.medscape.com/viewarticle/586673

Discussion

Antimicrobial Action of FAs From Edible Oils

VCO has a long tradition of use in treating infections. Like all edible oils, VCO is made up of triglycerides, each one with a simple glycerol core of three carbons, to each of which an FA is attached. In the stomach and the upper part of the small intestine, ingested VCO is digested by lipase enzymes into di- and monoglycerides, glycerol, and FFAs.[13]

Lipases are also present in the aerobic organisms of the normal skin flora. Holt reported that from the normal skin of adults and children, almost all 42 strains of isolated Micrococcaceae Sarcina, 40% of 50 aerobic skin diphtheroids, and 20% of 58 aerobic nasal diphtheroids produced strong or active lipases. The author postulated that action of these lipases on skin lipids accounts for the production of FAs that acidify the skin (average hydrogen ion concentration [pH], 5.5) and provide the surface of the skin its "acid mantle."[14]

Similarly, we postulated that these lipases (and those known to be produced bySA)[15] may hydrolyze the triglycerides of topical VCO to levels higher than the 1 to 7% monoglycerides and the 0.5% FFAs that are normally present in unhydrolyzed VCO.[16]

Studies on lipids in the 1960s by Kabara and colleagues showed medium-chain (C-8 to C-14) FAs and their monoglycerides to have antimicrobial effects against several laboratory organisms.[17] In the 1990s, more laboratory studies confirmed the antimicrobial activity of these lipids against gram-positive and some gram-negative organisms (including Neisseria gonorrhoeae,[18] Helicobacter pylori,[19] and Chlamydia trachomatis [20] ) as well as Candida albicans yeast[21] and enveloped viruses.[22]

Since 1998, some clinical studies have confirmed these laboratory data, specifically data on monolaurin, the monoglyceride of lauric acid from VCO. A 2% gel preparation of Lauricidin (Skin Sciences Laboratory, Inc, Pasig City, Philippines), which contains 90% pure monolaurin, significantly degermed SA cultured from health workers' hands after hospital duty.[23]

Another study cultured the skin lesions of 100 pediatric patients. The top isolates were SA, coagulase-negative SA, Streptococcus spp, Enterobacter spp, and Escherichia vulneris. The sensitivity of these organisms to penicillin, oxacillin, erythromycin, fusidic acid, mupirocin, and vancomycin varied significantly, demonstrating low to high susceptibility, across the different isolates (Fisher exact test = 0.000; p < .05). In marked contrast, sensitivity to monolaurin did not significantly differ across the different bacterial isolates (Fisher exact test = 0.110; p > .05), reflecting high antibacterial activity. There also was a statistically significant and marked difference in resistance rates. SA, coagulase-negative SA, and Streptococcus spp did not exhibit any resistance to monolaurin as opposed to the varying resistance observed with the other antibiotics in this study.[24]

Still another study showed significant activity against SA by 13 lauric monoester formulations in vitro and in vivo in mice.[25]

Mechanism of Action of Monolaurin

The mechanism of action (MOA) of monolaurin as an antimicrobial is "novel" in that it differs from that of most conventional antibiotics. A recent review of the many lipid studies conducted during the last 50 years (mostly in the laboratory), showed similar study results and similar proposed MOAs for the antimicrobial effects observed.[26] A common hypothesis explains the antimicrobial effects of monolaurin and the other medium-chain monoglycerides as being based on their capacity to alter the bacterial cell envelope. It is postulated that by virtue of size, these lipids are small enough to be readily dissolved in the lipid phase, to penetrate and physically disrupt cell membranes, and to inhibit enzymes involved in energy production and nutrient transfer, leading to reversible and irreversible changes that may lead to the death of the cell. A sophisticated electron microscopic and two-color fluorescent assay showed that on contact with these monoglycerides, bacteria show visible changes by 5 minutes and shrinkage and disintegration of cell membranes after 10 minutes, leading to the death of the bacteria.[27]

Conversely, conventional antibiotics are ionized molecules that do not readily bridge the membrane barrier because of charge or size and that act more on bacterial enzymes (although more antibiotics with similar action on the bacterial cell wall, called "novel," have been described recently[28] ).

Concurrent with this MOA in explaining the significant difference in the antimicrobial action of VCO versus VOO is the difference in the sizes of their monoglyceride FAs.[29]After lipase hydrolysis, all FAs produced by VOO are long-chain FAs, mostly C-18 (C-16 to C-24, except for 0.1% C-14). VCO produces 82% medium-chain FAs, mostly C-12 (C-6 to C-14) FA.[12] This may also explain the initial observations and pilot studies that prompted this study. At the authors' clinics, consistent improvement or clearing of inflamed or mildly to moderately infected psoriasis and AD lesions was noted after VCO application.[30]

VCO Natural FAs and AD Dry Skin

Emollients are a standard of care for prevention of dryness, steroid-sparing effect, and maintenance therapy in AD. Fixed vegetable oils coat the skin, occluding and protecting it by slowing down transepidermal water loss and increasing hydration within the stratum corneum and top layers of the dermis. They also "glue down" dry and desquamating skin cells, making the skin look less rough and scaly.[31] The AD patients who were treated with VCO in this study had significantly lower objective SCORAD scores for dryness and dryness-related conditions, such as excoriation and lichenification, and for erythema, edema, and papulation.

Adverse Reactions to Olive Oil, VCO, and Monolaurin

Olive oil is a very weak irritant, and adverse side effects from topical use are rare. Of 21 patients with reported cases of contact allergy to olive oil, 4 patients had occupation-related hand eczema; 1 of these 4 had positive patch-test and use-test results after 2 days.[32] One possible cause for these reactions may have been the gallates-antioxidants that may be used to stabilize the mostly monounsaturated (and some polyunsaturated) FAs of olive oil-that have been reported to produce contact dermatitis.[33] Antioxidants are not needed for (nor added to) stable and saturated VCO.

VCO has caused no reported contact dermatitis and should not be mistaken for the cocamides, which are VCO FAs treated with amidoamines. These popular surfactants and foam boosters in shampoos and cleansers have increasingly been reported to produce allergic reactions. However, a double-blind controlled pilot retest study of 12 patients previously allergic to cocamidopropyl betaine (CAPB) found that only 3 patients (25%) had doubtful reactions. The authors concluded that the results substantiated previous experience that doubtful and mild reactions to CAPB may represent irritant rather than true allergic reactions.[34] In this patch-testing study and in a toxicology report that implicated the nitrosylation of the FAs as a cause of reactions, the test results for CO and lauric acid were negative.[35]

The inadvertent intake of topical VCO and monolaurin is safe: CO has a long dietary history among tropical people, and monolaurin is a component of breast milk. Since 1964, monolaurin has been "generally recognized as safe" (GRAS) by the US Food and Drug Administration. A similar safety record has been shown in animals for which monolaurin constitutes up to 25% of the total diet.[29] The extensive topical use of VCO and the topical and oral use of monolaurin in our clinics have caused no adverse reactions.[30]

Conclusion 

A history of safe topical use and no known or reported cases of contact dermatitis, along with its dual effects as moisturizer and antiseptic, opens up more research and clinical possibilities for virgin coconut oil (VCO) and monolaurin. In the laboratory, VCO and monolaurin have also shown antimicrobial effects on fungi[36] and enveloped viruses[37] that (like Staphylococcus aureus) may infect or colonize sites of atopic dermatitis.