Novel Antibacterial and Emollient Effects of Coconut and Virgin Olive Oils in Adult Atopic Dermatitis

Vermén M. Verallo-Rowell; Kristine M. Dillague; Bertha S. Syah-Tjundawan


Dermatitis. 2008;19(6):308-315. 

In This Article


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 by SA)[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]

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]

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.

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]