Many essential oils possess antimicrobial properties, and in vitro testing often shows efficacy against resistant strains, such as MRSA. Tea tree is best known in this regard, though other anti-MRSA essential oils include eucalyptus, geranium, lavender, lemongrass, oregano and thyme. The most common medium used for massage is vegetable oil, and while this has some antimicrobial action, it’s minimal.

A Japanese research team wanted to find out whether massage would be “more hygienic” if essential oils were added to the vegetable oil. Initially they tested tea tree oil and lavender oil, separately, at 3% and 6%. Bacterial samples were taken from the therapist’s hands and the patient’s skin before, during and after a massage session. The 6% concentration of both essential oils was about 5 times more effective than the 3% concentration, but bacterial count was not reduced to zero. Only the ATCC 25923 strain of Staphylococcus aureus was measured (Donoyama et al 2005).

In a second study, oils of eucalyptus, niaouli, sage and thyme linalool were tested in addition to lavender and tea tree. Using the same strain of S. aureus, niaouli oil was found to be the most effective, reducing colony count to zero at 3.125%. Unlike the first study, these were all organic essential oils (Donoyama and Ichiman 2006). Although this suggests that niaouli oil is more effective than tea tree, or any of the other oils tested, one limitation of the research is that only one bacterium was tested. Another is that only two people, one giver and one receiver, were used.

In an in vitro study, 6 essential oils were tested for antibacterial activity against 10 bacteria. The oils were tea tree, niaouli, cajuput, eucalyptus, manuka and kanuka. Against S. aureus ATCC 6538, tea tree was twice as effective as niaouli, as it was against almost all the bacteria tested. However, manuka oil was more effective than tea tree, or any other oil, against 9 of the 10 bacteria. Manuka and tea tree were then tested against 7 resistant strains of Staphylococcus, and manuka was more effective in every instance.

The Japanese research is interesting because swabs were taken from an actual massage session where the essential oils were diluted. In other research, tea tree oil at 0.5% had little antimicrobial action in a body balm base (Kunicka-Styczynska et al 2011). In my own private research, I found that a mixture of tea tree, lavender and eucalyptus oil was only an effective antibacterial when used at 10% or more in a lotion base. It should be possible to identify mixtures of essential oils that work well in oily media at a dilution of around 3%. Much more than that would be too strong for a massage therapist. In the meantime, niaouli and mankua oils look like good candidates, and it may be too early to rule out tea tree, especially as we know it has excellent antifungal effects. Manuka oil is relatively expensive, but it smells better than tea tree or niaouli.

Massage therapists who use essential oils normally use them for therapeutic benefits, not simply for hygiene. But in these times of killer bacteria and widespread use of hand hygiene products, “hygienic massage” could be a sensible move.

References
Harkenthal M, Reichling J, Geiss H-K et al 1999 Comparative study on the in vitro antibacterial activity of Australian tea tree oil, cajuput oil, niaouli oil, manuka oil, kanuka oil, and eucalyptus oil. Pharmazie 54:460-463

Kunicka-Styczynska A, Sikora M, Kalemba D 2011 Lavender, tea tree and lemon oils as antimicrobials in washing liquids and soft body balms. International Journal of Cosmetic Science 33:53-61

Donoyama N, Wakuda T, Tanitsu T et al 2005 Using tea tree oil for hygeinic massage practice. The International Journal of Aromatherapy 15:106-109

Donoyama N, Ichiman Y 2006 Which essential oil is better for hygeinic massage practice? The International Journal of Aromatherapy 16:175-179

Ingredient tunnel vision is seriously bad for your health. It will turn you into an obsessive, paranoid, vicious, spitting fireball of righteous indignation. You will write searing blog posts, develop gastritis or worse, lose sleep, and die young. And for what? Essential oils and their constituent chemicals are very frequent targets. Because essential oils contain chemicals, and because almost all chemicals are, to some people, toxic by definition, many bloggers in the green movement have become anti-fragrance and anti-essential oils. For a while I though that, when they realize that linalool is found in lavender oil, and that limonene is in lemon oil, they will relent. I was wrong. Obsession is, in fact, relent-less. It allows no release, no vacation, no light side. It is all-consuming!

Because essential oils are alleged to contain “allergens”, they are also favorite targets of regulators and legislators, especially in Europe. And, we in North America know full well that whatever happens in Europe must be good, because Europeans are more intelligent. Their accents prove this. Since I have been living in the US (12 years now) my accent has slowly become less English English, and more American English, and my mental faculitoes have detturiated protortionisely, as you kan see.

Peer-not
More on Europe soon. But first, a new study financed by Silent Spring Institute, written by Robin Dodson et al, and published in Environmental Health Perspectives. EHP claims to be peer-reviewed, but if this report is anything to go by, its reviewers need replacing. In fact, they might as well not bother with peering, since it clearly accomplished nothing. The report is entitled: Endocrine Disruptors and Asthma-Associated Chemicals in Consumer Products. Classes of chemicals that were tested for include UV filters, cyclosiloxanes, glycol ethers, parabens, phthalates, alkylphenols and fragrances. The “fragrances” tested for include these essential oil constituents:

For your edification, I have highlighted one essential oil and also some foods that naturally contain said chemical. No rationale is given for why these particular substances were selected. This is important, not only because they have now become what might be called “target chemicals of concern”, but because the list could have been so much longer. It could include almost every essential oil constituent in existence. Now, at a rough guess, this is in the region of 1,000. The above list is said to represent “asthma-related chemicals”. This is not defined anywhere, but the article begins with “Laboratory and human studies raise concerns about endocrine disruption and asthma from exposure to chemicals in consumer products” and it goes on to talk about “asthma-related chemicals.”

Fragrance chemicals do not cause asthma, but they can exacerbate asthmatic symptoms. Many fragrance chemicals have this potential because they are very mild respiratory irritants in concentration. It’s the nature of the beast. However, listing limonene, isobornyl acetate, terpineol etc., is not helpful. If you are asthmatic, and you tend to react badly to fragrances, then you stay away from fragrances. Mounting a new campaign to list particular fragrance ingredients on consumer labels will not accomplish anything. It will not meaningfully make fragrances safer, and if consumers need a warning that a product is fragranced, this can be accomplished in either one word: “FRAGRANCE”. Or two: “CONTAINS FRAGRANCE”.

The paper states that, if a compound is “available from plant materials”, it was described as natural, and if “commonly synthesized”, then it was described as synthetic. But there is no list! No classification! So we don’t know which they regard as natural, and which as synthetic! In the text, limonene is mentioned as being natural (correct), isobornyl acetate as synthetic (incorrect) and hexyl cinnamaldehyde as natural (incorrect, since it is always synthesized. It is also spelled wrongly throughout the article. I’m Just saying…).

No direct evidence is provided for any adverse health effects for any of these compounds, and there is no discussion of the factors involved, although several papers are cited: “Fragrances, particularly terpenes such as limonene, are associated with secondary chemical reactions in indoor air, and can contribute to the production of formaldehyde, glycol ethers, ultrafine particles, and secondary organic aerosols (Nazaroff and Weschler 2004; Singer et al. 2006). Exposure to fragrances has been associated with a range of health effects, including allergic contact dermatitis, asthma and asthmatic exacerbations, headaches, and mucosal symptoms (Heydorn et al. 2003; Kumar et al. 1995; Steinemann 2009).”

Dodson and friends do not mention that moderate-to-high levels of ozone are required for these reactions to take place, nor that cleaning products (which can also contain volatiles such as formaldehyde, benzene, toluene and xylene) are the only ones that have been reported to cause actual health problems (Nazaroff and Weschler 2004). Ozone-limonene reactions can produce hydroxyl radicals, and these in turn can contribute to formaldehyde formation (Fan et al 2003). However, this was only observed under conditions that were admitted to be not typical of “nonindustrial indoor environments.” And, the statement that terpenes such as limonene can contribute to the formation of glycol ethers is not true. Nazaroff and Weschler (2004) state that both terpenes and glycol ethers were found in some cleaning products, not that one is formed from the other! And while I’m on my soapbox,, ultrafine particles and secondary organic aerosols are the same thing. Now, if I can find this many holes in a research paper without breaking a sweat, where is the so-called “peer-review”? And how much credence can we give any of the findings?

The Kumar et al (1995) study did find exacerbation of respiratory symptoms in asthma patients when they smelled perfume scent strips, as used in magazine advertising. And other research shows that if you give asthma patients strong fragrances to inhale, they may react adversely. The same is true for people with multiple chemical sensitivity, but it is not true of the general population.

Under extreme conditions terpenes such as limonene and pinene do form particles that are respiratory irritants. These conditions require (a) moderate-to-high ozone, and (b) substantial quantities of vaporized terpenes. These may be hazardous for vulnerable individuals, such as babies, older people, or people with asthma. However, it’s a leap to assume that fragrances cause health problems. They don’t. Yes, a fragrance could trigger an asthma attack in a person with asthma. But it cannot cause asthma. In a mostly supportive Forbes blog post based on Dodson’s article, Amy Westervelt quotes the following lines:

“This study presents a clear example of biased, advocacy-based research,” says William Troy, Ph.D., Scientific Advisor the International Fragrance Association North America. “It is a repackaging of older information and the methodology used defies basic principles and standards of scientific protocols and investigations. The advice to consumers based on study findings is simply wrong,” said Dr. Troy.

“There’s been a lot of work done on exposure to these chemicals in average households, and we know that these chemicals are found in air and dust in peoples’ homes, and the CDC [Center for Disease Control] has shown that we find them in our bodies as well,” says the study’s lead author Dr. Robin Dodson. “Now we’re trying to understand where the chemicals are coming from, and how people are exposed to them.”

There is a degree of naivete in this last statement. As far as the fragrant compounds are concerned, they are naturally found in some common foods (see Table), so that could be one reason that they are found in our bodies. Limonene and pinene are ubiquitous simply because so many trees produce them. If you have pine furniture, it is giving off limonene and pinene vapors. If you have paint thinned with turpentine, same deal, because turpentine is made from pine trees. If you live near trees…basically, if you’re breathing, you are inhaling limonene and pinene. How much you are inhaling, what the ambient ozone level is, and whether or not you have asthma are all considerations in whether these vapors might present a hazard. Some advice:

• If you are asthmatic, beware of strong fragrances.
• In high-ozone conditions (usually hot weather combined with factory exhalations and/or much vehicular traffic) beware of exposure to high levels of fragrant molecules.
• When using cleaning products, paints, glues or varnishes, ventilation is important.
• Note that some types of office equipment, such as photocopiers and fax machines, give off ozone.

Dodson advises avoiding fragranced products, and looking for ones with plant-based ingredients. So would that include or exclude essential oils? I’m baffled.

References
Dodson R, Nishioka M, Standley LJ et al 2012 Endocrine Disruptors and Asthma-Associated Chemicals in Consumer Products.

Fan Z, Lioy P, Weschler C et al 2003 Ozone-initiated reactions with mixtures of volatile organic compounds under simulated indoor conditions. Environmental Science & Technology 37:1811-1821

Heydorn S, Johansen JD, Andersen KE et al. 2003 Fragrance allergy in patients with hand eczema – a clinical study. Contact Dermatitis 48:317-323

Kumar P, Caradonna-Graham VM, Gupta S et al 1995 Inhalation challenge effects of perfume scent strips in patients with asthma. Annals of Allergy Asthma & Immunology 75:429-433

Nazaroff WW, Weschler CJ 2004 Cleaning products and air fresheners: exposure to primary and secondary air pollutants. Atmospheric Environment 38:2841-2865

Steinemann AC 2009 Fragranced consumer products and undisclosed ingredients. Environmental Impact Assessment Review 29:32-38

Aseyah

Methyl salicylate is good for some people, not for others. A blanket contraindication is not necessary, but it is best avoided in pregnancy – all salicylates are teratogenic in sufficient amount, including methyl salicylate and aspirin (acetyl salicylic acid). Methyl salicylate must be absolutely avoided by anyone taking blood-thinning drugs, as it increases the action of the drug, and this causes blood to leak into tissues and  internal bruising occurs. Knowing a lethal dose tells you very little about what (a) a therapeutic dose would be or (b) a safe dose would be, but it does tell you what dose not to use! Therapeutic dose is good to know of course, and this varies between essential oil and also between purpose. Wintergreen oil has some wonderful properties, but I would not like to see it used at more than 5%.
-Robert

Hi Tiffany,

A number of essential oils enhance the transcutaneous penetration of other substances. This is a widely-studied phenomenon, and research is ongoing. It happens because some essential oil constituents are very good at crossing the epidermis. In a 1991 paper, Williams and Barry found that 1,8-cineole, the major constituent of eucalyptus oil, enhanced the skin permeability of 5-FU by an incredible 95 times.

5-FU is only applied to the skin to treat skin cancers. In those situations, it would be prudent to avoid applying any essential oils or aromatherapy products to the same area of skin. When 5-FU is given intravenously (for internal tumors) applying essential oils to the skin will have no effect. Similarly, ingested essential oils will not affect the dermal delivery of 5-FU, or any other substance.

-Robert

Moss and Oliver exposed 20 subjects to varying levels of rosemary oil vapor, and assessed speed and accuracy tests in mathematical tasks, and mood assessments. Intriguingly, the results indicate that the concentration of 1,8-cineole in the blood is related to an individual’s cognitive performance – with higher concentrations resulting in improved performance. The researchers stress that both speed and accuracy were improved, suggesting that the relationship is not describing a speed-accuracy trade-off. They carefully designed their study to eliminate any effect of expectation, or of the perceived aroma.

In an earlier study, Moss and colleagues compared the effects of inhaled rosemary oil, lavender oil and no odor, in a larger group – 144 subjects. In the rosemary group, recall accuracy was significantly improved, but not speed (Moss et al 2003). The main difference between this and the new research was the tasks subjects were asked to perform. This suggests that rosemary oil inhalation improves accuracy in any type of mental task, but that speed is also improved only in mathematical calculation.

The new research also noted an effect on mood, and a negative correlation was seen between changes in contentment levels and blood levels of 1,8-cineole. This, say the researchers, suggests that rosemary affects subjective state and cognitive performance through different neurochemical pathways. “Contentedness possessed a significant relationship with 1,8-cineole levels, and interestingly to some of the cognitive performance outcomes, leading to the intriguing proposal that positive mood can improve performance whereas aroused mood cannot” said Moss.

The blood-brain barrier
Christy C. Tangney is quoted on WebMD as saying: “More study is needed to see how, or even if, rosemary affects how quickly and accurately we perform mental exercises.” Tangney is an associate professor of clinical nutrition at Rush University Medical Center in Chicago. She feels that the findings could be due to chance or something else besides the fragrance. “There is something here. I don’t know that I could conclude that it is the aroma of the rosemary that is associated with improvements though” Tangney says.

On the face of it this is an odd comment, since the researchers were at pains to clarify that it is not the “aroma” of the rosemary oil that is producing the effect, it is the fact that constituents of the oil enter the bloodstream, and thereby produce an effect. But, Tangney probably meant simply that the rosemary oil might not be doing anything at all. I suppose someone has to be the designated bearer of the “it’s only placebo” message.

As small, fat-soluble organic molecules, terpenes like 1,8-cineole can enter the blood stream via the nasal or pulmonary mucosa. We know they can cross the blood-brain barrier (i.e. move out of the cerebral blood vessels and into the brain), as interactions with various receptor sites in the brain have been seen after administration (Aoshima and Hamamoto 1999, Elisabetsky et al 1999). In a German study, whether mice were given rosemary oil orally, or it was evaporated in their cage, similar blood levels of 1,8-cineole were detected. This was associated with an increase in ‘locomotor activity’ – spontaneous movement – thus demonstrating a stimulant effect from inhalation of the oil (Kovar et al 1987). This shows that inhalation of rosemary oil produces an effect on the nervous system that is not purely psychological, or due to expectation. We don’t know whether mice like rosemary oil, or whether it might improve their mathematical skills. I’m just saying…

Acetylcholine
1,8-Cineole is found in many other essential oils including eucalyptus, sage, laurel, myrtle and cardamon. Previous research has shown that it inhibits acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) enzymes, which are important in brain and central nervous system neurochemistry. Acetylcholine is the principal neurotransmitter in the brain, so when the enzyme that breaks it down is inhibited, there’s more acetylcholine to help those synapses fire. The most commonly prescribed pharmaceuticals for treating loss of cognitive function in Alzheimer’s disease (AD) are AChE inhibitors, also known as cholinergic drugs.

A rosemary oil with 44.4% 1,8-cineole and 12.6% a-pinene inhibited AChE and BChE (Orhan et al 2008). All three of the major constituents of rosemary oil individually inhibit (AChE), as do three of its minor constituents. The AChE inhibiting effect is especially strong for 1,8-cineole and a-pinene, and less so for camphor. These three, and other constituents, act synergistically to produce the effect (Savelev et al 2003). There are several chemotypes of rosemary oil. The one used by Moss in all his research (from Tisserand Aromatherapy) is a 1,8-cineole chemotype. A typical analysis for this type of oil is shown in the Table below.

In a Japanese study, 17 AD patients were exposed to the vapors of rosemary and lemon oils in the morning, and lavender and orange oils in the afternoon for 28 days. Compared to similar pre-treatment and post-treatment periods, aromatherapy resulted in significant cognitive improvements (Jimbo et al 2009). In other clinical research, 11 AD patients were given small oral doses of Spanish sage (Salvia lavandulaefolia) oil, which is chemically very similar to the type of rosemary oil used by Mark Moss (see Table). Again, there were significant cognitive improvements (Perry et al 2003). When Spanish sage oil was taken orally by 24 healthy young volunteers in a placebo-controlled, double-blind crossover trial, both speed and accuracy significantly improved in tests of cognitive performance (Tildesley et al 2005).

Cholinergic function is surely not the whole story, and a number of other mechanisms are likely at work. For example, cognitive impairment in AD is also associated with low dopamine (Wolfe et al 1990), and 1,8-cineole increases dopamine release in brain cells (Kako et al 2008).

Mark Moss

Summary
Taken together, the evidence for a positive effect on cognitive function by rosemary oil, and similar oils, is strong. Effects are due to synergistic interactions of constituents. Since both rosemary and Spanish sage oil have similar effects, the precise composition of the oil does not seem to be critical. Whether the perception of the rosemary odor produces contentment or relaxation may not be directly relevant, since taking the oil orally has a similar effect. This gives credence to Mark Moss’s contention that it is blood-borne essential oil constituents that affect mental function.

“Rosemary. For weyknesse of ye brayne. Agaynst weyknesse of the brayne and coldeness thereof, sethe rosmarin in wyne and lete the pacyent receve the smoke at his nose and kepe his heed warme.” The Grete Herball, 1529

References
Aoshima H, Hamamoto K 1999 Potentiation of GABAA receptors expressed in Xenopus oocytes by perfume and phytoncid. Bioscience Biotechnology & Biochemistry 63:743-748

Elisabetsky E, Coelho de Souza GP, Dos Santos MA et al 1995 Sedative properties of linalool. Fitoterapia 66:407-414

Jimbo D, Kimura Y, Taniguchi M et al 2009 Effect of aromatherapy on patients with Alzheimer’s disease. Psychogeriatrics 9:173-179

Kako H, Fukumoto S, Kobayashi Y et al 2008 Effect of direct exposure of green odour components on dopamine release from rat brain striatal slices and PC12 cells. Brain Research Bulletin 75:706-712

Kovar KA, Gropper B, Friess D et al 1987 Blood levels of 1,8-cineole and locomotor activity of mice after inhalation and oral administration of rosemary oil. Planta Medica 53:315-318

Moss M, Oliver L 2012 Plasma 1,8-cineole correlates with cognitive performance following exposure to rosemary essential oil aroma. Therapeutic Advances in Psychopharmacology doi: 10.1177/2045125312436573

Moss M, Cook J, Wesnes K et al 2003 Aromas of rosemary and lavender essential oils differentially affect cognition and mood in healthy adults. International Journal of Neuroscience 113:15-38

Orhan I, Aslan S, Kartal M et al 2008 Inhibitory effect of Turkish Rosmarinus officinalis L. on acetylcholinesterase and butyrylcholinesterase enzymes. Food Chemistry 108:663-668

Perry NS, Bollen C, Perry EK, Ballard C et al 2003 Salvia for dementia therapy: review of pharmacological activity and pilot tolerability clinical trial. Pharmacology, Biochemistry & Behavior 75:651-659

Savelev S, Okello E, Perry NS et al 2003 Synergistic and antagonistic interactions of anticholinesterase terpenoids in Salvia lavandulaefolia essential oil. Pharmacology, Biochemistry & Behavior 75:661-668

Tildesley NT, Kennedy DO, Perry EK et al 2005 Positive modulation of mood and cognitive performance following administration of acute doses of Salvia lavandulaefolia essential oil to healthy young volunteers. Physiology &  Behavior 83:699-709

Wolfe N, Katz DI, Albert ML et al 1990 Neuropsychological profile linked to low dopamine: in Alzheimer’s disease, major depression, and Parkinson’s disease. Journal of Neurology, Neurosurgery, & Psychiatry 53:915-917

“Plants produce primary and secondary metabolites, which have been exploited by humans for many different beneficial purposes. Many secondary plant metabolites, e.g. terpenes, terpenoids, alkaloids and phenolic compounds have been well characterized. Essential oils are considered the chemical weapons of plants, as their compounds may deter insects or protect plants against bacterial and fungal infections. They also act as plant pheromones to attract insects. In traditional medicine, lots of plant products have been widely used for the treatment of neurologic diseases, cancer, inflammation and infectious diseases and plants represent an abundant source of new bioactive secondary metabolites.

According to the Communicable Diseases Centre in the US, about one third of prescribed antibiotics were inappropriate thus stating an overuse and misuse of antibiotics. Essential oils are also highly active against multi-resistant Staphylococcus aureus (MRSA), one of the so-called hospital super bugs, as well as more common and well-known infections like herpes labialis. In addition to antibacterial and antiviral effects, essential oils have been shown to possess many useful pharmacological properties, often being more effective than conventional drugs and revealing fewer side effects.

Oregano oil gland

Although the number of published papers on anti-infective properties of medicinal plants is increasing during the last years, most of these papers seem to somehow disappear and do not attract physicians and pharmacologists. On the other side, there is often lack of finance to continue research to the clinical trial level. This area is largely dominated by pharmaceutical companies, who can afford costly clinical trials. It also seems that natural and complementary therapies are pushed aside by pharmaceutical companies.

Although there is no shortage of research on the antimicrobial effects of medicinal and aromatic plants, it is somehow ignored in industrialized countries. Prescribed drugs are more convenient for patients and physicians, although natural products might offer an alternative in treatment of many different diseases. In resource-limited countries, conventional medications are often not affordable or not available and consequently natural products are the medication of choice.

Our goal is to provide scientific results that can be reproduced by others, thus standardized plant products are required. If more standardized and only high quality natural products are used in basic research as well as in clinical trials, the critics might be convinced and acceptance of medicinal plant products might be increased. Investigators are also encouraged to explore the potential of phytopreparations in combination with synthetic drugs in order to enhance pharmacological actions. High quality plant products and more clinical trials are urgently needed to establish rational phytotherapy.”

Why should I worry anyway, I don’t wear lipstick. And, since men have higher lead levels than women (because we shoot each other more often?) the lipstick factor isn’t making a huge difference. Average lead levels in US lipstick: 1 ppm (0.0001%). Found in one Chinese brand (not sold in the US): 3,760 ppm (0.37%). Two other Chinese-made lipsticks had over 2,000 ppm. If you live in China, don’t buy the lipstick. If you live in the US, this is one thing you don’t need to worry about. But if you enjoy worrying, there’s a facebook page called “There’s lead in your lipstick”.

It is true that there are few clinical trials involving essential oils. Randomized clinical trials (RCTs) are very expensive, and few other than pharmaceutical concerns (PCs) have that kind of disposable cash. PCs do sometimes fund RCTs, though more commonly for essential oil constituents than whole essential oils. A recent exception was a series of trials on lavender oil taken as a medicine for anxiety. In one RCT that recruited 221 adults suffering from anxiety disorder, lavender oil capsules reduced anxiety levels in 76.9%, compared to 49.1% in the placebo group (Kasper et al), a highly significant result.  The PC is based in Germany, and now markets this as an approved medicine there, under the brand name Lasea. (Can you patent an essential oil? No you can’t, but you can patent various aspects of a preparation containing essential oils.)

Depending on what you include and what you exclude, there are maybe 50 or so published RCTs involving essential oils. And yet, I have in my possession thousands of research papers. They consist of in vitro and animal studies, and there are more on single constituents than whole essential oils. When faced with the question – many years ago – of whether to read and make use of the animal research or ignore it, I decided on the former course of action. Ethical issues aside, I could see no reason to ignore good data. (Poor research, whether in vitro, in vivo or clinical, I’m happy to ignore.)

When I consider the biological action of an essential oil, I like to include all the information I can get my hands on, ranging from uses of the plant in Traditional Chinese Medicine, to the pharmacology and toxicology of key constituents. It’s nice when it all points in one direction, such as with lavender oil and its calming action. There is evidence across all phases – animal studies on the whole oil (Bradley et al 2007), animal studies on constituents and why they do what they do (Umezu et al 2006), and RCTs too. Sometimes there are conflicting data, and this compels you to try to figure out what is going on. This often leads to a more sophisticated understanding of biological action.

Two recent aromatherapy publications (Price & Price 2011, Schnaubelt 2011) have addressed the issue of animal/pharmacology testing, and both have made comments that I find odd and confusing. Schnaubelt’s comments are on page 12 of his book:

I agree that, if you are going to demonstrate how an essential oil works – its mechanism of action – you do need to study constituents. However, you don’t need to study all 100 or so, only the few major constituents. Some studies examine as many as 5 or 10. In many cases the researchers are looking for the most active compounds. Sometimes they find exactly that, and sometimes they don’t – instead they find that the whole essential oil is more active than any of its constituents. We call this synergy, and I believe it is the primary distinguishing factor, at least in scientific terminology, between a conventional medicine (invariably a single chemical) and plant-based medicine. Understanding mechanism of action for major constituents is, anyway, not an absolute requirement of therapy. If something can be shown to be significantly effective (and safe) it will be used. This is called evidence-based medicine.

And, I don’t agree that pharmacological testing cannot be used to demonstrate the efficacy of a whole essential oil. In fact, lemongrass oil has been tested in exactly the way Schaubelt describes above for sleep (Blanco et al 2009) and its main constituent is citral. On the next page of his book, Schnaubelt goes on to say: “To prepare for our foray into the biological explanations of essential oil efficacy, we shall first review some important examples of the therapeutic or curative effects of essential oils that have, despite the limitations just outlined, been recognized through conventional reductionist experimentation.” He seems to be saying that pharmacological testing can in fact be used to demonstrate essential oil efficacy! I’m not sure what the word “reductionist” is describing here – the testing of constituents, the focusing on one aspect of therapeutic action, or both – but I would argue that all information is potentially useful.

The second new publication has a section on page 42 headed “Animal testing“, and this is in the context of safety. It argues that toxicological testing on animals is not relevant to humans:

To pick up on the mains points:

• Animal physiology can absolutely be compared with human physiology, and this comparison is done with increasing sophistication, as more is learned about gene expression and metabolism. Some animal “models” prove to be substantially different, and some substantially similar to humans.
• Estragole is indeed a rodent carcinogen, but the use of an essential oil in aromatherapy is often much greater than the amounts present in foods, so estragole toxicity cannot be written off so easily. One microgram per kg is one part per million (in food).
• Skin absorption is indeed often different between animals and humans, though the data given above on amines has no relevance to essential oils.
• Isolated components. Here we are again with this question. I do not agree that toxicological research on single constituents is irrelevant, though I feel very strongly that an essential oil should not be viewed as if it was simply a vehicle for a single constituent. For example, antitumoral constituents should be considered relevant too, not just carcinogenic ones.
• The final point is a very strange criticism. If you want to find the lethal dose of a substance you have to administer a fatal overdose!

Both Schnaubelt and the Prices go on to cite animal research in their respective books. For example, on page 157, Schnaubelt says: “Sandalwood oil was used topically for twenty weeks and was found to decrease the incidence of skin papillomas.” He does not quote the source but it’s an animal study (Dwivedi and Abu-Ghazaleh 1997). Schnaubelt has been one of the major proponents of Functional Group Theory (FGT), which is based on the idea that the action of an essential oil is largely determined by the chemical class of its major constituent(s). One of the basic tenets of FGT is that all ketones are neurotoxic (i.e. have the potential to cause convulsions). The main evidence for this is a single animal study (Wenzel & Ross 1957). I’m not saying it’s good evidence, in fact I think it’s relevance is very questionable. My point is, it’s hypocritical to say that animal-based research is not relevant, but then to use animal-based data when convenient.

On page 59 of their book, Price & Price cite this very paper, saying: “It is thought that the ketone thujone…is toxic to the central nervous system, as is the ketone asarone (found in Acorus calamus) (Wenzel & Ross 1957).” Well, asarone is indeed found in A. calamus, but it is not a ketone (it’s a phenylpropanoid ether) nor is it mentioned in the Wenzel & Ross paper. Oops. The initial statement in Price & Price (2011) about animal physiology is a sweeping one, and suggests that no animal research has any relevance to humans. But, the reader only has to turn from page 42 to page 47, to find a Table showing LD50 (lethal dose) values for 44 essential oils and 11 constituents. The LD50 values are then extrapolated to the equivalent human dose. Animal data not relevant? Oops again.

Price & Price (2011) is a comprehensive practitioner manual with 11 contributors and two editors, and this is the fourth edition. There are many tables and charts, and the book is moderately well referenced, but much of the safety information is of questionable value. Schnaubelt (2011) is beautifully illustrated and contains much practical information. My main criticism is that the facts are molded to suit the philosophy, rather than the philosophy deriving from the facts.

For both safety and efficacy, more clinical data are always needed. In the meantime, let’s make use of what we have, and let’s not be afraid to acknowledge that much of what we know about the action of essential oils derives from animal research. I’m not saying it’s all good information, and I’m not saying it’s all relevant. It isn’t. But neither is it all irrelevant. I’m not trying to defend animal research per se, I’m just saying that we should be open and honest when citing it, and that if you take all the animal research out of the aromatherapy literature, you won’t be left with very much solid data to demonstrate efficacy and safety.

References
Blanco MM, Costa  CA, Freire AO et al 2009 Neurobehavioral effect of essential oil of Cymbopogon citratus in mice. Phytomedicine 16:265-270

Bradley BF, Starkey NJ, Brown SL et al (2007) Anxiolytic effects of Lavandula angustifolia odour on the Mongolian gerbil elevated plus maze. Journal of Ethnopharmacology 111:517-525

Dwivedi C, Abu-Ghazaleh A 1997 Chemopreventive effects of sandalwood oil on skin papillomas in mice. European Journal of Cancer Prevention 6:399-401

Kasper S, Gastpar M, Müller WE et al 2010 Silexan, an orally administered Lavandula oil preparation, is effective in the treatment of ‘subsyndromal’ anxiety disorder: a randomized, double-blind, placebo controlled trial. International Clinical Psychopharmacology 25:277-287

Price S, Price L (eds) 2011 Aromatherapy for health professionals. Churchill Livingstone, Edinburgh

Schnaubelt K 2011 The healing intelligence of essential oils. Healing Arts Press, Rochester

Umezu T, Nagano K, Ito H et al (2006) Anticonflict effects of lavender oil and identification of its active constituents. Pharmacology, Biochemistry, & Behavior 85:713-721

Wenzel DG, Ross CR 1957 Central stimulating properties of some terpenones. Journal of the American Pharmaceutical Association 46:77-82