A frequent criticism of aromatherapy is that there are few clinical trials demonstrating efficacy over placebo. Medical interests in both Australia and the UK have recently lobbied to withdraw government funding from university departments teaching any kind of alternative medicine. Books like Bad Science, Snake Oil Science and Trick or Treatment express the view that herbal medicine, aromatherapy, chiropractic, homeopathy etc. have no effect beyond placebo, but that they can be harmful. Trick or Treatment, amazingly, contains not a single citation to back up anything expressed in its vitriolic pages. To complain about lack of evidence, and then to provide none yourself constitutes extreme hypocrisy.
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
On the morning of Tuesday November 15th 2011 I drove to LAX (two hours of heavy traffic) and boarded an Air China flight direct to Beijing. I was the only non-Asian in my business class cabin. The food was excellent! After dinner and then two movies I remember thinking that I still had eight hours to go. I had hoped to get some sleep but it didn’t happen. I arrived at 4.40 pm on Wednesday.
I was welcomed like a long-lost relative! My host in Beijing was Darren Moore, a Canadian who settled there in 1996. He lives with his Chinese wife and their 3-year-old daughter Mollii (Jasmine) in a village on the outskirts of Eastern Beijing. His house is part of a square courtyard, and the other buildings are where his staff lives and works. Darren’s company, Organic Earth, makes organic soap and other personal care products. His soap is amazing, as is his packaging. I was very impressed with the opaque white bottles he uses for his pure essential oils.
I spent part of Thursday signing copies of The Art of Aromatherapy in Mandarin (the book, not my signature), and going over my slides with Darren’s wife Sharon, who would be translating for me over the next two days. On Friday we all drove to the center of Beijing and checked into the Swissotel (Chinese cuisine with a hint of Swiss). Just before we left, Darren was feeling a bit stressed. Here you can see me shaking him, telling him that everything was going to be fine! And it was. Much of the evening was spent setting up for the seminar.
The next day I delivered my presentation How to Harness the Healing Power of Essential Oils to an audience of over 100, including 40 journalists. My talk covered many aspect of aromatherapy, such as wound healing, acne, photo-ageing, obesity, post-surgical pain, skin cancer, diabetes and antibiotic-resistant infections! Sharon did an amazing job translating, and the preparation we had done together really paid off. (Unfortunately there is rarely time to go through every slide with a translator.)
After each break, we were called back to the seminar room with live saxophone music. Very cool. I repeated the seminar on the Sunday for a new 100+ audience, this time with no media. (The video incorporates clips from both days.) On the Monday we drove back to Darren’s place where I was interviewed by three journalists – one print magazine, one website, and one tv channel. You can see the internet report here, and below is a screenshot of Yoka.com’s home page 2 days after the seminar. Yoka.com is a very popular fashion/beauty/lifestyle website.
My last day in China (Tuesday) was spent sightseeing, mostly at the Forbidden City. I was expecting to find a large structure at the center, but it’s not built like that and seems like a series of massive courtyards. I did come across some 300-year-old bottles of essential oil, which you can see on the video. And some massive incense burners. At lunch time I met a literary agent (Jessie) and Yao, who distributes Shirley Price Aromatherapy products in China. On the Wednesday I departed for Seoul, Korea.
Doing some research on Cedarwood EO for an event I am doing. I do understand that it is very high in Sesquiterpenes (95% to 98%), but some sites are claiming that Cedarwood can oxygenate the brain and that it can repair DNA damage! I don’t know how much of those claims are true?
Thanks, Devita
Hi Devita,
There are several cedarwood oils, but unspecified usually means Virginian. Virginian cedarwood is indeed high in sesquiterpenes: alpha-cedrene, beta-cedrene and thujopsene being about 80% of the oil, plus 15% cedrol and many other minor constituents.
Sesquiterpenes are generally regarded as safe.
Oxygenate the brain – that’s a very odd claim for an essential oil! No essential oils oxygenate body tissues or organs – see my blog post on this: The Oxygenation Myth.
Repairing DNA damage would be a good thing (and antioxidants do this, not pro-oxidants!) but there’s no research showing that either cedarwood oil or any of its major constituents has this (antigenotoxic) action. This does not mean that cedarwood oil could not repair DNA damage, just that no-one has researched it, so we don’t know.
An alleged ingredient of geranium oil is now one of the latest performance-enhancing supplements, and has already been linked to two fatalities. In the 1940s, Eli Lilly developed and patented a nasal decongestant known as Forthane. The active ingredient was methylhexaneamine (MHA), also known as 2-amino-4-methylhexane, 1,3-dimethylpentylamine (1,3 DMAA) or “geranamine”. Some companies are now pitching this as “geranium oil extract”, citing various aromatherapy authors (including myself) to show that geranium oil is safe and harmless. But is MHA even a constituent of geranium oil?
A Chinese paper (Ping et al 1996) claims that MHA constitutes 0.66-1.0% of (presumably Chinese) geranium oil, though amines have never previously been reported in any essential oil. Volatile amines do exist, but their chemical structure makes occurrence in an essential oil extremely unlikely. Even if the MHA was being extracted from geranium oil, at current wholesale prices of the oil, and assuming a 1% concentration, the cost of the extracted MHA would be about $20 per gram. Then add the cost of extraction, product manufacture, plus distributor and retail mark-ups. Legally, “geranium oil extract” is not a banned substance, but this is looking like a very grey area.
In August 2011, Health Canada announced: “DMAA, a substance used in sports and weight loss supplements and reported by some to be a natural constituent of geranium oil, is not isolated from plants and products containing it need drug authorization.” In the same month, The American Herbal Products Association announced a trade requirement for the labeling of products containing the ingredient 1, 3-dimethylamylamine (DMAA). The trade requirement, which becomes effective on January 13, 2012, requires that “AHPA members do not label 1,3-dimethylamylamine, whether identified by this name or any synonym, as geranium oil or as any part of the geranium plant, whether by the common name of geranium or by the botanical name of any plant known as geranium”. In 2010, the World Anti-Doping agency banned MHA, under its “stimulants” category.
Why all the rukus? Because MHA is now suspected of causing the deaths of two US soldiers from cardiac arrest. Both had taken a pre-workout supplement thought to contain MHA, and toxicology tests confirmed its presence in their blood. The US military has now pulled all MHA-containing supplements from its stores, world-wide. The Army initiated a safety review after compiling records of several other MHA users reporting health problems such as “kidney and liver failure, seizures, loss of consciousness, heat injury and muscle breakdown during exertion and rapid heartbeat,” Army spokesperson Maria Tolleson told Stars and Stripes.
This has been a disaster waiting to happen. In February 2011, Nutrition Business Journal (NBJ) reported in depth on the chorus of voices raising alarms about “geranium extracts” in preworkout supplements, a category of sports nutrition with outsized growth rates and sales topping $100 million in geranium-inclusive products alone, according to industry sources. At the time, NBJ called this “the next nightmare” to hit the supplements industry and, through subsequent publications and presentations, called on industry to head off another ephedra by taking matters into its own hands. This did not happen, and now the expected nightmare is upon us.
Ping Z, Jun Q, Qing L 1996 A Study on the Chemical Constituents of Geranium Oil, Journal of Guizhou Institute of Technology 25 (1): 82–85
I met Kelly when I gave a talk in April 2011 in Sidney BC, for the British Columbia Association of Practicing Aromatherapists . Kelly is on the BCAPA Board and is working on her PhD dissertation in Chemical Ecology at Simon Fraser University. She recently returned from Java Indonesia, where she conducted research on slow loris toxin for a BBC film.
Robert
What is chemical ecology?
Kelly
Chemical ecology is the study of chemicals that mediate interactions between living organisms and their environment. These are known as semiochemicals. The subclass used for communication between the same species is known as pheromones. Pheromones are often classified according to their function and include sex pheromones, aggregation pheromones, and alarm pheromones (Figure 2). Many insect pheromones are also essential oil constituents; for example, linalool and geraniol are sex pheromones of the moth Spodoptera littoralis, and limonene and benzaldehyde are present in the airborne aggregation pheromone of bed bugs. (Aggregation pheromones function in mate selection, defense against predators, and overcoming host resistance by mass attack.)
Robert
What other types of semiochemicals are there?
Kelly
Semiochemicals acting between different species are known as allelochemicals, and are typically categorized contingent on the benefit(s) and cost(s) to the signaler and the receiver (see diagram). Allelochemicals that benefit the sender through deceit or propaganda are known as allomones. For example, this video shows how the female bolas spider catches male prey by mimicking various female moth sex pheromones.
Robert
That is truly one of the creepiest things I have ever seen!
Kelly
Yes, the bolas spider is totally bizarre! I gave a presentation last year on it, and the audience was completely freaked out. Generally, sex pheromone emission by female nocturnal moths peaks around midnight, but this isn’t always the case.
Robert
You were saying..
Kelly
Kairomones benefit an individual of a different species which receives it, without benefiting the emitter. For example, the aggregation pheromone of the female western bark beetle, Dendroctonus brevicomis,not only attracts males of the same species but also another beetle, Temnochila chloridia, which preys on the adult and larval bark beetles. Deterrents and repellents that are used for predator defense would also constitute allelochemicals. Plants use secondary metabolites in the form of toxins to fend off herbivores, and mammals who sequester secondary metabolites from a diet source (e.g. plants or insects), may be extremely unpalatable to consume. Essential oil constituents used by some tropical trees to deter predators are limonene and α-pinene.
The diagram shows the two semiochemical subclasses: pheromones (categorized by their function) and allelochemicals (categorized on the benefits [+] and costs [-] assigned to both signalers and receivers).
Lastly, synonomes benefit both signaler and receiver. An example of synonomes at work is pollination. Mammals and insects are attracted to many flowers or fruit-bearing plants and trees as a source of food. As a result, the pollen from flowers and seeds from fruit are dispersed which enhances reproductive success and genetic variability. It has recently been suggested that various types of flora have similarly evolved in taste and fragrance to attract human consumption and reliance on them. While thousands of types of flora perpetuate as a species because of this, we in turn benefit from their countless medicinal, therapeutic, and nutritional properties.
Robert
Is it a new field of study?
Kelly
Compared to many scientific fields, chemical ecology is not that old, and originated in the mid-to-late 1800s. During this time many significant contributions were made in the context of allelochemicals, specifically about plants producing toxins (alkaloids) that functioned as chemical defenses against predators. These ideas resurfaced in the late 1950s when scientists made similar discoveries that acted as the catalysts which put this field of study into universal motion.
Robert
How did you get involved in both aromatherapy and chemical ecology?
Kelly
My curiosity in aromatherapy heightened approximately 20 years ago when I was prescribed a cocktail of essential oils to help battle endless migraines. Their great efficacy led to my pronounced respect for aromatherapy, and it grew even more after reading your book The Art of Aromatherapy! The chemical properties of essential oils and their effects on humans fascinated me. I often wondered how or if other living organisms would similarly respond to essential oils, and what other functions chemicals served for all living organisms. As I became a certified aromatherapist, I learned that quite a few animals (e.g. horses, pigs, orangutans) mentally and/or physically benefit from essential oils. I also researched the behavioral effects of predator and non-predator olfactory cues on two slender loris species as part of my MSc thesis. Consequently, I was hooked on chemical ecology and in 2006 I decided to further my knowledge of the field by pursuing a doctoral degree. I plan on defending in Spring 2012, at which point I will be able to continue my professional practice of aromatherapy.
Robert
Tell me about your dissertation work.
Ooencyrtus kuvanae male (L) and female (R). (Photo by Sean McCann)
Kelly
My dissertation work focuses on facets of chemical ecology, behavioral ecology, and evolutionary biology of the small solitary parasitoid wasp Ooencyrtus kuvanae. Insects are exceptional model specimens in that they demonstrate the many classes of semiochemicals. I am amazed at how advanced this 2mm insect is when it comes to chemical communication! We have strong evidence that the pheromones we’ve identified function in individual recognition and mate assessment. Other living organisms that use chemicals for individual recognition include humans, badgers, and deer – to my knowledge this has yet to be seen in any other insect.
Robert
I can understand your fascination. How did you get involved with the BBC and the slow loris toxin project?
Kelly
The loris documentary is part of a research project initiated by Dr. Anna Nekaris, a leading authority on lorises. Since she was my primary MSc supervisor, and I presently conduct research in a chemical ecology lab, the BBC sent me to the Indonesian Institute of Sciences in Bandung, Indonesia with the objective that I add to my previous knowledge of loris behavior and ecology by conducting research on the source(s) of slow loris toxin. The toxin may likely contribute to a decrease in their parasite load, a predator deterrent, and/or an alarm pheromone, all of which are critical factors to their overall well-being and survival. *As many conservation efforts are underway to stabilize populations of this endangered species, an understanding of the toxin source could prove imperative for husbandry management protocol, and possible re-release initiatives, especially if the source of the toxin comes from their diet. The Javan slow loris is endangered primarily as a result of the illegal pet trade.
One of nine slow lorises Kelly found offered for sale by a poacher on the black market in Java (Photo by Ali Amran)
Robert
Is this a volatile toxin? Can you discuss its composition?
Kelly
The toxin likely has non-volatile and volatile properties. There is evidence that proteins play a functional role; and it is conjectured that secondary metabolites may be of equal importance.
Robert
In relation to aromatherapy as we know it, what can we learn from the world of animal / insect / plant communication?
Kelly
Much like humans, animals, insects, and plants also benefit from allelochemicals that can take the form of a warning message, a health remedy, a predator/ectoparasite repellent, and a fragrance to attract a much desired partner. What we have learned from their chemical displays have already been useful in the discovery of new medicines, the control of economic pests, and a better understanding of human courtship behavior. Since there is not one creature on this Earth that does not rely to some extent on chemical interactions, I think there are an endless number of beneficial findings we have yet to discover!
In a recent blog post an Environmental Working Group (EWG) research assistant suggests that lavender oil may be unsafe, saying: “the science is still evolving and safety can’t be assumed.” The science is still evolving? Isn’t that true of anything? Are we just sowing the seeds of doubt here?
I have written a number of posts about the EWG and sloppy science. Their modus operandi involves highlighting negative information, along with liberal use of the phrase “has been linked to”. Facts are so often distorted that their reputation in scientific circles is all but worthless. I have never read an EWG report in which both sides of an argument are presented. The problem I have with this approach is that the EWG audience is consumers, who have neither the scientific training nor the knowledge and expertise to challenge what is being said. In spite of this many do, because they instinctively feel that something is not right.
Skin allergy
Lavender oil “has been linked to” allergic reactions, it’s true. But how strong is that link? After all, if you look hard enough, you will find at least one allergic reaction report for almost every substance used in cosmetics. Cherry picking a few negative studies is not a useful way to help consumers assess product safety. What we need is a comparative rating that clearly flags high-risk ingredients, along with practical safety guidelines.
“Allergy epidemics” have occurred in the past, most often with preservatives. As use becomes more extensive, adverse reactions escalate, and eventually the substance is either banned or restricted. In spite of widespread use, this is not happening with lavender, which has been the most popular essential oil for aromatherapy use since the 1970s.
The EWG post is written by Swati Sharma. She tells us that: “Despite its ubiquity in cosmetics, researchers in Japan who compared eight essential oils found that lavender caused the greatest number of skin allergies.” No it did not, unless you only look at two of the nine years of the study! The Japanese researchers tested six essential oils, one absolute and two essential oil constituents. The essential oil that produced the most adverse reactions was ylang-ylang (tested at 5%), followed by geranium (tested at 20%) followed by lavender (also tested at 20%). And since all the other substances were tested at either 5% or 2%, the relative risk of each cannot be compared anyway. The higher the test concentration, the greater will be the number of reactions. And, the Japanese subjects were all dermatology patients “suspected of cosmetic dermatitis”, an especially high-risk group.
Considering that the lavender oil was patch tested at 20% in a high-risk population, and that only 1.4% (21 of 1,483) of patients had an adverse reaction, this does not suggest a significant allergen. Other research points to lavender oil presenting a very low risk. When 50 healthy volunteers were patch tested with the undiluted oil, there were no reactions (Meneghini et al 1971). Similarly, none were produced in 25 volunteers tested with lavender at 10% (Opdyke 1976 p451). In a study of 200 dermatitis patients in Poland, none were sensitive to 2% lavender oil (Rudzki et al 1976). In a Danish study, two of 217 dermatitis patients (0.9%) tested positive to 2% lavender oil (Veien et al 2004). Tested at 1%, lavender oil produced no reactions in 273 dermatitis patients (Meneghini et al 1971).
Taken together, these results show that two of 690 dermatitis patients (0.3%) reacted to lavender oil when patch tested at 1% or 2%. However, extrapolating from patch test data on dermatology patients to the general population is notoriously difficult (especially since the conditions of patch testing exaggerate risk) and the actual number of people with adverse reactions to lavender is very much less than 0.3%. Over a 15 year period (1986-2000) there have only been five cases of lavender oil allergy reported worldwide (Brandão 1986, De Groot 1996, Keane et al 2000, Schaller & Korting 1995, Selvaag et al 1995) and three were people with multiple allergies. This is in contrast to millions of bottles of undiluted lavender oil being sold to consumers per annum, and millions more personal care products containing lavender oil.
From all of the above we can conclude that a 20% concentration of lavender oil might be risky for Japanese consumers with cosmetic allergies, but 2% is not a risk to anyone, and even undiluted lavender is safe to use on healthy skin. Not only is lavender a very low-risk skin allergen, it possesses anti-allergic properties. Topically applied, the oil inhibited immediate-type allergic reactions by inhibiting the release of histamine from mast cells (Kim et al 1999). How is this possible? Probably because in most cases, allergies only occur from the use of oxidized lavender oil. The unoxidized oil is anti-allergic, and is even moderately antioxidant (Wei and Shibamoto 2007).
Oxidation
Sharma tells us that linalyl acetate, a major constituent of lavender oil, can oxidize in the presence of atmospheric oxygen, “forming allergens that can cause contact dermatitis” (Sköld et al 2008). Indeed it can, as can linalool, the other major constituent of lavender oil (Sköld et al 2004). However, these are theoretical risks, not actual risks, and lavender oil oxidation is a process that takes many months, even years. What this research suggests is that products containing lavender oil should be protected from oxidation by the addition of antioxidants, and that very old products should be discarded. The International Fragrance Association (IFRA) does not have a regulation for lavender oil, but it does for linalool. Referring to linalool-rich essential oils, the IFRA guideline recommends the addition of an antioxidant: “The addition of 0.1% BHT or a-tocopherol has shown great efficiency” (IFRA 2009).
Next, Sharma informs us that “lavender oil may be toxic to human skin cells” though curiously no reference is given (it’s Prashar et al 2004). I addressed this issue in a previous post about lavender, in which I explain how we know that the oil is not a skin irritant, and is not toxic to skin cells when applied to human skin.
Hormone disruption
Finally, Sharma raises the question of lavender oil and hormone disruption, an issue I have also addressed previously, in this article. To sum up, there was no established link between lavender oil and breast growth in three pre-perbertal boys, but lavender oil did show a weak in vitro estrogenic action in two (of the four possible) types of in vitro test for estrogenic activity (Henley et al 2007). None of this establishes that lavender oil disrupts hormones. To quote Diel et al (1999): “…even a combined use of several in vitro test systems is not able to predict the occurring action of a substance in the organism.” In other research, lavender oil was significantly toxic to human breast cancer cells (Zu et al 2010) suggesting that it would prevent breast cancer, and not increase risk.
Summary points
Consumer products containing lavender oil may benefit from the addition of an antioxidant, such as alpha-tocopherol. This should be used at 0.1-0.2% (note that using more is not more effective).
Bottles of lavender oil, or products containing lavender oil, that are more than 12 months old (after first use) should be discarded if they no longer smell fresh.
There is a theoretical risk of skin allergy from lavender oil, but this risk is extremely low. Restricting the percentage of lavender oil in leave-on products (skin creams, lotions, gels) to 2% would be over-cautious, but combined with the addition of an antioxidant, will make a product super-safe.
Lavender oil has a weak in vitro estrogenic activity, but there is no reason to believe that this translates to a hormone-disrupting effect in humans.
References
Brandão FM 1986 Occupational allergy to lavender oil. Contact Dermatitis 15:249-250
De Groot AC 1996 Airborne allergic contact dermatitis from tea tree oil. Contact Dermatitis 35:304-305
Diel P, Smolnikar K, Michna H 1999 In vitro test systems for the evaluation of the estrogenic activity of natural products. Planta Medica 65:197-203
Keane FM, Smith HR, White IR et al 2000 Occupational allergic contact dermatitis in two aromatherapists. Contact Dermatitis 43:49-51
Henley DV, Lipson N, Korach KS et al 2007 Prebubertal gynecomastia linked to
lavender and tea tree oils. New England Journal of Medicine 365: 479-485
IFRA 2009 Standards, including amendments as of October 14th 2009. International Fragrance Association, Brussels. http://www.ifraorg.org
Kim HM, Cho SH 1999 Lavender oil inhibits immediate-type allergic reaction in mice and rats. Journal of Pharmacy & Pharmacology 51:221-226
Meneghini CL, Rantuccio F, Lomuto M 1971 Additives, vehicles and active drugs of topical medicaments as causes of delayed-type allergic dermatitis. Dermatologica 143:137-147
Opdyke DL 1976 Monographs on fragrance raw materials. Food & Cosmetics Toxicology 14 supplement
Prashar A, Locke IC, Evans CS 2004 Cytotoxicity of lavender oil and its major components to human skin cells. Cell Proliferation 37:221-229
Rudzki E, Grzywa Z, Brud WS 1976 Sensitivity to 35 essential oils. Contact Dermatitis 2:196-200
Schaller M, Korting HC 1995 Allergic airborne contact dermatitis from essential oils used in aromatherapy. Clinical & Experimental Dermatology 20:143-145
Selvaag E, Holm JO, Thune P 1995 Allergic contact dermatitis in an aromatherapist with multiple sensitizations to essential oils. Contact Dermatitis 33:354-355
Sköld M, Börje A, Harambasic E et al 2004 Contact allergens formed on air exposure of linalool. Identification and quantification of primary and secondary oxidation products and the effect on skin sensitization. Chemical Research in Toxicology 17:1697-1705
Sköld M, Hagvall L, Karlberg AT et al 2008 Autoxidation of linalyl acetate, the main component of lavender oil, creates potent contact allergens. Contact Dermatitis 58:9-14
Sugiura M, Hayakawa R, Kato Y et al 2000 Results of patch testing with lavender oil in Japan. Contact Dermatitis 43:157-160
Veien NK, Rosner K, Skovgaard GL 2004 Is tea tree oil an important contact allergen? Contact Dermatitis 50:378-379
Wei A, Shibamoto T 2007 Antioxidant activities and volatile constituents of various essential oils. Journal of Agricultural & Food Chemistry 55:1737-1742
Zu Y, Yu H, Liang L et al 2010 Activities of ten essential oils towards Propionibacterium acnes and PC-3, A-549 and MCF-7 cancer cells. Molecules 15:3200-3210
Help please…today i was told that lavender essential oil can not be used when using estrogen cream therapy because of it’s phytoestrogen content…do you know of any research i could read about this or is this just an outrageous sweeping statement? Lauren, via Facebook
Lauryn, lavender oil has an in vitro estrogenic action, as do many foods and natural substances (phytoestrogens) but most of these have a negligible effect in reality. To start putting out contraindications for lavender oil until we know more is scaremongering in my opinion. No-one yet knows which constituent(s) of the oil interact with estrogen receptors, nor what the interaction involves (could promote estrogen, or block it). Either way, it’s very likely that the effect is so minimal as to be a non-issue, unless you are talking about ingesting the oil daily in quite large amounts.
-Robert
Rachel M. writes:
Dear Robert,
Greetings! Because you are an expert with regards to using essential oils I was wondering if you could offer some advice or direct to me to research with regards to using essential oils for an advanced case of HPV (Human papillomavirus). I appreciate any information that you could offer and thank you in advance for your time.
Be well, Rachel
Hi Rachel,
I could only find one relevant piece of research, which talks about tea tree oil successfully treating warts caused by HPV. I hope this may be of some help! Robert
Hi Robert,
I was able to be at your seminar in Ithaca and enjoyed it very much. You presented much needed information on essential oils research. That compelled me to pose the following question to you: Do you know of any research regarding if and how essential oils react with titanium?
My son had a titanium screw implanted into his skull to attach a hearing aid to it. While that area heals it can be prone to infection and skin reaction. Of course I would love to use essential oils to prevent that. I have heard of Essential Oils reacting in a destructive way with plastics. I think they are fine with stainless steel. I have no idea what they could do to titanium.
I would appreciate any advice you have.
Regards, Karin E.
Hi Karin,
Great to hear you enjoyed the seminar in Ithaca!
I don’t know of any research concerning essential oils and titanium. Undiluted essential oils can react with tin (over a period of many weeks), and tin is quite a soft metal, and subject to corrosion from some types of chemicals. Since titanium is a hard metal, and is known to be highly resistant to corrosion, it is very unlikely that it would be subject to any kind of interaction with essential oils, especially diluted ones.
Hi Robert, I wondered what the current advice/research is regarding the internal use of essential oils – specifically using oils on tampons? Any guidance would be much appreciated. Many thanks. Adele
Adele – one important point is that, as with all other ways essential oils are applied to the body, they must first be diluted in a suitable medium, such as a gel. The risk of not doing this is that any concentrated essential oil could cause irritation, or even an allergic reaction. I suggest using no more than one or two drops of essential oil, diluted to 1-5% of the total.
Best, Robert
Thanks for this Robert. Very much appreciated. Adele
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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.)
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.
Rachel M. writes:
