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Emu Oil - a natural anti-inflammatory
Research Data Published in INFLAMMOPHARMACOLOGY 1998
Emu Oil(s): A source of non-toxic transdermal anti-inflammatory agents in aboriginal medicine.
M.W. Whitehouse1 , A.G. Turner2 , C.K.C. Davis and M.S.Roberts3


Whitehouse M.W, Turner A.G., Davis C.K.C, Roberts M.S. Emu Oil(s): a source non-toxic transdermal
anti-inflammatory agents in aboriginal medicine, Inflammopharmacology. 1998;6:1-7
The ‘oil’ abstained from Emu fat can be very effective inhibitor of chronic inflammation in rats when
applied dermally (which is a skin penetration enhancer). Assays for this activity using the adjuvant-
induced arthritis model have shown:
i. Considerable variability in potency of some commercial oil samples;
ii. Little or no correlation of activity with colour or linolenic acid content of the oil;
iii. Relative stability of some active oils (to heal, aging at room temperature);
iv. The bulk of the anti-inflammatory activity was present in a low triglyceride fraction;
v. Potential arthritis-suppressant/immmuno-regulant activity of these active fractions.
These studies point to the need for more rigid quality control before considering such a (now proven)
traditional medicine as a complementary therapy. Repeated applications of selections of selected oils
did not induce any of the more prominent side effects associated with NSAIDs (e.g. platelet inhibition,
gastrotoxicity) or certain anti-arthritic drugs (Proteinuria, leukopenia)


The Emu (‘bush chook’), Dormaius (novae-hollandiae) is a free roving, large, flightless bird indigenous
to Australia now farmed in Australia, Canada, Europe and the USA. The native Aboriginal and early
white settlers in Australia rubbed on the liquid fat to facilitate wound healing and to alleviate pain and
disability from musculo-skeletal disorders.
An adult bird (15 months old) weighing 45 kg carries up to 10 kg of body fat, from which 7-8 L of a
thick oil is obtained by rendering at temperatures up to 15°C.
Filtering this semi-solid fat at 2°C yields 20 80% (v/v) of clear oil (CO); the proportion varying with
conditions of nurture and other factors (genetic stock, stress, etc.). These CO’s can vary greatly in
their content of (a) natural antioxidants (e.g. carotenoids, flavones), and (b) skin permeation-
enhancing (PE) factors (e.g. under-sterified oleic acid, plant-derived sesquiterpenes). The content of
a-linolenic acid (18:3) in the total triglyceride fraction varies notably from almost zero (many farmed
birds) up to 20% (some feral birds), also reflecting significant influences of the basal diet on oil
Evidence for the variability in anti-inflammatory potency of different emu oils was first obtained using
the rat adjuvant arthritis model. This report extends and amplifies previous observations that not all
Emu oils show similar therapeutic activity when applied dermally. To eliminate variations in the
endogenous PE content between clarified oils, 15% (v/v) cineole (eucalyptol) was routinely added to
all samples before testing.


Unless indicated otherwise, Emu fat samples were mixtures of both internal and external fat. These
fat samples, free of blood and extraneous matter, were freshly minced at the time of slaughter,
packed on ice (if not rendered immediately) and then rendered at controlled temperatures ranging
from 30°C to 95°C. The semi-liquid fat/oil thus obt ained showed considerable variations in clarity,
viscosity and colour (yellow). For routine testing, these oils and commercial samples were filtered at
25 C to remove solids and then diluted with sterile cold-pressed olive oil if necessary (e.g. for dose-
response studies).
After admixture with 15% (v/v) cineole (eucalyptol) samples were applied dermally (2.5ml kg -1 day-1)
for at least 4 days to shaved dorsum (6cm2) of female outbred Wistar rats (160-200g) developing
adjuvant-induced polyarthritis as previously described [1,2]. This protocol measures a therapeutic
action, the animals having a previously established disease, with the first dose being given at the time
of onset of arthritis. Signs of arthritis were measured before dosing (day 10 post-adjuvant), after
dosing (day 14) and again after a rebound/washout period 9 (day 17). The latter observation served to
eliminate those rats which were non-responders (n<15%) to the inoculated arthritigen given on day 0.
A blinded independent observer assessed the overall arthritic severity on day 14; giving each animal
a score (0 to 5+) based on paw and tail inflammation and general condition of the animal. Changes in
rear paw and maximal tail thickness were measured with a micrometer and forepaw inflammation was
assessed arbitrarily (on a scale of 0 to 4+). Data are presented as means from five or more rats per
experimental group. A second assay was based on treating female Dark Agouti (DA) rats (150.180g)
with test fractions/oil co-administered the arthritigenic adjuvant, i.e. treatment was prophylactic with a
single dose at the time triggering the arthritis. Wistar rats came from the University of Queensland
Animal Farm; DA from the Animal Resources Centre at Murdoch University (Western Australia). Oils
proved active in the above assays were further treated by various fractionation procedures, not
detailed here, to obtain (a) low-triglyceride (active) concentrates which were, 6% original oil volume,
and (b) triglyceride-rich oil residues (>94% (v/v)).


Anti-inflammatory activity of various oils
Tables 1 and 2 expand on data previously showing that Emu oils can differ greatly in their ability to
suppress the expression of an ongoing experimental arthritis in rats when given transdemally in a
therapeutic regime. Table 1 compares the activity of several oil samples carrying claims for potential
therapeutic activity, assessed as soon as possible after they were purchased from commercial
outlets. Some of these oils might have been subjected to vigorous processing (e.g. bleaching) to
attain cosmetic grade. Since these data were generated in several experiments over a 24-month
period, it is not feasible to record here full details of all measurements on the untreated controls.
Likewise, Table 2 gives the relative activities of some freshly prepared oils derived from the
internal/intestinal fat and the external/rump fat of the bird; these being feral (i.e. source from the wild,
farmed intensively and dependent wholly on feed rations, or farmed with free access to considerable
natural fodder. Although no simple correlation was evident between oil activity and food supply, the
intestinal fat seems to carry more activity than the rump fat in each instance.
Table 1
Variations in potency between some commercial emu oils

Percent Reduction (on day 14) of:
Source (country/brand)
Emu oils were applied for 4 days only (controls received no treatment). Only reductions > 32%
considered significant (n= 4/group)

Table 2

Variations in the potency of some freshly derived unprocessed Emu oils
% Reduction (on day 14) of:
Bird/Fat source
Emu oil was applied at 1 ml/kg (plus 1 ml/kg olive oil) with 15% (v/v) cineole for 4 days only. Controls received no treatment. Table 3 shows that the therapeutic activity was reasonably thermostable in some preliminary experiments on hearing selected oils. These were first obtained by rendering at 30 C before being divided into two lots for comparison: one lot was then heated to 85 C for 3 hours and the other
maintained at 25 C. In other experiments not detailed here, it was found that the colour of the oil (very
marked in some, but not all, feral Emu fat samples) did not correlate with its anti-inflammatory activity,
as disclosed in this bioassay. Some coloured oils showed marked deterioration in potency on being
exposed to sunlight, suggesting that the yellow pigment(s) might have photosensitizing activity and
may accelerate the deterioration of the active principles.
Table 4 compares an Emu oil with other oils claimed to have therapeutic value for inflammatory
disorders, when applied dermally with 15% cineole. These results indicate that Emu fat is a relatively
unique source for transdermal anti-inflammatory activity. Oils rich in a- or g-linoenates, e.g.
flax/linseed, evening primrose, showed some modest activity. By contrast, no correlation was found
between linolenate content of Emu oils (ranging from 0.2 to 19.7%) and overall anti-inflammatory
activity (data not shown).

Table 3

Thermostability of two Emu oil
Changing in arthritic signs (days 10-14)
Measurements represent mean (±SE) changes in arthritic signs between day 10 and 14 after applying
oils (1 ml kg-1 day –1) for 4 days, π = 5 rats/group. Each oil sample treated at 30°C or 85°C

Table 4

Emu Oil vs. Other oils: Transdermal efficiency for inhibiting arthritis
Percent Reduction (on day 14) of:
Controls were untreated. Oils applied for 4 days only

Preliminary observations regarding safety

Arthritic animals at autopsy after 10 dermal applications (2.5 ml kg –1 day), no macroscopic
abnormalities were noted in post-mortem examinations (π = 30 rats). Platelet aggregation, in
response to ADP or arachidonic acid ex vivo, was normal. Large doses of a ‘good’ oil (1 ml/rat)
administered orally caused no gastric irritation. By contrast, doses as low as 150 mg/kg of these good
oils (suspended in 0.04% Tween – 20) actually reduced the gastric irritation and bleeding caused by
50 mg/kg ibuprofen and 25 mg/kg naproxen PO in disease – stressed rats. We found no evidence for
increased proteinuria (beyond that seen in approximately 30% of the untreated arthritic animals) after
10 days treatment with active oil. The areas of skin exposed to emu oil (with or without admixed
cincole) showed very little/o irritation, in contrast to that seen after applying some other transdermally
active drugs notably certain ‘topical’ NSAID’s, E.g. piroxicam, copper salicylate, etc.


This progress report further confirms the likely validity of repeated claims and testimony available in
writing since 1820, that Aboriginal lore has located a natural medicine, transdermally active, for casing
inflammatory signs and symptoms of musculoskeletal disorders. This testimony, both historic and
contemporary, also indicates a likely analgesic action: the data presented here neither affirm or deny
this analgesic property.
Like many alternative medicines, the credibility of emu oil has suffered from overstated claims for
poorly characterized products that may sometimes even be adulterated (e.g. with chicken fat or
linseed oil) without recognition of this fact. It is of prime importance to assert continuous quality
control throughout the whole supply line, i.e. from selecting the best birds for (good/active) oil
production, their feed and nurture through to the rendering of the crude fat and subsequent
preservation of the extracted oil. This is yet another example of conditional pharmacology, often
overlooked when we take for granted the consistency and potency of synthetic drugs. It should be
recognized and more carefully defined in the context of using natural-sources remedies.
One great advantage of emu oils is that they require little refining, unlike most animal fats. They also
come from a renewable and Eco-sustainable resource, in contrast to so many petroleum-derived
1. Department of Medicine, University of Queensland, Princess Alexandra Hospital, Brisbane,
Queensland 4102
2. Department of Biological Sciences, Sydney Institute of Technology, Ultimo, NSW 2007
3. Centre for Food Technology, Department of Primary Industry, Hamilton, Queensland 4007,
Australia correspondence
a. From the Cherbourg Aboriginal Community. Queensland, Australia
b. Commercial sample (Pfeiffer Farm, St Thomas, ON Canada)
c. Pikasol (lube AS, Hadsund, Denmark)


1. Snowden JM, Whitehouse MW, Anti-inflammatory action of emu oils. Inflammopharmacology. 2. Whitehouse MW, Rainsford KD, Taylor RM, Vernon-Roberts B, and Zinc monoglyccrolate: a slow release source of zinc with anti-arthritic activity in rats, Agents Actions. 1990; 31:47-58 3. Rofe AM, Whitehouse MW, Bourgeois CS, Hayes DR, Vernon-Roberts B. Prevention of adjuvant induced cachexia in rats by cyclosporine – A Immunol Cell Biol. 1990; 68: 63-9. 4. Haynes DR, Gadd SJ, Whitehouse MW, Mayrhofer G, Vernon-Roberts B. Complete prevention of the clinical e xpression of adjuvant – induced arthritis in rats by cyclosporine – A and lobenzafit, Inflame Res. 1996; 45: 159-65


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