Aromatherapy in Psychiatric Disorders
Aromatherapy in Psychiatric Disorders
Aromatherapy in Psychiatric Disorders
1172-7047/06/0004-0257/$39.95/0
LEADING ARTICLE
Abstract
1. Background
Aromatherapy is the therapeutic use of plant essential oils, whether absorbed via the skin or olfactory system. The term aromatherapy, intended to
describe the compounds present in the essential oil
that are aromatic (i.e. have an aroma), is not entirely
precise, as effects are not necessarily related to the
aromatic properties of the agent; further terms such
258
Alpha-pinene
(monoterpene hydrocarbon)
Rosmarinus officinalis (22%)
Camphor
(monoterpene ketone)
Salvia officinalis (12%)
O
OH
Linalool
(monoterpene alcohol)
Lavandula angustifolia (38%)
Linalyl acetate
(acetate of linalool)
Lavandula angustifolia (45%)
O
H
O
Geranial
(monoterpene aldehyde)
Melissa officinalis (32%)
H
1,8-Cineole
(monoterpene oxide)
Salvia lavandulaefolia (21%)
O
H
Caryophyllene oxide
(sesquiterpenoid)
Lavandula latifolia (2.4%)
Fig. 1. Examples of frequently occurring essential oil terpenoids
from the different chemical classes. % indicates the amount of
terpenoids present in each oil, e.g. Lavandula angustifolia is 38%
linalool.
ranging list of therapeutic activities. The pharmacology behind the actions of many essential oils remains undefined and it is certain to be a long and
complex path to full medicinal and pharmacological
understanding, paralleling that of medical herbalism
and unlike any conventional medicinal substance.
Essential oils can be absorbed into the body in
three ways: (i) through the olfactory and respiratory
systems (vapour inhalation); (ii) transdermally via
lotions or compresses, often involving massage and
during bathing; or (iii) orally, via ingestion of essential oils in capsules or as additives to food or medical
preparations, for example. The latter option belongs
more to the realm of herbal medicine than aromatherapy.
The aromatic oils have been used for over 5000
years; ancient Egyptians used them as perfumes,[3]
and there are nearly 200 references in the Bible to
their use for mental, spiritual and physical healing.[7]
Modern aromatherapy originated in Germany in the
16th century.[8] Gattefosse, a French chemist, investigated the antibacterial and healing properties of
essential oils during World War I to treat wounded
soldiers[9] and Valnet, a French army surgeon, further revived the application of aromatherapy during
World War II.[7]
The effects of an aroma can be instantaneous and
include both direct and indirect psychological effects even thinking about a smell may have a
similar effect to the smell itself. However, accumulating evidence that inhaled or dermally applied
essential oils enter the blood stream and, in relevant
molecular, cellular or animal models, exert measurable psychological effects, indicates that the effects
are primarily pharmacological. This conclusion is
supported by increasingly reported benefits of
aromatherapy using specific essential oils in the
management of chronic pain, depression, anxiety
and some cognitive disorders, as well as insomnia
and stress-related disorders.[10] The subjective effects of aromatic plant oils relevant to CNS/cerebral
CNS Drugs 2006; 20 (4)
Latin name
Citrus bergamia
259
Table I. Subjective effects and chemical constituents of aromatic essential oils relevant to cerebral functiona
260
This review was submitted in May 2004 and accepted in March 2005.
Controlled clinical trials of aromatherapy in dementia were originally prompted by open-label trials demonstrating beneficial effects, e.g. increased
sleep with lavender vapourisation in patients with
dementia who were in residential care,[18] reduced
agitation in patients with severe dementia following
lavender oil vapourisation,[19] and a range of these
and other improved outcomes using a mixture of
lavender and other oils.[20] The results of the controlled trials are outlined in table II.
The most commonly used essential oils for dementia therapy in controlled trials have been lavender (Lavandula angustifolia) and lemon balm (Melissa officinalis), singly or in combination (table II).
The trials have involved people with advanced dementia in residential care and have generally assessed behavioural symptoms, particularly agitation,
as outcome measures, although one trial did assess
cognitive parameters.[25] The trials divide equally
between inhalation or dermal application, with a
duration of up to 4 weeks. What is remarkable, given
the diversity of trial design and type of aromatherapy, is that all treatments have resulted in significant
benefit. The benefits include reductions in agitation,
insomnia, wandering, difficult behaviour and social
withdrawal.
In a more recently published open-label trial, ten
patients with dementia were treated for 6 months
with a range of essential oils (vaporised mixtures of
orange, ylang ylang, patchouli, basil, rosemary, peppermint, rosewood, geranium, bergamot, chamomile
and jasmine). A marked decrease in disturbed behaviour was observed in the majority of patients, leading to reductions in psychotropic medications, with
overall cost savings.[26] However, Gray and Clair[27]
noted no reduction in combative, resistive
behaviours in 13 elderly people in residential care
treated in an open-label manner with lavender,
sweet orange or tea tree oil vapour (delivered, rather
2006 Adis Data Information BV. All rights reserved.
261
262
Table II. Controlled clinical trials of aromatherapy in patients with severe dementia
Essential oil
Study design
Outcome
Reference
21
aroma
massage alone)
10d
arms
Lavender aroma
22
23
24
and limbs
This open-label trial is included here because the patient numbers are substantial and the multiple outcomes were measured.
20
skina
25
al.[37]
Ferry et
conducted a survey of 80 cognitively normal, non-institutionalised patients with
Parkinsons disease. Over half of the patients (54%)
reported using complimentary therapies, and
aromatherapy was one of the most commonly used,
although no information is provided in the report on
2006 Adis Data Information BV. All rights reserved.
263
264
Many essential oils are associated with an improvement in mood (table I) indicative of potential
application for the treatment of depression. AnecdoCNS Drugs 2006; 20 (4)
265
266
267
268
Table III. CNS effects of lavender speciesa essential oil and constituents
Lavender species
[% constituents]
Lavandula angustifolia Mill.
(syn. Lavandula officinalis),
References
Anticonflict
Dose-dependent (4001600 mg/kg, SC) anti-conflict effects in the Geller conflict test,
with effects similar to diazepam
78
Anticonvulsant
Inhalation of oil blocked pentetrazol-, nicotine- and electroshock- but not strychnineinduced convulsions in mice. A dose of 33mg decreased motility of normal mice and
reversed caffeine-induced over-agitation in mice; serum concentration of linalool
correlated with effects on motility
72,79
Sedative/anticonvulsant
80
Neuroprotective
81
Spasmolytic
82
Anaesthetic
83,84
Lavandula
stoechas L.
Anticonvulsant/sedative
85
Anticonvulsant
44
Sedative
10300 mg/kg potentiated narcotic effects of hexobatbital sodium, alcohol and chloral
hydrate, and inhibited spontaneous motor activity in mice
Anticonvulsant
Competitive antagonism of [3H]-glutamate and non-competitive antagonism of [3H]dizocilpine (NMDA receptor antagonist) binding in rat cortical membranes. Evidence
that optically active linalools may have different CNS effects. Delayed NMDA-induced
convulsions and blocked QUIN-induced convulsions; partial inhibition and significant
delay of behavioural expression of pentylenetetrazole-induced kindling in mice.
Protection against pentylenetetrazol- and picrotoxin-induced convulsions and noncompetitive inhibition of [3H]-dizocilpine binding (IC50 2.97 mmol/L) but no effect on
[3H]-muscimol binding in mice. Significantly inhibited (at concentrations of 1 and 3
mmol/L) potassium-stimulated [3H]-glutamate release and decreased its uptake in
mice cortical synaptosomes
86-90
Sedative
Inhalation (of 27mg) decreased motility of normal mice and reversed caffeine-induced
over-agitation in mice
72,73
Anaesthetic
Modified the kinetics of the nicotinic receptor ion channel at the mouse neuromuscular
junction. Inhibited basal adenylate cyclase activity
86,91
Sedative
72,73,92
Linalool [3040%]
The main lavender species used in aromatherapy is Lavandula angustifolia, although other species include L. latifolia, L. stoechas and L. x intermedia. These species do
not have the same phytochemistry and may have differing biological activities.[67]
IC50 = concentration that inhibited the effect by 50%; IP = intraperitoneal; QUIN = quinolinic acid; SC = subcutaneous.
Some essential oils are traditionally used as stimulants, although there are fewer of these than sedative oils (table V). Essential oils with stimulant
properties include rosemary (Rosmarinus officinalis), sage (Salvia sp.) and jasmine (Jasminum
grandiflora). Data (mainly from studies on locomotor activity in animals) indicate that these oils have
pharmacological activity consistent with their therapeutic application (table I and table V). For example, inhalation and oral administration of rosemary
oil stimulated locomotor activity in mice and this
was correlated with blood concentrations of
2006 Adis Data Information BV. All rights reserved.
269
270
Table IV. The main essential oils used in aromatherapy and their constituents that show pharmacological sedative activities
Main CNS effect
References
Anticonvulsant,
neuroprotective,
sedative
94,95
Artemisia annua L.
(Asteraceae) [camphor 22.7%,
1,8-cineole 20.4%, p-cymeme
12.2%]
Sedative
96
CNS depressant
72,97
Sedative
98
Sedative
99
Sedative,
antidepressant
Increased duration of barbiturate-induced sleeping time and had motor relaxant effects
(100200 mg/kg IP) in rats. 0.1 mL/h significantly reduced total immobility time and
potentiated the imipramine-induced reduction of total immobility time in a forced
swimming test in rats
92,100
Anticonflict
400800 mg/kg (IP) possessed anticonflict effect similar to diazepam in Geller and
Vogel tests in mice
101,102
Anticonvulsant,
anxiolytic, sedative
0.5 g/kg peel essential oil increased latency period of tonic seizures in
pentylenetetrazole- and electroshock-induced convulsions in mice and 1 g/kg increased
the sleeping time induced by pentobarbital. Anxiolytic effect in the elevated plus maze
test. Inhalation of Subsp. aurantium reduced motility of mice by 65%. Inhalation
decreased motility of normal but not caffeine-injected mice
103
CNS depressant
1040 mg/kg (IP) nonvolatile extract of essential oil reduced spontaneous activity,
potentiated sodium pentobarbital-induced sleeping time and protected against
pentylenetetrazole-induced convulsions in mice
104
Anticonvulsant
105
Anticonvulsant,
sedative
106
References
Sedative
50200 mg/kg (IP) increased duration of barbiturate-induced sleeping time and had
motor relaxant effects
100
Anxiolytic
107
Anticonvulsant
108,109
CNS depressant,
anticonflict,
analgesic, sedative,
cholinergic,
antioxidative
Suppression of the population spike amplitude in the CA1 region of rat hippocampal
slice preparation following application of essential oil (IC50 128 g/mL), comparable to
the GABAA agonist muscimol. 3100 L/kg did not influence behavioural parameters in
the staircase test in mice and inhalation produced no effect on the motility of mice.
12800 mg/kg extract decreased behavioural parameters measured in a non-familiar
environment test (staircase test) and familiar environment test (two compartment test).
4001600 mg/kg extract produced peripheral analgesia by reducing acetic acid-induced
pain; 36 mg/kg extract (and not 100 L/kg essential oil) induced sleep in mice after
treatment with an infrahypnotic dose of pentobarbital; 6 and 50 mg/kg potentialised
sleep induced by pentobarbital. 25 and 50 mg/kg extract produced sedative and
hypnotic effects and potentiated barbiturate-induced sleep time. Extracts (ethanolic)
displaced [3H]-(N)-nicotine and [3H]-(N)-scopolamine in receptor binding studies using
human cerebral cortical cell membranes. Leaves contain compounds with 10-fold
greater radical scavenging ability than ascorbic acid and -tocopherol (Perry N et al.,
unpublished data)
110-115
Sedative
CNS depressant effect (100400 mg/kg) in spontaneous activity and curiosity test,
potentiation of pentobarbital-induced sleep (50 mg/kg) in mice and rats
116
Menthone
[in e.g. Calamintha sylvatica]
Sedative
99
Sedative
Decreased motility of caffeine-induced over-agitated mice but not normal mice following
inhalation
73
271
73
Sedative
Sedative
119
101,102
400800 mg/kg (IP) possessed anticonflict effect similar to diazepam in Geller and
Vogel tests in mice
30 mg/kg (IP) decreased motor activity in mice
400800 mg/kg (IP) possessed anticonflict effect similar to diazepam in Geller and
Vogel tests in mice. Inhalation produced no effects on pentobarbital-induced sleep time
in mice. Restorative effects on stress-induced immunosuppression in mice
100500 mg/kg (IP) reduced motor activity, impaired the performance in the rotarod
test and protected against electroshock-induced convulsions in mice
Inhalation decreased motility of normal and over-agitated mice
Anticonflict
Sedative
Anxiolytic
References
In vitro effects and in vivo pharmacology
Main CNS effect
99
101,102,117,118
272
Main effect
References
Antidepressant, stimulant,
neuroimmunomodulatory
0.1 mL/h vapour reduced total immobility time and potentiated the imipramineinduced reduction of total immobility time in a forced swimming test in rats.
Shortened pentobarbital-induced sleep time in normal but not anosmic (via zinc
sulphate) mice. Long-term inhalation of lemon fragrance in mice induced
suppression of plaque-forming cells in blood (immune response) induced by highpressure stress. Inhalation modulated the behavioural and neuronal (acetylcholine
release) responses related to nociception and pain differently in male and female
rats. Restorative effects on stress-induced immunosuppression in mice
92,117,118,121-123
Stimulant in normal,
anxiolytic in stressed
73
Stimulant, spasmolytic
7,8,10,78,97,117,124
400 and 800 mg/kg (IP and IV) increased ambulatory activity of mice. Note other
Mentha species with distinct photochemistry (e.g. Mentha longifolia) may have
CNS depressant activity (table IV)
116,125
64,108,126
Cholinergic, stimulatory,
GABAergic, antioxidant
29,76,110,127
273
Table V. The main essential oils used in aromatherapy that show pharmacological stimulant activities
= elimination half-life;
73
128-130
Essential oil (IC50 0.03 mg/mL) and certain constituent monoterpenoids inhibited
erythrocyte acetylcholinesterase. 20 and 50L essential oil inhibited rat striatal and
hippocampal acetylcholinesterase following oral administration. 0.07 mg/mL
increased population spike amplitude with no epileptiform activity in the CA1 region
of rat hippocampal slice preparation. Essential oil and certain monoterpenoid
constituents exhibit in vitro antioxidant and anti-inflammatory activity (Perry N et
al., unpublished data)
Tagetes minuta L.,
Anxiogenic
45 g/mL inhibited binding of the benzodiazepine [3H]-flunitrazepam to rat and
chinchilla (Asteraceae)
chick brain membranes. 0.3 mg/kg (SC) displayed anxiogenic and antidepressant[c-ocimene, t-ocimene,
like effects in rats in elevated plus maze and forced swimming tests. 0.040.45
dihydrotagetone]
mg/kg exhibited anxiogenic effects on chick behaviour in T-maze and tonic
immobility tests
Thymol
Stimulant in normal,
Inhalation increased locomotor activity of mice under normal conditions, though
anxiolytic in stressed
decreased it in over-agitated mice pretreated with caffeine
a Taken from the individual references or from Boelens BACIS ESO database;[6] principal chemical constituents listed in order of concentration, highest
proportions may vary according to source and that many oils contain hundreds of terpenoids.
cAMP = cyclic adenosine monophosphate; IC50 = concentration that caused 50% inhibition; IP = intraperitoneal; IV = intravenous; SC = subcutaneous; t1/2
TBPS = t-butylbicyclophosphorothionate.
Neurochemical/putative
memory-enhancing,
stimulatory, antioxidant,
anti-inflammatory
Table V. Contd
28,29,76,127
References
274
mitters, which are almost all amines or nitrogencontaining. Terpenoids, in contrast, generally being
hydrocarbons, may interact with the CNS in as yet
undiscovered ways, raising the exciting prospect of
uncovering novel receptors, molecular targets or
endogenous chemical signals in the CNS. This parallels the discovery of the endogenous cannabinoids
and their receptors, which were identified originally
based on the interaction of plant-based terpenoids
from Cannabis sativa with CNS receptors.
Some of the challenges for further research that
can presently be identified are summarised in table
VI. As well as considering potential contraindications and/or adverse effects of certain essential oils
(including skin sensitivities and toxicities and abortifacient effects), in the event that clinical efficacy is
established for particular oils and this efficacy is
attributable to specific terpenoids, the question then
arises as to whether future treatment should involve
the use of single chemical constituents or combinations of these. This would satisfy those that seek
simple, standardised formulations as medicines but
most probably not the vast majority of aromatherapeutic practitioners who believe in the value of the
whole essential oil.
The linking of subjective or objective behavioural evaluations to potential objective assessments, such as neuroimaging or EEG, when assessing essential oils would help establish aromatherapy
in clinical practice. Several studies have reported
results from such assessments. In healthy individuals, 810Hz EEG reductions in parietal and temporal regions were reported after lavender oil inhalation, associated with subjective ratings of feeling
comfortable.[146] In 15 healthy adults exposed to
lavender or single aromatic chemicals (e.g. ethyl
aceto acetate and camphor), autonomic measures
including skin potential and respiratory and heart
rates altered in conjunction with hedonic effects.[147]
Other potential physiological measures that are affected by lavender include auditory reaction time
CNS Drugs 2006; 20 (4)
275
Table VI. Challenges for further research into the use of aromatherapeutic agents for psychiatric disorders
Clinical trials
Conducting suitably powered, controlled trials, fulfilling the rigid criteria for blinded, randomised, controlled
trials, or developing other criteria for establishing clinical efficacy
Selection and
standardisation of oils
Selecting appropriate aromatic oil(s), based on relevant bioactivities and chemical composition as well as
traditional use, together with standardisation of commercial preparations, application procedure and dose
delivery
Chemical constituents
Establishing the active constituent(s) in order to understand the pharmacology, toxicology and interactions
that may occur between constituents
Anosmic issues
Identifying and separating the psychological and pharmacological effects and relevance to anosmic
patients
Adverse reactions,
interactions and
contraindications
Developing awareness of which essential oils do or no not have contraindications, potential interactions
with other medications, and individual dermal or other adverse reactions
Individuality
Aromatherapeutic practice tailors the application to the individual as opposed to standardised symptomatic
treatment; this poses obvious challenges
Acceptance
Bridging the gap between preferences and practices between nursing and medical practitioners;
accumulating scientific evidence, clinical trial data and relevant pharmacology to enable, e.g. general
practitioners, to consider prescribing the use of specific essential oils as an adjunct to conventional
medicine in psychiatric disorders; availability of standardised aromaceuticals with information on clinical
and pharmacological effects; including such information in medical student education; acceptance of
complex, synergistic effects of a therapeutic agent
Research support
Identifying research support the absence of economic incentives for the pharmaceutical industry and the
insufficient resources of commercial suppliers of essential oils indicate the need for government and
charity support
276
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Correspondence and offprints: Dr Nicolette Perry, Medicinal Plant Research Centre, Universities of Newcastle and
Northumbria, Newcastle General Hospital, MRC Building,
Newcastle upon Tyne, NE4 6BE, UK.
E-mail: [email protected]