Psychoaromatherapy in Mental Health "Aromatherapy seems to drive autonomic nervous activity toward a balanced state." Example: In anxiety and stress, sympathetic activity is often increased, together with decreased parasympathetic activity. It has been noted there are higher sympathetic activities for depressed and anxious subjects than for normal subjects. On the emotional level: "Positive emotions result in altered autonomic nervous system activity, characterized by increased parasympathetic nervous system activity, whereas negative emotions (e.g., anger) result in parasympathetic withdrawal and sympathetic activity" It is said there are parasympathetic-stimulating oils like lavender and the sympathetic-stimulating oils like rosemary but a study has noted that short inhalation of essential oils suppresses parasympathetic nervous activation while continuous inhalation suppresses sympathetic nervous activation [1] Oils that cause parasympathetic stimulation of the autonomic nervous system in turn are associated with decreased anxiety, improved mood, and increased sedation whereas the sympathetic-stimulating oils have been associated with increased arousal, improved cognition and memory, and enhanced performance on cognitive assessment tests [2] Essential oil inhalation is often effective in reducing the stress index, and that it effectively regulated the activity of the hypothalamus to provide stable and relaxing conditions by creating balance and harmony in the 1 sympathetic nervous system "A clinical study with depressed patients revealed that it was possible to reduce the needed antidepressants' doses by inhaling a mixture of citrus oils; moreover, inhalation of the oil by itself was antidepressive and normalized neuroendocrine hormone levels" [3] With regard to agitation and anxiety, in a clinical mental health population, there were significant reductions in needed medications for anxiety or agitation With regard to depression, significantly more improvement in scores on depression, anxiety, and severity of emotional symptoms, studies finding effects independent of personality traits, psychological status, and psychotherapeutic medication Inhalation of essential oils may induce stimulant or sedative effects [4] and peppermint is well known as a stimulating oil. Inhaled, a growing body of evidence that suggests aroma of peppermint essential oil may act as a positive and easy intervention delivering beneficial objective and subjective outcomes for measures of cognition and mood [5]. - increased physiological arousal producing increased awareness and attention to detail (potentially increasing self-other boundaries through a focused, more exclusive state [6]) - delivered an experience of less mental demand, perceived effort, and anxiety - improved participants overall mood - positively impacts accuracy of long-term memory - increased subjective arousal and associated engagement with tasks - enhanced concentration levels: peppermint facilitates the functioning of a cognitive control mechanism that inhibits inappropriate responses [7] Single doses of volatile monoterpenes derived from edible herbs such as peppermint (Mentha piperita) have been shown to enhance relevant aspects of cognitive function and alertness when administered orally [8] It beneficially modulated performance of demanding cognitive tasks and attenuated increases in mental fatigue but it "seems likely that 100 μL of M. piperita essential oil may represent the lower reaches of this oil’s dose-response profile". 2 drops of essential oil is approximately 100 μL Peppermint oil exhibited in vitro concentration-dependent GABAA and nicotinic receptor binding properties and inhibited acetylcholinesterase. Menthol [9] and other constituents 2 (menthone etc) have effects mediated by the dopamine system and menthol has been shown to modulate nicotinic receptor populations and sensitivity and inhibit nicotinic receptor mediated activity. Menthol (the (-)-menthol is mainly produced by plants) is negative allosteric modulator of α4β2 nAChRs, (2) a noncompetitive antagonist of α7 and α3β4 nAChRs, (3) a noncompetitive antagonist of 5-HT3 receptors, (4) a positive allosteric modulator of GABAA receptors, (5) a positive modulator of glycine receptors and (6) TRPM8 agonist, responsible for the cooling sensation It has antidepressant properties via 5-HT, DA and GABAergic systems [10] Other constituents show stimulant properties [11] Interaction with nicotine Menthol by itself upregulates nAChRs and alters midbrain dopamine neuron firing and possesses the potential risk of enhancing nicotine reward and reinforcement, enhancing nicotine reward through nAChRs on dopamine neurons [12]. Interestingly, in some studies menthol sex dependently increases oral nicotine consumption [13] and in others "pharmacological interactions of menthol with nicotine reduce, rather than increase, nicotine's reinforcing effects and some measures of relapse vulnerability" [14]. On a deeper level - Lavender oil 3 Linalool is a potent VDCC blocker, similar to pregabalin and exerts antidepressant and anxiolytic effects clinically Lavender and linalool inhibits serotonergic targets, such as SERT and 5-HT1A binding, which might explain why lavender has shown antidepressant-like effects in animal and human models and it seems to have glutamatergic properties, including via mGlu2/3 receptors ⦁ (-)-linalool modulates NMDA receptors, inhibits VDCCs and stimulates the opioidergic, cholinergic M2 and dopaminergic D2 systems. PAM at α1β2 GABAARs With oral lavender oil (Silexan) for generalised anxiety disorder, responder rates exceeded 60% on the basis of HAMA and Clinical Global Impressions criteria. For the 80 mg/day dosage, superiority over placebo could be shown in one trial as well as in the pooled analysis. The risk of adverse events under silexan was similar to placebo for all dosages investigated. In GAD silexan 160 mg/day is efficacious whereas 80 mg/day may represent the lower end of the therapeutic range. Daily doses up to 160 mg were well tolerated. The anxiolytic effect of Silexan (3 mg/kg) was comparable with that of the active controls diazepam (2.5 mg/kg) and pregabalin (100 mg/kg). Silexan also elevated the pentobarbital sleeping time at similar concentrations (3–30 mg/kg). However, this finding rather suggests sleep promoting activity following its anxiolytic effects as no sedative effect by itself was observed. Silexan bears some similarities with the established anxiolytic pregabalin as it non- selectively inhibits voltage-operated calcium channels (VOCCs) already at nanomolar concentrations. Silexan, however, does not primarily interact with the a2d subunit of P/Qtype calcium channels, which is the binding site of pregabalin. Instead, Silexan non-selectively reduces the calcium influx through several different types of VOCCs (e.g. N-type, P/Q-type and T-type VOCCs). It has been speculated that under pathological conditions, such as anxiety or stress disorders, an enhanced Ca influx through N-type and P/Q-type VOCCs may increase the release of neurotransmitters such as glutamate and norepinephrine (Musazzi et al. 2011; Kalk et al. 2011), which are involved in the pathogenesis of these diseases. By inhibiting VOCCs, Silexan may have a normalising effect on hyperactive nerve cells and counteract the symptomatic expressions such as spinning thoughts and anxious moods. ...the interoceptive stimulus properties inherent in the benzodiazepine diazepam are absent in Silexan, thus suggesting the absence of a dependence-inducing potential as is known of benzodiazepines. Based on their findings, Silenieks et al. (2013) also conclude there is little likelihood of a benzodiazepine-like anxiolytic action of Silexan via interaction with GABAA receptors, which supports the findings reported by Schuwald et al. (2013). Baldinger et al. (2015) provided supportive information on the anxiolytic mode of action of Silexan by reporting data from a 4 placebo-controlled clinical trial with a cross-over design. In order to elucidate the effect of Silexan on 5-HT1A receptor binding, 17 healthy men underwent positron emission tomography measurements using the radioligand [carbonyl-11C] WAY-100635 following a daily intake of 160mg Silexan or placebo for a minimum of 8 weeks. It was shown that the serotonin-1A receptor binding potential was significantly reduced following the intake of Silexan in comparison with placebo in two large clusters encompassing the temporal gyrus, the fusiform gyrus and the hippocampus, as well as the insula and anterior cingulate cortex. These findings provide strong evidence that in humans, as in rodents (Chioca et al. 2013), the anxiolytic effect of Silexan is mediated via the serotonergic neurotransmitter system, particularly the 5-HT1A receptor, and not through a GABAergic mechanism. Silexan is devoid of adverse effects and does not cause drug interactions or withdrawal symptoms at daily doses of 80 or 160 mg. Silexan neither inhibits nor induces the activity of cytochrome P450 enzymes, and thus does not interfere with the expected metabolism of major marketed drugs. Either oral administration or inhalation of lavender essential oil exerts CNS effects. Exposure to lavender odor showed an anxiolytic profile similar to diazepam in animal models and showed anxiolytic properties, increased social interaction, and decreased aggressive behaviour. Inhalation of linalool restored the expression of 560 stress-induced probe sets to a normal status after stress, these genes were associated with synaptic transmission via neurotransmitters including anxiolytic neuropeptides such as oxytocin and neuropeptide Y. These genes also included several major histocompatibility complex (MHC) class I molecules necessary for neural development and plasticity. Studies using EEG and brain imaging using fMRI show significant changes during lavender aromatherapy consistent with its relaxing effects. In a neurology in-patient department, there were increased mood scores and reduced psychological distress following aromatherapy with lavender accompanied with rosemary Scans after inhalation of lavender showed neuronal enhancement in the orbitofrontal, posterior cingulate gyrus, brainstem, thalamus, and cerebellum and reduction of activity in the pre/post-central gyrus and frontal eye field. Functional magnetic resonance imaging showed significant activation in major olfactory brain structures, including the primary olfactory cortex, entorhinal cortex, hippocampus and parahippocampal cortex, thalamus, hypothalamus, orbitofrontal cortex, and insular cortex and its extension into the inferior lateral frontal region. A significant activation was observed in gyrus rectus, orbitofrontal cortex, and superior temporal cortical areas. Lavender aromatherapy in addition to relaxation effect may enhance arousal level in some subjects. Inhalation of lavender for 3 minutes increases alpha power of EEG as decreases anxiety and brings the subject to a better mood in 40 healthy adults - it increases in theta (4–8 Hz) and alpha (8–13 Hz) wave activity. Lavender oil administered alone in an aroma stream shows modest efficacy in the treatment of agitated behaviour in patients with severe dementia and causes a significant improvement in cognitive function in elderly patients suffering from 5 different forms of dementia Lavender elicited a significant dose-dependent reduction in both inhibitory and excitatory transmission, with a net depressant effect on neurotransmission References [1] https://www.researchgate.net/publication/288053919 _Effects_of_essential_oils_used_in_aromatherapy_on_the_autonomic_nervous_system_A_ study_using_three_different_methods [2] http://libres.uncg.edu/ir/uncg/f/M_Shattell_HealingScents_2008.pdf [3] https://www.mitchmedical.us/essential-oils/psychopharmacology-of-essential-oils.html [4] https://www.ncbi.nlm.nih.gov/pubmed/16114490 [5] https://www.scirp.org/Journal/PaperInformation.aspx ... [6] https://dx.doi.org/10.3758/s13414-015-0955-9 [7] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3231408/ [8] https://www.ncbi.nlm.nih.gov/pubmed/30087294 [9] https://www.ncbi.nlm.nih.gov/pubmed/12686756 [10] https://www.ncbi.nlm.nih.gov/pubmed/30956723 [11] https://www.ncbi.nlm.nih.gov/pubmed/11509195 [12] https://www.ncbi.nlm.nih.gov/pubmed/30627659 [13] https://www.ncbi.nlm.nih.gov/pubmed/30753589 [14] https://www.ncbi.nlm.nih.gov/pubmed/30483833 6