Essential oils, smell, brain, healing

Connie b. Dellobuono
Connie b. Dellobuono, Health author and blogger at , student of nurse midwifery

Most inhaled oils can have psychoactive properties since they are electrically charged chemicals and the brain is also charged.


Citrus Scent Inhibits Liver Cancer

Citrus Scent Inhibits Liver Cancer

Essential oils protect not only from bacteria, viruses and fungi

Essential oils occur in many plants, protecting them through their antibacterial, antiviral and fungicidal properties. It has been recently discovered that terpenes, the oils’ main components, can also inhibit the growth of different cancer cells, including liver cancer. Their function had not previously been fully understood.

Olfactory receptors not just in the nose

Terpenes can trigger signalling processes in cells by activating olfactory receptors. Those receptors are mainly located in the nose, but they have been proved to occur in all types of human tissue, including skin, prostate and spermatozoa. Carcinogenesis and cancer growth are likewise significantly affected by terpenes, even though it has not been understood which function exactly they fulfil.

This image shows the calcium influx into the liver cancer cells.

Terpene triggers signalling pathway in the cell

In order to find this out, the researchers from Bochum utilised a cellular model of hepatocellular carcinoma, a common liver tumour. They exposed the cells to a subset of terpenes with different concentrations, and monitored their reactions. It emerged that two of the eleven terpenes tested resulted in a significant increase in calcium concentration in the cells: (-)-citronellal and citronellol. During a follow-up analysis, the researchers focused on (-)-citronellal and scanned for a receptor into which the terpene has to fit like a key into a lock. They demonstrated that the decisive olfactory receptor OR1A2 occurs in liver cells and is responsible for detection of the citrus scent and cellular reaction. If the option for producing that receptor had been removed from the cells, they did no longer react to the terpene. The researchers, moreover, succeeded in tracking the signalling pathway which the terpene uses for increasing calcium concentration inside the cells, thus reducing cell growth. “These results are yet another example for the significance of olfactory receptors outside the nose, and they give rise to hope that new drugs with no severe side effects may be developed for cancer therapy.”


The hepatocellular carcinoma is the most common primary tumour of the liver. It is the third most common tumour-induced cause of death. According to current estimations, approx. 8,900 people (6,200 men, 2,700 women) contract this form of cancer in Germany every year.

Contact: Dr Hanns Hatt – Ruhr-University Bochum
Source: Ruhr-University Bochum press release
Image Source: The image is credited to RUB, Lehrstuhl Hatt and is adapted from the press release
Original Research: Abstract for “Monoterpene (-)-citronellal affects hepatocarcinoma cell signaling via an olfactory receptor” by Désirée Maßberg, Annika Simon, Dieter Häussinger, Verena Keitel, Günter Gisselmann, Heike Conrad, and Hanns Hatt in Archives of Biochemistry and Biophysics. Published online December 13 2014 doi:10.1016/

Hospital aroma and smell of Rosemary can aid children’s working memory

Do you like the smell of the hospital?

If you are recovering from your illness, it is best to stay at home in the company of a caring caregiver.

The brain is influenced by the smell of our environment. Some carbon monoxide poisoning and other toxic chemicals affect our brain. Some essential oils can influence our brain. Can you heal your cells from the aroma of various plants and oils?

I use lavender essential oils to our senior clients to calm them during the massage. I cooked cinnamon, vanilla and rosemary in many dishes to increase appetite.


Image shows a fat mouse and a thin mouse.


According to a new study, your sense of smell could be responsible for weight gain. Using mice, researchers noticed that those who lost their sense of smell also lost weight, while those mice with a super sense of smell gained more weight on a high fat diet than mice with a regular sense of smell. Findings suggest odor may play an important role in calorie burning processes; if you can’t smell your food, you may burn it rather than store it. READ MORE…

Artificially intelligent nanoarray analyzes 17 diseases from breaths


Schematic representation of the concept and design of the study. It involved collection of breath samples from 1404 subjects in 14 departments in nine clinical centers in five different countries (Israel, France, USA, Latvia, and China). The population included 591 healthy controls and 813 patients diagnosed with one of 17 different diseases: lung cancer, colorectal cancer, head and neck cancer, ovarian cancer, bladder cancer, prostate cancer, kidney cancer, gastric cancer, Crohn’s disease, ulcerative colitis, irritable bowel syndrome, idiopathic Parkinson’s, atypical Parkinsonism, multiple sclerosis, pulmonary arterial hypertension, pre-eclampsia, and chronic kidney disease. One breath sample obtained from each subject was analyzed with the artificially intelligent nanoarray for disease diagnosis and classification, and a second was analyzed with GC-MS for exploring its chemical composition.

The present study reports on an artificially intelligent nanoarray based on molecularly modified gold nanoparticles and random network of single-wall carbon nanotubes for noninvasive diagnosis and classification of 17 different diseases from exhaled breath. The nanoarray was used for the practical evaluation of 1404 subjects in nine clinical settings worldwide. Blind experiments with the artificially intelligent nanoarray showed that 86% accuracy could be achieved, allowing discrimination between each pair of the diseases, and that each disease has its own unique volatile molecular print compared to both healthy controls and other diseases.

The artificially intelligent nanoarray had a low or no vulnerability to clinical and demographical confounding factors. The findings by nanoarray were examined by an independent analytical technique, GC-MS. This analysis found 13 exhaled VOCs associated with various diseases, and their composition differs from one disease to another, thereby validating the nanoarray results. While further and larger translational studies are required to validate these findings, this work provides a shuttling pad for in statu nascendi “volatolomics” field (the omics of volatile biomarkers), as well as a method for obtaining affordable, easy-to-use, inexpensive, and miniaturized tools for personalized screening, diagnosis, and follow-up of a range of diseases.

Control samples ruled out the possibility of coincidence and/or external biases. Of special importance, results from the artificially intelligent nanoarrays support the hypothesis that similarities in pathophysiological processes are expressed in quite similar breath patterns. The results also indicated that the adjustment for confounding factors was successful. The subgroups were not clustered according to similarities in demographic features or geographical location, which also stresses that the artificially intelligent nanoarray analysis is less sensitive to possible confounding factors since we have seen in some cases trends in the control groups that were like those seen among the diseases.

In some cases, two or more diseases shared the same control group, as in (1) Crohn’s disease, ulcerative colitis, and irritable bowel syndrome; (2) kidney and bladder cancer; and (3) idiopathic and atypical Parkinsonism. Therefore, the last analysis was not applicable in these cases (Figure 3, hatched boxes). In contrast to the high accuracy achieved among diseases (86%), the classification of the control samples resulted in random results with a total accuracy of 58%, ruling out the possibility of coincidence. In certain comparisons, the results were higher than the arbitrary classification of the control subjects.

In some cases, two or more diseases shared the same control group, as in (1) Crohn’s disease, ulcerative colitis, and irritable bowel syndrome; (2) kidney and bladder cancer; and (3) idiopathic and atypical Parkinsonism. Therefore, the last analysis was not applicable in these cases (Figure 3, hatched boxes). In contrast to the high accuracy achieved among diseases (86%), the classification of the control samples resulted in random results with a total accuracy of 58%, ruling out the possibility of coincidence. In certain comparisons, the results were higher than the arbitrary classification of the control subjects.

The artificially intelligent nanoarray analyzes the collective breath VOC patterns in a black-box approach. To identify and quantify the specific VOCs associated with each disease state, a second breath sample obtained from all participants was analyzed by GC-MS. This identified over 150 different VOCs in the different cohorts, but only 35 VOCs were selected for further investigation. The choice was made on the following criteria: (i) they were common to >70% of the total population (patients and controls); (ii) they were easily identified and verified by the analysis of pure standards; and (iii) they had concentrations in ambient air samples at least 10-fold lower (on average) than in the equivalent breath samples. Owing to the demographic differences between the groups, multiple linear regression for the abundance of each VOCs was first carried out to explore any possible correlation between abundance and the covariates (age, sex, location, and smoking status). The results indicate that the abundances of 15 VOCs were negatively correlated with age and/or smoking; three of them were also correlated with gender. However, there was no significant correlation between the abundance of those VOCs and the sampling site. Therefore, each VOC with significant correlations (p < 0.05) was adjusted according to the calculated coefficient corresponding to the confounding element (see SI, Table S16).

Regression models applied to the raw GC-MS data showed that the abundance of exhaled VOCs was affected by some common confounding factors. A number of the VOCs was affected by age and/or smoking habits (e.g., 2-ethylhexanol, 3-methylhexane, 5-ethyl-3-methyloctane, acetone, ethanol, ethyl acetate, ethylbenzene, isononane, isoprene, nonanal, styrene, toluene, and undecane), whereas three of them were also affected by the gender of the subject (isononane, nonanal, and undecane). This effect stemming from the first part of the VOCs could be explained by the relationship between the anatomical and physiological changes in the respiratory system and circulation associated with aging and/or smoking injury.(65) It includes stiffness and degeneration of the elastic fibers, fibrosis, aging-associated destruction of lung parenchyma, emphysema, and chronic bronchitis, mainly among smokers.(66) These alterations could easily affect the diffusion of VOCs through the blood–air barrier by altering the thickness or permeability of the epithelium (the so-called membrane conductance) or by reducing the total surface area of the membrane.(66) These factors could easily alter the flux, according to Fick’s first law, affecting the diffusion of gases in the exhaled air, eventually reducing/stressing the expression and/or concentrations of a wide range of the exhaled VOC components.(5) The effect stemming from the second part of the VOCs might be attributed to hormonal or structural gender-related differences.(67)

Neurons ‘Predict’ Drinking’s Restorative Effects Well Before They Unfold

By Leigh Beeson

A new UC San Francisco study shows that specialized brain cells in mice “predict” the hydrating effects of drinking, deactivating long before the liquids imbibed can actually change the composition of the bloodstream. The results stand in stark contrast to current views of thirst regulation, which hold that the brain signals for drinking to stop when it detects liquid-induced changes in blood concentration or volume.

Thirst neurons, located in the subfornical organ (SFO) of the brain, do make us thirsty when they sense that blood volume has dipped or when blood becomes too concentrated. But the same signaling mechanism can’t operate in reverse to alert us to stop drinking because thirst is satiated too soon after a person begins to drink, said UCSF’s Zachary Knight, PhD, senior author of the study, which appears in the August 3, 2016 issue of Nature. Nor can current theories explain why we usually like to drink something while we eat.

“You drink a glass of water and you instantly feel like your thirst is quenched, but it actually takes tens of minutes for that water to reach your blood,” said Knight, assistant professor of physiology. “You eat something salty and you instantly beginning to feel thirsty even though that food is just in your mouth. The dominant model that thirst is a response to changes in the blood didn’t explain that.”

After employing a technique that causes specific, targeted populations of neurons in the mouse brain to fluoresce brightly when active, they used fiber optic probes to measure the activity of SFO neurons when mice drank water. They found that SFO neuron activity shut off almost immediately after the mice started to drink and that the mice stopped drinking shortly thereafter. The brief time scale of these events suggests that, rather than acting only as monitors of blood composition, the SFO must also be linked to sensors in the mouth and throat that rapidly detect food and water consumption.

To confirm the relationship between oral-cavity sensors and SFO neurons, the research group deprived the mice of water overnight and used optogenetic methods – in which particular cells are genetically altered so light delivered via fiber optics can activate or inhibit those cells — to shut down SFO neuron activity when they were again given access to water. Despite the water deprivation, and the presumed changes in the blood that would cause, the mice didn’t drink. But as soon as the researchers stopped silencing the SFO neurons, the mice drank copiously.

The researchers used similar methods to explore why eating often prompts people to drink and why a drink’s temperature affects how refreshing we find it.

“When you sit down at a meal, it’s such a universal experience to have a beverage with you, and we’ve never understood why that is — why you take a bite of food and then take a drink of water,” said Christopher Zimmerman, lead author of the study and a UCSF Discovery Fellow in the Knight laboratory. “And almost everyone has had the experience of exercising or doing some sort of activity and becoming really thirsty, and almost viscerally feeling better after drinking a cold glass of water. But why does cold water seem to quench your thirst so much more rapidly?”

To answer the first question, mice that went without food for a night were given food the following morning but no water. SFO neurons lit up almost immediately as the mice began to eat. Mice who were allowed both food and water also experienced the increase in thirst neuron activity, and when the researchers tamped down the neurons’ activity, the mice reduced their water consumption (though they continued to eat).

When mice were given access to water bottles of varied temperatures, the researchers found that although all the mice drank enough water to turn off their SFO neurons, it required significantly fewer licks to deactivate SFO neurons if the water the mice drank was cold. The scientists zeroed in on temperature as a crucial factor in SFO activity by applying cold metal, similar to that found on animal water-bottle droppers, to the mice’s mouths. This proved as effective as cold water in shutting down the activity of SFO cells.

The new study is an extension of Knight’s previous work on hunger neurons in mice, for which he was awarded a National Institutes of Health New Innovator Award in 2015. In that research his team used similar techniques to record the activity of hunger neurons in mice for the first time and showed that these neurons shut off in response to the sight and smell of food well before the mice actually consumed anything — a surprising finding that parallels those in the new Nature study — just as thirst neurons “anticipate” the bodily changes that drinking will produce, hunger neurons shut down long before mice are actually satiated by eating.

The study was co-authored by Yen-Chu Lin, Erica Huey, and Gwendolyn Daly, research specialists in the Knight Lab, as well as David Leib, Ling Guo and Yiming Chen, students in the UCSF Neuroscience Graduate Program. The study was funded by a UCSF Discovery Fellowship, the New York Stem Cell Foundation, the the American Diabetes Association, Rita Allen Foundation, the McKnight Foundation, the Alfred P. Sloan Foundation, the Brain and Behavior Research Foundation, the Esther A. and Joseph Klingenstein Foundation, the Program for Breakthrough Biomedical Research, an NIH New Innovator Award, the UCSF Diabetes and Obesity Centers, and grants from the National Science Foundation and the National Institutes of Health.

UCSF is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. It includes top-ranked graduate schools of dentistry, medicine, nursing and pharmacy; a graduate division with nationally renowned programs in basic, biomedical, translational and population sciences; and a preeminent biomedical research enterprise. It also includes UCSF Health, which comprises two top-ranked hospitals, UCSF Medical Center and UCSF Benioff Children’s Hospital San Francisco, and other partner and affiliated hospitals and healthcare providers throughout the Bay Area.

Smell test could identify Alzheimer’s disease

sense of smell AD

New research suggests that the decreased ability to identify certain odors may signal early-stage Alzheimer’s disease and future cognitive decline.

The test – dubbed the University of Pennsylvania Smell Identification Test – was the focus of two studies presented at the Alzheimer’s Association International Conference in Toronto. Both studies were funded by the National Institute on Aging.

The memory area is the same area in the brain where odor information is stored. The lowest smell recognition has the greatest risk for Alzheimer’s disease.  Loss of sense of smell for peanut butter can be indicative of the presence of Alzheimer’s.


Olfactory sensory neurons project axons to the brain within the olfactory nerve, (cranial nerve I). These nerve fibers, lacking myelin sheaths, pass to the olfactory bulb of the brain through perforations in the cribriform plate, which in turn projects olfactory information to the olfactory cortex and other areas. The axons from the olfactory receptors converge in the outer layer of the olfactory bulb within small (~50 micrometers in diameter) structures called glomeruli.

Mitral cells, located in the inner layer of the olfactory bulb, form synapses with the axons of the sensory neurons within glomeruli and send the information about the odor to other parts of the olfactory system, where multiple signals may be processed to form a synthesized olfactory perception.

A large degree of convergence occurs, with twenty-five thousand axons synapsing on twenty-five or so mitral cells, and with each of these mitral cells projecting to multiple glomeruli. Mitral cells also project to periglomerular cells and granular cells that inhibit the mitral cells surrounding it (lateral inhibition).

Granular cells also mediate inhibition and excitation of mitral cells through pathways from centrifugal fibers and the anterior olfactory nuclei. Neuromodulators like Acetylcholine, Serotonin and Norepinephrine all send axons to the olfactory bulb and have been implicated in gain modulation, pattern separation and memory functions, respectively.

The mitral cells leave the olfactory bulb in the lateral olfactory tract, which synapses on five major regions of the cerebrum: the anterior olfactory nucleus, the olfactory tubercle, the amygdala, the piriform cortex, and the entorhinal cortex. The anterior olfactory nucleus projects, via the anterior commissure, to the contralateral olfactory bulb, inhibiting it.

The piriform cortex has two major divisions with anatomically distinct organizations and functions. The anterior piriform cortex (APC) is better associated with determining the chemical structure of the odorant molecules and whereas the posterior piriform cortex (PPC) is best known for its strong role in categorizing odors and assessing similarities between odors (e.g. minty, woody, citrus are odors which can be distinguished via the PPC despite being highly-variant chemicals and in a concentration-independent manner).

The piriform cortex projects to the medial dorsal nucleus of the thalamus, which then projects to the orbitofrontal cortex. The orbitofrontal cortex mediates conscious perception of the odor. The 3-layered piriform cortex projects to a number of thalamic and hypothalamic nuclei, the hippocampus and amygdala and the orbitofrontal cortex but its function is largely unknown. The entorhinal cortex projects to the amygdala and is involved in emotional and autonomic responses to odor. It also projects to the hippocampus and is involved in motivation and memory.

Odor information is stored in long-term memory and has strong connections to emotional memory. This is possibly due to the olfactory system’s close anatomical ties to the limbic system and hippocampus, areas of the brain that have long been known to be involved in emotion and place memory, respectively.

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