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ANXIETY/FEAR/STRESS –our health and what can we do.




It was always there in covid and post covid world it’s a global concern nightmare with no treatment and with health care we have –there happens to be just no hope.


Fear and anxiety are so interwoven that separating them is too scholastic. Almost right from toddler age and we are not even talking of the trauma of passage through a nine-inch tube from a mother’s womb to this earth. While infants feel stranger anxiety, toddlers fear separation anxiety. Young kids go through what is called “pretend” a mixture of imaginative creativity and older kids fear real-life dangers and it continues --- as we keep growing the baggage keeps growing bigger and bigger. The fear/anxiety syndrome just keeps changing shapes.


It’s like a load on a camel’s back whether in the sub-conscious mind or conscious mind –it’s in the mind. That means whether one takes its cognizance or not – it’s there.

This whole process is like a steel spring –its inherent strength permits it to keep expanding but then a time comes it can’t stretch anymore and with one extra load, it collapses . The mind works in the same way.


So fear/anxiety is a constant feature with humans and they impact human health via a lot of different paths ----there is no system in the body that is not impacted by them. Hormones in the body are extremely sensitive functions and impact all functions of the body and all of them are impacted by stress /anxiety /fear. So it’s very important to understand it.

Fear/anxiety and stress caused by it is just a thought and as Budha said –it’s not a stone being hurled by some outsider. It’s our own creation of reality (which physically does not exist) hence more dangerous as we can easily keep on adding its values.


In this note, we talk about what is and how essential oils can be used as a simple tool to reduce their impact.

Fear is an automatic neurophysiological state of alarm characterized by a fight or flight response to a cognitive appraisal of present or imminent danger (real or perceived). Anxiety is linked to fear and manifests as a future-oriented mood state that consists of a complex cognitive, affective, physiological, and behavioral response system associated with preparation for the anticipated events or circumstances perceived as threatening.

The significant mediators of anxiety in the central nervous system are thought to be norepinephrine, serotonin, dopamine, and gamma-aminobutyric acid (GABA). The autonomic nervous system, especially the sympathetic nervous system, mediates most of the symptoms.


The amygdala plays an important role in tempering fear and anxiety. Patients with anxiety disorders have been found to show heightened amygdala response to anxiety cues. The amygdala and limbic system structures are connected to prefrontal cortex regions, and prefrontal-limbic activation abnormalities may be reversed with psychological or pharmacologic interventions.

It is an established fact that the psychological path is far superior and sensible. The pharmacologic method is just not successful with a lot of side effects.


Pathophysiology


The exact mechanism is not entirely known. Anxiety can be a normal phenomenon in children. Stranger anxiety begins at seven to nine months of life (Munir et al., 2019). Anxiety symptoms and the resulting disorders are thought to be due to disrupted modulation within the central nervous system. Physical and emotional manifestations of this dysregulation are the result of heightened sympathetic arousal of varying degrees (Kaplan and Sadock, 1995).

Several neurotransmitter systems have been implicated to have a role in one or several of the modulatory steps involved. The most commonly considered are the serotonergic and noradrenergic neurotransmitter systems. In very general terms, it is thought that an under-activation of the serotonergic system and an over-activation of the noradrenergic system are involved (Ressler and Nemeroff, 2000, Munir et al., 2019). These systems regulate and are regulated by other pathways and neuronal circuits in various regions of the brain, resulting in the dysregulation of physiological arousal and the emotional experience of this arousal (Ressler and Nemeroff, 2000). Many believe that low serotonin system activity and elevated noradrenergic system activity are responsible for its development. Is, therefore, selective serotonin reuptake inhibitors (SSRI) and serotoninnorepinephrine reuptake inhibitors (SNRI) are the first-line agents for its treatment (Munir et al., 2019). Disruption of the gamma-aminobutyric acid (GABA) system has also been implicated because of the response of many anxiety spectrum disorders to treatment with benzodiazepines (Nutt, 2001). There has been some interest in the role of corticosteroid regulation and its relationship to symptoms of fear and anxiety. Corticosteroids may increase or decrease the activity of certain neural pathways, affecting not only behavior under stress but also the brain's processing of fear-inducing stimuli (Korte, 2001). Cholecystokinin has long been viewed as a neurotransmitter involved in regulating emotional states (Korte, 2001).


There is such careful orchestration between these neurotransmitters that changes in one neurotransmitter system invariably elicit changes in another, including extensive feedback mechanisms. Serotonin and GABA are inhibitory neurotransmitters that quieten the stress response (Coplan and Lydiard, 1998; Rush et al., 1998). All of these neurotransmitters have become important targets for therapeutic agents.

Many studies indicate that a genetic predisposition to developing an anxiety disorder is likely. However, environmental stressors clearly play a role, in varying degrees. All of the disorders are affected in some way by external cues and how they are processed and reacted to (Kaplan and Sadock, 1995).

Several studies have found elevated WBC count among depressed and anxious individuals (Pitsavos et al., 2006; Kobrosly and van Wijngaarden, 2010; Duivis et al., 2013; Aydin et al., 2016; Shafiee et al., 2017). Shafiee et al., 2017 reported that the mean WBC count increased with increasing severity of symptoms of depression and anxiety among men. Men (but not women) with severe anxiety symptoms had significantly higher values of RDW (p<0.001). Moreover, there was a negative association between red blood cells (RBC) and mean corpuscular hemoglobin (MCH) and symptoms of depression/anxiety. Pitsavos et al. (2006) observed that anxiety score is positively correlated with WBC count in women, but not in men. Since WBC count is an independent predictor of atherosclerosis and cardiovascular diseases (Loimaala et al., 2006; Madjid et al., 2004, Shafiee et al., 2017). RDW is a strong predictor of mortality and has an association with a variety of cardiovascular and thrombotic disorders (Montagnana et al., 2012; Patel et al., 2009, Shafiee et al., 2017). Therefore, higher levels of RDW among depressed and anxious individuals may predict a greater risk of developing cardiovascular diseases in these patients (Shafiee et al., 2017).

Shafiee et al., 2017 concluded that a positive association between depression/anxiety symptoms and levels of hematological inflammatory markers including WBC and RDW, persisted despite adjustment by potential confounders.


Biochemical Basis of Anxiety:

An exciting new line of research proposes that anxiety engages a wide range of neurocircuits. This line of research catapults to prominence two key regulatory centers found in the cerebral hemispheres of the brain— the hippocampus and the amygdala. These centers, in turn, are thought to activate the hypothalamic-pituitaryadrenocortical (HPA) axis (Goddard & Charney, 1997; Coplan & Lydiard, 1998; Sullivan et al., 1998). Researchers have long established the contribution of the HPA axis to anxiety but have been perplexed by how it is regulated. They are buoyed by new findings about the roles of the hippocampus and the amygdala.


The hippocampus and the amygdala govern memory storage and emotions, respectively, among their other functions. The hippocampus is considered important in verbal memory, especially of time and place for events with strong emotional overtones (McEwen, 1998). The hippocampus and amygdala are major nuclei of the limbic system, a pathway known to underlying emotions. There are anatomical projections between the hippocampus, amygdala, and hypothalamus (Jacobson & Sapolsky, 1991; Charney & Deutch, 1996; Coplan & Lydiard, 1998).


Amygdala is critical to fear responses. Sensory information enters the lateral amygdala, from which processed information is passed to the central nucleus, the major output nucleus of the amygdala. The central nucleus projects, in turn, to multiple brain systems involved in the physiologic and behavioral responses to fear. Projections to different regions of the hypothalamus activate the sympathetic nervous system and induce the release of stress hormones, such as CRH. The production of CRH in the paraventricular nucleus of the hypothalamus activates a cascade leading to the release of glucocorticoids from the adrenal cortex. Projections from the central nucleus innervate different parts of the periaqueductal gray matter, which initiates descending analgesic responses (involving the body's endogenous opioids) that can suppress pain in an emergency, and which also activates species-typical defensive responses (e.g., many animals freeze when fearful) (Davis, 1997 ).

Anxiety differs from fear in that the fear-producing stimulus is either not present or not immediately threatening, but in anticipation of danger, the same arousal, vigilance, physiologic preparedness, and negative effects and cognitions occur (LeDoux, 1996). Different types of internal or external factors or triggers act to produce the anxiety symptoms of panic disorder, agoraphobia, post-traumatic stress disorder, specific phobias, generalized anxiety disorder, and the prominent anxiety that commonly occurs in major depression. It is currently a matter of research to determine whether dysregulation of these fear pathways leads to the symptoms of anxiety disorders. It has now been established, using noninvasive neuroimaging, that the human amygdala is also involved in fear responses (Breiter et al., 1996). Fearful facial expressions have been shown to activate the amygdala in MRI studies of normal human subjects (Breiter et al., 1996). Functional imaging studies in anxiety disorders, such as PET studies of brain activation in phobias (Rauch et al., 1995), are also beginning to investigate the precise neural circuits involved in anxiety disorders.


What is especially exciting is that neuroimaging has furnished direct evidence in humans of the damaging effects of glucocorticoids. In people with post-traumatic stress disorder, neuroimaging studies have found a reduction in the size of the hippocampus. The reduced volume appears to reflect the atrophy of dendrites—the receptive portion of nerve cells—in a select region of the hippocampus. Similarly, animals exposed to chronic psychosocial stress display atrophy in the same hippocampal region (McEwen & Magarinos, 1997). Stress-induced increases in glucocorticoids specially corticosterone are thought to be responsible for the atrophy (McEwen, 1998). If the hippocampus is impaired, the individual is thought to be less able to draw on memory to evaluate the nature of the stressor (McEwen, 1998).

Pharmacological protocols include

Serotonin Receptor Modulators and Reuptake Inhibitors

Γ-Aminobutyric Acid Receptor Modulators (Benzodiazepines and Related Drugs)

Corticotrophin-Releasing Factor Modulators

Neurokinin Receptor Antagonists

Cholecystokinin B antagonists


And personally, I will say none of them are successful.

Therapeutic Effects of EOs


EOs are effective in alleviating symptoms of depression, anxiety, and stress in adults both below and over 60 years of age, respectively (Tsang, H.W and others 2015, Fung, J.K.K 2018) A great updated survey by (Fung and others 2021). And these sorts of facts have been now established. Even in hospital conditions, surgery patients and cancer patients and pushed as a positive adjacent protocol for anxiety management.


Based on what is known five years back we developed an anti-anxiety blend that has been pretty successful. And as we learned along the way a roll-on Vicks-type inhaler is more convenient, cheaper, and practical.

From Jan 1st it will be offered at an introductory price of rs 100. Inhaled via the nose (as that breaks the blood-brain barrier fastest). Depending on the level of anxiety one has inhalation can be for 1 to 3 minutes and continue with life.


Advantages

1. No side effects

2. Can be used on day to day basis even when symptoms are not strong.

3. The volume/ effect can be adjusted by time/number of times used.

4. Can be used by all age groups

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Please I need two

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