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The Future of CBD in Georgia

Stress-Induced Anxiety Acute



  • Stress-Induced Anxiety Acute
  • Stress Takes a Toll on Your Body and Mind
  • Explore Everyday Health
  • Nov 28, In the weeks after a traumatic event, you may develop an anxiety disorder called acute stress disorder (ASD). People with ASD have symptoms similar to those seen in post-traumatic stress disorder (PTSD). Who’s at risk for acute stress disorder?. May 25, Stress and anxiety are a normal part of life, but in some people, they can become bigger issues. Learn what causes stress and anxiety and how. Whether in good times or bad, most people say that stress interferes at least moderately with their lives. Chronic stress can affect your health, causing symptoms.

    Stress-Induced Anxiety Acute

    The effects of stress can include forgetfulness, sexual problems, insomnia, and hair loss. When most of us think of the physical effects of stress , our minds jump to common complaints like headaches and upset stomachs. Stress, however, can affect many aspects of physical and mental health, ranging from hair, teeth, and skin to memory and concentration skills, and even how well we sleep.

    The good news is while these problems may seem serious, stress relief can lead to real improvements in your overall health and well-being. The United States of Stress. Some amount of hair loss is normal — strands fall out over time and get replaced by new ones. Known as telogen effluvium, this diffuse and often stress-induced hair loss may not happen right away. In fact, it may take weeks or months after the stressful event for the hair to actually shed. Fortunately, after six to eight months this type of hair loss often improves.

    We all have our moments of not being able to find our car keys, but research shows that the more stress we are under, the more frequent these mental lapses may become. But before jumping to conclusions, take a step back and consider whether any chronic stress in your life may be playing a role in memory issues. Regular brushing, flossing, and dental check-ups — most of us are well-versed in what it takes to keep our teeth healthy. But how many of us realize that the effects of stress can impact dental health?

    During the day and even while sleeping, people under stress may clench their teeth or grind them back and forth against one another.

    This action, called bruxism, can not only wear down and damage your teeth, but may also cause temporomandibular joint problems TMJ , leading to severe jaw and neck pain. According to the American Academy of Dermatology, our internal thoughts and feelings can actually affect our external appearance. This is particularly true when it comes to stress. Stress can worsen pre-existing conditions including rosacea, psoriasis , and acne, as well as dehydrate the skin, permitting allergens, bacteria, and pollutants to irritate it.

    For individuals struggling with alcohol or drugs , stress can wreak havoc on efforts to remain substance-free. Even for people who have abstained for a long time, stress can play a significant role in contributing to a relapse. Interestingly, not only can stress in adulthood contribute to substance abuse, but experiencing a severe psychosocial stressor during childhood can also increase your risk for drug or alcohol abuse as an adult.

    The effects of stress can extend to the bedroom. While most men may experience erectile dysfunction from time to time, when it happens frequently, its underlying cause should be investigated. Administration of a selective CRF1 receptor antagonist reversed the high corticosterone-induced anxiety-like behavior Myers et al.

    It was found that administration of urocortin, a CRF1 and 2 receptors agonist, into the BLA promoted a long lasting anxiety-like behavior in rats, which showed a prominent reduction in both spontaneous and stimulation-evoked inhibitory postsynaptic currents IPSCs Rainnie et al.

    These results suggest that stress-induced excessive CRF might induce a depression of local GABAergic inhibition and a resultant hyperexcitability of the amygdala. Other than the internal activation of HPA axis and excess secretion of stress hormones, short-term or long-term exposure to external stressors can induce hyperactivity of amygdala.

    Stress can induce various alterations of neurotransmission system in amygdala, mainly in GABA receptors adaption, the GABAergic inhibition and the synaptic neurotransmission. Lasting hyperactivity in amygdala might contribute to higher susceptibility to stress-related neuropsychiatric diseases. Enduring high GABAergic inhibition in amygdala contributes to the resistance from various physiological and environmental stressors stimuli.

    Whether the impaired GABAergic control and hyperactivity in amygdala under stress exposure contribute to the pathogenesis of the neuropsychiatric diseases is worthy of investigation. Amygdala activation followed stress exposure is extensively reported in electrophysiology studies, while the majority of such studies focus on effect of single external stressor on the firing rate or action potentials in amygdala neurons.

    Few researches put emphasis on the long lasting stress animal models and their consequent anxiety- or depression-like behavior alterations. A striking literature investigated the effects of both chronic immobilization and unpredictable stress on the GABAergic inhibitory modulation in amygdala. In contrast to the phasic inhibition, tonic inhibition is characterized by persistent inhibitory currents via continuously activation of extrasynaptic GABAA-Rs resulting from ambient GABA release Carver and Reddy, GABAergic inhibitory control in BLA depends on both GABAergic phasic and tonic inhibition under resting state and the latter one contributes to sustaining a high threshold of activating the amygdala Davern et al.

    A possible explanation for the unaffected phasic inhibition is that the impairment of phasic inhibition might occur instantly following exposure to stressor and recover in the stress-free phase. Furthermore, they also found that the long-lasting loss of tonic inhibition impaired the ability of GABA to suppress neuronal firing. Another interesting result was that long-term exposure 6—8 days and daily 2 h exposure both reduced the tonic currents while no significance was detected in short-term exposure group and daily 15 min exposure group Liu et al.

    In addition, Aroniadou-Anderjaska1 et al. Notably, Rajbhandari et al. Taken together, acute or chronic exposure to external stressors can dampen the GABAergic inhibition of BLA in different manner through which both acute and chronic stress can overly activate the downstream brain regions and contribute to abnormal anxiogenic-like responses. Whereas the opposite results exist, Tzanoulinou S et al. These results suggest that stress-induced reduction of GABAA-Rs expression, indicating an impaired GABAergic transmission in amygdala, might affect the vulnerability to stress-induced behavioral abnormality.

    Different experimental conditions and procedure might explain the paradoxical results. Also, genetic factors, affecting the adaptive expression of GABAA-Rs followed stress, might result in the susceptivity to stress-induced neuropsychiatric diseases Sarro et al.

    As we mentioned above, impaired extrasynaptic GABA receptors-mediated tonic inhibition contributes to the neuronal hyperactivity induced by chronic stress in BLA. The available studies mainly focus on the expression and sensitivity changes of GABAA-Rs followed stress and few of them discriminate these two types of receptors. Since the expression of GABAA-Rs displayed a tendency to be reduced followed stress exposure, this might explain the suppressed GABAergic inhibition in amygdala under stress conditions at molecular level.

    Previous research has found that patients with mood disorder, particular depression and anxiety, had a lower GABA levels in plasma and cerebral spinal fluid than control Petty and Sherman, Stress caused a reduction of glutamic acid decarboxylase GAD expression in amygdala, both in mRNA level and protein level in amygdala of stressed mice Gilabert-Juan et al. However, opposite results showing that increased GABA levels in the venous blood of amygdala were also reported followed exposure to predator stress Cook, Taken together, due to the limitation of current experimental methods, the neurotransmitter level remains relatively low-sensitivity to be an indicator or biomarker to assess amygdala's response to different stressor stimuli.

    Contradictory results still exist and need to be further studied. Lately, an emerging hypothesis revealed that the N-methyl-D-aspartate receptor NMDAR -dependent synaptic plasticity changes might implicate the pathogenesis of mood disorders Gerhard et al. Thus it's appropriate to investigate the stress-induced synaptic plasticity alterations in amygdala and its interrelation with neuropsychiatric diseases. Although the behavioral evidence is still absent, the glutamate-mediated synaptic neurotransmission alterations appear to be involved in the potential mechanism of stress-induced hyperactivity of amygdala.

    Chronic restraint stress can reduce cannabinoid receptor type 1 CB1 -mediated decrement of GABAergic synaptic transmission in BLA, in contrast with that, exposure to adverse acute stressors can cause a transient enhancement in short-term eCB signaling in the CeA Ramikie and Patel, Pharmacology experiments showed that intra-CeA administration of CB1-selective antagonists prevented the acute stress-induced behavior impairment Li et al.

    Thus, eCB-CB1 signaling-mediated synaptic alterations in BLA-CeA microcircuits of amygdala might play a critical role in the emotional processing following external stressors.

    The neuronal and synaptic alterations induced by stress appear to manifest as long-lasting morphological changes and structural adaption in amygdala, which might underlie the development of anxiety or other mood disorders Kim et al. It was found that after 21 days of stress-free recovery, chronic immobilization stress can even exhibit dendritic growth on spiny neurons of BLA, accompanying with enhanced long-lasting anxiety behaviors Vyas et al.

    It was found that a single immobilization stress led to a gradual increment of spine density on principal neurons of the BLA accompanying with enhanced anxiety-like behavior.

    Such morphological and behavioral alterations showed up 10 days after the acute stress exposure Mitra et al. These results indicate that the generation of acute stress-induced synaptic alterations needs more time.

    However, chronic or repeated stress can instantly lead to a robust and persistent enhancement of spinogenesis and anxiety-like behaviors. Stress causes reduction of brain derived neurotrophic factor BDNF expression and the mechanistic target of rapamycin mTOR in synapse, consequently contributing to the loss and atrophy of specific synapse in the brain regions implicated in depression, particularly the PFC and the hippocampus Marsden, ; Abelaira et al. Mounts of evidence have showed that the expression of BDNF in amygdala was increased after exposure to stress Bennett and Lagopoulos, The PSD and synaptophysin are well known as synapse-related proteins which can act as markers of synaptogenesis or synaptic potentiation.

    Furthermore, Yi et al. Thus, the expression of BDNF in amygdala exhibited a tendency to increase followed restraint stress and this detected increment is in accordance with the promotion of spinogenesis in BLA induced by chronic stress.

    Together, chronic stress might induce synaptogenesis and synaptic incorporation in BLA synapses, while the precise relationship between the structural and functional synaptic changes of other nucleus of amygdala and the development of stress-related neuropsychiatric disease is still obscure. Thus, further evidence is needed to elucidate the deeper mechanisms. Above all, three remarkable issues arise up and need further investigation. The first is the distinct regulatory role of different subregions within the amygdala.

    Furthermore, majority of electrophysiology studies illuminated that the neurons of BLA prefer to be evoked comparing with the neurons of CeA and other subregions of amygdala. The distinct role of these different subregions within the amygdala needs to be further investigated. The second issue is that whether the individual difference of GABAA-Rs adaption and morphological alterations induced by long lasting stress is affected by inherited genetic factors, which ultimately contribute to the individual susceptibility to the stress-induced neuropsychiatric diseases.

    The last one is the different pathological mechanisms of amygdala adapted to acute and chronic stress. Electrophysiology results indicated that acute stress could impair the phasic inhibition which occurred instantly following exposure to stressor and then recovered in the stress-free phase. In contrast to the acute stress, chronic stress was reported to impair the tonic inhibition in amygdala and consequently affect the ability of GABA to suppress neuronal firing.

    The morphological alterations of amygdala to acute stress can be accumulated. The effect of long lasting synaptic alterations induced by stress is manifested as synaptic morphological adaption. Significantly, the restructuring of dendrite and spines in amygdala is companied by stress-related behavior abnormalities.

    However, whether regulating the synaptic plasticity is involved in the underlying mechanisms of available antidepressant and anxiolytic therapy is still unclarified. In conclusion, at the cellular and molecular level there are still inconsistent neurological alterations of the amygdala in various stress models. It's still argued that the hyperactivity and hyperresponsiveness of amygdala induced by stress is the primary predisposing factor of neuropsychiatric diseases.

    Although intra-amygdala administration of antidepressants or anxiolytic agents has been reported to inhibit the hyperactivity of amygdala and reverse the impairment of anxiety and depressive behaviors, the potential therapeutic property of amygdala needs to be deeply investigated. Future studies should take the severity and duration of stressor stimuli into consideration. Mounts of animal studies have shown that stress-related disorders, especially anxiety, depression and PTSD, are characterized by hyperactivity or hyperreactivity of the amygdala.

    It is well known that the amygdala plays a critical role in integrating sensory information. Amygdala can integrate the sensory information and subsequently transform them into behavioral output as a response to external stimuli through specific neural circuit.

    Besides, an important physiologic response to stress is the hyperactivity of the HPA axis, which is paralleled with the amygdala's response. The stress-induced HPA axis hyperactivity strengthens the amygdala through regulating the neuroendocrine system. In turn, the activated amygdala can reciprocally stimulate the neuronal projection to PVN.

    The crucial alterations of stress-induced neurotransmission and synaptic plasticity in amygdala are intricate. The hyperactivity and hyperresponsiveness of amygdala followed stress attributes to the impaired GABAergic inhibition.

    The molecular mechanisms and potential role of stress-induced synaptic remodeling and increment of BDNF in specific amygdala nucleus are still obscure and need further investigations. All authors approved the final version of the manuscript for submission. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

    The role of mTOR in depression and antidepressant responses. The central nucleus of the amygdaloid body of the brain: Reduced GABAergic inhibition in the basolateral amygdala and the development of anxiety-like behaviors after mild traumatic brain injury. Importance of the glucocorticoid stress response in a changing world: Behavioral profiling as a translational approach in an animal model of posttraumatic stress disorder.

    Mechanisms regulating GABAergic inhibitory transmission in the basolateral amygdala: Amino Acids 32, — Stress sensitivity and the development of affective disorders. BDNF control of dendritic-spine formation and regression. Enhanced amygdala and medial prefrontal activation during nonconscious processing of fear in posttraumatic stress disorder: Inhibition of corticotropin releasing factor expression in the central nucleus of the amygdala attenuates stress-induced behavioral and endocrine responses.

    Control of the serotonergic system by the medial prefrontal cortex: Structural and synaptic plasticity in stress-related disorders. Chronic restraint stress down-regulates amygdaloid expression of polysialylated neural cell adhesion molecule. GABAA receptor dysfunction contributes to high blood pressure and exaggerated response to stress in Schlager genetically hypertensive mice. Role of dopamine receptor mechanisms in the amygdaloid modulation of fear and anxiety: GABA receptors inhibited by benzodiazepines mediate fast inhibitory transmission in the central amygdala.

    Synaptic plasticity and depression: Amygdala microcircuits controlling learned fear. Amygdala inhibitory circuits and the control of fear memory. Social stress in tree shrews as an animal model of depression: The role of the forebrain glucocorticoid receptor in acute and chronic stress. Emerging treatment mechanisms for depression: Chronic stress induces changes in the structure of interneurons and in the expression of molecules related to neuronal structural plasticity and inhibitory neurotransmission in the amygdala of adult mice.

    The central amygdala as an integrative hub for anxiety and alcohol use disorders. Role in autonomic, neuroendocrine, and behavioral responses to stress. Cortical connectivity and sensory coding. The role of CRF in behavioral aspects of stress. Stress, the brain, and mental illness. Neurobiology of chronic mild stress: Lack of feedback inhibition on rat basolateral amygdala following stress or withdrawal from sedative-hypnotic drugs.

    GABA A receptor trafficking and its role in the dynamic modulation of neuronal inhibition. Short- and long-term effects of juvenile stressor exposure on the expression of GABAA receptor subunits in rats.

    Stress Takes a Toll on Your Body and Mind

    Children with acute stress disorder may also experience anxiety related to their Causes. A person must be exposed to a traumatic event to be at risk for acute. Mar 8, The extended amygdala is critically implicated in mediating acute and chronic stress responsivity and anxiety-like behaviors. The bed nucleus. May 16, Role of allopregnanolone biosynthesis in acute stress-induced anxiety-like behaviors in mice. Yoshizawa K(1), Okumura A(1), Nakashima K(1).

    Explore Everyday Health



    Children with acute stress disorder may also experience anxiety related to their Causes. A person must be exposed to a traumatic event to be at risk for acute.


    Mar 8, The extended amygdala is critically implicated in mediating acute and chronic stress responsivity and anxiety-like behaviors. The bed nucleus.


    May 16, Role of allopregnanolone biosynthesis in acute stress-induced anxiety-like behaviors in mice. Yoshizawa K(1), Okumura A(1), Nakashima K(1).


    Feb 13, Stress and anxiety share many of the same physical symptoms, making it you pull off that deadline you thought was a lost cause, it's positive.


    Acute stress reaction is a psychological condition arising in response to a terrifying or traumatic event, or witnessing a traumatic event that induces a strong emotional response within . Symptoms include depression, anxiety, withdrawal, confusion, paranoia and sympathetic hyperactivity. The APA officially included the term.

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