Nervous System, Trauma, and Shinrin Yoku

Trauma is considered to be a result of a single event, series of events, or set of circumstances, that is physically or emotionally harmful or threatening and that has lasting adverse effects on the individual’s functioning and well-being [1].

Individuals who have experienced traumatic events especially in childhood are at much higher risk of mental health problems throughout their lives [2].

Post-traumatic stress disorder (PTSD) is a consequence of trauma characterised by increased anxiety.

The feature of anxiety disorders is the prevalence of a displaced stress response in a situation when a stressor is not there or when it is not immediately cautionary. Therefore, a key to understanding anxiety is to understand how the stress response is regulated by the brain [3].

The stress response
is the coordinated reaction to threatening stimuli.
Its hallmarks are:
– avoidance behaviour
– increased arousal and vigilance
– activation of the sympathetic nervous system
– release of cortisol, a stress hormone, from the adrenal glands

Shinrin Yoku can serve as a preventive medicine agains stress to induce a relaxing state. Research shows that forest environments act on the endocrine system to reduce blood cortisol [4].

To understand how this response is regulated, we must focus on humeral reaction to stress, which is facilitated by the hypothalamic-pituitary-adrenal axis (HPA), of which hypothalamus is involved in coordinating suitable somatic-motor,  humoral, and viscero-motor, responses. 

In other words, The HPA axis regulates the secretion of cortisol from the adrenal gland [5]:

  • the hormone cortisol is released from the adrenal cortex in response to an elevation in the blood level of adrenocorticotropic hormone (ACTH); 
  • ACTH is released by the anterior pituitary gland in response to corticotropin-releasing hormone (CRH), which is the chemical messenger between the paraventricular nucleus of the hypothalamus and the anterior pituitary gland;
  • ACTH released by the pituitary gland is carried in the bloodstream to the adrenal gland (located above the kidney), where it prompts cortisol freeing;
  •  cortisol contributes to the body’s physiological response to stress.

It is clear thus that stress response is linked to hypothalamus’s neurones that contains CRH. 

As an example, studies on mice shows that when CRH is over-expressed in genetically engineered mice, they show increased anxiety-like behaviours, but  when the receptors for CRH are genetically removed, the animals have less anxiety-like behaviour compare with normal mice [6].

The CRH neurons are controlled by the amygdala and the hippocampus. 

The amygdala is critical to fear responses: sensory information enters the baso-lateral amygdala, where it is processed and passed on to neurons in the central nucleus of amygdala – the stress response follows, when it is activated.  fMRI research indicates that the activation of undesirable nature is associated with some anxiety disorders [7]. In addition neurons  of the bed nucleus of the stria terminalis (BNST), so called the extended amygdala and located in the basal forebrain, activate HPA axis and the stress response [8].

The HPA axis is also regulated by the hippocampus by inhibiting CRH release  when circulating cortisol levels get too high [9]. The hippocampus contains also  numerous glucocorticoid receptors that respond to the cortisol released from the adrenal gland and are found in frontal cortex and amygdala – regions involved in memory processing and emotional regulation [11].

Studies on animals shows that constant exposure to chronic stress (high levels of cortisol for a prolong period of time) can cause damage to hippocampal neurons [10]. This finding has been confirmed in the human brain of people suffering for PTSD [12].

Anxiety disorders have been related to both hyperactivity of the amygdala and diminished activity of the hippocampus caused by high levels of circulating cortisol, which may effect human cognition.


[1] Center for Substance Abuse Treatment (US). (2014). Trauma-Informed Care in Behavioral Health Services. Substance Abuse and Mental Health Services Administration (US).

[2] Devi, F., Shahwan, S., Teh, W. L., Sambasivam, R., Zhang, Y. J., Lau, Y. W., Ong, S. H., Fung, D., Gupta, B., Chong, S. A., & Subramaniam, M. (2019). The prevalence of childhood trauma in psychiatric outpatients. Annals of general psychiatry, 18, 15.

[3] McEwen, B. S., Bowles, N. P., Gray, J. D., Hill, M. N., Hunter, R. G., Karatsoreos, I. N., & Nasca, C. (2015). Mechanisms of stress in the brain. Nature neuroscience, 18(10), 1353–1363.

[4] Park, B. J., Tsunetsugu, Y., Kasetani, T., Kagawa, T., & Miyazaki, Y. (2010). The physiological effects of Shinrin-yoku (taking in the forest atmosphere or forest bathing): evidence from field experiments in 24 forests across Japan. Environmental health and preventive medicine, 15(1), 18–26.

[5] Herman, J. P., McKlveen, J. M., Ghosal, S., Kopp, B., Wulsin, A., Makinson, R., Scheimann, J., & Myers, B. (2016). Regulation of the Hypothalamic-Pituitary-Adrenocortical Stress Response. Comprehensive Physiology, 6(2), 603–621.

[6] van Gaalen, M. M., Stenzel-Poore, M. P., Holsboer, F., & Steckler, T. (2002). Effects of transgenic overproduction of CRH on anxiety-like behaviour. The European journal of neuroscience, 15(12), 2007–2015.

[7] Etkin, A., & Wager, T. D. (2007). Functional neuroimaging of anxiety: a meta-analysis of emotional processing in PTSD, social anxiety disorder, and specific phobia. The American journal of psychiatry, 164(10), 1476–1488.

[8] Lebow, M., Chen, A. Overshadowed by the amygdala: the bed nucleus of the stria terminalis emerges as key to psychiatric disorders. Mol Psychiatry 21, 450–463 (2016).

[9] Dahmen, B., Puetz, V. B., Scharke, W., von Polier, G. G., Herpertz-Dahlmann, B., & Konrad, K. (2018). Effects of Early-Life Adversity on Hippocampal Structures and Associated HPA Axis Functions. Developmental neuroscience, 40(1), 13–22. 

[10] McEwen, B. S., Nasca, C., & Gray, J. D. (2016). Stress Effects on Neuronal Structure: Hippocampus, Amygdala, and Prefrontal Cortex. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 41(1), 3–23.

[11] Lupien, S. J., Juster, R. P., Raymond, C., & Marin, M. F. (2018). The effects of chronic stress on the human brain: From neurotoxicity, to vulnerability, to opportunity. Frontiers in neuroendocrinology, 49, 91–105.

[12] Logue, M. W., van Rooij, S., Dennis, E. L., Davis, S. L., Hayes, J. P., Stevens, J. S., Densmore, M., Haswell, C. C., Ipser, J., Koch, S., Korgaonkar, M., Lebois, L., Peverill, M., Baker, J. T., Boedhoe, P., Frijling, J. L., Gruber, S. A., Harpaz-Rotem, I., Jahanshad, N., Koopowitz, S., … Morey, R. A. (2018). Smaller Hippocampal Volume in Posttraumatic Stress Disorder: A Multisite ENIGMA-PGC Study: Subcortical Volumetry Results From Posttraumatic Stress Disorder Consortia. Biological psychiatry, 83(3), 244–253.

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