The philosophical concept of ‘well-being’ refers to how well a person’s life is going for them, encompassing more than just health. Health may contribute to well-being, but it is not the sole component. Philosophers also consider the ‘negative’ aspects of a person’s life, such as experiencing terrible agony, which might result in a negative well-being state. They distinguish well-being from terms like ‘welfare’ and ‘happiness,’ the latter of which may refer to short-lived states of contentment in everyday language but often has a broader scope in philosophical discussions. The term ‘well-being’ is preferred over ‘happiness’ to encompass the broader notion of what makes life good for an individual, including non-human entities like plants. This concept, linked to the Greek term ‘eudaimonia,’ highlights the idea of flourishing rather than mere happiness. Aristotle’s view that a friend’s well-being is closely tied to one’s own suggests that well-being can be interconnected without conflating individual interests.

While understanding well-being from a philosophical perspective is important, we must also consider the physiological evidence on well-being, which will be useful in the context of forest bathing, forest therapy, or Shinrin Yoku. Mental health, as defined by the World Health Organization, is “a state of well-being in which the individual realizes their own abilities, can cope with the normal stresses of life, can work productively, and is able to make a contribution to their community” (World Health Organization, 2005). This definition emphasizes that mental health encompasses more than just the absence of mental disorders, including the broader concept of well-being. 

In the past two decades, interest in well-being and happiness has surged, with an increasing number of scientific publications across various disciplines. Well-being is recognized as a protective factor linked to overall physical and mental health (Diener et al., 2017; Greenspoon and Saklofske, 2001). Research shows that the positive effects of well-being are independent of the negative impacts of conditions like depression, highlighting the importance of studying well-being (Howell et al., 2007). Additionally, well-being is associated with positive life outcomes, including longer, healthier lives (James et al., 2019; Kim et al., 2019; Zaninotto and Steptoe, 2019), academic achievement, happy marriages, and increased productivity at work ( Lyubomirsky et al., 2005; Maccagnan et al., 2019; Oswald et al., 2015).

Behavioral and molecular genetics studies indicate that biological and physiological factors significantly influence individual differences in well-being. Recent genome-wide association studies (GWAS) have identified specific genetic variants associated with well-being with findings suggesting gene enrichment in the subiculum (part of the hippocampus) and GABAergic interneurons as related to the well-being spectrum (Baselmans et al., 2019a). These genetic discoveries provide insights into the physiology of well-being, though comprehensive research on physiological measures remains limited as of today.

So what are these physiological markers?

HORMONES

Hormones are chemical messengers produced by the endocrine glands and released into the bloodstream, traveling to various organs and tissues to regulate physiological processes, including growth, metabolism, and reproduction. These hormones are present in different biological fluids such as blood, urine, saliva, and even hair. Although both hormones and neurotransmitters serve as messengers, they differ significantly in their site of release, action, and speed. Hormones act throughout the entire body and have slower, longer-lasting effects, while neurotransmitters operate locally within the central nervous system and act more rapidly.

There are three primary stress hormones: adrenaline (indicating mental stress), noradrenaline (indicating physical stress), and cortisol (indicating both) (de Vries et al., 2021). Adrenaline, released from the adrenal medulla, increasee anticipation, unpredictability, and emotional arousal. Noradrenaline, predominantly a neurotransmitter of the sympathetic system, rises during physical activity. Cortisol is released by the hypothalamic-pituitary-adrenal axis in response to stress.

A review by Rector and Friedman (2018) highlighted the association between well-being and hormones. Adrenal hormones like cortisol can cross the blood-brain barrier and influence subjective experiences, including well-being. The most commonly studied hormone in this context is cortisol, which can be measured through various means, including overall levels, daily decline (diurnal slope), and the response after waking up (cortisol awakening response, CAR) (Chida and Steptoe, 2009; Fries et al., 2009). 

In relation to forest therapy,  forest bathing or Shinrin Yoku, research has shown that  forest atmosphere (phytoncides) can reduce stress hormones like adrenaline, noradrenaline, and cortisol, aiding in stress management (Park et al., 2010). The effect of forest bathing on adrenaline is more significant than on noradrenaline, suggesting a greater impact on mental stress than physical stress. The very first study conducted inJapan (Miyazaki, 1990, 1996) and other studies also support the finding that Shinrin Yoku reduces cortisol levels in saliva, further indicating its efficacy in stress reduction.

In addition, recent research has highlighted the complex interactions between the hypothalamic-pituitary-adrenal (HPA) axis and the autonomic nervous system (ANS) throughout the lifespan. These interactions are crucial in understanding how stress affects overall well-being.

The HPA axis plays a central role in the body’s response to stress by regulating cortisol release, a hormone often associated with stress. The autonomic nervous system, which includes the sympathetic and parasympathetic nervous systems, controls involuntary bodily functions such as heart rate and digestion. The parasympathetic nervous system, in particular, is involved in promoting relaxation and recovery.

Studies in healthy adults and adolescents have shown that higher cortisol levels are often associated with lower heart rate variability (HRV), a measure of the variation in time between heartbeats. HRV is driven by parasympathetic activity, with higher HRV indicating better autonomic flexibility and a greater ability to adapt to stress. Therefore, the finding that higher cortisol levels correspond to lower HRV suggests a link between elevated stress levels and reduced autonomic function (Philippi et. al., 2024)

This relationship has significant implications for stress and well-being. Chronic stress can lead to sustained high cortisol levels, which may impair the body’s ability to regulate stress responses effectively. This impairment can manifest as reduced HRV, indicating a decreased capacity for physiological recovery and relaxation. Consequently, this can negatively impact overall well-being, as the body remains in a heightened state of stress.

Understanding the interplay between the HPA axis and ANS can inform interventions aimed at improving well-being. For instance, practices like Shinrin-yoku (forest bathing) have been shown to reduce cortisol levels and increase HRV, promoting relaxation and stress recovery. By enhancing parasympathetic activity and lowering cortisol levels, such interventions can help mitigate the adverse effects of chronic stress on well-being (Li, 2022)

INFLAMMATORY MARKERS

The immune system is the body’s defense mechanism against infections and diseases, involving various biological structures and processes. When the immune system is activated, it triggers an inflammatory response, leading to the production of inflammatory markers like interleukin (IL)-1β, IL-6, interferon (IFN)-γ, tumor necrosis factor (TNF)-α, and C-reactive protein (CRP). These cytokines act as chemical messengers, activating different parts of the immune response. Baseline levels of these cytokines have been associated with various traits and behaviors. For instance, CRP levels rise in response to acute stress, and individuals with depression often have higher baseline CRP levels (Khandaker et al., 2014; Osimo et al., 2019).

Proinflammatory cytokines are signaling molecules that play a crucial role in the body’s immune response by promoting inflammation. When these cytokines increase, it typically indicates an ongoing immune response to injury, infection, or stress. Conversely, a decrease in proinflammatory cytokines suggests a reduction in inflammation, which can be beneficial in managing chronic diseases and improving overall health.

In relation to forest therapy, shinrin yoku or forest bathing, several studies have investigated the effects of forest-based interventions like walking in forest environments on the levels of proinflammatory cytokines. 

A. Walking Intervention in Healthy Male University Students:

Measured Cytokines: IL-6 and TNF-α.

Findings: Significant changes were observed in both cytokines, indicating a modulation of the immune response through physical activity in a forest setting.

B. Walking Intervention for Patients with Chronic Obstructive Pulmonary Disease (COPD):

Measured Cytokines: IL-6, IL-8, IFN-γ, IL-1β, and TNF-α.

Findings: Significant changes were reported in IL-6, IL-8, IFN-γ, and IL-1β, but not in TNF-α. This suggests that the intervention had a broad impact on reducing inflammation, although the response of TNF-α varied.

B. Walking Intervention for Chronic Heart Failure Patients:

Measured Cytokines: IL-6 and TNF-α.

Findings: A significant decrease in IL-6 levels was observed, while no significant change was reported in TNF-α levels. This indicates that IL-6 might be more sensitive to the intervention in this patient population.

C. Additional studies further support these findings:

IL-6: In four studies, IL-6 levels were measured, and two of them reported significant decreases. This suggests that interventions in natural settings can effectively reduce IL-6, a marker of inflammation.

 IL-8: Two studies reported significant decreases in IL-8 levels indicating a reduction in inflammation.

TNF-α: In three studies, TNF-α levels were measured, with two reporting significant decreases . This suggests a potential but variable impact on TNF-α.

C-Reactive Protein (CRP): CRP levels were measured in three studies, with one reporting a significant decrease .CRP is another marker of inflammation, and its reduction indicates a positive anti-inflammatory effect.

D. Other Markers:

One study  measured several other markers, including IL-1β, IFN-γ, pulmonary and activation-regulated chemokine, tissue inhibitor of metalloproteinase-1, and surfactant protein D, all of which were significantly decreased. This comprehensive reduction indicates a broad anti-inflammatory effect of the intervention.

The interplay between stress, inflammation, and the hypothalamic-pituitary-adrenal (HPA)

Stress and Inflammation: When the body experiences stress, it activates inflammatory responses both in the brain and throughout the body (peripherally). This has been supported by substantial evidence (Rohleder, 2014; Calcia et al., 2016).

Communication Between Systems: The neuroendocrine system (which regulates hormones) and the immune system communicate with each other. During stress, this communication involves the activation of the HPA axis through the secretion of corticotropin-releasing hormone (CRH).

Role of CRH: CRH is a hormone that plays a key role in stress response. It typically suppresses immune responses by prompting the release of glucocorticoids (GCs) from the adrenal glands. GCs are known for their immunosuppressive and anti-inflammatory properties (Sorrells et al., 2009).

Pro-inflammatory Effects of GCs: While GCs are generally anti-inflammatory, recent research has shown that they can also have pro-inflammatory effects (Elenkov, 2008). They can enhance the expression of inflammasomes like NLRP3, which promote the secretion of pro-inflammatory cytokines such as IL-1β in response to signals like adenosine triphosphate (ATP) (Busillo et al., 2011).

Feedback Loop: Pro-inflammatory cytokines (IL-1, IL-6, and TNF-α) further stimulate the HPA axis, leading to increased levels of adrenocorticotropic hormone (ACTH) and glucocorticoids. These hormones then act to inhibit the production of the cytokines, creating a feedback loop (Alley et al., 2006; Danese et al., 2007; Steptoe et al., 2007; Miller et al., 2008).

The connection between stress, the hypothalamic-pituitary-adrenal (HPA) axis, inflammation, and the nervous system 

Stress and the Nervous System

Stress Response Activation: When the body perceives stress, the nervous system, specifically the sympathetic nervous system (SNS), is activated. This triggers the “fight or flight” response, preparing the body to respond to the threat.

Hypothalamic-Pituitary-Adrenal (HPA) Axis: The hypothalamus, a region in the brain, responds to stress by releasing corticotropin-releasing hormone (CRH). CRH signals the pituitary gland to release adrenocorticotropic hormone (ACTH), which then prompts the adrenal glands to release glucocorticoids (GCs) such as cortisol.

Glucocorticoids (GCs) and Immune System

Immune Suppression: Initially, GCs help to suppress the immune response and reduce inflammation, preventing the body from overreacting to stress.

Pro-inflammatory Role: Despite their anti-inflammatory properties, GCs can also enhance the expression of inflammasomes like NLRP3, promoting the secretion of pro-inflammatory cytokines such as IL-1β in response to signals like adenosine triphosphate (ATP). This dual role means that while GCs can reduce inflammation, they can also contribute to it under certain conditions.

Pro-inflammatory Cytokines and the Nervous System

Cytokine Signaling: Pro-inflammatory cytokines (IL-1, IL-6, TNF-α) can communicate with the nervous system, influencing brain function and behavior. These cytokines can stimulate the HPA axis, leading to further production of ACTH and cortisol, creating a feedback loop that regulates both stress and inflammation.

Nervous System Influence: Chronic stress and sustained high levels of pro-inflammatory cytokines can affect the nervous system, leading to alterations in neurotransmitter function and potentially contributing to mental health disorders such as depression and anxiety.

Autonomic Nervous System (ANS)

Sympathetic Nervous System (SNS): The SNS, part of the autonomic nervous system, is responsible for the immediate “fight or flight” response, releasing adrenaline and noradrenaline, which prepare the body for rapid action.

Parasympathetic Nervous System (PNS): The PNS promotes relaxation and recovery, counterbalancing the SNS. High levels of stress can impair the PNS, leading to a reduced ability to relax and recover, which can affect overall well-being.

Heart Rate Variability (HRV) and Well-being

HRV as an Indicator: HRV, which measures the variation in time between heartbeats, is driven by parasympathetic activity. Higher HRV indicates better autonomic flexibility and a greater ability to adapt to stress. Lower HRV, often associated with higher cortisol levels, suggests reduced autonomic function and a decreased capacity for physiological recovery.

The body’s response to stress is designed to protect you by managing inflammation and preventing the immune system from overreacting. However,  if stress is constant or chronic, this system can become unbalanced. Chronic stress can lead to prolonged inflammation, which can be harmful and contribute to various health issue

Abbreviations

CRH (Corticotropin-Releasing Hormone): A hormone released by the hypothalamus that stimulates the release of ACTH from the pituitary gland, initiating the body’s response to stress.

GCs (Glucocorticoids): A class of steroid hormones released by the adrenal glands. They are known for their ability to suppress immune responses and reduce inflammation. However, recent research suggests they can also have pro-inflammatory effects under certain conditions.

NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3): A type of inflammasome, which is a multi-protein complex involved in the activation of inflammatory responses. It plays a key role in the secretion of pro-inflammatory cytokines like IL-1β.

IL-1β (Interleukin-1 beta): A pro-inflammatory cytokine produced by activated macrophages. It is part of the body’s immune response to infections and injuries and plays a role in the development of inflammation.

ATP (Adenosine Triphosphate): A molecule that carries energy within cells. It can act as a danger signal in the extracellular space, activating inflammasomes like NLRP3.

IL-1 (Interleukin-1): A group of 11 cytokines, of which IL-1β is a prominent member, involved in the regulation of immune and inflammatory responses.

IL-6 (Interleukin-6): A cytokine that plays a role in inflammation and infection responses. It is produced by various cell types, including T cells and macrophages.

TNF-α (Tumor Necrosis Factor-alpha): A cytokine involved in systemic inflammation and the acute phase reaction. It is produced primarily by macrophages.

ACTH (Adrenocorticotropic Hormone): A hormone produced by the pituitary gland that stimulates the production and release of glucocorticoids (like cortisol) from the adrenal cortex.

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Writing in progress.

Miyazaki, Y., 1990. 森林浴の心理的効果と唾液中コルチゾール. 日生気誌(Jpn.J.Biometeor.)27(Suppl.). 

Miyzaki, Y., 1996. 森の香. ISBN 97849383446