Effects of forest bathing on older COPD patients

Relation

Jia BB, Yang ZX, Mao GX, et al. Health effects of forest bathing in older patients with chronic obstructive pulmonary disease.Biomed Environ Sci. 2016;29(3):212-218.

Design and participants

Eighteen patients (aged 61–79) with chronic obstructive pulmonary disease (COPD) living in Hangzhou, China, were taken to either a forest or an urban environment and allowed to walk around for 3 hours (1.5 h in the morning and afternoon on the same day). All participants had gone at least 6 weeks without a significant respiratory event before the study date, and there were no statistically significant differences in key medical parameters (body mass index [BMI], resting blood pressure or heart rate, forced expiratory volume [FEV]1, FEV1/forced vital capacity [FVC]modified Medical Research Council (mMRC) dyspnea scale and COPD assessment test result) between groups at baseline.

Target parameters

To measure the physiological effects of the forest versus the urban environment, blood levels of the following biomarkers were measured before and after exposure:

• Immunologische T-Zellantwort: CD8+, natürliche Killerzellen (NK) und NKT-ähnliche Zellen, insbesondere Zellen, die die zytolytischen Enzyme Perforin und Granzyme exprimieren, die Hauptkomponenten der Pathogenese von COPD;¹ mittels Durchflusszytometrie gemessen.
• Entzündungsfördernde Zytokine: Interferon (IFN)-γInterleukin (IL)-6, IL-8, IL-1β, Tumornekrosefaktor (TNF)-aund C-reaktives Protein (CRP), die alle als Teil des Pathomechanismus von COPD erhöht sind;² gemessen mittels Enzyme-linked Immunosorbent Assay (ELISA).
• COPD-Biomarker: Lungen- und aktivierungsreguliertes Chemokin (PARC)/Chemokin (CC-Motiv) Ligand 18 (CCL-18); Surfactant-pulmonal-assoziiertes Protein D (SP-D); Gewebeinhibitor von Metalloproteinase (TIMP)-1; gemessen über ELISA.
• Neuroendokrine Marker: Serumcortisol und Epinephrin

In addition, a pre-post psychometric measurement was carried out using the Profile of Mood States (POMS).

Key insights

Flow cytometry showed a significant reduction in the proportion of perforin-expressing CD8+, NK- and NKT-like cells. This decline was found in both the forest and urban groups, but was much larger (and statistically significant) in the forest group. The levels of total and granzyme-expressing T cells did not change significantly in either the forest or urban groups.

Is it possible that forest therapy upregulates immune function to fight cancer while downregulating it to prevent further damage in COPD?

The enzyme-linked immunosorbent assay showed significant decreases in all inflammatory cytokines and COPD biomarkers only in the Wald group participants. Statistical significance was achieved for the reduction in IFN cytokines.γ, IL-6, IL-8, IL-1β and CRP as well as the biomarkers PARC/CCL-18 and TIMP-1. The urban group had inflammatory cytokine and biomarker results that either did not change or increased pre-post exposure (IL-8, TIMP-1). Serum levels of cortisol and epinephrine also decreased (P<0.05) for the forest group, while it increases for the urban group.

Psychometric tests revealed statistically significant decreases in POMS measures of tension-anxiety, depression-dejection, and anger-aggression for the forest group. No significant changes were measured for the urban group.

Practice implications

This study extends the empirical work on forest air bathing (Shinrin-yokuin Japanese) by recruiting from a clinically relevant population – patients with COPD. To date, research on forest therapy has primarily used healthy subjects in an exploratory attempt to understand relevant psychophysiological mechanisms.^3.4The number of studies examining clinical outcomes in diseased populations is small and currently limited primarily to cancer treatment.^5.6In this current study, the decrease of such an extensive variety of immunological, inflammatory, neuroendocrine and COPD biomarkers after only 3 hours of exposure in a forested environment provides strong initial support for the beneficial effects of forest therapy for patients with respiratory diseases.

Previous studies of forest therapy have tended to rely on cardiovascular biomarkers (e.g., heart rate variability). [HRV]blood pressure) or the psycho-neuro-immuno-endocrinology tetrad.⁷The collection of data about conditions of other organ systems, such as: B. lung diseases, helps extend the benefits of forest therapy beyond a purely “stress reduction” model to a broadly applicable and truly holistic intervention.

It is interesting to note the decrease in perforin-expressing T cells in this study. The majority of papers onShinrin-yokuincluding the study that made this aspect of forest therapy famous, show oneincreasein NK cell and perforin/granzyme activity after forest exposure.^8.9There are too many unknowns between these series of studies to say why such divergent results occur at similar exposures. Despite the statistical significance of the results, this was only a pilot study, so any interpretation of the data is premature.

With this in mind, one of the purposes of pilot studies is to generate more hypotheses. It is possible that different types of forest flora produced different phytoncidal terpenes, resulting in a decrease in NK cells rather than the typically measured increaseShinrin-yokuStudies. Vegetation and/or air concentration analysis of aromatherapeutic compounds would help answer this question.¹⁰Or perhaps Forest Therapy has some sort of modulating or “experiential amphoteric” property that helps a person’s physiology recognize what is needed to restore health. Is it possible that forest therapy upregulates immune function to fight cancer while downregulating it to prevent further damage in COPD? Could the same ability be used for immunoregulatory diseases such as autoimmune diseases? These questions are purely speculative, but are worth exploring with further research.

restrictions

As mentioned above, this pilot study cannot be interpreted as clinically relevant due to its small sample size. However, the essential biomarker decreases (many at theP<0.05 level) from forest vs. urban exposure suggests that clinically significant physiological changes occur. Larger study populations with greater demographic variation would be required to make more robust claims.

The study authors did not include any of the numerical data in their paper, choosing instead to present their results exclusively via bar charts. While this provides an indication of relative change in measures pre-post and between forest and urban groups, it limits useful discussion of numerical percent change with academic and clinical audiences. It would be helpful to include the raw data in a table.

Finally, functional measurements of COPD severity were not performed after forest/urban exposure to assess changes in pulmonary function status. Further research using pre-post FEV1 and/or FEV1/FVC measures is needed to understand how forest therapy might benefit patients with lung disease.

Conclusion

This study advances the understanding and therapeutic potential of forest therapy by examining its effects in the context of a new clinical disease (COPD) and provides compelling preliminary results. It also raises more questions than it answers; most importantly, how does the tested mechanism of action (cytotoxic T cells) respond in contrast to other studies that have used the same intervention? That the ultimate outcome can be the same (i.e. patients move away from disease and closer to a state of health) regardless of the clinical condition being treated by time in the forest speaks to the wonders and mysteries of the human body and the healing power of thecompared to medicatrix naturae.