What is the impact of nature on human health? A scoping review of the literature.

Background: The burden of non-communicable diseases (including poor mental health) is increasing, and some practitioners are turning to nature to provide the solution. Nature-based interventions (NBIs) could offer cost-effective solutions by reconnecting individuals with nature, but the success of these interventions depends partially on the way in which people engage with blue and green spaces. Methods: We conducted a scoping review in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) and Cochrane guidelines to establish the evidence base for treating poor mental and physical health with NBIs. We searched five databases and the grey literature. Exposure was the active engagement with natural environments. The primary outcome was mental health and the secondary outcome was physical health defined using established metrics. All data were extracted to a charting table and reported as a narrative synthesis. Results: 952 studies were identified, of which 39 met the inclusion criteria. 92% demonstrated consistent improvements across any health outcome where individuals engaged with natural outdoor environments. Mental health outcomes improved across 98% of studies while physical and cognitive health outcomes showed improvement across 83% and 75% of studies respectively. Additionally, we identified 153 factors affecting engagement with nature, 78% of which facilitated engagement compared with 22% that reduced engagement. Aspects such as the sense of wilderness, accessibility, opportunities for physical activity and the absence of noise/ air pollution all increased engagement. Conclusions: Further research (accompanied by a global improvement in study design) is needed to establish the magnitude and relative effect of nature-based interventions, and to quantify the compounding effect of factors that improve engagement with green and blue spaces. Nevertheless, this review has documented the increasing body of evidence in support of NBIs as effective tools to improve mental, physical, and cognitive health outcomes, and highlighted key factors that improve engagement with the natural world. Registration: Open Science Framework: https://doi.org/10.17605/OSF.IO/8J5Q3.

Olfactory exposure to late-pregnant and lactating mice causes stress-induced analgesia in male mice.

In an attempt to improve reproducibility, more attention is being paid to potential sources of stress in the laboratory environment. Here, we report that the mere proximity of pregnant or lactating female mice causes olfactory-mediated stress-induced analgesia, to a variety of noxious stimuli, in gonadally intact male mice. We show that exposure to volatile compounds released in the urine of pregnant and lactating female mice can themselves produce stress and associated pain inhibition. This phenomenon, a novel form of female-to-male chemosignaling, is mediated by female scent marking of urinary volatiles, such as n-pentyl-acetate, and likely signals potential maternal aggression aimed at defending against infanticide by stranger males.

Long-term male-specific chronic pain via telomere- and p53­mediated spinal cord cellular senescence.

Mice with experimental nerve damage can display long­lasting neuropathic pain behavior. We show here that 4 months and later after nerve injury, male but not female mice displayed telomere length (TL) reduction and p53­mediated cellular senescence in the spinal cord, resulting in maintenance of pain and associated with decreased lifespan. Nerve injury increased the number of p53­positive spinal cord neurons, astrocytes, and microglia, but only in microglia was the increase male­specific, matching a robust sex specificity of TL reduction in this cell type, which has been previously implicated in male­specific pain processing. Pain hypersensitivity was reversed by repeated intrathecal administration of a p53­specific senolytic peptide, only in male mice and only many months after injury. Analysis of UK Biobank data revealed sex-specific relevance of this pathway in humans, featuring male­specific genetic association of the human p53 locus (TP53) with chronic pain and a male-specific effect of chronic pain on mortality. Our findings demonstrate the existence of a biological mechanism maintaining pain behavior, at least in males, occurring much later than the time span of virtually all extant preclinical studies.