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There is growing recognition that interactions with nature provide many desirable human well-being outcomes, yet increasing urbanization is degrading the quality and quantity of nature experiences. Thus, it has become increasingly important to understand how and why urban dwellers interact with nature. Studies of urban green space use have largely focused on the availability and ease of access to green space, suggesting that greater opportunities to experience such space will lead to increased use. However, a growing literature emphasizes the potential for an individual's nature orientation to affect their interaction with green space. Here we measure the importance of both opportunity and orientation factors in explaining urban park use. An urban lifestyle survey was deployed across Brisbane, Australia in November 2012 to assess patterns of green space use. Participants (n=1479) were asked to provide information on demographics, private yard use, park visitations in the past week, and their orientation toward nature. About 60% of those surveyed had visited a park in the past week, and while this park user population had significantly greater nearby park coverage (within a 250 m radius; p=0.006), a much stronger determinant of visitation was their higher nature orientation (p<0.00001), suggesting that while both opportunity and orientation are important drivers for park visitation, nature orientation is the primary effect. Park users also spent significantly more time in their yards than non-park users (p<0.00001), suggesting that yard use does not necessarily compensate for lower park use. Park users with stronger nature orientation (i) spent more time in their yard, (ii) traveled further to green spaces, and (iii) made longer visits than park visitors with weaker nature orientation. Overall, our results suggest that measures to increase people's connection to nature could be more important than measures to increase urban green space availability if we want to encourage park visitation.

Evidence that experiences of nature can benefit people has accumulated rapidly. Yet perhaps because of the domination of the visual sense in humans, most research has focused on the visual aspects of nature experiences. However, humans are multisensory, and it seems likely that many benefits are delivered through the non-visual senses and these are potentially avenues through which a physiological mechanism could occur. Here we review the evidence around these lesser studied sensory pathways—through sound, smell, taste, touch, and three non-sensory pathways. Natural sounds and smells underpin experiences of nature for many people, and this may well be rooted in evolutionary psychology. Tactile experiences of nature, particularly beyond animal petting, are understudied yet potentially fundamentally important. Tastes of nature, through growing and consuming natural foods, have been linked with a range of health and well-being benefits. Beyond the five senses, evidence is emerging for other non-visual pathways for nature experiences to be effective. These include ingestion or inhalation of phytoncides, negative air ions and microbes. We conclude that (i) these non-visual avenues are potentially important for delivering benefits from nature experiences; (ii) the evidence base is relatively weak and often based on correlational studies; and (iii) deeper exploration of these sensory and non-sensory avenues is needed.

Bacterial colonisation of the intestine has a major role in the post-natal development and maturation of the immune and endocrine systems. These processes are key factors underpinning central nervous system (CNS) signalling. Regulation of the microbiome–gut–brain axis is essential for maintaining homeostasis, including that of the CNS. However, there is a paucity of data pertaining to the influence of microbiome on the serotonergic system. Germ-free (GF) animals represent an effective preclinical tool to investigate such phenomena. Here we show that male GF animals have a significant elevation in the hippocampal concentration of 5-hydroxytryptamine and 5-hydroxyindoleacetic acid, its main metabolite, compared with conventionally colonised control animals. Moreover, this alteration is sex specific in contrast with the immunological and neuroendocrine effects which are evident in both sexes. Concentrations of tryptophan, the precursor of serotonin, are increased in the plasma of male GF animals, suggesting a humoral route through which the microbiota can influence CNS serotonergic neurotransmission. Interestingly, colonisation of the GF animals post weaning is insufficient to reverse the CNS neurochemical consequences in adulthood of an absent microbiota in early life despite the peripheral availability of tryptophan being restored to baseline values. In addition, reduced anxiety in GF animals is also normalised following restoration of the intestinal microbiota. These results demonstrate that CNS neurotransmission can be profoundly disturbed by the absence of a normal gut microbiota and that this aberrant neurochemical, but not behavioural, profile is resistant to restoration of a normal gut flora in later life.

The prefrontal cortex (PFC) is a key region implicated in a range of neuropsychiatric disorders such as depression, schizophrenia and autism. In parallel, the role of the gut microbiota in contributing to these disorders is emerging. Germ-free (GF) animals, microbiota-deficient throughout life, have been instrumental in elucidating the role of the microbiota in many aspects of physiology, especially the role of the microbiota in anxiety-related behaviours, impaired social cognition and stress responsivity. Here we aim to further elucidate the mechanisms of the microbial influence by investigating changes in the homeostatic regulation of neuronal transcription of GF mice within the PFC using a genome-wide transcriptome profiling approach. Our results reveal a marked, concerted upregulation of genes linked to myelination and myelin plasticity. This coincided with upregulation of neural activity-induced pathways, potentially driving myelin plasticity. Subsequent investigation at the ultrastructural level demonstrated the presence of hypermyelinated axons within the PFC of GF mice. Notably, these changes in myelin and activity-related gene expression could be reversed by colonization with a conventional microbiota following weaning. In summary, we believe we demonstrate for the first time that the microbiome is necessary for appropriate and dynamic regulation of myelin-related genes with clear implications for cortical myelination at an ultrastructural level. The microbiota is therefore a potential therapeutic target for psychiatric disorders involving dynamic myelination in the PFC.

The amygdala is a key brain region that is critically involved in the processing and expression of anxiety and fear-related signals. In parallel, a growing number of preclinical and human studies have implicated the microbiome-gut-brain in regulating anxiety and stress-related responses. However, the role of the microbiome in fear-related behaviours is unclear. To this end we investigated the importance of the host microbiome on amygdala-dependent behavioural readouts using the cued fear conditioning paradigm. We also assessed changes in neuronal transcription and post-transcriptional regulation in the amygdala of naive and stimulated germ-free (GF) mice, using a genome-wide transcriptome profiling approach. Our results reveal that GF mice display reduced freezing during the cued memory retention test. Moreover, we demonstrate that under baseline conditions, GF mice display altered transcriptional profile with a marked increase in immediate-early genes (for example, Fos, Egr2, Fosb, Arc) as well as genes implicated in neural activity, synaptic transmission and nervous system development. We also found a predicted interaction between mRNA and specific microRNAs that are differentially regulated in GF mice. Interestingly, colonized GF mice (ex-GF) were behaviourally comparable to conventionally raised (CON) mice. Together, our data demonstrates a unique transcriptional response in GF animals, likely because of already elevated levels of immediate-early gene expression and the potentially underlying neuronal hyperactivity that in turn primes the amygdala for a different transcriptional response. Thus, we demonstrate for what is to our knowledge the first time that the presence of the host microbiome is crucial for the appropriate behavioural response during amygdala-dependent memory retention.

Over 30 years of research has shown that urban nature is a promising tool for enhancing the physical, psychological, and social well-being of the world’s growing urban population. However, little is known about the type and amount of nature people require in order to receive different health benefits, preventing the development of recommendations for minimum levels of exposure and targeted city planning guidelines for public health outcomes. Dose–response modelling, when a dose of nature is modeled against a health response, could provide a key method for addressing this knowledge gap. In this overview, we explore how “nature dose” and health response have been conceptualized and examine the evidence for different shapes of dose–response curves. We highlight the crucial need to move beyond simplistic measures of nature dose to understand how urban nature can be manipulated to enhance human health.

Nature within cities will have a central role in helping address key global public health challenges associated with urbanization. However, there is almost no guidance on how much or how frequently people need to engage with nature, and what types or characteristics of nature need to be incorporated in cities for the best health outcomes. Here we use a nature dose framework to examine the associations between the duration, frequency and intensity of exposure to nature and health in an urban population. We show that people who made long visits to green spaces had lower rates of depression and high blood pressure, and those who visited more frequently had greater social cohesion. Higher levels of physical activity were linked to both duration and frequency of green space visits. A dose-response analysis for depression and high blood pressure suggest that visits to outdoor green spaces of 30 minutes or more during the course of a week could reduce the population prevalence of these illnesses by up to 7% and 9% respectively. Given that the societal costs of depression alone in Australia are estimated at AUD$12.6 billion per annum, savings to public health budgets across all health outcomes could be immense.

Studies of inflammatory bowel disease (IBD) have been inconclusive in relating microbiota with distribution of inflammation. We report microbiota, host transcriptomics, epigenomics and genetics from matched inflamed and non-inflamed colonic mucosa [50 Crohn’s disease (CD); 80 ulcerative colitis (UC); 31 controls]. Changes in community-wide and within-patient microbiota are linked with inflammation, but we find no evidence for a distinct microbial diagnostic signature, probably due to heterogeneous host-microbe interactions, and show only marginal microbiota associations with habitual diet. Epithelial DNA methylation improves disease classification and is associated with both inflammation and microbiota composition. Microbiota sub-groups are driven by dominant Enterbacteriaceae and Bacteroides species, representative strains of which are pro-inflammatory in vitro, are also associated with immune-related epigenetic markers. In conclusion, inflamed and non-inflamed colonic segments in both CD and UC differ in microbiota composition and epigenetic profiles. Inflammatory bowel disease (IBD) has been linked to host-microbiota interactions. Here, the authors investigate mucosa-associated microbiota using endoscopically-targeted biopsies from inflamed and non-inflamed colon in patients with Crohn’s disease and ulcerative colitis, finding associations with inflammation and host epigenomic alterations.

Background and AimsIncreased efficiency of energy harvest, due to alterations in the gut microbiota (increased Firmicutes and decreased Bacteroidetes), has been implicated in obesity in mice and humans. However, a causal relationship is unproven and contributory variables include diet, genetics and age. Therefore, we explored the effect of a high-fat (HF) diet and genetically determined obesity (ob/ob) for changes in microbiota and energy harvesting capacity over time.MethodsSeven-week-old male ob/ob mice were fed a low-fat diet and wild-type mice were fed either a low-fat diet or a HF-diet for 8 weeks (n=8/group). They were assessed at 7, 11 and 15 weeks of age for: fat and lean body mass (by NMR); faecal and caecal short-chain fatty acids (SCFA, by gas chromatography); faecal energy content (by bomb calorimetry) and microbial composition (by metagenomic pyrosequencing).ResultsA progressive increase in Firmicutes was confirmed in both HF-fed and ob/ob mice reaching statistical significance in the former, but this phylum was unchanged over time in the lean controls. Reductions in Bacteroidetes were also found in ob/ob mice. However, changes in the microbiota were dissociated from markers of energy harvest. Thus, although the faecal energy in the ob/ob mice was significantly decreased at 7 weeks, and caecal SCFA increased, these did not persist and faecal acetate diminished over time in both ob/ob and HF-fed mice, but not in lean controls. Furthermore, the proportion of the major phyla did not correlate with energy harvest markers.ConclusionThe relationship between the microbial composition and energy harvesting capacity is more complex than previously considered. While compositional changes in the faecal microbiota were confirmed, this was primarily a feature of high-fat feeding rather than genetically induced obesity. In addition, changes in the proportions of the major phyla were unrelated to markers of energy harvest which changed over time. The possibility of microbial adaptation to diet and time should be considered in future studies.