Non-communicable diseases (NCDs) including obesity, diabetes, and allergy are chronic, multi-factorial conditions that are affected by both genetic and environmental factors. Over the last decade, the microbiome has emerged as a possible contributor to the pathogenesis of NCDs. Microbiome profiles were altered in patients with NCDs, and shift in microbial communities was associated with improvement in these health conditions. Since the genetic component of these diseases cannot be altered, the ability to manipulate the microbiome holds great promise for design of novel therapies in the prevention and treatment of NCDs. Together, the Developmental Origins of Health and Disease concept and the microbial hypothesis propose that early life exposure to environmental stimuli will alter the development and composition of the human microbiome, resulting in health consequences. Recent studies indicated that the environment we are exposed to in early life is instrumental in shaping robust immune development, possibly through modulation of the human microbiome (skin, airway, and gut). Despite much research into human microbiome, the origin of their constituent microbiota remains unclear. Dust (also known as particulate matter) is a key determinant of poor air quality in the modern urban environment. It is ubiquitous and serves as a major source and reservoir of microbial communities that modulates the human microbiome, contributing to health and disease. There are evidence that reported significant associations between environmental dust and NCDs. In this review, we will focus on the impact of dust exposure in shaping the human microbiome and its possible contribution to the development of NCDs.

Low- and middle-income countries (LMICs) are disproportionately affected by non-communicable diseases (NCDs), accounting for more than 80% of NCD-related deaths globally. Research into early-life influences on these diseases via the developmental origins of health and disease (DOHaD) paradigm has informed health promotion interventions and policies focused on optimising early-life health. However, little is known about where this research occurs and whether it reaches and reflects the countries most affected by NCDs. This review searched for DOHaD studies that investigated relationships between factors during pregnancy and at birth, with later-life NCD incidence, risk and related mortality. The aim of this review was to identify where DOHaD research has been conducted and whether this focus is appropriate and relevant, given the differential burden of NCDs. Embase, MEDLINE and Scopus were searched, and eligibility screening processes identified 136 final articles. This review found that 49.7% of DOHaD research was conducted on populations within Western Europe, 15.9% in East Asia, 12.7% in North America, 8.3% in Latin America and the Caribbean, and fewer in Australasia, South Asia, the Middle East, the Africas, and Central Asia. When categorised by income, this review found that 76.4% of studies were based in high-income countries, 19.1% in upper-middle-income and 4.5% in lower-middle-income countries. No studies were based in low-income countries. There is therefore a marked disconnect between where DOHaD research is undertaken and where the greatest NCD disease burden exists. Increasing DOHaD research capacity in LMICs is crucial to informing local strategies that can contribute to reducing the incidence of NCDs.

Developmental origins of health and disease research have cemented relationships between the early-life environment and later risk of non-communicable diseases (NCDs). However, there is limited translation of this knowledge in developing-economy nations, such as the Cook Islands, that carry exceptionally high NCD burdens. Considering the evidence, Cook Islands leaders identified a need for increased community awareness of the importance of early-life nutrition. Using a community-based participatory research approach, this study aimed to engage Cook Islands community representatives in the co-construction of a contextually relevant early-life nutrition resource. A booklet distributed to mothers in Australia and New Zealand was used as a starting point. Ten semi-structured focus groups (n = 60) explored views regarding the existing resource and options for contextual adaptation. Three core themes were identified: knowledge of the importance of early-life nutrition, recognition of the need for an early-life nutrition resource and the importance of resources being context specific. A draft booklet was created based on these discussions. Participants were invited to give feedback via a second round of focus groups. This confirmed that the voice of the community was represented in the draft booklet. Suggestions for additional material not included in the original resource were also identified. We report on the process and outcomes of the co-construction with community representatives of a resource that has the potential to be used to stimulate community-level discussion about the importance of early-life nutrition. It is crucial that communities have an active voice in research and in making decisions about interventions for their population.

Nearly 80% of new cases of myopia arise between 9 and 13 years old when puberty development also progresses rapidly. However, little is known about the association between myopia and puberty. We aim to evaluate the association between myopia and menarche, the most important puberty indicator for girls, and to test whether menarche could modify the effects of myopia-related behaviors. The participants came from two consecutive national surveys conducted in 30 provinces in mainland China in 2010 and 2014. We included 102,883 girls (61% had experienced menarche) aged 10–15 years. Risk behaviors for myopia which included sleep duration, homework time, and outdoor activity were measured by self-administrated questionnaire. Myopia was defined according to a validated method, and its relationships with menarche status and behaviors were evaluated by robust Poisson regression models based on generalized estimated equation adjusting for cluster effect of school. We found that postmenarche girls were at 13% (95% confidence interval: 11%–16%) higher risk of myopia than premenarche girls, after adjusting for exact age, urban–rural location, survey year, and four behavioral covariates. Short sleep duration (<7 h/d), long homework time (>1 h/d) and low frequency of weekend outdoor activity tended to be stronger (with higher prevalence ratios associated with myopia) risk factors for myopia in postmenarche girls than in premenarche girls, and their interaction with menarche status was all statistically significant (P < 0.05). Overall, our study suggests that menarche onset may be associated with increased risk of myopia among school-aged girls and could also enhance girls’ sensitivity to myopia-related risk behaviors.

Shifts in the maternal gut microbiota have been implicated in the development of gestational diabetes mellitus (GDM). Understanding the interaction between gut microbiota and host glucose metabolism will provide a new target of prediction and treatment. In this nested case-control study, we aimed to investigate the causal effects of gut microbiota from GDM patients on the glucose metabolism of germ-free (GF) mice. Stool and peripheral blood samples, as well as clinical information, were collected from 45 GDM patients and 45 healthy controls (matched by age and prepregnancy body mass index (BMI)) in the first and second trimester. Gut microbiota profiles were explored by next-generation sequencing of the 16S rRNA gene, and inflammatory factors in peripheral blood were analyzed by enzyme-linked immunosorbent assay. Fecal samples from GDM and non-GDM donors were transferred to GF mice. The gut microbiota of women with GDM showed reduced richness, specifically decreased Bacteroides and Akkermansia, as well as increased Faecalibacterium. The relative abundance of Akkermansia was negatively associated with blood glucose levels, and the relative abundance of Faecalibacterium was positively related to inflammatory factor concentrations. The transfer of fecal microbiota from GDM and non-GDM donors to GF mice resulted in different gut microbiota colonization patterns, and hyperglycemia was induced in mice that received GDM donor microbiota. These results suggested that the shifting pattern of gut microbiota in GDM patients contributed to disease pathogenesis.

Systematic reviews and meta-analyses suggest that behaviour change interventions have modest effect sizes, struggle to demonstrate effect in the long term and that there is high heterogeneity between studies. Such interventions take huge effort to design and run for relatively small returns in terms of changes to behaviour.

So why do behaviour change interventions not work and how can we make them more effective? This article offers some ideas about what may underpin the failure of behaviour change interventions. We propose three main reasons that may explain why our current methods of conducting behaviour change interventions struggle to achieve the changes we expect: 1) our current model for testing the efficacy or effectiveness of interventions tends to a mean effect size. This ignores individual differences in response to interventions; 2) our interventions tend to assume that everyone values health in the way we do as health professionals; and 3) the great majority of our interventions focus on addressing cognitions as mechanisms of change. We appeal to people’s logic and rationality rather than recognising that much of what we do and how we behave, including our health behaviours, is governed as much by how we feel and how engaged we are emotionally as it is with what we plan and intend to do.

Drawing on our team’s experience of developing multiple interventions to promote and support health behaviour change with a variety of populations in different global contexts, this article explores strategies with potential to address these issues.