Modifiable health behaviours, including suboptimal dietary patterns, contribute to the global burden of disease. Messaging to raise awareness about health and nutrition behaviours is an important first step toward behaviour change and promotion of healthy dietary patterns. The aim of this rapid review was to systematically identify best practice recommendations and evidence for the development and characteristics of persuasive health and nutrition messages for awareness raising among adults. Academic reviews and grey literature reports published in English after 2010 that focused on the development or characteristics of general health or nutrition-specific messaging for awareness raising were eligible. MEDLINE Complete, CINHAL, Global Health, Embase and websites of public health organisations were searched between April and July 2024. Data was synthesised narratively. From 12 507 records, 31 were included (27 reviews and 4 reports). There was consistent support for an audience-centred approach to messaging, including audience segmentation, message tailoring and testing with target audiences. It was recommended that messages be disseminated through multiple channels, including mass and social media to facilitate repeat exposure. Message characteristics, including use of narratives, simple language, keeping messages short, conveying the general gist rather than detailed information and utilising imagery, were considered best practice for persuasive messaging. Nutrition messages that are audience-centred, tailored, thoroughly tested and incorporate elements such as narratives, imagery and simple language are likely to be accepted and persuasive among adults. Findings can be used to inform effective nutrition messaging for awareness raising in research and nutrition promotion settings.

Collagen supplementation (CS) has emerged as a promising therapeutic approach with potential benefits for managing metabolic syndrome (MetS)-related risk factors. This narrative review integrates human evidence with preclinical mechanistic insights into the metabolic actions of collagen. Anti-obesity effects are attributed to increased satiety, gastric distension, GLP-1 secretion and enhanced fatty acid oxidation mediated by PPAR-α activation and AMPK signalling. In type 2 diabetes, collagen improves glucose homeostasis by enhancing insulin sensitivity, upregulating GLUT-4 and inhibiting dipeptidyl peptidase IV (DPP-IV), thereby prolonging incretin activity (GLP-1 and GIP) and supporting β-cell function. The antihypertensive effect of collagen peptides (CP) is primarily linked to angiotensin-converting enzyme (ACE) inhibition, which reduces angiotensin II levels while promoting bradykinin-mediated vasodilation and nitric oxide release. In addition, CP has shown potential in improving lipid profiles by modulating PPAR-γ and AMPK, increasing HDL-C and reducing LDL-C and triacylglycerols. Emerging evidence also supports a role for collagen in restoring gut microbiota balance, increasing short-chain fatty acid production and reducing pro-inflammatory and oxidative pathways, contributing to systemic metabolic regulation. Overall, these findings suggest CS exerts multi-targeted benefits on MetS components through modulation of endocrine, inflammatory and metabolic pathways. Nevertheless, larger, long-term clinical trials are warranted to determine optimal dosing regimens, evaluate long-term efficacy, and further elucidate microbiota-mediated effects.

The increasing focus on longevity and cellular health has brought into the spotlight two key compounds, urolithin A (UroA) and spermidine, for their promising roles in autophagy and mitophagy. Urolithin A, a natural metabolite derived from ellagitannins, stimulates mitophagy through pathways such as PTEN induced kinase 1 (PINK1)/Parkin RBR E3 ubiquitin protein ligase (PRKN), leading to improved mitochondrial health and enhanced muscle function. However, spermidine, a polyamine found in various food sources, induces autophagy by regulating key signaling pathways such as 5′ AMP-activated protein kinase (AMPK) and sirtuin 1, thus mitigating age-related cellular decline and promoting cardiovascular and cognitive health. While both UroA and spermidine target cellular maintenance, they affect overlapping as well as distinct signalling pathways. Thus, they do not have completely identical effects, although they overlap in many ways, and offer varying benefits in terms of metabolic function, oxidative stress reduction and longevity. This review article aims to describe the mechanisms of action of UroA and spermidine not only on the maintenance of cellular health, which is mediated by the induction and maintenance of autophagy and mitophagy, but also on their potential clinical relevance. The analysis presented here suggests that although both compounds are safe and offer substantial health benefits and are involved in both autophagy and mitophagy, the role of UroA in mitophagy places it as a targeted intervention for mitochondrial health, whereas the broader influence of spermidine on autophagy and metabolic regulation may provide more comprehensive anti-ageing effects.

Cognitive decline is a hallmark of brain ageing. Leucocyte telomere length (LTL) has emerged as a candidate biomarker related to brain ageing and neurodegeneration; however, reported associations with cognition and brain structure vary across cohorts. Long-chain omega-3 polyunsaturated fatty acids (PUFA), notably docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), exert anti-inflammatory and antioxidant effects that may, in some contexts, relate to slower telomere attrition. Here, we synthesise evidence on n-3 PUFA, telomere biology and cognitive outcomes, integrating clinical, epidemiologic and experimental data. We emphasise biological plausibility (oxidative stress/inflammation, membrane remodelling, mitochondrial function and expression of telomerase reverse transcriptase (TERT) through PI3K/Akt/mTOR, NRF2 and epigenetic modifications) while acknowledging heterogeneous human findings and methodological considerations (assay variability, life-course timing, cognitive domains and biomarker stratification). We outline priorities for future studies to clarify causal pathways and inform dietary strategies that support healthy cognitive ageing.

This systematic review examined the associations of dietary factors such as nutrients, food intake, dietary patterns and dietary biomarkers with structural and functional brain MRI biomarkers, focusing on macrostructural, microstructural, lesion and perfusion measures, and functional activity/connectivity. Articles published in English were systematically searched in PubMed, Embase and PsycInfo up to 19 July 2024. A total of thirty-eight prospective cohort studies (twenty-three cross-sectional and fifteen longitudinal analyses) and thirteen intervention studies were included. Cross-sectional analyses revealed heterogenous associations: baked fish correlated with larger hippocampal volumes (β = 0·21), while oily fish, dairy products and tofu adversely related to ventricle grade. Pro-inflammatory dietary patterns were positively associated with silent infarct risk (DII Q4 v. Q1, OR = 1·77), whereas anti-inflammatory patterns tended to favour brain preservation. Longitudinal studies demonstrated more consistent protective associations: green tea consumption (+100 mL/d) reduced hippocampal atrophy by 0·024%/year, prudent dietary patterns preserved +203 mm3 left hippocampal volume over 4 years and higher plasma carotenoids decreased medial temporal lobe loss by 0·02 cm3/year. However, null findings were common across multiple dietary factors. Interventions showed limited structural benefits (effective in only two of six studies), while polyphenol-rich supplements more consistently improved cerebral perfusion and functional connectivity. Longitudinal and intervention studies demonstrated more consistent patterns than cross-sectional analyses; however, current evidence remains limited for clinical translation. Findings from cross-sectional analyses, despite being from prospective cohorts, require careful interpretation. Further replication across diverse populations and standardised long-term studies are needed before translating these associations into clinical practice.

Malnutrition results from inadequate nutrient intake, assimilation or utilisation, negatively impacting clinical outcomes and quality of life. It likely compromises gut barrier integrity, increasing intestinal permeability (IP), which impairs nutrient absorption or utilisation and increases the risk of infections and inflammation. This systematic review aims to examine the current evidence on the association between malnutrition and IP, identifying existing research gaps. A systematic search was conducted on PubMed, Scopus and Web of Science up to June 2024. According to PECOS strategy, ‘P’ = malnourished individuals or at risk of malnutrition, assessed for intestinal permeability; ‘E’ = malnutrition or risk of malnutrition; ‘C’ = well-nourished individuals; ‘O’ = increased intestinal permeability; and ‘S’ = all study types. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) checklist was followed, and Study Quality Assessment Tools (NIH) were used for methodological quality analysis. Sixteen studies met the inclusion criteria, with a moderate/high risk of bias. Malnourished individuals exhibited increased IP across various conditions (e.g. anorexia nervosa, cancer and liver cirrhosis) or setting (hospital and community). A wide heterogeneity was observed in malnutrition assessment tools, which consider different parameters such as body mass index, body weight loss and food intake. Similarly, diverse biomarkers/methods for assessing IP, including direct and indirect approaches, were used. Despite methodological heterogeneity, findings show an association between malnutrition and increased IP. Standardised research, including comprehensive biomarker panels, is needed to improve comparability, facilitating the development of targeted interventions for preventing malnutrition and managing its complications.

A major driver of the link between poor water, sanitation and hygiene (WASH) and child stunting is hypothesised to be a sub-clinical condition of the small intestine termed environmental enteric dysfunction (EED). This systematic review aimed to collate research investigating the association between biomarkers of EED and child linear growth outcomes. A systematic search of literature was conducted to identify articles that contain a measure of a domain of EED and its association with linear growth outcomes published up to 31 December 2024. Data pertaining to the measure of EED and child linear growth, as well as study characteristics, were extracted and tabulated. A total of eighty-one studies comprising 31 996 children were included, which suggested that all EED domains, including intestinal damage and repair, intestinal absorption and permeability, microbial translocation, intestinal inflammation and systemic inflammation, were associated with child linear growth. Nuances in the measurement of association were apparent and impacted the observation of significant associations. This review found that whilst the role of EED in child stunting is relatively well established, there are challenges faced in measuring biomarkers in relation to linear growth with possible ambiguities. These issues are discussed in detail to provide aid in interpretation of existing studies and to inform future studies of this kind.

Sub-Saharan Africa (SSA) is currently undergoing rapid urbanisation, a transition that is closely linked to the adoption of sedentary lifestyles and Westernised dietary habits. This shift has contributed to a substantial rise in obesity and diet-related non-communicable diseases (DR-NCDs), placing a significant strain on already burdened healthcare systems. Among the key modifiable risk factors driving this epidemiological transition are changes in dietary patterns. Western-style diets have been shown to promote inflammation and trigger metabolic and immune dysregulation, factors that underlie the development of DR-NCDs. Conversely, many Tanzanian heritage diets incorporate a diverse array of nutrient-rich foods prepared using techniques that minimise the use of oils, sweeteners and preservatives. These diets predominantly use whole grains, legumes and fruits, foods high in dietary fibre and nutraceuticals. Nutraceuticals are known to have both immunomodulatory and metabolic benefits and could potentially counteract the negative effects associated with Western-style diets. However, the limited scientific documentation of these heritage diets endangers future research into their potential health benefits. This underscores the need for targeted efforts to preserve and promote traditional dietary practices. In this review, we summarise the diversity of heritage diets from four distinct tribes in Northern Tanzania – the Maasai, Chagga, Pare and Hadzabe – who have historically exhibited low rates of DR-NCDs but are now experiencing rapid urbanisation and lifestyle changes. We briefly describe the dietary patterns of these tribes and examine the potential links between the declining usage of traditional dietary practices and the rising prevalence of DR-NCDs in Tanzania.

Frailty is an ageing-related syndrome of physiological decline, heightening vulnerability and increasing risk of adverse health outcomes. Nutritional deficiencies, particularly in vitamins B9, B12 and D, are prevalent among the elderly owing to physiological changes and reduced food intake. Research suggests a correlation between low levels of these vitamins and an elevated risk of frailty. Vitamin B9, crucial for DNA synthesis and cell division, shows potential in frailty prevention, although evidence regarding supplementation remains inconclusive. Similarly, vitamin B12, essential for nerve function and red blood cell formation, presents conflicting findings regarding its impact on frailty prevention. Vitamin D, essential for bone health and muscle function, is linked to frailty risk, yet studies on the efficacy of supplementation yielded mixed results. The mechanisms involving these vitamins, including their roles in DNA methylation and inflammation regulation, highlight the need for further research to clarify their direct impact on frailty prevention. Maintaining optimal levels of vitamins B9, B12 and D may reduce frailty, but older individuals need a complete approach that includes proper nutrition, physical activity and other preventive measures.