A high intake of fruit and vegetables (FV) has consistently been associated with a reduced risk of a number of non-communicable diseases. This evidence base is largely from prospective cohort studies, with meta-analyses demonstrating an association between increased FV intake and reduced risk of both CHD and stroke, although the evidence is less certain for cancer and diabetes. Controlled intervention trials examining either clinical or intermediate risk factor endpoints are more scarce. Therefore, evidence that FV consumption reduces the risk of disease is so far largely confined to observational epidemiology, which is hampered by some methodological uncertainties. Although increased FV intake is promoted across all dietary guidelines, national surveys confirm that dietary intakes are suboptimal and are not increasing over time. A range of barriers to increasing FV intake exist, including economic, physical and behavioural barriers that must be considered when exploring potential opportunities to change this, considering the feasibility of different approaches to encourage increased FV consumption. Such interventions must include consideration of context, for example, challenges and uncertainties which exist with the whole food system.

Age-related frailty and cognitive decline are complex multidimensional conditions that significantly impact the ability of older adults to sustain functional capacity and independence. While underlying causes remain poorly understood, nutrition continually emerges as one associated risk element. Many studies have addressed the importance of adequate nutrition in delaying the onset of these conditions, but the specific role of micronutrients is not well established. The consideration of pre-frailty as an outcome variable is also limited in the current literature. In this review, we focus on the potential value of maintaining micronutrient sufficiency to sustaining the health of the ageing population. Using data from the Irish longitudinal study on ageing, we consider several vitamins known to have a high prevalence of low status in older adults and their impact on pre-frailty, frailty and cognitive impairment. They include vitamin B12 and folate, both of which are associated with multiple biological mechanisms involved in long-term health, in particular in cognitive function; vitamin D, which has been associated with increased risk of musculoskeletal disorders, depression and other chronic diseases; and the carotenoids, lutein and zeaxanthin, that may help mitigate the risk of frailty and cognitive decline via their antioxidant and anti-inflammatory properties. We show that low concentrations of folate and carotenoids are implicated in poorer cognitive health and that the co-occurrence of multiple nutrient deficiencies confers greatest risk for frailty and pre-frailty in the Irish longitudinal study on ageing cohort. These health associations contribute to evidence needed to optimise micronutrient status for health in the older adult population.

Changing consumer behaviour has potential benefits for health, the economy and the environment. Change is possible, and behavioural change has been the purpose of much research; nevertheless we can still observe limited success, as in the case of food in public policies or individual diets. One reason is that models driving behavioural change interventions tend to neglect some important contextual factors. The three layers of components that channel behaviour (‘installations’ in the material, embodied and social realms) are described here and how this channelling can be hacked, modified and leveraged to foster behavioural change. Installations scaffold and control individual and collective behaviour at each step of the behavioural path with their three-layered and partly redundant structure. This redundancy makes the channelling resilient enough to train novices and to guide and repair behaviour. The three layers, physical affordances, embodied competences and social regulation are described in detail. To change eating behaviour, installations must be adapted at all steps of behaviour, from procurement to storage, preparation, meal and disposal. This adaptation can be done through the various layers in an opportunistic way, according to the agency of those who endeavour to change behaviour (e.g. budget, time, political power, etc.) Finally the steps necessary to design behavioural change interventions leveraging installations are listed.

This review summarises evidence relating to a potential role for vitamin D supplementation in the prevention or treatment of coronavirus disease 2019 (COVID-19). Laboratory studies show that the active vitamin D metabolite 1,25-dihydroxyvitamin D induces innate antiviral responses and regulates immunopathological inflammation with potentially favourable implications for the host response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Meta-analyses of cross-sectional, case-control and longitudinal studies report consistent protective associations between higher circulating 25-hydroxyvitamin D [25(OH)D] concentrations or vitamin D supplement use and reduced risk and severity of COVID-19. However, Mendelian randomisation studies testing for associations between genetically predicted circulating 25(OH)D concentrations and COVID-19 outcomes have yielded consistently null results. Positive findings from observational epidemiological studies may therefore have arisen as a result of residual or unmeasured confounding or reverse causality. Randomised controlled trials of prophylactic or therapeutic vitamin D supplementation to reduce risk or severity of COVID-19 reporting to date have yielded inconsistent findings. Results of further intervention studies are pending, but current evidence is insufficient to support routine use of vitamin D supplements as a therapeutic or prophylactic agent for COVID-19, or as an adjunct to augment immunogenicity of SARS-CoV-2 vaccination. Accordingly, national and international bodies have not made any recommendations regarding a role for vitamin D in the prevention or treatment of COVID-19.

Type 2 diabetes (T2D) and CVD are major causes of mortality and chronic morbidity. Whilst mortality from CVD has decreased they remain the largest cause of death in Europe and the prevalence of T2D is increasing rapidly. A consistent component of public health advice is to reduce intake of SFA to reduce CVD in particular, which implies limiting dairy food consumption. The prospective studies and randomised controlled trials included in this review show that for dairy foods at least, SFA are not consistently associated with CVD or T2D risk. For CVD the association with dairy foods is generally neutral despite dairy foods being the major source of SFA in many diets. This creates considerable doubt, at least for dairy foods, concerning the validity of the traditional diet-heart hypothesis which positively relates SFA intake to increased serum LDL-cholesterol and subsequent increased CVD. There is now emerging evidence to explain this which is highly relevant to dairy foods. These include the potentially counterbalancing effect of SFA-stimulated HDL-cholesterol and specific food matrix factors. In addition, SFA are associated with the less atherogenic large buoyant LDL particles and possible counterbalancing hypotensive effects of dairy proteins. Overall, dairy foods have either a neutral or beneficial association with CVD and T2D. Beneficial associations are seen for blood pressure and the reduced T2D risk linked to yoghurt consumption, a subject that needs urgent attention given the sharp rise in T2D prevalence in many countries.

The precision nutrition paradigm is based on the premise that substantial variation exists between human subjects in terms of diet-related disease risk and response to dietary interventions. In terms of better defining, ‘the right diet for the right person at the right time’ may be more appropriate than ‘one-diet-fits-all’. This review will explore how systems biology and nutrigenomics approaches have advanced the precision nutrition paradigm. We will draw upon a number of elegant mechanistic studies that have enhanced our understanding with respect to the complex biology and inter-organ crosstalk, relating to inflammation and metabolism, that underpin cardio-metabolic health. Also, this review will explore the extent to which more targeted, precision nutrition approaches may attenuate adverse risk factors associated with cardio-metabolic disease. We will focus on the key characteristics or ‘metabotypes’ of high- v. low-risk individuals and response v. non-response to interventions, to generate greater insights with respect to risk stratification and therapeutic interventions to enhance disease prevention. The goal is to utilise systems biology to enhance understanding by underpinning more targeted nutritional approaches, which may improve efficacy of personalised nutrition interventions.

Phenotypic flexibility is a methodology that accurately assesses health in terms of mechanistic understanding of the interrelationship of multiple metabolic and physiological processes. This starts from the perspective that a healthy person is better able to cope with changes in environmental stressors that affect homeostasis compared to people with a compromised health state. The term ‘phenotypic flexibility’ expresses the cumulative ability of overarching physiological processes to return to homeostatic levels after short-term perturbations. The concept of phenotypic flexibility to define biomarkers for nutrition-related health was introduced in 2009 in the area of health optimisation and prevention and delay of non-communicable disease. The core approach consists of the combination of imposing a challenge test to the body followed by time-resolved analysis of multiple biomarkers. This new approach may better facilitate nutritional health research in intervention studies since it may show effects on early derailed physiological markers and the biomarker response can be extended by perturbing the system, thereby making them more sensitive in detecting health effects from food and nutrition. At the same time, interindividual variation can also be extended and compressed by challenge tests, facilitating the bridge to personalised nutrition. This review will overview where the science is in this research arena and what the phenotypic flexibility potential is for the nutrition field.