Nutrition plays a pivotal role in health and disease prevention and management and through its interactions with social and personal factors, influences an individual's growth, development and life chances, as well as long-term health and longevity. These factors include amongst others, genetic inheritance, ethnicity, socio-cultural context, sex and gender. Although different interpretations exist, in general sex refers to the genetic, biological and physiological attributes that distinguish females, males and intersex whereas gender refers to socio-cultural and politically constructed roles and behaviours associated with a feminine, masculine or non-binary identity, which vary from society to society. Sex has implications for key biological processes involving food and nutrients as well as life-stage differences in nutritional requirements. Sex and gender may have implications in how individuals engage in different dietary behaviours and respond to nutrition interventions. The Irish Section Nutrition Society 2023 Conference sought to enhance understanding of the role of sex and gender in nutrition research; explore the influence of sex and gender on risk of non-communicable diseases and examine sex- and gender-specific considerations across the life course. This short editorial provides an overview and highlights of the conference.

The analysis of food using a perspective centred on nutrients seems inadequate for understanding the dietary transition and its impact on the growth of obesity and chronic diseases. Industrial food processing is now proposed as the key to explain the relationship between food and health. The NOVA food classification considers the degree and the purpose of food processing, which includes physical, biological and chemical processes used after foods are separated from nature, and before being consumed or prepared as dishes and meals. NOVA has four food groups: (1) unprocessed and minimally processed foods; (2) processed culinary ingredients; (3) processed foods and (4) ultra-processed foods, which are formulations made mostly or entirely from substances derived from group 1 foods and additives, with little if any intact group 1 food. Many investigations linking high ultra-processed food consumption with deterioration of diets and adverse health outcomes are reinforced by prospective studies, systematic reviews and meta-analyses. There are various plausible explanations of why diets high in ultra-processed foods are harmful. Their production and consumption continue to rise worldwide. Efficient and effective public policies and actions that reduce production and consumption of ultra-processed products are needed, to protect human health now and in future.

The FAO states that the term food sovereignty focuses on food for the people by placing people’s need for food at the centre of policies and insists that food is more than just a commodity. Food Sovereignty also promotes knowledge and skills by building on traditional knowledge; using research to support and pass on this knowledge to future generations; and rejecting technologies that undermine local food systems. It is essentially a movement that “recognizes that control over the food system needs to remain in the hands of producers, and is clearly focused primarily on small-scale agriculture of a non-industrial nature, preferably organic”(1). In Māori terms, Kai Sovereignty is drawn first from the relationship of foods to our needs; it is expressed through whakapapa, and has an overarching contribution to food security. Traditional foods abound in Aotearoa. The relationships are longstanding, expressive and contribute to our wellbeing in various ways(2). But the true cultural value of traditional foods is diminishing as new foods, lifestyles and experiences succeed them. Kai sovereignty therefore is at risk of being relegated to historical discourse. The FAO acknowledgement of the intergenerational role of traditional knowledge to support food sovereignty aligns well to the Māori experience. This knowledge covers a myriad of food relationships including foraging, producing, harvesting, processing, cooking and manaakitanga. We are in a renaissance period that seeks to rediscover our relationship with the pātaka, the food store. So much knowledge has been lost, but much also remains. How we draw that together in a way that acknowledges the whakapapa or historical relationship alongside the present and future. The right to achieving kai sovereignty is yet to be properly understood within our communities. The first steps lie in the knowledge space; sharing and acknowledgement of our food traditions before they are lost or misinterpreted.

The fungal cell wall facilitates an immune response and may be involved in intestinal immune training (1,2). It is also fermentable by the gut microbiome, thus, consumption of fungi changes gut microbial ecology (3). Yet, the specific effects of consuming fungal foods on the gut mycobiota (i.e., gut fungi) have not been well studied. An interesting case study is mycoprotein, a fungal based protein produced from Fusarium Venenatum (4). We have previously reported that mycoprotein consumption attenuates faecal water genotoxicity, a surrogate marker of colorectal cancer risk, as well as modulates faecal metabolite excretion and gut bacterial composition (5). Here, we aimed to evaluate the impact of consuming a diet high in mycoprotein on gut mycobial ecology, and to explore relationships between mycobial composition and faecal genotoxicity.

Here we leverage stool samples from Mycomeat: a randomised crossover-controlled trial, recruiting 20 healthy male adults to adhere to 2-week diets comprising 240 g/day of mycoprotein based foods or red and processed meat, separated by a 4-week washout. Internal transcriber spacer (ITS) sequencing was performed to characterise the mycobiota. Alpha diversity before and after study phases was compared using Wilcoxon tests. Beta diversity was compared by permutational multivariate analysis of variance (PERMANOVA) based on Bay-Curtis dissimilarities. Differences in mycobial taxa within and between study phases were compared using Wilcoxon tests. Changes in mycobiota composition was then regressed against faecal excretion of metabolites using mixed- effects models to understand the impact of myco-ecology on the wider colonic environment. Finally, given the abundance of mycobial genotoxins in nature, we regressed mycobial taxa against faecal water genotoxicity.

There were significant shifts in the abundance of several taxa following both diets. Notably, mycoprotein consumption was associated with an increase in the abundance of Malasseziales sp. (P = 0.02) and a reduction in Candida Albicans (P = 0.01). Meat consumption was associated with an increase in Phaeoacremonium Tuscanum (P = 0.01) and Rhodotorula Mucilaginosa (P = 0.008), and reduction in Penicillium Commune (P = 0.02). In addition, Aspergillus Caesiellus was associated with lower faecal genotoxicity (P = 0.04), whereas Penicillium Commune (P = 0.04) and Penicillium Olsonii (P = 0.03) were both associated with higher genotoxicity. Regressing mycobial taxa against faecal metabolites revealed a number of significant associations, including between Penicillium Commune and austdiol, a putative mycotoxin (P < 0.001) as well as 1-methyladenine, a methylated DNA base with cytotoxic properties (P = 0.001).

The gut mycobiota is malleable through a fungi rich diet alongside changes within the wider microbiome. Members of the gut mycobiota predicted faecal genotoxicity and faecal excretion of toxins in this model, and there may be value in further exploring the gut mycobiota and the contribution of mycotoxins in gut health and colorectal cancer risk.

Pacific Island communities are disproportionally impacted by the effects of climate change, and as teina (younger sibling) to our Pacific tuakana (older sibling), it is our responsibility to ensure these communities have resilience through co-developed solutions to these real-world problems. We focus on marine and freshwater ecosystems, understand their intrinsic links to Pacific communities, while, in partnership with science, empower and enable local knowledge to steer the waka. With more than 20 years’ experience of supporting Pacific communities, we deliver our positive impact through knowledge exchange, capability and capacity development, and problem solving. We strive to learn and grow our own capability, while brokering knowledge between Aotearoa, the Pacific, and our world leading research partners. Our aim is that Pacific Island communities gain a deeper scientific understanding of their aquatic systems, have the tools to rejuvenate and conserve these ecosystems, are empowered to transform their food systems towards more healthy, sustainable, and resilient pathways, and can adapt to the impacts of climate change. We take a systems approach that incorporates adaptive solutions, which are community-led, thereby ensuring a long-lasting positive impact into the future. Our Kete is filled with world-leading expertise from different organizations, which ensures a greater collective impact where it is needed most. This presentation will cover the seven themes within our Pacific Impact area, with a particular focus on food safety and security in relation to ciguatera poisoning (the number one cause of non-bacterial seafood illness affecting Pacific Island communities) (1,2), analytical laboratory development, and transforming food systems.

This review presents evidence related to the postprandial responses after consumption of dairy products focusing on the effect of the dairy matrix and lipid response, which was also presented as part of a speech at the Nutrition Society Winter Conference, January 2023. The key findings are that the dairy product(s) that differentiate from others in the postprandial TAG response are products with a semi-solid structure. There were no differences in lipid responses between cheese and butter. The main factors viscosity, fat globule size and milk fat globule membrane do not seem to explain the effect of the dairy matrix in the acute postprandial response. In summary, it is very difficult to investigate the effects of the dairy matrix per see and with the few studies conducted to date, no clear cause and effect can be established. Future research should focus on the semi-solid dairy matrix, and studies investigating specifically the yoghurt matrix are warranted.

Atopic diseases, including asthma and eczema, represent a substantial public health problem in children and adolescents globally; asthma is the commonest chronic disorder of childhood(1). Research suggests that the origins of childhood asthma lie in utero, and several components of the maternal diet during pregnancy have been investigated in relation to atopic outcomes in children. Epidemiological evidence suggests that a higher intake of sugar during pregnancy is associated with a higher risk of childhood asthma and atopy(2,3). However, randomised trial evidence supporting such a link is lacking.

Aims

1. 1. To examine whether a low glycaemic index (GI) dietary intervention during pregnancy decreases the risk of asthma and eczema in childhood.

2. 2. To assess observationally whether maternal intake of sugar during pregnancy is positively associated with asthma and eczema in childhood.

This is a secondary analysis of children from the ROLO trial. Healthy women were randomised to receive an intervention of low GI dietary advice or routine antenatal care from early pregnancy. All women completed a 3-day food diary in each trimester of pregnancy. Estimates of maternal intake of sugar in each trimester were averaged to provide mean intakes during pregnancy. Mothers reported current doctor-diagnosed eczema in their children at 2-years of age (n=271), and current doctor-diagnosed asthma and eczema in their children at 5 (n=357) and 9-11 years (n=391) of age. Multivariable logistic regression models were used a) to test the effect of the intervention on child outcomes overall, and stratified by maternal education level (with, versus without, a complete tertiary level education), and b), in observational analyses, to analyse the relation between sugar and carbohydrate intake in pregnancy and child outcomes.

There was weak evidence overall for a reduction in asthma at 5-years of age in children whose mothers received the low GI dietary intervention during pregnancy compared to usual care [adjusted odds ratio (OR) 0.43 (95% CI 0.18, 1.03); P=0.06]. However, in stratified analyses the intervention was associated with a marked reduction in risk of asthma at 5-years of age in children born to mothers with lower educational attainment [adjusted OR 0.16 (0.03, 0.85); P=0.032]. Intake of sugar during pregnancy was positively associated with the development of asthma at any time point in childhood [adjusted OR per quartile of mean sugar intake 1.40 (0.99, 1.97), P-trend=0.048] and at 5-years of age [adjusted OR per quartile 1.55 (1.00, 2.40), P-trend=0.046]. No associations with eczema outcomes were found.

This novel study provides stronger evidence that higher sugar intake during pregnancy is associated with an increased risk of asthma among offspring. An intervention to reduce sugar intake in pregnancy may have potential as a primary prevention strategy, particularly amongst children born to mothers with lower educational attainment.

For some 20 years, science funding bodies have been asking for the integration of sex- and gender-related factors into the content of research and innovation. The rationale for those requirements has been the accumulated evidence that sex and gender are important determinants of health and disease. The European Commission (EC) has been the first, since 2002, to seriously ask for the integration of sex and gender into research and innovation in the context of their multi-annual framework programmes. When introduced, this condition was not immediately applauded by the research community, who perhaps lacked training in methods for the integration of sex- and gender-related factors. The EC Expert Group on Gendered Innovations sought to fill this gap. This review describes the work of this international collaborative project which has resulted in the development of general and field-specific methods for sex and gender analysis and 38 case studies for various research domains (science, health and medicine, environment, engineering) to illustrate how, by applying methods of sex and gender analysis, new knowledge could be created. Since 2010, science funding bodies in Canada, the USA and several EU member states have followed the example of the EC issuing similar conditions. Although the effects of nutritional patterns on a range of (physiological and health) outcomes may differ for men and women, sex and gender analyses are rarely conducted in nutrition research. In this review, we provide examples of how gender is connected to dietary intake, and how advancing gender analysis may inform gender-sensitive policies and dietary recommendations.

Fructose-containing sugars can exaggerate postprandial lipaemia and stimulate hepatic de novo lipogenesis (DNL) when compared to glucose-based carbohydrates(1). Galactose has recently been shown to increase postprandial lipaemia compared to glucose(2), but mechanisms remain uncharacterised. The aim of this study was to assess the effect and mechanisms of lactose-induced lipaemia.

Twenty-four non-obese adults (12 male and 12 female) completed three trials in a randomised, crossover design (28 ± 7-day washout). During trials, participants consumed test drinks containing 50 g fat with 100 g of carbohydrate. The control carbohydrate was a glucose polymer (maltodextrin), the experimental carbohydrate was galactose-containing carbohydrate (lactose) and the active comparator was fructose-containing carbohydrate (sucrose). Hepatic DNL was assessed by the 2H2O method and [U-13C]-palmitate was added to the test drink to trace the fate of the ingested fat. Blood and breath samples were taken to determine plasma metabolite and hormone concentrations, in addition to plasma and breath 2H and 13C enrichments. Data were converted into incremental under the curve (iAUC) and were checked for normality by visual inspection of residuals. Differences between trials were assessed by one-way ANOVA. Where a main effect of trial was detected, post- hoc t-tests were performed to determine which trials differed from lactose according to the principle of closed-loop testing.

The plasma triacylglycerol iAUC (mean ± SD) in response to maltodextrin was 51 ± 68 mmol/L*360 min. Following lactose ingestion, plasma triacylglycerol iAUC increased to 98 ± 88 mmol/L*360 min (p<0.001 vs maltodextrin), which was comparable to sucrose [90 ± 95 mmol/L*360 min (p=0.41 vs lactose)]. Hepatic DNL in response to maltodextrin was 6.6 ± 3.0%. Following ingestion of lactose, hepatic DNL increased to 12.4 ± 6.9% (p=0.02 vs maltodextrin), which was comparable to sucrose [12.2 ± 6.9% (p=0.96 vs lactose)]. Exhaled 13CO2 in response to maltodextrin was 10.4 ± 4.1 mmol/kgFFM*360 min. Following ingestion of lactose, exhaled 13CO2 was 8.8 ± 4.9 mmol/kgFFM*360 min (p=0.09 vs maltodextrin), which was lower than sucrose [11.1 ± 3.9 mmol/kgFFM*360 min (p=0.01 vs lactose)].

These data are consistent with the hypothesis that hepatic de novo lipogenesis contributes to both lactose and sucrose-induced lipaemia and provide a rationale to investigate the longer-term effects of lactose and sucrose on metabolism.

The purpose of the present article is to describe the current state of sex and gender data collection in nutrition science research, discuss the effects of flawed data collection practices, highlight considerations for transgender and gender non-conforming populations and propose a sex- and gender-informed approach to human subjects research. Sex and gender are separate constructs that are often conflated in nutrition research and practice. Current nutrition surveillance programmes in the United States, United Kingdom and Ireland do not accurately capture sex and gender data, which undermines the accuracy of the analyses and excludes gender minorities. Transgender and gender non-conforming populations have distinct clinical and psychosocial nutrition considerations that require further research to inform nutrition policy and practice, such as anthropometric and biochemical changes with hormone therapy, eating disorders, food insecurity and nutrition as a source of empowerment or expression of gender identity. Researchers can apply a sex- and gender-informed approach to human subjects research by treating sex and gender as separate, relevant demographic data, appreciating gender as a fluid construct, and approaching data collection on gender minorities with sensitivity to privacy and confidentiality.

A diet low in fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAP) improves functional bowel symptoms and is a second-line dietary management strategy for the treatment of irritable bowel syndrome (IBS). The diet is complex and involves three stages: restriction, reintroduction and personalisation and clinical effectiveness is achieved with dietitian-led education; however, this is not always available. The aim of this review is to provide an update on the evidence for using the low FODMAP diet, with a focus on the impact of FODMAP restriction and reintroduction considering long-term management of IBS in a clinical setting. Randomised controlled trials have assessed symptom response, quality of life, dietary intake and changes to the gut microbiota during FODMAP restriction. Systematic reviews and meta-analyses consistently report that FODMAP restriction has a better symptom response compared with control diets and a network analysis reports the low FODMAP diet is superior to other dietary treatments for IBS. Research focused on FODMAP reintroduction and personalisation is limited and of lower quality, however common dietary triggers include wheat, onion, garlic, pulses and milk. Dietitian-led delivery of the low FODMAP diet is not always available and alternative education delivery methods, e.g. webinars, apps and leaflets, are available but remove the personalised approach and may be less acceptable to patients and may introduce safety concerns in terms of nutritional adequacy. Predicting response to the low FODMAP diet using symptom severity or a biomarker is of great interest. More evidence on less restrictive approaches and non-dietitian-led education delivery methods are needed.

A range of metrics have been developed and used to measure components of dietary patterns (e.g., adequacy, quality, diversity). However, no existing dietary metric simultaneously captures the three key dimensions of sustainable healthy diets recommended by the Food and Agriculture Organization of the United Nations and the World Health Organization: food processing; dietary diversity; and intake of animal products(1). This study aimed to identify indicators of a global sustainable healthy diet and translate these features into a multidimensional diet quality score (SUSDIET). Informed by our scoping review(1), a Delphi method was adopted in the form of a three-round online survey of 13 national and international experts in nutritional epidemiology, environmental health, dietary assessment and/or food and nutrition policy. Surveys were conducted between November 2022 and May 2023. Participants were asked about procedures to establish an operational definition for a global sustainable healthy diet. Based on consensus from global experts, we developed the SUSDIET, a food-based diet quality score incorporating variety of plant foods, intake of animal products, and dietary contribution of ultra-processed foods (the ‘dimensions’). Categories and amounts of foods consumed were informed by the Global Diet Quality Score(2), EAT Lancet Planetary Health(3) and a meta-analysis of the relationship between ultra-processed foods and all-cause mortality(4). The variety of plant foods is measured based on 12 food groups (citrus fruits, deep orange fruits, other fruits, dark green leafy vegetables, cruciferous vegetables, deep orange vegetables, other vegetables, legumes, deep orange tubers, nuts and seeds, whole grains, white roots and tubers), animal intake based on 5 food groups (egg, dairy, poultry, fish and seafood, red meat), and ultra-processed foods as one food group. Three categories of consumed amounts (in grams per day) are defined for variety of plant foods and animal intake, scoring as 0, 0.5 or 1. Ultra-processed food consumption is scored as 0 or 1 using ≤10% or >10% of total dietary intake as cut-offs. The components of each dimension are weighted so the three dimensions equally range from 0-5. SUSDIET overall score ranges from 0-15 (up to 5 points per dimension), with a higher score indicating a more healthy and sustainable diet. SUSDIET will be of immediate use for research aiming to assess the impact of diets on both health and environmental sustainability outcomes among the general adult population. This multidimensional diet quality score can also be used to inform and assess the effectiveness of policy actions that promote sustainable healthy diets, including the monitoring and surveillance of diets globally.

The trace element selenium is known to protect against oxidative damage which is known to contribute to cognitive impairment with ageing (1,2). The aim of this study was to explore the association between selenium status (serum selenium and selenoprotein P (SELENOP)) and global cognitive performance at baseline and after 5 years in 85-year-olds living in the Northeast of England.

Serum selenium and SELENOP concentrations were measured at baseline by total reflection X-ray fluorescence (TXRF) and enzyme-linked immunosorbent assay (ELISA), respectively, in 757 participants from the Newcastle 85+ study. Global cognitive performance was assessed using the Standardized Mini-Mental State Examination (SMMSE) where scores ≤25 out of 30 indicated cognitive impairment. Logistic regressions explored the associations between selenium status and global cognition at baseline. Linear mixed models explored associations between selenium status and global cognition prospectively after 5 years. Covariates included sex, body mass index, physical activity, high sensitivity C-reactive protein, alcohol intake, self-rated health, medications and smoking status.

At baseline, in fully adjusted models, there was no increase in odds of cognitive impairment with serum selenium (OR 1.004, 95% CI 0.993-1.015, p = 0.512) or between SELENOP (OR 1.006, 95% CI 0.881-1.149, p = 0.930). Likewise, over 5 years, in fully adjusted models there was no association between serum selenium and cognitive impairment (β 7.20E-4 ± 5.57E-4, p = 0.197), or between SELENOP and cognitive impairment (β 3.50E-3 ± 6.85E-3, p = 0.610).

In this UK cohort of very old adults, serum selenium or SELENOP was not associated with cognitive impairment at baseline and 5 years. This was an unexpected finding despite SELENOP’s key role in the brain and the observed associations in other studies. Further research is needed to explore the effect of selenium on global cognition in very old adults.

Malnutrition affects over half the world’s population, manifesting in myriad forms. Nearly 1 in 4 children never reach their full growth potential, while 1 in 2 lack key micronutrients essential for health and development.1 Furthermore, 1 in 3 women suffer from anemia, and 2 in 3 do not get enough vital micronutrients. At the same time, over 2 in 5 adults are overweight or obese, and 1 in 5 live with high blood pressure. These various forms of malnutrition lead to physical and cognitive impairments, increased susceptibility to infections and chronic diseases, and reduced quality and length of life. They also impose immense economic, social, and health burdens. In addition to harming human health, our food system damages the planet, generating greenhouse gas emissions that drive climate change and depleting freshwater reserves. It also causes deforestation and habitat destruction which drive species to extinction. These grave harms to both human and environmental wellbeing demand urgent action. Transforming our food systems is imperative to promote nutritious diets that deliver adequate nutrition and protect against noncommunicable diseases, while simultaneously protecting our planet, its biodiversity, and natural resources. As a response, many call for drastically limiting consumption of animal source foods like meat, eggs, and dairy. They argue that these foods jeopardize both human health and environmental sustainability. However, is it possible to meet the nutritional needs of the global population with few animal source foods? What are the full impacts, both positive and negative, of animal source foods on human health and the environment? In this presentation, I will review the latest scientific evidence surrounding these questions. I will examine whether mindfully produced and consumed animal source foods can be part of the solution. Join me to explore these critical issues concerning sustainable nutrition and the role of animal source foods in our food system transformation.

The aim of the paper is to review the current evidence on the impact of ‘the timing of energy intake’ on the risk of developing obesity and obesity-related metabolic diseases. The prevalence of obesity is currently increasing worldwide thus becoming a severe health burden for most countries. Indeed, obesity represents a risk factor for several non-communicable diseases such as cancer, type 2 diabetes, dyslipidaemia, CVD and overall mortality. In order to treat obesity, several pharmacological approaches have been developed and are indicated for subjects with obesity with a BMI ≥ 30 kg/m2 or ≥ 27 kg/m2 and obesity-related comorbidities. For severe obesity (BMI ≥ 40 kg/m2), bariatric surgery represents a promising approach. The most common bariatric surgical procedures are represented by the Roux-en-Y gastric bypass, laparoscopic adjustable band, laparoscopic gastric sleeve and biliopancreatic diversion with duodenal switch. Both anti-obesity pharmacological and surgical treatments require change in lifestyle. When a nutritional plan is established, attention is usually paid to macronutrient composition and energy intake, while ‘the time of food’ is not taken into account. Chronotype, which is the attitude of a subject to carry out most of their daily activities in the first (morning chronotype) or second half (evening chronotype) of the day, has been reported to have a role in the pathogenesis of obesity and obesity-related cardiometabolic diseases as well as eating speed. Thus, adopting a physiological timing of energy intake could be an additional strategy to potentiate the current anti-obesity approaches.

The high levels of non-communicable diseases such as CVD and type 2 diabetes mellitus are linked to obesity and poor diet. This continuing emphasis on health in relation to food is proving a powerful driver for the development of cheap but palatable and more functional foods. However, the efficacy of such foods is often hard to prove in human subjects. Thus, a suite of tools has been developed including in silico and in vitro simulations and animal models. Although animal models offer physiologically relevant platforms for research, their use for experimentation is problematic for consumers. Thus, in vitro methods such as Infogest protocols have been developed to provide digestion endpoints or even an indication of the kinetics of digestion. These protocols have been validated for a range of food systems but they still miss the final absorption step. This review discusses the use of such in vitro models and what further steps need to be included to make the bioaccessibility determination more relevant to bioavailability and human health.

New Zealand has committed to a 50% reduction in greenhouse gas emissions (GHGEs) from 2005 levels by 2030. Dietary changes within New Zealand could simultaneously improve population health and contribute towards the nation’s emissions reduction target, as agricultural emissions are estimated to account for half of New Zealand’s GHGEs(1). This research aimed to quantify the GHGEs associated with household purchases of major food groups in New Zealand and identify the sociodemographic characteristics that are associated with per capita household dietary emissions. Household dietary emissions were estimated using the NielsenIQ Homescan(R) consumer panel — a large sample of households within New Zealand who report purchasing data of take-home food and beverages. The sample is nationally representative in terms of broad geographical regions and selected key demographic characteristics. Carbon emission estimates were assigned to 1,908,485 total food and beverage purchases from 1,775 households over one year (2019) using a process-based life cycle assessment (LCA) dataset initially constructed in the United Kingdom (UK) and adapted for New Zealand(2). This LCA dataset contains estimates of greenhouse gas emissions generated over the life cycle of the production of food products from the following stages: farming and processing, transit packaging, consumer packaging, transport, warehouse and distribution, refrigeration, and overheads. Greenhouse gas emissions are expressed in kg of carbon dioxide equivalents per kg of food product over a 100-year time horizon. Total emissions from purchases of major food groups were then estimated. Multiple linear regression was used to examine the relationships between household variables and per capita dietary emissions. Overall purchases of red and processed meat (35%) and dairy products (19%) were responsible for the greatest proportion of emissions. The age group of the primary household shopper as well as household size were predictors of per capita dietary emissions — households with primary shoppers > 65 years had, on average, 33% (95% CI: 20% to 49%) higher per capita dietary emissions, compared to households with primary shoppers 34 years; and every additional household member was associated with, on average, 11% (95% CI: 9% to 13%) lower per capita dietary emissions. We have shown in this large representative sample of New Zealand households that purchases of just two food groups — red and processed meat, and dairy — were responsible for approximately half of dietary greenhouse gas emissions. Larger households had lower per capita dietary greenhouse gas emissions, and older shoppers had relatively higher greenhouse gas emissions. Whilst similar associations have been reported elsewhere more research is needed to confirm these latter findings. With enhanced understanding of the observed association between age of a household’s primary shopper and per capita dietary emissions, interventions may be devised that encourage shoppers to purchase lower-emitting foods, particularly less meat and dairy.

Calcium and vitamin D have well-established roles in maintaining calcium balance and bone health. Decades of research in human subjects and animals have revealed that calcium and vitamin D also have effects on many other organs including male reproductive organs. The presence of calcium-sensing receptor, vitamin D receptor, vitamin D activating and inactivating enzymes and calcium channels in the testes, male reproductive tract and human spermatozoa suggests that vitamin D and calcium may modify male reproductive function. Functional animal models have shown that vitamin D deficiency in male rodents leads to a decrease in successful mating and fewer pregnancies, often caused by impaired sperm motility and poor sperm morphology. Human studies have to a lesser extent validated these findings; however, newer studies suggest a positive effect of vitamin D supplementation on semen quality in cases with vitamin D deficiency, which highlights the need for initiatives to prevent vitamin D deficiency. Calcium channels in male reproductive organs and spermatozoa contribute to the regulation of sperm motility and capacitation, both essential for successful fertilisation, which supports a need to avoid calcium deficiency. Studies have demonstrated that vitamin D, as a regulator of calcium homoeostasis, influences calcium influx in the testis and spermatozoa. Emerging evidence suggests a potential link between vitamin D deficiency and male infertility, although further investigation is needed to establish a definitive causal relationship. Understanding the interplay between vitamin D, calcium and male reproductive health may open new avenues for improving fertility outcomes in men.

The development of multiple long-term conditions (MLTC) has been shown to be associated with low-grade chronic inflammation(1). The Dietary Inflammatory Index (DII®) is a literature-based dietary score that was developed to measure the potential impact of diet on the inflammatory status of an individual(2). In this study, we aimed to validate the DII® score against biomarkers, including high- sensitivity C-reactive protein (hs-CRP), and plasma concentrations of vitamin C, retinol and α- tocopherol in European Prospective Investigation Into Cancer and Nutrition (EPIC)-Norfolk participants, aged 39–79 years at baseline(3).

The DII® score was calculated using a 130-item Food Frequency Questionnaire collected at baseline, between 1993 and 1997. The dietary intakes were adjusted to a 2000 kcal/day diet, to assess diet quality independently of diet quantity. Non-fasting serum cholesterol, hs-CRP, and plasma α- tocopherol, vitamin C and retinol concentrations were also measured at this time-point. Data collected via a self-administered Health and Lifestyle Questionnaire were used to establish classification of a number of variables. Analyses were conducted on sub-samples with a DII® score and measures of hs-CRP (8,034 men and 9,861 women), and concentrations of vitamin C (9,866 men and 11,702 women), retinol (3,673 men and 3,517 women) and cholesterol-adjusted α- tocopherol (3,623 men and 3,476 women). Analysis of covariance and linear regression were used to study associations across sex-specific quintiles of the DII® score (adjusted for age, BMI, smoking status, physical activity, social class and educational level), where a higher score indicates a more pro-inflammatory diet.

Mean concentrations in men and women were 2.99 and 3.09 mg/L for hs-crp, 47 and 59 μmol/L for vitamin C, 53 and 50 μg/dL for retinol and 4.34 and 4.42 μmol/mmol for cholesterol-adjusted α- tocopherol, respectively. In both men and women, mean hs-CRP was higher if the diet was more pro-inflammatory (p-trend = 0.02 in men and 0.07 in women), while concentrations of vitamin C, retinol and α-tocopherol were significantly lower (p-trend < 0.001). Positive associations for hs-CRP, but negative associations for plasma concentrations of vitamin C, retinol and α-tocopherol were evident in both men and women, after adjustments for covariates (p-trend < 0.001). The differences between Q1 and Q5 adjusted means for hs-CRP, vitamin C, retinol and α-tocopherol were +9.4%, -22.1%, -3.9% and -8.6% in men and +7.9%, -17.5%, -4.8% and -7.6% in women, respectively.

We observed statistically significant positive associations between the DII® score and hs-CRP, a well-known inflammatory biomarker, whilst significant negative associations were found for circulating concentrations of three anti-inflammatory vitamins, after adjustment for covariates. These findings indicate that the DII® score is a valid measure of the inflammatory potential of diet in these middle-aged and old adults, making it possible to study the inflammatory role of diet in MLTC development.