Coeliac disease (CD) is an autoimmune gastrointestinal disorder whereby the ingestion of gluten, a storage protein found in wheat, barley and rye, causes damage to intestinal mucosa with resultant malabsorption, increased risk of anaemia and osteoporosis. Worldwide estimates suggest 1% of the population have CD. With no cure, the only treatment is a gluten-free diet (GFD). Adhering to a GFD can be very challenging; it requires knowledge, motivation and modified behaviours. Assessing adherence to a GFD is methodologically challenging. This review aims to provide an overview of the literature reporting adherence to a GFD in people with CD and the methodological challenges encountered. From six studies it has been reported that rates of adherence to a GFD range between 45 and 90% in patients of different ethnicities with CD. GF dietary adherence can be influenced by age at diagnosis, coexisting depression, symptoms on ingestion of gluten, nutrition counselling, knowledge of GF foods, understanding of food labels, cost and availability of GF foods, receiving GF foods on prescription and membership of a coeliac society. To date only five intervention studies in adults with CD have been undertaken to improve GF dietary adherence. These have included dietary and psychological counselling, and the use of online training programmes, apps, text messages and telephonic clinics. Future interventions should include people of all ethnicities, consider patient convenience and the cost-effectiveness for the healthcare environment.

Colorectal cancer (CRC) is the third most common cancer globally. CRC risk is increased by obesity, and by its lifestyle determinants notably physical inactivity and poor nutrition. Obesity results in increased inflammation and oxidative stress which cause genomic damage and contribute to mitochondrial dysregulation and CRC risk. The mitochondrial dysfunction associated with obesity includes abnormal mitochondrial size, morphology and reduced autophagy, mitochondrial biogenesis and expression of key mitochondrial regulators. Although there is strong evidence that increased adiposity increases CRC risk, evidence for the effects of intentional weight loss on CRC risk is much more limited. In model systems, energy depletion leads to enhanced mitochondrial integrity, capacity, function and biogenesis but the effects of obesity and weight loss on mitochondria in the human colon are not known. We are using weight loss following bariatric surgery to investigate the effects of altered adiposity on mitochondrial structure and function in human colonocytes. In summary, there is strong and consistent evidence in model systems and more limited evidence in human subjects that over-feeding and/or obesity result in mitochondrial dysfunction and that weight loss might mitigate or reverse some of these effects.

Menopause, the permanent cessation of the menstrual cycle, marks the end of a woman's reproductive lifespan. In addition to changes in sex hormone levels associated with menopause, its timing is another predictor of future health outcomes such as duration of the presence of vasomotor symptoms (VMS) and the risk of hormone-related cancers. With ageing of the population, it is estimated that worldwide 1·2 billion women will be menopausal by the year 2030. Previously the effects of reproductive factors (e.g. parity, age at menarche, pregnancy) and socio-demographic factors on intermediate and long-term health outcomes of menopause have been widely documented. However, little is known about whether diet could have an impact on these. Therefore, we review current evidence on the associations of diet with menopause, presence of VMS and the risk of hormone-related cancers such as ovarian, endometrial and breast cancer. Dietary factors could influence the lifespan of the ovaries and sex-hormones levels, hence the timing of natural menopause. Few studies reported an association between diet, in particular soya consumption, and a reduced risk of VMS. Sustained oestrogen exposure has been associated with a higher risk of hormone-related cancers and thus high-fat and meat diets have been linked with an increased risk of these cancers. However, to better understand the mechanistic pathways involved and to make stronger conclusions for these relationships, further studies investigating the associations of dietary intakes and dietary patterns with menopause, presence of VMS and the risk of hormone-related cancers are required.

The functional effects of folate within C1 metabolism involve interrelationships with vitamin B12, vitamin B6 and riboflavin, and related gene–nutrient interactions. These B vitamins have important roles throughout life, from pregnancy, through childhood, to middle and older age. Achieving optimal nutritional status for preventing folate-related disease is challenging, however, primarily as a result of the poor stability and incomplete bioavailability of folate from natural food sources when compared with the synthetic vitamin form, folic acid. Thus, in European countries, measures to prevent neural tube defects (NTD) have been largely ineffective because of the generally poor compliance of women with folic acid supplementation as recommended before and in early pregnancy. In contrast, countries worldwide with mandatory folic acid fortification policies have experienced marked reductions in NTD. Low vitamin B12 status is associated with increased risk of cognitive dysfunction, CVD and osteoporosis. Achieving optimal B12 status can be problematic for older people, however, primarily owing to food-bound B12 malabsorption which leads to sub-clinical deficiency even with high dietary B12 intakes. Optimising B-vitamin intake may be particularly important for sub-populations with impaired folate metabolism owing to genetic characteristics, most notably the 677C→T variant in the gene encoding the enzyme methylenetetrahydrofolate reductase (MTHFR). This common folate polymorphism is linked with several adverse health outcomes, including stroke, however, recent evidence has identified its novel interaction with riboflavin (the MTHFR cofactor) in relation to blood pressure and risk of developing hypertension. This review addresses why and how the optimal status of folate-related B vitamins should be achieved through the lifecycle.

The term ‘sweeteners’ encompasses both nutritive and non-nutritive sweeteners, which when added to food/beverages, can enhance the flavour and other functional properties of food/beverage products. This review considers how dietary biomarker approaches may enhance current understanding of nutritive sweetener (namely free sugars) and non-nutritive or low-energy sweetener (LES) intakes and how these may impact health. Recent public health strategies to reduce free sugar consumption will help contribute to challenging sugar intake targets. Robust evaluation is needed to determine the effectiveness of these approaches to reducing free sugar consumption. LES provides a sweet taste without the addition of appreciable energy and can help maintain the palatability of reformulated products. All LES undergo rigorous safety evaluations prior to approval for use. Whilst intervention data suggest LES can be beneficial for health (relating to weight status and glycaemic control), debate persists on their use and findings from population-based research are mixed, in part because of potential contributing factors such as reverse causality. Additionally, assessments often consider only certain sources of LES (e.g. LES-beverages) and/or LES as a homogeneous group despite differing biological fates, thus not adequately capturing intakes of individual LES or allowing for reliable estimation of overall intakes. Urinary biomarker approaches developed/investigated for sweetener consumption have the potential to overcome existing limitations of dietary data by providing more objective intake data, thereby enhancing population-based research. In conclusion, such biomarker approaches to the concomitant study of free sugars and LES intakes are timely and represent interesting developments in an area of significant public health interest.