Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline associated with oxidative stress, neuroinflammation, tau neurofibrillary tangles, amyloid-beta plaque deposition, and metabolic dysfunction. Increasing evidence suggests that the gut microbiota plays an important role in AD pathogenesis through the microbiota–gut–brain axis. This review aims to provide a comprehensive overview of the role of the gut microbiota in AD and healthy aging, with a particular focus on microbiota-targeted preventive and therapeutic strategies and their potential to influence disease progression. Recent studies have demonstrated that alterations in gut microbial composition are closely associated with AD. Patients with AD commonly exhibit a reduced abundance of short-chain fatty acid–producing bacteria and an increased prevalence of lipopolysaccharide-producing taxa, supporting a mechanistic link between microbial dysbiosis, systemic inflammation, and neurodegeneration. Emerging evidence indicates that dietary patterns, prebiotics, probiotics, synbiotics, postbiotics, and microbiota-based therapies, including fecal microbiota transplantation (FMT), may beneficially modulate gut microbial composition and influence AD-related pathophysiological processes. In addition, lifestyle factors such as sleep quality and physical activity have been increasingly recognized for their interactions with the gut–brain axis and their potential to affect cognitive health. Current evidence highlights the gut microbiota as a promising therapeutic target in AD prevention and management. Microbiota-directed interventions, together with healthy dietary and lifestyle modifications, may help attenuate neuroinflammation, improve metabolic homeostasis, and delay cognitive decline. Furthermore, given the substantial global economic burden of AD, microbiota-focused preventive strategies may contribute not only to improving clinical outcomes but also to reducing long-term healthcare and societal costs. Future longitudinal and interventional studies are needed to establish causal relationships and determine the efficacy of microbiota-based therapies in AD.
This systematic review evaluates the association between nut consumption and kidney health outcomes, including kidney function markers and chronic kidney disease (CKD) incidence, prevalence, and mortality. Given the nutritional benefits of nuts and the growing burden of CKD, we aimed to assess whether nut consumption is associated with kidney-related outcomes and to assess the strength and consistency of the available evidence. Recent observational studies and cohort analyses provide emerging but heterogeneous evidence on the relationship between nut intake and kidney outcomes. Higher nut consumption and substitution of red and processed meat with nuts are associated with lower CKD risk or prevalence in some populations. However, findings for specific kidney function markers, such as estimated glomerular filtration rate and albuminuria, remain inconsistent across studies. Nuts have also been evaluated within plant-based dietary indices and through biomarker-based approaches, yielding complementary but non-uniform results. Evidence in individuals with established CKD or high-risk populations is limited. Overall, variability in exposure definitions, outcome measures, and study populations contributes to uncertainty in the strength and consistency of associations. Current evidence suggests that nut consumption, particularly when nuts replace red and processed meat, may be associated with favorable kidney-related outcomes in some populations. However, the evidence is predominantly observational and does not establish causality or an optimal level of nut consumption for kidney health. The heterogeneity in study design and outcome assessment further constrains definitive conclusions. Future research should prioritize well-designed prospective studies and randomized controlled trials to establish causality, clarify dose–response relationships, and determine the role of nuts in CKD-specific dietary recommendations for its prevention and management.
Questions challenging the healthfulness of diets high in linoleic acid (LA) and seed oils, which are major sources of this essential fatty acid, have recently arisen. These questions are especially relevant to adherents of plant-based diets as their LA intake is higher than the general population. Some maintain that LA increases inflammation and oxidative stress and for these reasons, despite its ability to lower circulating LDL-cholesterol levels when replacing saturated fat, does not lower cardiovascular disease (CVD) risk. Because most of the discussion about LA has focused on CVD, the primary focus of this manuscript is to examine the effects of LA on health outcomes aside from CVD. Interventional and observational studies indicate increasing LA intake lowers risk of CVD. Beyond CVD, possible benefits include preventing hepatic fat accumulation, increasing muscle mass, decreasing risk of skin cancer, decreasing epigenetic aging, increasing the healthspan, and improving cognitive function and decreasing risk of developing neurocognitive disorders. Support for these proposed benefits comes from observational studies and randomized controlled trials (RCTs), although more from the former. The observational evidence is especially robust in the case of cognitive function and neurological disorders, as the results of all but one of the eight recently published cohort studies show LA exposure, as assessed by dietary intake or circulating levels, is supportive of benefit, although much of the data come from analyses of one cohort. While it is premature to conclude that LA intake exerts benefits beyond CVD, evidence is sufficient to warrant that this possibility should be included in discussions about the role of LA and seed oils in the diet. Given the large contribution LA makes to energy intake, particularly among consumers of plant-based diets, research aimed at more definitively determining the range of possible benefits, especially related to cognitive function, is warranted.
Excessive intake of added sugars, particularly from sugar-sweetened beverages (SSBs), is an important global public health concern associated with increased risks of obesity, type 2 diabetes, cardiovascular diseases, and other non-communicable diseases. However, the health impacts of sugar consumption are influenced by broader dietary patterns, total energy intake, and overall diet quality. Although sugar plays important sensory and functional roles in food, including flavour enhancement, texture, colour development, and shelf-life extension, growing concerns regarding excessive added sugar intake have driven global efforts to reduce sugar content in processed foods. This review outlines current strategies undertaken by the food industry and regulatory authorities to address this challenge. Industry-driven initiatives include product reformulation, substitution with natural and artificial sweeteners, intrinsic sugar reduction through processing innovations, and portion-control strategies. In parallel, regulatory actions, such as sugar taxation, mandatory nutritional labelling, and public awareness campaigns have been implemented to promote healthier purchasing behaviours and dietary choices. While these interventions have contributed to progress in sugar reduction, challenges persist concerning consumer acceptability, labelling transparency, cross-regional policy inconsistencies, and limited long-term evidence regarding population-level health impacts. Emerging technologies, including enzymatic sugar modification, rare sugar production, and fermentation-derived sweeteners, offer promising solutions but require further validation regarding safety, scalability, sustainability, and consumer acceptance. Effective sugar reduction strategies demand an integrated framework that combines technological innovation, policy alignment, and behavioural change. Strengthened collaboration between industry, governments, and consumers is essential to developing healthier and more sustainable food systems.
Food loss and waste represent major challenges for food systems, while fruit and vegetable by-products generated during processing are underused sources of bioactive compounds with potential applications in functional food development. The present review aims to examine the valorization of beetroot and watermelon by-products as functional ingredients associated with nitric oxide (NO) bioavailability, vascular function, and cardiovascular health. Given that impaired NO signaling is a hallmark of endothelial dysfunction and cardiometabolic disease, nutritional strategies capable of modulating NO-related pathways are of growing interest. Beetroot by-products, including peels and pomace, contain betalains, phenolic compounds, dietary fiber, and other constituents of potential functional relevance. However, nitrate content is rarely measured in these materials, and direct evidence that their consumption increases nitrate bioavailability or improves vascular function is currently lacking. Their proposed contribution to the nitrate–nitrite–NO pathway is therefore based mainly on evidence from conventional nitrate-rich beetroot products. In contrast, watermelon rind is a natural source of L-citrulline, which is bioavailable after ingestion and may support NO production through the citrulline–arginine–eNOS pathway. Human studies have demonstrated the bioavailability of L-citrulline derived from watermelon rind, while studies using a microencapsulated rind juice providing 4 g of L-citrulline have reported improvements in conduit artery endothelial function. Antioxidant compounds present in these by-products may also help limit oxidative degradation of NO, although this effect has not been directly demonstrated. Beetroot and watermelon by-products are linked to distinct pathways of NO generation but are currently supported by different levels of evidence. Future studies should quantify nitrate in beetroot by-products and L-citrulline in watermelon rind, including in the corresponding final food products, and evaluate changes in circulating nitrate, nitrite, and amino acids together with vascular function in well-controlled clinical studies.
