Stroke is one of the leading causes of long-term disability and mortality. Mounting evidence from observational studies suggests that among lifestyle factors, diet may play an important role for the prevention of stroke. Neuroimaging markers, particularly white matter hyperintensity (WMH) and brain infarcts (BI), are more sensitive measurements of cerebrovascular disease than clinical assessments. We reviewed published observational and clinical studies that evaluate the association between dietary factors and WMH and BI. The few existing studies examined only a handful individual nutrients or foods (dietary intake of alcohol, B vitamins, fish, choline, serum markers of antioxidants) and a few food groups, Mediterranean-style diet, and nutrient biomarker patterns. Findings from these studies are inconclusive either due to conflicting results from different studies or due to lack of replication. Further studies are necessary to replicate the existing findings. Many other foods or nutrients or dietary patterns may worth investigating and longitudinal studies are needed.

Mounting evidence continues to point to dietary habits as a modifier of cancer risk and tumor behavior; although it is clear that considerable variability occurs across studies. While genetic public health messages can be developed, the use of mean values may result in underexposure to some essential and nonessential food components, yet precipitate overexposure to nutrients. Undeniably, inconsistencies in the literature may reflect variation in timing of exposures to specific dietary constituents, interactions with the food matrix, processing technologies, or the genomic variation among individuals, which can influence absorption, metabolism, and/or the molecular target. Interindividual variability in genetics, epigenetics, transcriptomics, proteomics, metabolomics, or microbiomics can influence the magnitude and direction of response to bioactive food components, as briefly reviewed in this article. Unquestionably, understanding nutrigenomics holds promise to reveal those who will benefit most from dietary interventions plus identify any who might be placed at risk due to overexposures.

Cardiovascular disease (CVD) is the leading cause of death worldwide. Risk of CVD is determined by genetic and environmental factors. Numerous dietary factors have been linked to CVD beyond the conventional risk factors. In the past few years, genome-wide association studies have also identified more than 30 genomic loci that determine the susceptibility to cardiovascular events. Genetic background may interact with habitual dietary compositions in predisposition to CVD. In this context, large-scale studies of gene–diet interaction in prospective cohorts or randomized intervention trials have emerged to integrate genetic and dietary risk factors in predicting cardiovascular risk. The use of genetic variants to estimate a causal effect between dietary factors and CVD, namely mendelian randomization analysis, has also been considered in the nutritional epidemiology field. The purpose of this review is to present recent advances in research into dietary and genetic risk factors, gene–diet interactions, and mendelian randomization with regard to CVD risk.

The cardiometabolic syndrome is a cluster of metabolic factors that increase an individual’s risk of developing cardiovascular disease and type 2 diabetes mellitus. The metabolic risk factors that cluster in the syndrome include insulin resistance, hypertension, impaired glucose tolerance, central obesity, and dyslipidemia. Other abnormalities, such as chronic proinflammatory and prothrombotic states and oxidative stress, have been added to the syndrome. Magnesium (Mg) plays a key role in regulating insulin action, glucose uptake, and vascular tone. Many experimental, clinical, and epidemiologic studies have shown a clear link between Mg status and any component included in the constellation. Increasing evidence suggests a role for Mg deficiency as a possible unifying mechanism underlying the coincidence among those apparently disparate clinical conditions clustering in the syndrome. Although the use of Mg supplements has been suggested as a potential tool in the prevention of the cardiometabolic syndrome, this needs to be demonstrated by future prospective studies.

Vitamin D deficiency has become a major public health problem worldwide due to its increasing prevalence and potential health risks. There is growing evidence from experimental studies to suggest that vitamin D may influence risk of cardiometabolic disease through multiple pathways, including inhibition of the release of proinflammatory cytokines; regulation of the renin-angiotensin system; and favorable effects on lipids, blood pressure, insulin secretion and action, and thrombosis. Human observational data, primarily from cross-sectional studies, have shown that low dietary vitamin D intake or vitamin D levels are inversely related to various cardiometabolic risk factors. Prospective studies have suggested the relationship between low 25(OH)D and increased risk of cardiometabolic disease, including hypertension, type 2 diabetes, and cardiovascular disease. Evidence from small randomized trials and post-hoc analyses of large clinical trials for the effect of vitamin D supplements on cardiometabolic risk factors, however, remains inconsistent. This article aims to summarize epidemiologic data on the relationship between vitamin D and major cardiometabolic disease and highlight the challenges in translating observational evidence to future intervention studies.

Obesity and overweight status is growing rapidly worldwide. Although there have been enormous advances in explaining the genetic basis of obesity in recent years, the pathways that lead to a high body weight are still not fully understood. Interactions between genetic and environmental factors, including nutrient exposures and dietary behaviors, can influence the development of obesity. Specifically, genes play a decisive role under the permissive circumstances of an obesogenic environment (increase in energy intake with a decrease in physical activity). Given the many factors that influence obesity, as well as the dynamic nature of this health problem (weight gain, weight loss, weight maintenance, variability in body composition), genomic tools have been used to evaluate all possible contributions of genes to the obesity problem. In this report, we present recently discovered gene–diet interaction studies in human obesity. Although existing literature in this specific area is fairly limited, various investigations utilizing large cohorts corroborate the potential for personalized interventions that take into account genetic patterns.

The 2009 review of human carcinogens by the International Agency for Research on Cancer (IARC) determined that there is sufficient evidence in humans to confirm the carcinogenicity of alcohol consumption. From the ample evidence provided, the positive association between alcohol intake and colorectal cancer risk is convincing. Although the site-specific mechanism by which alcohol intake influences colorectal carcinogenesis remains unknown, one notable mechanism is via an effect on the folate pathway. Genetic polymorphisms, such as aldehyde dehydrogenase 2 (ALDH2) and 5,10-methylenetetrahydrofolate reductase (MTHFR), also are suggested to influence the effect of alcohol on colorectal carcinogenesis. Although the mechanism of this carcinogenesis requires further clarification, the avoidance of excess alcohol consumption will substantially contribute to reducing the risk and burden of colorectal cancer attributable to alcohol consumption.

Vitamin D and its potential role in the prevention of cancer have received widespread attention in recent years. A broad range of potential vitamin D–related mechanisms affecting carcinogenesis have been identified. Epidemiology now provides evidence for a cancer protective role of elevated levels of serum vitamin D, particularly for colorectal cancer, and less clearly for breast cancer, while for many other cancers, including cancer of the prostate, no associations have been demonstrated. There continues to be a gap between results from observational trials assessing vitamin D status and those from randomized trials of vitamin D supplementation that cannot be resolved easily. However, whether new randomized trials on vitamin D and cancer development should be conducted in the future remains debatable.

Vitamin D is hypothesized to prevent cancer development, and its potential anticarcinogenic effect against colorectal cancer has been explored in epidemiologic studies. Epidemiologic studies found that a low circulating level of 25-hydroxyvitamin D was associated with higher risk of colorectal cancer, whereas the association for vitamin D intake has not been as clear as for circulating vitamin D levels. A large intervention study on vitamin D supplementation and colorectal cancer did not show a protective benefit against colorectal cancer development, but several possible explanations remain open. Genetic polymorphisms in the pathway of vitamin D metabolism also have drawn attention, and single polymorphism studies and Genome Wide Association Studies (GWAS) have been conducted. Given a relatively high prevalence of vitamin D insufficiency among industrialized populations, further research on the optimal dose and duration of vitamin D supplementation, interaction with other nutrients or genes, and the appropriate timing of vitamin D interventions is warranted.