Lifestyle modifications that include adherence to healthy dietary patterns that are low in saturated fat have been associated with reduced risk for cardiovascular disease, the leading cause of death globally. Whole-milk dairy foods including milk, cheese, and yogurt, are leading sources of saturated fat in the diet. Dietary guidelines around the world recommend the consumption of low-fat and fat-free dairy foods to obtain overall healthy dietary patterns that help meet nutrient recommendations while keeping within recommended calorie and saturated fat limitations. A body of observational and clinical evidence indicates, however, that whole-milk dairy food consumption, despite saturated fat content, does not increase risk for cardiovascular disease. This review describes the proposed biological mechanisms underlying inverse associations between whole-milk dairy food consumption and risk markers for cardiometabolic health, such as altered lipid digestion, absorption, and metabolism; influence on the gut microflora; and regulation of oxidative stress and inflammatory responses. The dairy food matrix, a term used to describe how the macro- and micronutrients and other bioactive components of dairy foods are differentially packaged and compartmentalized among fluid milk, cheese, and yogurt, may dictate how each affects cardiovascular risk. Current evidence indicates consideration of dairy foods as complex food matrices, rather than delivery systems for isolated nutrients, such as saturated fatty acids, is warranted.

Carotenoids have been associated with risk reduction for several chronic diseases, including the association of their dietary intake/circulating levels with reduced incidence of obesity, type 2 diabetes, certain types of cancer, and even lower total mortality. In addition to some carotenoids constituting vitamin A precursors, they are implicated in potential antioxidant effects and pathways related to inflammation and oxidative stress, including transcription factors such as nuclear factor kappa B (NF-κB) and nuclear factor erythroid 2-related factor 2 (Nrf2). Carotenoids and metabolites may also interact with nuclear receptors, mainly retinoic acid receptor/retinoid X receptor (RAR/RXR) and peroxisome proliferator-activated receptors (PPARs) that play a role in the immune system and cellular differentiation. Therefore, a large number of downstream targets are likely influenced by carotenoids, including but not limited to genes, proteins implicated in oxidative stress and inflammation, antioxidant enzymes and cellular differentiation processes. Furthermore, recent studies also propose an association between carotenoid intake and gut microbiota. While all these endpoints could be individually assessed, a more complete/integrative way to determine a multitude of health-related aspects of carotenoids includes (multi)-omics-related techniques, especially transcriptomics, proteomics, lipidomics and metabolomics, but also metagenomics, measured in a variety of biospecimens including plasma, urine, stool, white blood cells or other tissue cellular extracts. In this review, we highlight the use of -omics technologies to assess health-related effects of carotenoids in mammalian organisms and models.