Evidence from observational studies, prospective cohort studies and randomized clinical intervention studies indicate that moderate doses of long-chain n-3 polyunsaturated fatty acids (LC n-3 PUFA) significantly decrease risk of fatal coronary heart disease (CHD). Higher doses and longer duration of intervention may also protect from non-fatal CHD events. The exact mechanisms through which LC n-3 PUFA has an effect on CHD are not well established but may include a decrease in fasting and postprandial triacylglycerol levels, a decrease in arrhythmias, modulation of platelet aggregation and decreased synthesis of pro-inflammatory agents. The mechanistic relation between LC n-3 PUFA and inflammation has attracted great interest, and in vitro studies have revealed that these fatty acids decrease endothelial activation, affect eicosanoid metabolism (including epoxygenation pathways) and induce inflammatory resolution. However, the effects of LC n-3 PUFA on established biomarkers of inflammation and endothelial activation in vivo are not strong. Consequently we need new and more sensitive and systemic biomarkers to reveal the effects of LC n-3 PUFA on localized inflammatory processes.

Low folate intake is associated with colon cancer. We combined a proteomics and biochemical approach to identify proteins and pathways affected by folate deficiency in human colonocytes. Folate differentially altered activity and expression of proteins involved in proliferation [e.g., PCNA], DNA repair [e.g., XRCC5, MSH2], apoptosis [e.g., BAG family chaperone protein, DIABLO and porin], cytoskeletal organization [e.g., actin, ezrin, elfin], and expression of proteins implicated in malignant transformation [COMT, Nit2].

Salt sensitivity, which is an increase in blood pressure in response to high dietary salt intake, is an independent risk factor for cardiovascular disease and mortality. It is associated with physiological, environmental, demographic, and genetic factors. This review focuses on the physiological mechanisms of salt sensitivity in populations at particular risk, along with the associated dietary factors. The interplay of mechanisms such as the renin-angiotensin aldosterone system, endothelial dysfunction, ion transport, and estrogen decrease in women contributes to development of salt sensitivity. Because of their effects on these mechanisms, higher dietary intakes of potassium, calcium, vitamin D, antioxidant vitamins, and proteins rich in L-arginine, as well as adherence to dietary patterns similar to the DASH (Dietary Approaches to Stop Hypertension) diet, can be beneficial to salt-sensitive populations. In contrast, diets similar to the typical Western diet, which is rich in saturated fats, sucrose, and fructose, together with excessive alcohol consumption, may exacerbate salt-sensitive changes in blood pressure. Identifying potential mechanisms of salt sensitivity in susceptible populations and linking them to protective or harmful dietary and lifestyle factors can lead to more specific guidelines for the prevention of hypertension and cardiovascular disease.

Salt sensitivity is an independent CVD and mortality risk factor, which is present in both hypertensive and normotensive populations. It is genetically determined and it may affect the relationship between salt taste perception and salt intake. The aim of this study was to explore the genetic predisposition to salt sensitivity in a young and a middle-aged adult population and its effects on salt taste perception and salt intake. The effects of Na loading on blood pressure (BP) were investigated in twenty normotensive subjects and salt sensitivity defined as the change in BP after 7 d of low-Na (51·3 mmol Na/d) and 7 d of high-Na diet (307·8 mmol Na/d). Salt taste perception was identified using the British Standards Institution sensory analysis method (BS ISO 3972:2011). Salt intake was assessed with a validated FFQ. DNA was genotyped for SNP in the SLC4A5, SCNN1B and TRPV1 genes. The subjects with AA genotype of the SLC4A5 rs7571842 exhibited the highest increase in BP (∆ systolic BP=7·75 mmHg, P=0·002, d=2·4; ∆ diastolic BP=6·25 mmHg, P=0·044, d=1·3; ∆ mean arterial pressure=6·5 mmHg, P=0·014, d=1·7). The SLC4A5 rs10177833 was associated with salt intake (P=0·037), and there was an association between salt taste perception and salt sensitivity (r s 0·551, P=0·041). In conclusion, there is a genetic predisposition to salt sensitivity and it is associated with salt taste perception. The association between salt taste perception and discretionary salt use suggests that preference for salty taste may be a driver of salt intake in a healthy population and warrants further investigation.