Phytosterols/phytostanols are bioactive compounds found in vegetable oils, nuts and seeds and added to a range of commercial food products. Consumption of phytosterols/phytostanols reduces levels of circulating LDL-cholesterol, a causative biomarker of CVD, and is linked to a reduced risk of some cancers. Individuals who consume phytosterols/phytostanols in their diet may do so for many years as part of a non-pharmacological route to lower cholesterol or as part of a healthy diet. However, the impact of long term or high intakes of dietary phytosterols/phytostanols has not been on whole-body epigenetic changes before. The aim of this systematic review was to identify all publications that have evaluated changes to epigenetic mechanisms (post-translation modification of histones, DNA methylation and miRNA expression) in response to phytosterols/phytostanols. A systematic search was performed that returned 226 records, of which eleven were eligible for full-text analysis. Multiple phytosterols were found to inhibit expression of histone deacetylase (HDAC) enzymes and were also predicted to directly bind and impair HDAC activity. Phytosterols were found to inhibit the expression and activity of DNA methyl transferase enzyme 1 and reverse cancer-associated gene silencing. Finally, phytosterols have been shown to regulate over 200 miRNA, although only five of these were reported in multiple publications. Five tissue types (breast, prostate, macrophage, aortic epithelia and lung) were represented across the studies, and although phytosterols/phytostanols alter the molecular mechanisms of epigenetic inheritance in these mammalian cells, studies exploring meiotic or transgenerational inheritance were not found.

We evaluated whether plant stanol esters mixed with different vegetable oil spreads improved arterial health. A total of 200 adults with serum cholesterol >5 mmol/l were randomised to consume camelina, rapeseed or sunflower oil spread with stanol (2 g/d) ester or sunflower oil spread without stanol ester (controls) for 3 months. Non-invasive ultrasound was used to measure carotid artery compliance (CAC) and brachial artery flow-mediated endothelial dependent vasodilatation (FMD) at baseline and after the intervention as markers of arterial health. Plant stanol esters reduced LDL-cholesterol by 9 % compared with controls (P < 0·001) similarly in the different treatment groups. In the combined treatment groups (n 147), CAC or FMD were not changed from controls (n 47). In a subgroup analysis, division of subjects at baseline into below and over sex-specific 50th percentiles of CAC and FMD revealed that low CAC was improved from 1·23 to 1·59 % per 10 mmHg in the treatment group (n 69), and from 1·42 to 1·47 % per 10 mmHg in controls (n 25), (P = 0·0035 between groups). Low FMD was improved from 6·9 % to 8·6 % in the treatment group (n 73) and from 6·6 % to 6·8 % in controls (n 24) (P = 0·05 between groups). In the respective high-median groups, CAC and FMD were not changed in spite of significantly lowered LDL-cholesterol. In conclusion, consumption of plant stanol ester for 3 months had no overall significant effect on arterial elasticity and endothelial function. A controlled study is needed to test whether beneficial changes are obtained in subjects with initially reduced arterial elasticity and endothelial function.

Phagostimulant activities of sucrose, sitosterol, stigmasterol, campesterol, and soybean leaf extractables were evaluated towards the third-instar larvae of the cabbage looper, Trichoplusia ni Hubner (Lepidoptera: Noctuidae) on elderberry-pith discs under laboratory conditions. There was a linear relationship between sucrose dosage and larval feeding on the pith discs. Water fraction from PI 227687 soybean leaf extractables at dosages > 400 μg/disc inhibited feeding by T. ni larvae. Ethyl acetate fraction showed phagostimulant properties comparable to sucrose. Sterols (5 μg/disc) and soybean leaf extractables (40 μg/disc) in combination with sucrose (400 μg/disc) showed synergistic effect as phagostimulants. Implications of genotypic differences in sterol content in relation to host plant resistance are discussed.