Inflammation is a normal process that is part of host defence and tissue healing. However, excessive or unresolved inflammation can lead to uncontrolled tissue damage, pathology and disease. In humans on a Western diet, the omega-6 polyunsaturated fatty acid arachidonic acid (ARA) makes a significant contribution to the fatty acids present in the membrane phospholipids of cells involved in inflammation. ARA is a precursor to a number of potent pro-inflammatory mediators including well described prostaglandins and leukotrienes, which has led to the development of anti-inflammatory pharmaceuticals that target the ARA pathway to successfully control inflammation. Hence, it is commonly believed that increasing dietary intake of the omega-6 fatty acids ARA or its precursor linoleic acid (LA) will increase inflammation. However, studies in healthy human adults have found that increased intake of ARA or LA does not increase the concentrations of many inflammatory markers. Epidemiological studies have even suggested that ARA and LA may be linked to reduced inflammation. Contrastingly, there is also evidence that a high omega-6 fatty acid diet inhibits the anti-inflammatory and inflammation-resolving effect of the omega-3 fatty acids. Thus, the interaction of omega-3 and omega-6 fatty acids and their lipid mediators in the context of inflammation is complex and still not properly understood.

acid-rich vegetable oil-based enteral and parenteral nutrition is still widely used, newer lipid 53 components such as medium-chain triglycerides and olive oil are safe and well tolerated. Fish 54 oil (FO)-enriched enteral and parenteral nutrition appears to be well tolerated and confers 55 additional clinical benefits, particularly in surgical patients, due to its anti-inflammatory and 56immune-modulating effects. Whilst the evidence base is not conclusive, there appears to be a 57 potential for FO-enriched nutrition, particularly administered peri-operatively, to reduce the rate 58 of complications and intensive care unit (ICU) and hospital stay in surgical ICU patients. The 59 evidence for FO-enriched nutrition in non-surgical ICU patients is less clear regarding its clinical 60 benefits and additional, well-designed large-scale clinical trials need to be conducted in this 61 area. The ESPEN Expert Group supports the use of olive oil and FO in nutrition support in 62 surgical and non-surgical ICU patients but considers that further research is required to provide 63 a more robust evidence base. 64 65 Page 4 of 77 Nutrition support of the critically ill patient 66Patients in an intensive care unit (ICU) are heterogeneous and include surgical and medical 67 patients, mechanically-ventilated or non-ventilated, obese or undernourished, preterm infants to 68 older adults, requiring either short-term or long-term intensive care [1]. Nutrition support is 69 critical in maintaining homeostasis in the ICU patient and to provide nutrients for the 70 maintenance of lean body mass as well as repair and maintenance of organ function and 71 support of defense and healing processes. 72Enteral nutrition (EN) comprises specialized liquid nutrition delivered through a nasogastric or 73 post-pyloric feeding tube into the stomach or small intestine (duodenum/jejunum), respectively 74[2]. The European Society for Clinical Nutrition and Metabolism (ESPEN) guidelines recommend 75 that EN should be given to all ICU patients who are not expected to be taking a full oral diet 76 within three days [3]. 77Whilst ESPEN acknowledges that there are no definitive data supporting the early use of EN in 78 terms of clinical outcomes, its guidelines recommend that hemodynamically stable critically ill 79 patients who have a functioning gastrointestinal tract should be fed early (< 24 hours) using an 80 appropriate amount of feed [3]. Early initiation of EN is also recommended by the American 81 Society for Parenteral and Enteral Nutrition (ASPEN) and the Canadian Society of Critical Care 82Medicine (SCCM) [4], as well as the European Society of Intensive Care Medicine (ESICM) [5]. 83Administration of early EN in critically ill patients appears to also have a positive economic 84 impact, with analysis suggesting that it is associated with significantly reduced costs relating to 85 reduction in ICU stay and duration of mechanical ventilation compared with standard care [6]. 86There are a number of nutritional and non-nutritional benefits associa...

The omega-3 (n-3) fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are found in seafood (especially fatty fish), supplements and concentrated pharmaceutical preparations. Long-term prospective cohort studies consistently demonstrate an association between higher intakes of fish, fatty fish and marine n-3 fatty acids (EPA + DHA) or higher levels of EPA and DHA in the body and lower risk of developing cardiovascular disease (CVD), especially coronary heart disease (CHD) and myocardial infarction (MI), and cardiovascular mortality in the general population. This cardioprotective effect of EPA and DHA is most likely due to the beneficial modulation of a number of known risk factors for CVD, such as blood lipids, blood pressure, heart rate and heart rate variability, platelet aggregation, endothelial function, and inflammation. Evidence for primary prevention of CVD through randomised controlled trials (RCTs) is relatively weak. In high-risk patients, especially in the secondary prevention setting (e.g., post-MI), a number of large RCTs support the use of EPA + DHA (or EPA alone) as confirmed through a recent meta-analysis. This review presents some of the key studies that have investigated EPA and DHA in the primary and secondary prevention of CVD, describes potential mechanisms for their cardioprotective effect, and evaluates the more recently published RCTs in the context of existing scientific literature.

A large body of evidence supports the cardioprotective effects of the long-chain omega-3 polyunsaturated fatty acids (PUFAs), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). There is increasing interest in the independent effects of EPA and DHA in the modulation of cardiometabolic risk factors. This systematic review aims to appraise the latest available evidence of the differential effects of EPA and DHA on such risk factors. A systematic literature review was conducted up to May 2017. Randomised controlled trials were included if they met strict eligibility criteria, including EPA or DHA > 2 g/day and purity ≥ 90%. Eighteen identified articles were included, corresponding to six unique studies involving 527 participants. Both EPA and DHA lowered triglyceride concentration, with DHA having a greater triglyceride-lowering effect. Whilst total cholesterol levels were largely unchanged by EPA and DHA, DHA increased high-density lipoprotein (HDL) cholesterol concentration, particularly HDL2, and increased low-density lipoprotein (LDL) cholesterol concentration and LDL particle size. Both EPA and DHA inhibited platelet activity, whilst DHA improved vascular function and lowered heart rate and blood pressure to a greater extent than EPA. The effects of EPA and DHA on inflammatory markers and glycaemic control were inconclusive; however both lowered oxidative stress. Thus, EPA and DHA appear to have differential effects on cardiometabolic risk factors, but these need to be confirmed by larger clinical studies.