Effects of aronia melanocarpa juice on plasma and liver phospholipid fatty acid composition in wistar rats

A nutritional placebo-controlled study was performed in Wistar rats in order to investigate the effects of 5-weeks aronia juice consumption towards fatty acid (FA) composition of phospholipids in the plasma and liver, as well as plasma glucose (Glu) and cholesterol levels. The animals were divided into 3 groups of 8 animals each, and randomized to receive either the full polyphenol dose of Aronia melanocarpa juice (AMJ), 4 times less polyphenol dose (1/4-AMJ) or polyphenol-lacking placebo beverage (PLB). Each group of 8 male adult Wistar rats received the liquid ad libitum. AMJ decreased the levels of low-density lipoprotein (LDL) (P lt 0.05) vs. PLB. AMJ increased dihomo-gamma-linoleic acid (DGLA, 20: 3n-6) (P lt 0.05) and decreased arachidonic acid content (AA, 20: 4n-6) (P lt 0.05) vs. PLB in liver phospholipids. AMJ significantly increased monounsaturated fatty acids (MUFA) levels both in the liver (P lt 0.05) and plasma (P lt 0.05). Both aronia juice doses elevated the levels of beneficial n-3 polyunsaturated fatty acids (PUFA) in the plasma and liver. There was a dose-dependent, significant increase (P lt 0.001) in cis-vaccenic acid (VA, 18: 1n-7) in phospholipids in the plasma and liver. Our results indicate favorable effects of aronia juice intake on lipid parameters in Wistar rats. These findings suggest the potential of aronia dietary intake in cardiometabolic diseases primary prevention strategies in the human population

Omega-3 PUFA metabolism and brain modifications during aging

In Canada, 5.5 million (16% of Canadians) adults are >65 years old and projections suggest this number will be approximately 20% of Canadians by 2024. A major concern regarding old age is a decline in health, especially if this entails a loss of self-sufficiency and independence caused by a decline in cognition. The brain contains 60% of fat and is one of the most concentrated organs in long chain omega-3 fatty acids such as docosahexaenoic acid (DHA). During aging, there are physiological modifications in the metabolism of lipids that could also have consequences on brain structure and levels of DHA. This review will hence discuss the physiological modifications in the metabolism of lipids during aging with a focus on long chain omega-3 and omega-6 fatty acids and also outline the structural and functional modifications of the brain during aging including brain lipid modifications and its relation to higher levels of DHA and cognition. Therefore, in this review, we outline the importance of collecting more data on the biology of aging since it might highly improve our understanding about what are «normal» modifications occurring during aging and what can become pathological

Low Levels of the Omega-3 Index are Associated with Sudden Cardiac Arrest and Remain Stable in Survivors in the Subacute Phase

In previous studies, low blood levels of n-3 fatty acids (FA) have been associated with increased risk of cardiac death, and the omega-3 index (red blood cell (RBC) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) expressed as weight percentage of total FA) has recently been proposed as a new risk factor for death from coronary artery disease, especially following sudden cardiac arrest (SCA). As blood samples often haven been harvested after the event, the aim of our study was to evaluate the stability of RBC fatty acids following SCA. The total FA profile, including the omega-3 index, was measured three times during the first 48 h in 25 survivors of out-of-hospital cardiac arrest (OHCA), in 15 patients with a myocardial infarction (MI) without SCA and in 5 healthy subjects. We could not demonstrate significant changes in the FA measurements in any of the groups, this also applied to the omega-6/omega-3 ratio and the arachidonic acid (AA)/EPA ratio. Furthermore, we compared the omega-3 index in 14 OHCA-patients suffering their first MI with that of 185 first-time MI-patients without SCA; mean values being 4.59% and 6.48%, respectively (p = 0.002). In a multivariate logistic regression analysis, a 1% increase of the omega-3 index was associated with a 58% (95% CI: 0.25–0.76%) reduction in risk of ventricular fibrillation (VF). In conclusion, the omega-3 index remained stable after an event of SCA and predicted the risk of VF

Chemokine ligand 18 predicts all-cause mortality in patients hospitalized with chest pain of suspected coronary origin

Introduction Chemokines mediate recruitment and activation of leucocytes. Chemokine ligand 18 (CCL18) is mainly expressed by monocytes/macrophages and dendritic cells. It is highly expressed in chronic inflammatory diseases, and locally in atherosclerotic plaques, particularly at sites of reduced stability, and systemically in acute coronary syndrome patients. Reports on its prognostic utility in the latter condition, including myocardial infarction (MI), are scarce. Aim To assess the utility of CCL18 as a prognostic marker of recurrent cardiovascular events in patients hospitalized with chest pain of suspected coronary origin. Methods The population consisted of 871 consecutive chest-pain patients, of whom 386 were diagnosed with acute myocardial infarction (AMI) based on Troponin-T (TnT) levels >50 ng/L. Stepwise Cox regression models, applying normalized continuous loge/SD values, were fitted for the biomarkers with cardiac mortality within 2 years and total mortality within 2 and 7 years as the dependent variables. Results Plasma samples from 849 patients were available. By 2 years follow-up, 138 (15.8%) patients had died, of which 86 were cardiac deaths. Univariate analysis showed a positive, significant association between CCL18 and total death [HR 1.55 (95% 1.30–1.83), p < 0.001], and for cardiac death [HR 1.32 (95% 1.06–1.64), p = 0.013]. Associations after adjustment were non-significant. By 7 years follow-up, 332 (38.1%) patients had died. CLL18 was independently associated with all-cause mortality [HR 1.14 (95% CI, 1.01–1.29), p = 0.030], but not with MI (n = 203) or stroke (n = 55). Conclusion CCL18 independently predicts long-term all-cause mortality but had no independent prognostic bearing on short-term cardiac death and CVD events