Impact of Work-Life Balance on the Quality of Life of Spanish Nurses during the Sixth Wave of the COVID-19 Pandemic: A Cross-Sectional Study.

This study addresses the health-related quality of life (HRQoL) of Spanish nurses during the sixth wave of the COVID-19 pandemic, assessed through the EQ-5D and EQ-VAS indices. METHODS: This cross-sectional 334 study used online surveys, recruiting 305 Spanish nurses. RESULTS: Nurses generally perceived a good HRQoL. "Negative work-family interaction" is adversely associated with the EQ-VAS (ß = -0.337, 95% CI [-1.733, -0.723]) and EQ-5D (ß = -0.399, 95% CI [-0.021, -0.01]) indices, while "positive work-family interaction" shows a positive relationship with the EQ-VAS (ß = 0.218, 95% CI [0.381, 1.759]). The presence of a "paid supportive caregiver" is positively associated with the EQ-VAS (ß = 0.18, 95% CI [1.47, 12.3]) and EQ-5D (ß = 0.149, 95% CI [0.004, 0.117]) indices, but a higher "number of children" is negatively linked with the EQ-5D index (ß = -0.146, 95% CI [-0.061, -0.002]). In addition, living with a partner (EQ-VAS ß = 0.16, 95% CI [1.094, 14.67] and EQ-5D index ß = 0.174, 95% CI [0.018, 0.163]) and working a "rotating shift" (EQ-5D index ß = 0.158, 95% CI [0.005, 0.098]) are positively associated. CONCLUSIONS: These findings highlight the need to comprehensively address nurses' well-being, considering both their working conditions and their home environment, especially in crisis contexts such as the current pandemic.

Does Metformin Modulate Mitochondrial Dynamics and Function in Type 2 Diabetic Patients?

Metformin is an effective drug against type 2 diabetes (T2D), a pathogenesis in which mitochondrial dysfunction is one of the main players. Thus, our first aim was to describe the effect of metformin on mitochondrial function in an outpatient population with T2D. For analyzing this hypothesis, we performed a preliminary cross-sectional study complying with the STROBE requirements. We studied leukocytes from 139 healthy controls, 39 T2D patients without metformin treatment, and 81 T2D patients who had been on said treatment for at least 1 year. Leukocytes from T2D patients displayed higher total and mitochondrial reactive oxygen species levels, lower mitochondrial membrane potential, and lower oxygen consumption. Moreover, their mitochondria expressed lower mRNA and protein levels of fusion proteins mitofusin-1 (MFN1), mitofusin-2 (MFN2), and optic atrophy 1 (OPA1), and higher protein and gene expression levels of mitochondrial fission protein 1 (FIS1) and dynamin-related protein 1 (DRP-1). In addition, we observed enhanced leukocyte/endothelial interactions in T2D patients. Metformin reversed most of these effects, ameliorating mitochondrial function and dynamics, and reducing the leukocyte/endothelial interactions observed in T2D patients. These results raise the question of whether metformin tackles T2D by improving mitochondrial dysfunction and regulating mitochondrial dynamics. Furthermore, it would seem that metformin modulates the alteration of interactions between leukocytes and the endothelium, a subclinical marker of early atherosclerosis. Antioxid. Redox Signal. 35, 377-385.

[Outpatient breech birth attendance.] / Atención al parto en presentación podálica en el medio extrahospitalario.

Nowadays, care for a breech delivery in the out-of-hospital environment through the vaginal route can be a frequent process caused by the change in the scientific literature favoring the free evolution of the delivery of a breech presentation compared to the previous literature where the Caesarean section scheduled at week 37 of gestation, avoiding its free evolution. Furthermore, among the statistical data consulted at the INE (Instituto Nacional de Estadística), there is an increase in preterm deliveries outside the hospital, which increases the presentation of buttocks more frequently, between 25-32 weeks, around 42%. Therefore, the objective of this manuscript was to instruct the health professionals of the out-of-hospital emergency services in the event of imminent delivery in breech presentation. This type of training would consist of maintaining an expectant attitude during the expulsion period until the lower angle of the newborn's scapula is visible, followed by manual assistance by detaching the shoulders while gently and slowly removing the fetal head.

Hoy en día la atención a un parto de nalgas en el medio extrahospitalario por vía vaginal puede ser un proceso frecuente ocasionado por el cambio en la literatura científica, que favorece la libre evolución del parto de una presentación podálica frente a la literatura anterior donde se llevaba a cabo la cesárea programada en la semana 37 de gestación, evitando la libre evolución del mismo. Además, entre los datos estadísticos consultados en el INE (Instituto Nacional de Estadística) existe un incremento de partos prematuros fuera del hospital que aumenta que la presentación de nalgas sea más frecuente, entre las 25-32 semanas entorno a un 42%. Por lo tanto, el objetivo de este manuscrito fue instruir a los profesionales sanitarios de los servicios de urgencias extrahospitalaria ante una situación de parto inminente en presentación podálica. Este tipo de formación consistiría en mantener una actitud expectante durante el periodo expulsivo hasta que el ángulo inferior de la escápula del recién nacido sea visible, seguido de la ayuda manual desprendiendo los hombros mientras se extrae con suavidad y lentitud la cabeza fetal.

Relationship between PMN-endothelium interactions, ROS production and Beclin-1 in type 2 diabetes.

Type 2 diabetes is closely related to oxidative stress and cardiovascular diseases. In this study, we hypothesized that polymorphonuclear leukocytes (PMN)-endothelium interactions and autophagy are associated. We evaluated PMN-endothelial interactions, ROS production and autophagy parameters in 47 type 2 diabetic patients and 57 control subjects. PMNs from type 2 diabetic patients exhibited slower rolling velocity (p < 0.001), higher rolling flux (p < 0.001) and adhesion (p < 0.001) in parallel to higher levels of total (p < 0.05) and mitochondrial ROS (p < 0.05). When the protein expression of autophagy markers was analysed, an increase of Beclin-1 (p < 0.05), LC3I (p < 0.05), LC3II (p < 0.01) and LC3II/LC3I ratio (p < 0.05) was observed. Several correlations between ROS and leukocyte-endothelium parameters were found. Interestingly, in control subjects, an increase of Beclin-1 levels was accompanied by a decrease in the number of rolling (r = 0.561) and adhering PMNs (r = 0.560) and a rise in the velocity of the rolling PMNs (r = 0.593). In contrast, in the type 2 diabetic population, a rise in Beclin-1 levels was related to an increase in the number of rolling (r = 0.437), and adhering PMNs (r = 0.467). These results support the hypothesis that PMN-endothelium interactions, ROS levels and formation of autophagosomes, especially Beclin-1 levels, are enhanced in type 2 diabetes.

The effect of prioritization over cognitive-motor interference in people with relapsing-remitting multiple sclerosis and healthy controls.

The cognitive-motor interference (CMI) produced by simultaneous performance of a cognitive and a motor task has been proposed as a marker of real-life impairment of people with Multiple Sclerosis (pwMS), yet there is no consensus on the dual task (DT) procedure. This study aimed to compare DT performance of pwMS and healthy controls (HC) under different instructions and to examine its association with neuropsychological and clinical variables. PwMS (N = 23; relapsing-remitting course) and HC (N = 24) completed the cognitive (Verbal Fluency) and motor (walking) tasks under three conditions: independently or as single task (ST), both tasks simultaneously at best capacity or double prioritization (DT-DP), and only the cognitive task at best capacity while walking at preferred speed or cognitive prioritization (DT-CP). Compared to HC, pwMS walked significantly slower and produced less correct words under all conditions. The distance walked by pwMS and HC significantly differed between conditions (DT-CP< DT-DP< ST). PwMS produced more words during ST respective to DT-DP and DT-CP, with no difference between both DT conditions. HC showed no differences in cognitive performance between conditions. Motor and cognitive dual-task costs (DTC) were similar between groups. Only in pwMS, the cognitive DTC of DT-DP was different from zero. CMI measures correlated with neuropsychological, symptomatic, physiological (cognitive event-related potentials) and clinical variables. These results suggest that cognitive performance while walking is impaired in pwMS, but not in HC. CMI over cognitive performance might be a potential early marker of cognitive decline in pwMS, which may be enhanced by the instruction to prioritize both tasks in DT.

Relationship Between Oxidative Stress, ER Stress, and Inflammation in Type 2 Diabetes: The Battle Continues.

Type 2 diabetes (T2D) is a metabolic disorder characterized by hyperglycemia and insulin resistance in which oxidative stress is thought to be a primary cause. Considering that mitochondria are the main source of ROS, we have set out to provide a general overview on how oxidative stress is generated and related to T2D. Enhanced generation of reactive oxygen species (ROS) and oxidative stress occurs in mitochondria as a consequence of an overload of glucose and oxidative phosphorylation. Endoplasmic reticulum (ER) stress plays an important role in oxidative stress, as it is also a source of ROS. The tight interconnection between both organelles through mitochondrial-associated membranes (MAMs) means that the ROS generated in mitochondria promote ER stress. Therefore, a state of stress and mitochondrial dysfunction are consequences of this vicious cycle. The implication of mitochondria in insulin release and the exposure of pancreatic ß-cells to hyperglycemia make them especially susceptible to oxidative stress and mitochondrial dysfunction. In fact, crosstalk between both mechanisms is related with alterations in glucose homeostasis and can lead to the diabetes-associated insulin-resistance status. In the present review, we discuss the current knowledge of the relationship between oxidative stress, mitochondria, ER stress, inflammation, and lipotoxicity in T2D.

Downregulation of miR-31 in Diabetic Nephropathy and its Relationship with Inflammation.

BACKGROUND/AIMS: There is a lack of reliable biological markers for the early diagnosis of diabetic nephropathy (DN) during type 2 diabetes. In this pilot study we aim to assess whether miR-31 levels are modulated by the presence of DN and whether the expression of this miRNA is related to leukocyte-endothelial interactions and inflammation. METHODS: Thirty-one T2D patients were enrolled in this pilot study; 18 with no diabetic complications and 13 with diabetic nephropathy. 24 non-diabetic subjects and 13 T2D patients with retinopathy (absent of other complications) were included to test the specificity of miR-31. Following anthropometric and biochemical evaluation, serum miR-31 levels were assessed by Real Time-PCR. Leukocyte-endothelial interactions were evaluated by a parallel flow chamber in vitro model. Serum TNFα, IL-6 and ICAM-1 levels were determined by XMAP-technology in a flow cytometry-based Luminex 200 instrument. RESULTS: Serum miR-31 levels were similar between control and T2D subjects. However, T2D patients with DN displayed reduced levels of miR-31 with respect to patients without complications. This decrease in miR-31 was more pronounced in patients with macroalbuminuria than in those with microalbuminuria and was specific for DN, since patients with retinopathy displayed unaltered miR-31 levels. The presence of DN involved a lower leukocyte rolling velocity and an increased rolling flux and adhesion. miR-31 levels were positively correlated with leukocyte rolling velocity and negatively associated to leukocyte adhesion, TNFα, IL-6 and ICAM-1 levels. CONCLUSION: Serum miR-31 may be a biomarker for DN in T2D patients. The regulation of this miRNA seems to be related to the recruitment of leukocytes to vascular walls induced by pro-inflammatory and adhesion molecules.

Does Metformin Protect Diabetic Patients from Oxidative Stress and Leukocyte-Endothelium Interactions?

Since metformin can exert beneficial vascular effects, we aimed at studying its effect on reactive oxygen species (ROS) production, antioxidant enzyme expression, levels of adhesion molecules, and leukocyte-endothelium interactions in the leukocytes from type 2 diabetic (T2D) patients. The study was carried out in 72 T2D patients (41 of whom were treated with metformin for at least 12 months at a dose of 1700 mg per day), and in 40 sex- and age-matched control subjects. Leukocytes from T2D patients exhibited enhanced levels of mitochondrial ROS and decreased mRNA levels of glutathione peroxidase 1 (gpx1) and sirtuin 3 (sirt3) with respect to controls, whereas metformin was shown to revert these effects. No changes were observed on total ROS production and the expression levels of superoxide dismutase 1 and catalase. Furthermore, increases in leukocyte-endothelial interactions and intercellular adhesion molecule-1 and P-selectin levels were found in T2D and were also restored in metformin-treated patients. Our findings raise the question of whether metformin could modulate the appearance of atherosclerosis in T2D patients and reduce vascular events by decreasing leukocyte oxidative stress through an increase in gpx1 and sirt3 expression, and undermining adhesion molecule levels and leukocyte-endothelium interactions. Antioxid. Redox Signal. 27, 1439-1445.

Metabolic syndrome enhances endoplasmic reticulum, oxidative stress and leukocyte-endothelium interactions in PCOS.

OBJECTIVE: Polycystic ovary syndrome (PCOS) is associated with insulin resistance, which can lead to metabolic syndrome (MetS). Oxidative stress and leukocyte-endothelium interactions are related to PCOS. Our aim was to evaluate whether the presence of MetS in PCOS patients can influence endoplasmic reticulum (ER) and oxidative stress and leukocyte-endothelium interactions. MATERIAL AND METHODS: This was a prospective controlled study conducted in an academic medical center. The study population consisted of 148 PCOS women (116 without/32 with MetS) and 112 control subjects (87 without / 25 with MetS). Metabolic parameters, reactive oxygen species (ROS) production, ER stress markers (GRP78, sXBP1, ATF6), leukocyte-endothelium interactions, adhesion molecules (VCAM-1, ICAM-1, E-Selectin), TNF-α and IL-6 were determined. RESULTS: Total ROS, inflammatory parameters and adhesion molecules were enhanced in the presence of MetS (p<0.05), and the PCOS+MetS group showed higher levels of IL-6 and ICAM-1 than controls (p<0.05). Increased adhesion and leukocyte rolling flux were observed in PCOS and PCOS+MetS groups vs their respective controls (p<0.05). GRP78 protein expression was higher in the PCOS groups (p<0.05 vs controls) and sXBP1 was associated with the presence of MetS (p<0.05 vs controls without MetS). Furthermore, PCOS+MetS patients exhibited higher GRP78 and ATF6 levels than controls and PCOS patients without MetS (p<0.05). In PCOS women, HOMA-IR was positively correlated with ICAM-1 (r=0.501; p<0.01), ROS (r=0.604; p<0.01), rolling flux (r=0.455;p<0.05) and GRP78 (r=0.574; p<0.001). CONCLUSION: Our findings support the hypothesis of an association between altered metabolic status, increased ROS production, ER stress and leukocyte-endothelium interactions in PCOS, all of which are related to vascular complications.

Low testosterone levels are related to oxidative stress, mitochondrial dysfunction and altered subclinical atherosclerotic markers in type 2 diabetic male patients.

INTRODUCTION: Low testosterone levels in men are associated with type 2 diabetes and cardiovascular risk. However, the role of testosterone in mitochondrial function and leukocyte-endothelium interactions is unknown. Our aim was to evaluate the relationship between testosterone levels, metabolic parameters, oxidative stress, mitochondrial function, inflammation and leukocyte-endothelium interactions in type 2 diabetic patients. MATERIALS AND METHODS: The study was performed in 280 male type 2 diabetic patients and 50 control subjects. Anthropometric and metabolic parameters, testosterone levels, reactive oxygen species (ROS) production, mitochondrial membrane potential, TNFα, adhesion molecules and leukocyte-endothelium cell interactions were evaluated. RESULTS: Testosterone levels were lower in diabetic patients. Total and mitochondrial ROS were increased and mitochondrial membrane potential, SOD and GSR expression levels were reduced in diabetic patients. TNFα, ICAM-1 and VCAM-1 levels, leukocyte rolling flux and adhesion were all enhanced in diabetic patients, while rolling velocity was reduced. Testosterone levels correlated negatively with glucose, HOMA-IR, HbA1c, triglycerides, nonHDL-c, ApoB, hs-CRP and AIP, and positively with HDL-c and ApoA1. The multivariable regression model showed that HDL-c, HOMA-IR and age were independently associated with testosterone. Furthermore, testosterone levels correlated positively with membrane potential and rolling velocity and negatively with ROS production, VCAM-1, rolling flux and adhesion. CONCLUSIONS: Our data highlight that low testosterone levels in diabetic men are related to impaired metabolic profile and mitochondrial function and enhanced inflammation and leukocyte-endothelium cell interaction, which leaves said patients at risk of cardiovascular events.

Are Mitochondrial Fusion and Fission Impaired in Leukocytes of Type 2 Diabetic Patients?

Mitochondrial fusion/fission alterations have been evaluated in different tissues of type 2 diabetic (T2D) patients. However, it is not known whether mitochondrial dynamics is disturbed in the leukocytes of T2D patients and whether glycemic control affects its regulation. Anthropometric and metabolic parameters in 91 T2D patients (48 with glycated hemoglobin [HbA1c] <6.5% and 43 with HbA1c >6.5%) were characteristic of the disease when compared with 78 control subjects. We observed increased reactive oxygen species production in leukocytes from diabetic patients, together with a reduced mitochondrial oxygen consumption rate, especially in poorly controlled patients. Mitochondrial fusion was reduced and fission was increased in diabetic patients, and both features were accentuated in patients with poor glycemic control. Furthermore, leukocyte rolling flux rose in parallel to HbA1c levels. The induction of leukocyte-endothelial interactions in diabetic patients was related to reduced mitochondrial fusion and higher mitochondrial fission. Our findings suggest that mitochondrial dynamics could be influenced by glycemic control in leukocytes of diabetic patients, in which there is decreased mitochondrial fusion and elevated fission related to enhanced leukocyte-endothelial interactions. These findings lead to the hypothesis that poor glycemic control during T2D may alter mitochondrial dynamics and could eventually promote leukocyte-endothelial interactions and the onset of cardiovascular diseases. Antioxid. Redox Signal. 25, 108-115.

Role of Oxidative Stress and Mitochondrial Dysfunction in Skeletal Muscle in Type 2 Diabetic Patients.

Type 2 diabetes can increase the risk of skeletal muscle dysfunction and, consequently, that of cardiovascular diseases, including coronary artery disease and stroke. It is also related to a reduced capacity for exercise, but the underlying mechanism is only partially understood. There are several factors that contribute to the development of skeletal muscle dysfunction, of which oxidative stress and mitochondrial dysfunction are among the most important. This review discusses the role of oxidative stress in the development and progression of skeletal and cardiac dysfunction associated with diabetes. It also provides an overview of the potential actions of antioxidants in general and mitochondria-targeted antioxidants in particular in the treatment of muscle dysfunction in type 2 diabetes.

Is Autophagy Altered in the Leukocytes of Type 2 Diabetic Patients?

It is unknown whether autophagy is altered in the leukocytes of type 2 diabetes (T2D) patients and whether oxidative and endoplasmic reticulum (ER) stresses regulate this mechanism. We studied anthropometric and metabolic parameters and evaluated oxidative stress, chromatin condensation, ER stress, and autophagy parameters in leukocytes of 103 T2D patients versus 109 sex- and age-matched controls. Patients showed increases in glucose, insulin, homeostasis model assessment of insulin resistance, and glycated hemoglobin (HbA1c) compared with controls (p < 0.001). Leukocytes displayed enhanced total and mitochondrial reactive oxygen species (ROS), reduced mitochondrial mass, and increased chromatin condensation (p < 0.05). ER stress was also activated in diabetic patients, who displayed augmented glucose-regulated protein 78 kDa (GRP78), phosphorylated eukaryotic translation initiation factor 2, subunit 1 alpha (P-eIF2α), and activating transcription factor 6 (ATF6) levels (p < 0.05). We also observed an increase in the autophagy markers, microtubule-associated protein light chain 3 (LC3)-II and Beclin 1 (p < 0.05), and significant positive correlations between Beclin 1 and total ROS (r = 0.667), GRP78 (r = 0.925) and P-eIF2α (r = 0.644), and between LC3-II and P-eIF2α (r = 0.636) and ATF6 (r = 0.601). Our results lead to the hypothesis that autophagy is activated in the leukocytes of T2D patients and that both oxidative and ER stress signaling pathways may be implicated in the induction of autophagy.

A single acute dose of pinitol from a naturally-occurring food ingredient decreases hyperglycaemia and circulating insulin levels in healthy subjects.

A limited amount of research suggests that oral ingestion of pinitol (3-O-methyl-d-chiro-inositol) positively influences glucose tolerance in humans. This study assessed the effects of different doses of pinitol supplementation on glucose tolerance, insulin sensitivity and plasma pinitol concentrations. Thirty healthy subjects underwent two one-day trials in which they consumed a nutritive beverage (Fruit Up®) containing 2.5, 4.0 or 6.0g of pinitol and a corresponding placebo equivalent in both energy and carbohydrates. Blood samples were collected frequently over the 240-min test period. The pinitol-enriched beverage reduced serum glucose and insulin at 45 and 60min, but only at a dose of 6.0g. Plasma pinitol concentrations, maximum concentration and AUC increased according to the dose administered. The results show that a single dose of pinitol from a naturally-occurring food ingredient at the highest dose administered acutely influences indices of whole-body glucose tolerance and insulin sensitivity in healthy subjects.

Is myeloperoxidase a key component in the ROS-induced vascular damage related to nephropathy in type 2 diabetes?

It is still unclear whether microvascular complications of type 2 diabetes correlate with leukocyte-endothelium interactions and/or myeloperoxidase (MPO) levels. In the present study, we found that serum levels of glucose, the rate of ROS and MPO concentration were higher in type 2 diabetic patients. Patients with nephropathy (39.6%) presented higher MPO levels that correlate positively with the albumin/creatinine ratio (r = 0.59, p<0.05). In addition, nephropatic patients showed increased leukocyte-endothelium interactions due to an undermining of polymorphonuclear leukocytes (PMN) rolling velocity and increased rolling flux and adhesion, which was accompanied by a rise in levels of the proinflammatory cytokine tumour necrosis factor alpha (TNFα) and the adhesion molecule E-selectin. Furthermore, MPO levels were positively correlated with PMN rolling flux (r = 0.855, p < 0.01) and adhesion (r = 0.682, p<0.05). Our results lead to the hypothesis that type 2 diabetes induces oxidative stress and an increase in MPO levels and leukocyte-endothelium interactions, and that these effects correlate with the development of nephropathy.

Effect of weight loss on C3 and C4 components of complement in obese patients.

BACKGROUND: Circulating C3 levels are elevated in obese patients, but how this factor is affected after weight loss through diet is a question that is yet unanswered. Therefore, the aim of this study was to evaluate the effects of weight loss on lipid and hydrocarbonated metabolism parameters and on the levels of C3 and C4 components of complement in obese patients. DESIGN: This is a longitudinal intervention study based on a 6-week very low-calorie diet (VLCD), a liquid formula of 603 kcal/day. A total of 131 middle-aged patients were distributed among grades II, III and IV of obesity. Anthropometric parameters, total cholesterol, triglycerides, high-density lipoprotein cholesterol, LDLc, apolipoproteins A-I and B-100, glucose, insulin, HOMA-IR and C3 and C4 levels were evaluated at baseline and after 6 weeks of intervention. RESULTS: After VLCD, the moderate weight loss was accompanied by a significant reduction in C3 levels in grade III and grade IV patients (10.2% and 15.4%, respectively; P < 0.001). C4 levels were not altered. Adherence to the diet improved anthropometric parameters and was accompanied by a significant decrease in all lipid profile parameters (P < 0.001). In addition, weight loss was associated with an improvement in hydrocarbonated metabolism as shown by the decrease in glucose levels and HOMA-IR (P < 0.01). CONCLUSIONS: Our findings show that in severely obese patients following a VLCD for 6 weeks produces reductions in factor C3, a biomarker of cardiovascular disease, and a significant improvement in some features of metabolic syndrome. In this way, the abovementioned diet may represent an effective strategy for treating obesity and related cardiovascular risk factors.

Comparability of two different polyacrylamide gel electrophoresis methods for the classification of LDL pattern type.

BACKGROUND: The measurement of small dense low-density lipoprotein (sdLDL) particles is relevant when assessing cardiovascular risk. However, there is as yet no referenced method for the determination of LDL subfractions or a standardized comparison of the methods currently available. Therefore, the aim of this study was to compare the pattern of LDL particles measured by polyacrylamide tube gel electrophoresis (PTGE) and polyacrylamide gradient gel electrophoresis (PGGE) and to correlate the results with triglyceride concentration. MATERIALS AND METHODS: Serum samples were collected from 177 patients. Lipid profile and LDL particle size were assessed using PTGE and PGGE. RESULTS: Pearson correlation and kappa index revealed a very good agreement between the methods. There was 81.3% concordance for classification of sdLDL particles and 97.2% concordance for classification of large LDL when PTGE and PGGE were compared. LDL size correlated with triglyceride in subjects with triglyceride levels >116 mg/dl, pointing to a high CAD risk, as reflected by their higher prevalence of pattern B. CONCLUSIONS: PTGE correlates favourably and is in very good agreement with PGGE. The determination of LDL particle size may be an appropriate analytical procedure to estimate CAD risk in patients with high triglyceride levels.

A review on the role of phytosterols: new insights into cardiovascular risk.

Phytosterols, which are structurally related to cholesterol, are found in all plant foods with highest concentration occurring in vegetable oils and nuts. Phytosterols are known to reduce serum low-density lipoprotein cholesterol level without changing high-density lipoprotein cholesterol or triglyceride levels. Daily consumption of phytosterols-enriched foods is widely used as a therapeutic option to lower plasma cholesterol and atherosclerotic disease risk. The cholesterol-lowering action of phytosterols is thought to occur, at least in part, through competitive replacement of dietary and biliary cholesterol in mixed micelles, which undermines the absorption of cholesterol. The aim of this review is to provide a general overview of available evidence regarding the effects of phytosterols on cholesterol metabolism and addressing issues related to efficacy as dose, length, frequency of consumption, type of phytosterol (sterols versus stanols) or food matrix. Furthermore, we will explore the factors that influence the response of individuals to phytosterol therapy and evaluate their safety and the possibility that elevated plasma phytosterol concentrations contribute to the development of premature coronary artery disease.