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Atherosclerosis (AS) is one of the most common causes of death from cardiovascular disease, and low folic acid (FA) levels have been reported to be strongly associated with an increased risk of AS. We aimed to obtain causal estimates of the association between FA and AS and to quantify the mediating role of known modifiable risk factors. Based on the largest genome-wide association study (GWAS) from the IEU Open GWAS Project for all human studies, we conducted a two-sample Mendelian randomization (MR) study of genetically predicted FA and AS. A two-step MR design was then used to assess the causal mediating effect of low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) on the relationship between FA and AS. This MR analysis showed that genetically determined FA levels [IVW: Odds Ratio (OR) = 0.623, 95% CI 0.421–0.924, P = 0.018] were associated with a reduced risk of AS. Inverse variance weighted (IVW) MR analysis also showed that genetically predicted FA was positively correlated with HDL-C levels (OR = 1.358, 95% CI 1.029–1.792, P = 0.031) and negatively correlated with LDL-C (OR = 0.956, 95% CI 0.920–0.994, P = 0.023) and TG levels (OR = 0.929, 95% CI 0.886–0.974, P = 0.003). LDL-C, HDL-C, and TG mediate 3.00%, 6.80%, and 4.40%, respectively, of the total impact of FA on AS. The combined effect of these three factors accounts for 13.04% of the total effect. Sensitivity analysis verifies the stability and reliability of the results. These results support a potential causal protective effect of FA on AS, with considerable mediation through many modifiable risk factors. Thus, interventions on levels of LDL-C, HDL-C, and TG have the potential to substantially reduce the burden of AS caused by low FA. [ABSTRACT FROM AUTHOR]

This study aimed to compare the accuracy of novel lipid indices, including the visceral adiposity index (VAI), lipid accumulation product (LAP), triglycerides and glucose (TyG) index, TyG-body mass index (TyG-BMI), and TyG-waist circumference (TyG-WC), in identifying insulin resistance and establish valid cutoff values. This cross-sectional study used the data of 11,378 adults, derived from the United States National Health and Nutrition Examination Survey (1999–2016). Insulin resistance was defined as a homeostasis model assessment-insulin resistance value above the 75th percentile for each sex and race/ethnicities. The area under the curves (AUCs) were as follows: VAI, 0.735; LAP, 0.796; TyG index, 0.723; TyG-BMI, 0.823, and; TyG-WC, 0.822. The AUCs for TyG-BMI and TyG-WC were significantly higher than those for VAI, LAP, and TyG index (vs. TyG-BMI, p < 0.001; vs. TyG-WC, p < 0.001). The cutoff values were as follows: VAI: men 1.65, women 1.65; LAP: men 42.5, women 42.5; TyG index: men 4.665, women 4.575; TyG-BMI: men 135.5, women 135.5; and TyG-WC: men 461.5, women 440.5. Given that lipid indices can be easily calculated with routine laboratory tests, these values may be useful markers for insulin resistance risk assessments in clinical settings. [ABSTRACT FROM AUTHOR]

Whether the lipid profile in diabetic patients is associated with diabetic neuropathy (DN) development remains ambiguous, as does the predictive value of serum lipid levels in the risk of DN. Here, we performed the first meta-analysis designed to investigate the relationship between DN and the serum levels of triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL), and low-density lipoprotein cholesterol (LDL). Candidate studies were comprehensively identified by searching PubMed, Embase, Cochrane Library and Web of Science databases up to May 2020. Observational methodological meta-analysis was conducted to assess the relationships of TG, TC, HDL, and LDL levels with DN. Changes in blood lipids were used to estimate the effect size. The results were pooled using a random-effects or fixed-effects model. Potential sources of heterogeneity were explored by subgroup analysis. Various outcomes were included, and statistical analyses were performed using STATA (Version 12.0). Mean differences (MDs) and odds ratios (ORs) with 95% confidence intervals (CIs) were estimated. The Newcastle–Ottawa Scale (NOS) was applied to assess the methodological quality. I2 statistics were calculated to evaluate statistical heterogeneity. Funnel plots were utilized to test for publication bias. A sensitivity analysis was performed by omitting each study one by one. Thirty-nine clinical trials containing 32,668 patients were included in the meta-analysis. The results demonstrated that DN patients showed higher TG and lower HDL levels (MD = 0.34, 95% CI: 0.20–0.48 for TG; MD = -0.05, 95% CI: -0.08–-0.02, I2 = 81.3% for HDL) than controls. Subgroup analysis showed that patients with type 1 diabetes mellitus (T1DM) neuropathy had elevated TG levels in their serum (MD = 0.25, 95% CI: 0.16–0.35,I2 = 64.4% for T1DM). However, only patients with T1DM neuropathy had reduced serum HDL levels, and there was no significant difference in serum HDL levels between patients with T2DM neuropathy and controls (MD = -0.07, 95% CI: -0.10–-0.03, I2 = 12.4% for T1DM; MD = -0.02, 95% CI: -0.07–0.03, I2 = 80.2% for T2DM). TC and LDL levels were not significantly different between DN patients and controls (MD = -0.03, 95% CI: -0.14–0.09, I2 = 82.9% for TC; MD = -0.00, 95% CI: -0.08–0.08, I2 = 78.9% for LDL). In addition, compared with mild or painless DN patients, those with moderate or severe pain DN pain had significantly reduced serum TC and LDL levels (MD = -0.31, 95% CI: -0.49–-0.13, I2 = 0% for TC; MD = -0.19, 95% CI: -0.32–-0.08, I2 = 0% for LDL). TG levels and HDL levels did not vary considerably between patients with mild or painless DN and those with moderate or severe DN pain patients (MD = 0.12, 95% CI: -0.28–0.51, I2 = 83.2% for TG; MD = -0.07, 95% CI:-0.14–0.01, I2 = 58.8% for HDL). Furthermore, people with higher TG and LDL levels had higher risk of DN (OR = 1.36, 95% CI: 1.20–1.54, I2 = 86.1% for TG and OR = 1.10, 95% CI: 1.02–1.19, I2 = 17.8% for LDL). Conversely, high serum HDL levels reduced the risk of DN (OR = 0.85, 95% CI: 0.75–0.96, I2 = 72.6%), while TC levels made no significant difference with the risk of DN (OR = 1.02, 95% CI: 1.00–1.04, I2 = 84.7%). This meta-analysis indicated that serum lipid profile changes are among the biological characteristics of DN. Lipid levels should be explored as routine laboratory markers for predicting the risk of DN, as they will help clinicians choose appropriate therapies, and thus optimize the use of available resources. [ABSTRACT FROM AUTHOR]

Lipids play a significant role in regulation of health and disease. To enhance our understanding of the role of lipids in regulation of lifespan and healthspan additional studies are required. Here, UHPLC-MS/MS lipidomics was used to measure dynamic changes in lipid composition as a function of age and gender in genetically identical male and female Daphnia magna with different average lifespans. We demonstrate statistically significant age-related changes in triglycerides (TG), diglycerides (DG), phosphatidylcholine, phosphatidylethanolamine, ceramide and sphingomyelin lipid groups, for example, in males, 17.04% of TG lipid species decline with age whilst 37.86% increase in relative intensity with age. In females, 23.16% decrease and 25.31% increase in relative intensity with age. Most interestingly, the rate and direction of change can differ between genetically identical female and male Daphnia magna, which could be the cause and/or the consequence of the different average lifespans between the two genetically identical genders. This study provides a benchmark dataset to understand how lipids alter as a function of age in genetically identical female and male species with different average lifespan and ageing rate. [ABSTRACT FROM AUTHOR]

Lipoprotein a (Lp(a) is an independent risk factor for atherosclerotic cardiovascular disease. The prevalence of high Lipoprotein (a) (Lp(a)) in the Lebanese pediatric population is unknown. Our study aims to assess this prevalence and to study the relationship of Lp(a) with the lipid profile, age, body mass index (BMI) and socio-economic status (SES) in Lebanese schoolchildren. A total of 961 children aged 8–18 years (497 boys and 464 girls) were recruited from ten private and public schools in 2013–2014 using a stratified random sample. Schools were selected from the Greater Beirut and Mount Lebanon areas, and were categorized into three subgroups according to the schools' SES status (high, medium, low). Lp(a) was assayed in 2018 on samples previously frozen at − 80 °C. Abnormal Lp(a) levels (≥ 75 nmol/L) were observed in 14.4% of the overall sample (13.5% for boys,15.3% of girls p = 0.56). The median of Lp(a) was 20(10–50) in the whole sample with no significant gender difference. No significant relationship was found between Lp(a) and age. However, Lp(a) was significantly correlated with BMI in whole sample, as well as in boys and girls (p = 0.02, p = 0.03, p = 0.03, respectively). A significant correlation was found between Lp(a) and non-HDL-C in the whole sample as well as in boys and girls (respectively p < 0.001,p = 0.024 and p = 0.03), but not with triglycerides and HDL-C. In a multivariate linear regression analysis, Lp(a) was only independently associated with BMI and non-HDL-C in boys and girls. Lp(a) was independently associated with BMI and non-HDL-C while no significant relationship was observed with age and sex confirming the strong genetic determination of Lp(a). [ABSTRACT FROM AUTHOR]