An updated systematic review and dose-response meta-analysis of the randomized controlled trials on the effects of alpha-lipoic acid supplementation on inflammatory biomarkers.

Data about the effects of alpha-lipoic acid (ALA) supplementation on inflammatory markers are inconsistent. This systematic review and dose-response meta-analysis of randomized controlled trials was performed to summarize the effects of ALA supplementation on inflammatory markers such as C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in adults. A comprehensive literature search was conducted in the electronic databases of PubMed, Web of Science, ProQuest, Embase, and SCOPUS from inception to February 2020. Among all of the eligible studies, 20 articles were selected. The weighted mean differences (WMD) and 95% confidence intervals (CI) were calculated to evaluate the pooled effect size. Between-study heterogeneity was evaluated using Cochran's Q test and I2. Subgroup analysis was done to evaluate the potential sources of heterogeneity. The dose-response relationship was evaluated using fractional polynomial modeling. Twenty eligible studies with a total sample size of 947 participants were included in the current meta-analysis. The findings of the meta-analysis showed that ALA supplementation significantly reduced CRP (WMD: -0.69 mg/L, 95% CI: -1.13, -0.26, P=0.002), IL-6 (WMD: -1.83 pg/ml, 95% CI: -2.90, -0.76, P=0.001), and TNF-α concentrations (WMD: -0.45 pg/ml, 95% CI: -0.85, -0.04, P=0.032). No evidence of departure from linearity was observed between dose and duration of the ALA supplementation on serum CRP, IL-6 and TNF-α concentration. In subgroup analysis, ALA dosage, baseline concentrations of the parameter, sample size, and gender were considered as possible sources of heterogeneity. In summary, ALA supplementation improves inflammatory markers without any evidence of non-linear association to dose or duration of the trial.

Dietary inflammatory index significantly affects lipids profile among adults: An updated systematic review and meta-analysis.

Background: The available data on the relationship between dietary inflammatory index (DII®) and serum lipids are controversial. This systematic review and meta-analysis aimed to investigate the relationship between DII® and serum lipids, including total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglyceride (TG) in general populations. Methods: PubMed, Web of Science, SCOPUS, and Cochrane electronic databases were systematically searched from inception to December 2019. Case-control, cohort or cross-sectional studies that evaluated the relationship between DII® and serum lipids were included. The random-effects model was applied to evaluate the pooled weighted mean difference (WMD) and 95% confidence intervals (CI). Results: In total, twenty-four cross-sectional and one case-control studies with a total sample size of 129,759 were included in the meta-analysis. The pooled results showed that the highest category of DII® was associated with 5.16 mg/dl increase in TC (Pooled WMD: 5.16; 95% CI: 0.58-9.73, p = 0.02) and 3.99 mg/dl increase in LDL-C (Pooled WMD: 3.99; 95% CI: 1.16-6.81, p = 0.006). However, no significant association between DII® scores, HDL-C and TG was found. In subgroup analysis, the geographical region, gender, and dietary assessment methods were potent sources of heterogeneity. Conclusion: This study showed that a higher level of DII® was associated with higher levels of TC and LDL-C in apparently healthy populations. Since the included studies had observational designs, therefore, no conclusion of causality was possible. More studies with interventional designs are required to elucidate the causality of the observed association between DII® and the risk of abnormal lipid profile.

Cocaine and amphetamine-regulated transcript prepropeptide gene (CARTPT) polymorphism interacts with Diet Quality Index-International (DQI-I) and Healthy Eating Index (HEI) to affect hypothalamic hormones and cardio-metabolic risk factors among obese individuals.

BACKGROUND: Epidemiologic studies show that cocaine- and amphetamine-regulated transcript prepropeptide (CARTPT) gene polymorphism modifies diet-obesity relationships. However, the interaction between CARTPT gene polymorphism and diet quality indices have not been investigated yet. The current study was aimed to evaluate the interaction between major dietary indices including Diet Quality Index-International (DQI-I) and Healthy Eating Index (HEI)-2015 and CARTPT gene rs2239670 variants among apparently healthy obese Iranians. METHODS: This cross-sectional study was carried out by employing 288 apparently healthy obese adults aged 20-50 years with a BMI of 30-40 kg/m2. Diet quality was evaluated by Diet Quality Index-International (DQI-I) and Healthy Eating Index-2015 (HEI-2015) using a 132-items semi-quantitative validated food frequency questionnaire. The CARTPT gene rs2239670 polymorphism was genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Blood concentrations of glycemic markers, lipid profile, α-melanocyte stimulating hormone (MSH) and agouti-related peptide (AgRP) were also measured. ANCOVA multivariate interaction model was used to analyze gene-diet interactions. RESULTS: The significant interactions were identified between CARTPT gene polymorphism and HEI, affecting BMR (PInteraction = 0.003), serum glucose (PInteraction = 0.009) and high density lipoprotein cholesterol HDL concentrations (PInteraction = 0.03) after adjusting for the effects of sex and age. Also we found gene-diet interaction between CARTPT genotypes and DQI-I in terms of fat mass (FM; PInteraction = 0.02), waist circumference (WC; PInteraction < 0.001), body mass index (BMI; PInteraction < 0.001), basal metabolic rate (BMR, PInteraction < 0.001), serum fasting glucose (PInteraction < 0.01) and AgRP (PInteraction = 0.05) in individuals even after adjusting for potential confounders. CONCLUSION: Current study showed the effects of interaction between CARTPT genotype with adherence to HEI and DQI-I scores on obesity-related anthropometric and metabolic risk-factors.

An updated systematic review and dose-response meta-analysis of the effects of α-lipoic acid supplementation on glycemic markers in adults.

This systematic review and dose-response meta-analysis was conducted to summarize data from available clinical trials on the effects of α-lipoic acid (ALA) supplementation on glycemic markers including glucose, hemoglobin A1c (HbA1c), insulin, homeostatic model assessment of insulin resistance (HOMA-IR), HOMA-ß, and quantitative insulin check index in adults. A comprehensive literature search was conducted in the electronic databases of PubMed, Web of Science, ProQuest, Embase and SCOPUS from inception to February 2020. Among all of the eligible studies, 28 articles were selected. The weighted mean differences (WMD) and 95% confidence intervals (CI) were calculated to evaluate the pooled effect size. Between-study heterogeneity was evaluated using Cochran's Q test and I2. Subgroup analysis was done to evaluate the potential sources of heterogeneity. The dose-response relationship was evaluated using fractional polynomial modeling. Twenty eight eligible studies with a total sample size of 1,016 participants were included in the current meta-analysis. The findings of the meta-analysis showed that ALA supplementation significantly reduced insulin (WMD: -0.64; CI: -1.287 to 0.004, P = .04), HOMA-IR (WMD: -0.48; 95% CI: -0.79 to -0.16; P = .002). No change in glucose or HbA1C was reported. Moreover, the effect of ALA on insulin was duration-dependent (Pnon-linearity = 0.04). No evidence of departure from linearity was observed between dose and duration of the ALA supplementation on other markers. The subgrouping revealed that ALA dosage and duration of ALA supplementation, health status of participants, geographic locations and the studies' quality are possible sources of heterogeneity. In summary, ALA supplementation improves serum insulin and insulin resistance in a two-class and duration dependent non-linear analysis.