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Background: Previous studies have linked sports-related concussions and repeated subconcussive head impacts in contact sport athletes to elevated brain injury biomarkers. Docosahexaenoic acid (DHA), the primary omega-3 (n-3) highly unsaturated fatty acid (HUFA) in the brain, has shown neuroprotective effects in animal models after brain injury, but clinical research has shown mixed results. Methods: We conducted a randomized, double-blind, placebo-controlled study on 29 Division 1 collegiate American football players, exploring the impact of DHA (2.5 g) and eicosapentaenoic acid (EPA) (1.0 g) supplied as ethyl esters, on levels of plasma lipids shown to cross the blood-brain barrier. Dietary intake data was collected using food frequency questionnaires (FFQ). Complex lipids and unesterified fatty acids were isolated from plasma, separated via reversed-phase liquid chromatography and analyzed by targeted lipidomics analysis. Results: FFQ results indicated that participants had low dietary n-3 HUFA intake and high omega-6 (n-6):n-3 polyunsaturated fatty acids (PUFA) and HUFA ratios at baseline. After DHA + EPA supplementation, plasma lysophosphatidylcholine (LPC) containing DHA and EPA significantly increased at all timepoints (weeks 17, 21, and 26; p < 0.0001), surpassing placebo at Weeks 17 (p < 0.05) and 21 (p < 0.05). Phosphatidylcholine (PC) molecular species containing DHA or EPA, PC38:6 PC36:6, PC38:7, PC40:6, and PC40:8, increased significantly in the DHA + EPA treatment group at Weeks 17 (and 21. Plasma concentrations of non-esterified DHA and EPA rose post-supplementation in Weeks 17 and 21. Conclusions: This study demonstrates that n-3 HUFA supplementation, in the form of ethyl esters, increased the DHA and EPA containing plasma lipid pools the have the capacity to enrich brain lipids and the potential to mitigate the effects of sports-related concussions and repeated subconcussive head impacts. Trial Registration: All deidentified data are available at ClinicalTrials.gov #NCT0479207. [ABSTRACT FROM AUTHOR]

Background: Several studies showed the hypoglycemic and hypolipidemic effects of Satureja Khuzestanica (SK) in animal models. This study aimed to determine the effect of SK supplementation on glycemic and lipid outcomes of patients with type 2 diabetes mellitus (T2DM). Methods: The study was designed as a double-blind, placebo-controlled, randomized clinical trial using block randomization. Seventy-eight T2DM patients were randomly assigned to intervention (n = 39) or placebo (n = 39) groups. They received SK or placebo in 500 mg capsules daily for 12 weeks. Anthropometric, blood pressure, liver enzymes, glycemic, and lipid outcomes were measured before and after the intervention. Results: At baseline, there were no significant differences in age, sex, or glycated hemoglobin (HbA1c) levels between the groups. SK supplementation led to a significant decrease in FBS (-12.6 ± 20.7 mg/dl in the intervention group versus 3.5 ± 31.9 mg/dl; p = 0.007), HbA1c (-0.28 ± 0.45 in the intervention group versus 0.11 ± 0.54% in the placebo group; p = < 0.001), insulin (-1.65 ± 6.18 in the intervention group versus 2.09 ± 5.90 mIU/L in the placebo group; p = 0.03), total cholesterol (-14.6 ± 21.1 mg/dl in the intervention group versus 8.2 ± 30.9 mg/dl in the placebo group; p < 0.001), LDL-cholesterol (-4.6 ± 15.2 mg/dl in the intervention group versus 5.8 ± 14.6 mg/dl in placebo group; p < 0.001) levels, and significant increase in HDL-cholesterol (3.9 ± 4.9 mg/dl in the intervention group versus 0.9 ± 5.2 mg/dl in placebo group; p = 0.005). Conclusion: Based on the study results, SK supplementation may improve glycemic indices and lipid profile of patients with T2DM. Our findings may provide novel complementary treatments without adverse effects for diabetes complications. These results need to be further confirmed in clinical trials. Registration: : This trial has been registered in the Iranian Registry of Clinical Trials (IRCT ID: IRCT20190715044214N1, registration date: 21/02/2021). [ABSTRACT FROM AUTHOR]

Background: Rosa species are rich sources of polyphenols with physiological functions. In this study a polyphenol-rich Rosa multiflora (var. platyphylala) petal extract (RoseFit™) was investigated for weight loss in humans. Methods: In a randomized, placebo-controlled, parallel-group, double-blind clinical trial seventy overweight male and female subjects (20–50 years) with body mass index (BMI) 25–30 kg/m2 were randomly allocated to the active treatment group (RoseFit) and placebo group in a 1:1 ratio. The subjects received 300 mg capsules twice daily for 12 weeks. The primary efficacy outcome measures included body weight, BMI, and body composition, as determined using Dual-energy X-ray absorptiometry (DEXA). Secondary measures consisted of serum lipid profile and appetite marker (leptin and ghrelin) analyses. Safety analyses included biochemical and hematological assessments. Results: At the end of the study, a marked reduction in body weight (-1.20 ± 2.62 kg, p < 0.05) and BMI from baseline was observed in the RoseFit group. In addition, the body fat % (RoseFit = -1.69 ± 2.59%, placebo = 0.96 ± 3.21%; p < 0.001) and fat mass (RoseFit = -1.75 ± 1.80 kg, placebo = 1.61 ± 3.82 kg; p < 0.001) were significantly abated in RoseFit group. Importantly, the lean mass was maintained during the intervention. RoseFit ingestion significantly increased the serum leptin levels compared to the placebo (4.85%; p < 0.05). Further, RoseFit group showed reduction in the hunger hormone ghrelin level (2.27%; p < 0.001) from baseline to the end of study, compared to the placebo. The subjective evaluation of appetite using visual analog scale (VAS) questionnaires further confirmed the appetite-suppression effects of RoseFit. The lipid profile significantly improved in RoseFit-treated subjects. No serious adverse events were observed during the study, indicating the tolerability of RoseFit. Conclusions: Supplementation with RoseFit significantly impacts body weight management and can thus be a potential nutraceutical ingredient for sustainable weight loss. Trial registration: CTRI/2019/10/021584 dated 09/10/2019 [ABSTRACT FROM AUTHOR]

Background: Chitosan is one of dietary fiber that has received great attention in improving obesity-related markers, but little is known on its effects on adolescents.Objectives: To analyze the effects of chitosan supplementation on obesity-related cardiometabolic markers and appetite-related hormones in adolescents with overweight or obesity.Methods and Analysis: A randomized clinical trial was performed on 64 adolescents with overweight and obesity, who were randomly allocated to receive chitosan supplementation (n = 32) or placebo as control (n = 32) for 12 weeks. Anthropometric measures, lipid and glycemic profiles, and appetite-related hormones were examined.Results: Sixty-one participants completed study (chitosan = 31, placebo = 30). Chitosan supplementation significantly improved anthropometric indicators of obesity (body weight: - 3.58 ± 2.17 kg, waist circumference: - 5.00 ± 3.11 cm, and body mass index: - 1.61 ± 0.99 kg/m2 and - 0.28 ± 0.19 Z-score), lipid (triglycerides: - 5.67 ± 9.24, total cholesterol: - 14.12 ± 13.34, LDL-C: - 7.18 ± 10.16, and HDL-C: 1.83 ± 4.64 mg/dL) and glycemic markers (insulin: - 5.51 ± 7.52 μIU/mL, fasting blood glucose: - 5.77 ± 6.93 mg/dL, and homeostasis model assessment of insulin resistance: - 0.24 ± 0.44), and appetite-related hormones (adiponectin: 1.69 ± 2.13 ng/dL, leptin - 19.40 ± 16.89, and neuropeptide Y: - 41.96 ± 79.34 ng/dL). When compared with the placebo group, chitosan supplementation had greater improvement in body weight, body mass index (kg/m2 and Z-score), waist circumference, as well as insulin, adiponectin, and leptin levels. Differences were significant according to P-value < 0.05.Conclusion: Chitosan supplementation can improve cardiometabolic parameters (anthropometric indicators of obesity and lipid and glycemic markers) and appetite-related hormones (adiponectin, leptin, and NPY) in adolescents with overweight or obesity. [ABSTRACT FROM AUTHOR]

Background: Despite significant advances in the management of cardiovascular disease (CVDs), there is still a large burden of CVD in the world. The inclusion of functional foods in the diet may provide beneficial effects on CVD. Purple-black barberry due to its richness in anthocyanins and berberine has shown beneficial effects on cardiometabolic factors. We investigated the effects of barberry on plasma lipids as well as inflammatory biomarkers in subjects with cardiovascular risk factors. Methods: This was an 8-weeks, single-blinded, randomized controlled clinical trial that the participants were randomly assigned to a barberry (10 g/day dried barberry) or placebo group. At baseline and end of the study, plasma lipid profiles including total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), small-dense LDL-C (sd-LDL-C), non-HDL-C, and TC/HDL-C, as well as inflammatory biomarkers including C-reactive protein (CRP) and interleukin-6 (IL-6), were determined. An intention-to-treat analysis was performed. Results: Eighty-four participants were randomly assigned to study groups. The mean (± SD) participants' age was 54.06 ± 10.19 years. Body weight, body mass index (BMI), physical activity, and dietary intake were not different between the two groups at baseline and the end of the study. After adjusting for baseline values, we observed a significant decrease in plasma levels of TG, TC, LDL-C, sd-LDL-C, non-HDL-C, and TC/HDL-C (p < 0.001, p = 0.011, p = 0.015, p = 0.019, p = 0.004, and p = 0.039 respectively) as well as CRP (p = 0.020) in the barberry group compared to the placebo group. Conclusions: Our results indicate that purple-black barberry consumption decreases plasma levels of CRP and improves lipid profile in subjects with cardiovascular risk factors. Trial registration: This clinical trial was registered at ClinicalTrials.gov (NCT number: NCT04084847). [ABSTRACT FROM AUTHOR]

Background: In previous study, we found that coenzyme Q10 (CoQ10) improved glucolipid profile in dyslipidemic individuals, but the mechanism is not yet clear. Adipokines have been demonstrated to be vital targets of metabolic diseases. The hypothesis that adipokines mediate the association of CoQ10 on glucolipid metabolism needs to be further studied in human. Methods: In this randomized, double-blinded, placebo-controlled trial, 101 dyslipidemic individuals were administrated to 120 mg CoQ10 or placebo for 24 weeks. Anthropometric parameters, glucolipid profile, serum total adiponectin, leptin, and resistin were evaluated at baseline, week 12 and week 24. Results: CoQ10 treatment significantly increased serum adiponectin levels at week 12 (165 [0, 362] ng/mL, p < 0.001) and at week 24 (523 [0, 1056] ng/mL, p < 0.001]), which was significant different compared with placebo (p < 0.001). The increase of adiponectin was negative associated with decrease in index of homeostasis model assessment of insulin resistance (HOMA-IR, r = − 0.465, p = 0.001), triglyceride (TG, r = − 0.297, p = 0.047), and low-density lipoprotein cholesterol (LDL-c, r = − 0.440, p = 0.002) at week 24 only in CoQ10-treated group. Resistin was reduced by CoQ10 only at week 24 (− 1.19 [− 4.35, 0.00] ng/mL, p < 0.001), which was significant different compared with placebo (p < 0.001). Reduction of resistin was positively correlated with the change in HOMA-IR (r = 0.343, p = 0.021) and TG (r = 0.323, p = 0.030) at week 24 in CoQ10-treated group but not placebo group. Leptin was not influenced by CoQ10 treatment. Mediation analysis indicated that the improvement of HOMA-IR, TG and LDL-c by CoQ10 was mediated by adiponectin but not resistin. Conclusions: Our study shows that CoQ10 ameliorates glucolipid profile and adipokines dysfunction in dyslipidemic patients in 24 weeks' intervention. The beneficial effect of CoQ10 on glucolipid profile was mediated by adiponectin. Trial registration: ClinicalTrials.gov, NCT02407548. Registered on April 3, 2015, https://clinicaltrials.gov/ct2/show/NCT02407548. [ABSTRACT FROM AUTHOR]