1.
Essential Hypertension and Oxidative Stress: Novel Future Perspectives.
Franco, C, Sciatti, E, Favero, G, Bonomini, F, Vizzardi, E, Rezzani, R
International journal of molecular sciences. 2022;23(22)
-
-
-
Free full text
Plain language summary
High blood pressure is one of the main risk factors for cardiovascular disease and a significant contributor to the development of strokes, heart attacks, and heart and kidney failure leading to early disability and reduced life expectancy. Essential or primary hypotension makes up 95% of high blood pressure cases, which is abnormally elevated blood pressure that is not a result of any other medical condition. Essential hypertension arises from various factors such as diet, lifestyle, environmental and genetic influences. Despite many available medications, not all patients attain well-managed blood pressure levels. Unmanaged high blood pressure can, over time, lead to narrowing and stiffening of the blood vessels and ultimately to structural and functional changes in the blood tissues. In part, this is mediated by oxidative stress, changes in antioxidant capacity and chronic low-grade inflammation, which damage the blood vessels' endothelial tissue and result in vascular stiffness. Melatonin is one of the most potent antioxidants found in nature and has been studied in short-term trials for its blood pressure lowering, antioxidant and vascular protective effects. This small open-label randomised study sought to get a better understanding of the long-term use of melatonin. Initially, the study assessed endothelial tissue damage, oxidative status and vascular stiffness in patients with high blood pressure. Subsequently, some of the participants received a low-dose melatonin supplement (1 mg/day) for one year, whilst being monitored for clinical and structural vascular changes. The study included 23 patients and 14 in the final analysis. After one year, the results showed a significant improvement in arterial stiffness in the melatonin group (11) and an improvement in endothelial tissue function, though the latter was not at statistically significant levels. Improvement in arterial stiffness seemed to be linked to a reduction in total antioxidant capacity (TAC). These findings suggest that melatonin can contribute to restoring oxidative balance in blood plasma, which reflects improved arterial stiffness. The study also demonstrated that besides being a well-tolerated intervention, melatonin also has clinical benefits even when administered at lower doses than normal.
Abstract
Among cardiovascular diseases, hypertension is one of the main risk factors predisposing to fatal complications. Oxidative stress and chronic inflammation have been identified as potentially responsible for the development of endothelial damage and vascular stiffness, two of the primum movens of hypertension and cardiovascular diseases. Based on these data, we conducted an open-label randomized study, first, to evaluate the endothelial damage and vascular stiffness in hypertense patients; second, to test the effect of supplementation with a physiological antioxidant (melatonin 1 mg/day for 1 year) in patients with essential hypertension vs. hypertensive controls. Twenty-three patients of either gender were enrolled and randomized 1:1 in two groups (control and supplemented group). The plasmatic total antioxidant capacity (as a marker of oxidative stress), blood pressure, arterial stiffness, and peripheral endothelial function were evaluated at the beginning of the study and after 1 year in both groups. Our results showed that arterial stiffness improved significantly (p = 0.022) in supplemented patients. The endothelial function increased too, even if not significantly (p = 0.688), after 1 year of melatonin administration. Moreover, the supplemented group showed a significative reduction in TAC levels (p = 0.041) correlated with the improvement of arterial stiffness. These data suggest that melatonin may play an important role in reducing the serum levels of TAC and, consequently, in improving arterial stiffness.
2.
Effect of Omega-3 Dosage on Cardiovascular Outcomes: An Updated Meta-Analysis and Meta-Regression of Interventional Trials.
Bernasconi, AA, Wiest, MM, Lavie, CJ, Milani, RV, Laukkanen, JA
Mayo Clinic proceedings. 2021;96(2):304-313
-
-
-
Free full text
Plain language summary
There is mixed evidence to support the use of omega-3 fatty acids for the prevention and treatment of cardiovascular disease. Animal studies have shown promising results, but randomised control trials are inconsistent, possibly due to differing doses used, or differences in the subject’s omega-3 levels at the start of the trial. This meta-analysis of 40 studies with over 135,000 subjects aimed to determine whether omega-3 supplementation reduces heart disease risk and whether dosage has a role. The results showed that omega-3 supplementation reduced the risk of heart attacks, death from heart attacks and deaths due to heart disease, and the higher the dose, the greater the protection. The majority of studies were on individuals who had already had a heart attack or who had suffered from a related condition. It was concluded that supplementation with omega-3 is effective in preventing heart disease and heart attacks and the protective effect increases with dosage. This study could be used by healthcare professionals to prevent further heart disease and heart attacks in individuals who have already suffered from one of these conditions.
Abstract
OBJECTIVES To quantify the effect of eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids on cardiovascular disease (CVD) prevention and the effect of dosage. METHODS This study is designed as a random effects meta-analysis and meta-regression of randomized control trials with EPA/DHA supplementation. This is an update and expanded analysis of a previously published meta-analysis which covers all randomized control trials with EPA/DHA interventions and cardiovascular outcomes published before August 2019. The outcomes included are myocardial infarction (MI), coronary heart disease (CHD) events, CVD events (a composite of MI, angina, stroke, heart failure, peripheral arterial disease, sudden death, and non-scheduled cardiovascular surgical interventions), CHD mortality and fatal MI. The strength of evidence was assessed using the Grading of Recommendations Assessment, Development, and Evaluation framework. RESULTS A total of 40 studies with a combined 135,267 participants were included. Supplementation was associated with reduced risk of MI (relative risk [RR], 0.87; 95% CI, 0.80 to 0.96), high certainty number needed to treat (NNT) of 272; CHD events (RR, 0.90; 95% CI, 0.84 to 0.97), high certainty NNT of 192; fatal MI (RR, 0.65; 95% CI, 0.46 to 0.91]), moderate certainty NNT = 128; and CHD mortality (RR, 0.91; 95% CI, 0.85 to 0.98), low certainty NNT = 431, but not CVD events (RR, 0.95; 95% CI, 0.90 to 1.00). The effect is dose dependent for CVD events and MI. CONCLUSION Cardiovascular disease remains the leading cause of death worldwide. Supplementation with EPA and DHA is an effective lifestyle strategy for CVD prevention, and the protective effect probably increases with dosage.
3.
The effects of coenzyme Q10 supplementation on biomarkers of inflammation and oxidative stress in among coronary artery disease: a systematic review and meta-analysis of randomized controlled trials.
Jorat, MV, Tabrizi, R, Kolahdooz, F, Akbari, M, Salami, M, Heydari, ST, Asemi, Z
Inflammopharmacology. 2019;27(2):233-248
-
-
Plain language summary
Cardiovascular disease is the leading cause of death worldwide. Systemic inflammation and oxidative stress significantly contribute to the narrowing of the blood supply to the heart leading to coronary artery disease (CAD). Increased levels of several markers of inflammation, such as C-reactive protein (CRP), tumour necrosis factor-α (TNF- α), and interleukin-6 (IL-6), appear to be indicative of heart attack risk. Coenzyme Q10 (CoQ10) is a naturally occurring nutrient made in the body but can also be found in some foods or taken via supplements. It is an antioxidant that protects cell membranes and mitochondria against oxidative damage and also does so in the heart by preventing endothelial damage and the associated narrowing of blood vessels. Several trials investigated the effects of CoQ10 on inflammation and oxidative stress, with some noteworthy results and yet also some conflicting evidence. Hence this systematic review and meta-analysis aimed to shed some light on the controversial findings regarding coenzyme Q10 (CoQ10) supplementation on biomarkers of inflammation and oxidative stress amongst patients with CAD. The authors included 13 clinical randomised controlled trials, amounting to 364 cardiac patients in the intervention groups. The treatment duration ranged from 4 to 48 weeks, and the dosage of CoQ10 varied between 60 to 300 mg/day. In conclusion, the meta-analysis showed that CoQ10 supplementation increased antioxidant markers of superoxide dismutase (SOD) and catalase (CAT), and decreased the oxidative stress marker malondialdehyde (MDA) and its derivative forms. There was no consistent effect on inflammatory markers of CRP, TNF-α, IL-6 or the levels of the antioxidant glutathione peroxidase. The discrepancies amongst the different studies may be a result of the divergent study designs, different population characteristics, the dosage of CoQ10 used and the duration of intervention.
Abstract
OBJECTIVE Systemic inflammation and oxidative stress significantly contribute in developing coronary artery disease (CAD). This systematic review and meta-analysis was aimed to determine the effects of coenzyme Q10 (CoQ10) supplementation on biomarkers of inflammation and oxidative stress among patients with CAD. METHODS The electronic databases including MEDLINE, EMBASE, Scopus, Web of Science, and Cochrane Library databases were systematically searched until Oct 2018. The quality assessment and heterogeneity of the selected randomized clinical Trials (RCTs) were examined using the Cochrane Collaboration risk of bias tool, and Q and I2 tests, respectively. Given the presence of heterogeneity, random-effects model or fixed-effect model were used to pool standardized mean differences (SMDs) as summary effect sizes. RESULTS A total of 13 clinical RCTs of 912 potential citations were found to be eligible for the current meta-analysis. The pooled findings for biomarkers of inflammation and oxidative stress demonstrated that CoQ10 supplementation significantly increased superoxide dismutase (SOD) (SMD 2.63; 95% CI, 1.17, 4.09, P < 0.001; I2 = 94.5%) and catalase (CAT) levels (SMD 1.00; 95% CI, 0.57, 1.43, P < 0.001; I2 = 24.5%), and significantly reduced malondialdehyde (MDA) (SMD - 4.29; 95% CI - 6.72, - 1.86, P = 0.001; I2 = 97.6%) and diene levels (SMD - 2.40; 95% CI - 3.11, - 1.68, P < 0.001; I2 = 72.6%). We did not observe any significant effect of CoQ10 supplementation on C-reactive protein (CRP) (SMD - 0.62; 95% CI - 1.31, 0.08, P = 0.08; I2 = 87.9%), tumor necrosis factor alpha (TNF-α) (SMD 0.22; 95% CI - 1.07, 1.51, P = 0.73; I2 = 89.7%), interleukin-6 (IL-6) (SMD - 1.63; 95% CI - 3.43, 0.17, P = 0.07; I2 = 95.2%), and glutathione peroxidase (GPx) levels (SMD 0.14; 95% CI - 0.77, 1.04, P = 0.76; I2 = 78.7%). CONCLUSIONS Overall, this meta-analysis demonstrated CoQ10 supplementation increased SOD and CAT, and decreased MDA and diene levels, but did not affect CRP, TNF-α, IL-6, and GPx levels among patients with CAD.
4.
Systematic review of palm oil consumption and the risk of cardiovascular disease.
Ismail, SR, Maarof, SK, Siedar Ali, S, Ali, A
PloS one. 2018;13(2):e0193533
-
-
-
Free full text
Plain language summary
Palm oil, the most widely consumed vegetable oil in the world, derives from the palm tree fruit with a balanced ratio of unsaturated and saturated fatty acids. Studies have shown an association between high contents of saturated fats in palm oil with the detrimental atherogenic profile. The review aims at synthesising the available evidence reporting the association of palm oil consumption with cardiovascular disease risk and cardiovascular disease-specific mortality, including specifically Coronary Heart Disease (CHD) and stroke. The authors systematically searched three databases up to June 2017 without restriction on setting or language. Published interventional and observational studies that evaluated palm oil consumption with coronary heart disease or stroke in adults were searched. Separate searches were performed depending on the outcome. The study did not find a clear association between palm oil consumption and risk or mortality of cardiovascular disease, namely coronary heart disease and stroke. The health effects found between association of palm oil consumption and risk of coronary heart disease were not unique to just palm oil consumption as other food items were also included in the analysis. The review could not establish strong evidence for or against palm oil consumption relating to cardiovascular disease risk and cardiovascular disease-specific mortality. A healthy overall diet is suggested for good cardiometabolic health.
Abstract
BACKGROUND The high amount of saturated fatty acids (SFA) coupled with the rising availability and consumption of palm oil have lead to the assumption that palm oil contributes to the increased prevalence of cardiovascular diseases worldwide. We aimed at systematically synthesising the association of palm oil consumption with cardiovascular disease risk and cardiovascular disease-specific mortality. METHODS We systematically searched Central, Medline and Embase databases up to June 2017 without restriction on setting or language. We performed separate searches based on the outcomes: coronary heart disease and stroke, using keywords related to these outcomes and palm oil. We searched for published interventional and observational studies in adults (Age: >18 years old). Two investigators extracted data and a consensus was reached with involvement of a third. Only narrative synthesis was performed for all of the studies, as the data could not be pooled. RESULTS Our search retrieved 2,738 citations for stroke with one included study and 1,777 citations for coronary heart disease (CHD) with four included studies. Palmitic acid was reported to be associated with risk of myocardial infarction (MI) (OR 2.76; 95%CI = 1.39-5.47). Total SFA intake was reported to be not significant for risk of MI. Varying intake of fried foods, highest contributor to total SFA with 36% of households using palm oil for frying, showed no significant associations to risk of MI. Odds of developing first non-fatal acute MI was higher in palm oil compared to soybean oil with 5% trans-fat (OR = 1.33; 95%CI = 1.09-1.62) than palm oil compared to soybean oil with 22% trans-fat (OR = 1.16; 95%CI = 0.86-1.56). Nevertheless, these risk estimates were non-significant and imprecise. The trend amongst those taking staple pattern diet (characterised by higher palm oil, red meat and added sugar consumption) was inconsistent across the factor score quintiles. During the years of 1980 and 1997, for every additional kilogram of palm oil consumed per-capita annually, CHD mortality risk was 68 deaths per 100,000 (95% CI = 21-115) in developing countries and 17 deaths per 100,000 (95%CI = 5.3-29) in high-income countries, whereas stroke was associated with 19 deaths per 100,000 (95%CI = -12-49) and 5.1 deaths per 100,000 (95% CI: -1.2-11) respectively. The evidence for the outcomes of this review were all graded as very low. The findings of this review should be interpreted with some caution, owing to the lack of a pooled effect estimate of the association, significant bias in selection criteria and confounding factors, inclusion of other food items together with palm oil, and the possible out-dated trend in the ecological study. CONCLUSION In view of the abundance of palm oil in the market, quantifying its true association with CVD outcomes is challenging. The present review could not establish strong evidence for or against palm oil consumption relating to cardiovascular disease risk and cardiovascular disease-specific mortality. Further studies are needed to establish the association of palm oil with CVD. A healthy overall diet should still be prioritised for good cardiometabolic health.