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1.
The Effect of a Multivitamin and Mineral Supplement on Immune Function in Healthy Older Adults: A Double-Blind, Randomized, Controlled Trial.
Fantacone, ML, Lowry, MB, Uesugi, SL, Michels, AJ, Choi, J, Leonard, SW, Gombart, SK, Gombart, JS, Bobe, G, Gombart, AF
Nutrients. 2020;12(8)
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Vitamins and minerals are essential for a healthy immune system. The prevalence of vitamin and mineral deficiencies increases with age, and this may contribute to age-related decline of the immune system. The aim of this study was to investigate whether a daily multivitamin and mineral (MVM) supplement could improve the immune function of older people. 42 healthy adults aged between 55 and 75 took part in this single-centre, two-armed, parallel, randomised, double-blinded study. Half of the group was given a MVM supplement called Redoxon Vita Immune (VI) containing the vitamins A, D, E, C, B6, B12 and folate plus iron, copper, zinc and selenium daily for 12 weeks, whilst the other half was given placebo tablets for 12 weeks. Participants were instructed to avoid certain foods high in vitamins and minerals such as oily fish, red meat, liver, and citrus fruits during the study period. Blood and saliva samples were taken from all participants at the beginning and end of the study period, to measure vitamin and mineral status and markers of immune function. Participants also kept a diary to record any illnesses or symptoms. At the end of the study, participants given the MVM supplement had increased their blood levels of vitamin C by 126% and zinc by 43%. There was no significant change in blood levels of vitamin D. There was no significant difference in the potential of blood to kill the introduced bacteria Staphylococcus aureus, or in neutrophil activity, nor were there any significant changes in blood levels of cytokines and chemokines. Participants taking the supplement did however report a shorter length, and lower severity of illnesses compared to those taking the placebo. The authors concluded that their findings support further research to test whether MVM supplementation can improve immune outcomes in older adults.
Abstract
Older adults are at increased risk for vitamin and mineral deficiencies that contribute to age-related immune system decline. Several lines of evidence suggest that taking a multi-vitamin and mineral supplement (MVM) could improve immune function in individuals 55 and older. To test this hypothesis, we provided healthy older adults with either an MVM supplement formulated to improve immune function (Redoxon® VI, Singapore) or an identical, inactive placebo control to take daily for 12 weeks. Prior to and after treatment, we measured (1) their blood mineral and vitamin status (i.e., vitamin C, zinc and vitamin D); (2) immune function (i.e., whole blood bacterial killing activity, neutrophil phagocytic activity, and reactive oxygen species production); (3) immune status (salivary IgA and plasma cytokine/chemokine levels); and (4) self-reported health status. MVM supplementation improved vitamin C and zinc status in blood and self-reported health-status without altering measures of immune function or status or vitamin D levels, suggesting that healthy older adults may benefit from MVM supplementation. Further development of functional assays and larger study populations should improve detection of specific changes in immune function after supplementation in healthy older adults. Clinical Trials Registration: ClinicalTrials.gov #NCT02876315.
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Selenium, antioxidants, cardiovascular disease, and all-cause mortality: a systematic review and meta-analysis of randomized controlled trials.
Jenkins, DJA, Kitts, D, Giovannucci, EL, Sahye-Pudaruth, S, Paquette, M, Blanco Mejia, S, Patel, D, Kavanagh, M, Tsirakis, T, Kendall, CWC, et al
The American journal of clinical nutrition. 2020;112(6):1642-1652
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Oxidative damage is a shared characteristic in chronic diseases such as cardiovascular disease (CVD), diabetes, cancer and ageing. Antioxidants mitigate the impact of oxidants and have been widely investigated in ageing and disease. However, the evidence for supplementary antioxidants has been mixed and some authorities have advised against the use of certain single nutrients for the prevention of CVD or cancer. This systematic review and meta-analysis focused on selenium due to its vital role in the antioxidant system and associations of low selenium blood levels with increased risk of CVD, cancers and death. The study included 43 randomised controlled trials (RCTs) evaluating the effect of supplemental selenium and antioxidants with or without selenium and their impact on CVD risk, cancer and all-cause mortality. Overall supplemental selenium or antioxidants alone did not seem to be associated with CVD outcomes, cancer, CVD and cancer mortality, or all-cause mortality. On close examination, a decreased risk was seen for CVD mortality when antioxidants were combined with selenium, whilst antioxidant mixtures without selenium demonstrated an increased risk in all-cause mortality. The findings did not seem to be influenced by dietary selenium intake. The authors suggested that inclusion of selenium as part of an antioxidant mix could be key for an antioxidant associated risk reduction. However, in the absence of further long term studies, a balanced antioxidant-rich diet was advocated as the safest approach. In clinical practice, where antioxidant support beyond diet is warranted, supplemental antioxidant use should be concurrent with adequate selenium supplementation, with dose benefits of 50-200mcg observed.
Abstract
BACKGROUND Antioxidants have been promoted for cardiovascular disease (CVD) risk reduction and for the prevention of cancer. Our preliminary analysis suggested that only when selenium was present were antioxidant mixtures associated with reduced all-cause mortality. OBJECTIVE We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) to determine the effect of selenium supplementation alone and of antioxidant mixtures with or without selenium on the risk of CVD, cancer, and mortality. METHODS We identified studies using the Cochrane Library, Medline, and Embase for potential CVD outcomes, cancer, and all-cause mortality following selenium supplementation alone or after antioxidant supplement mixtures with and without selenium up to June 5, 2020. RCTs of ≥24 wk were included and data were analyzed using random-effects models and classified by the Grading of Recommendations, Assessment, Development, and Evaluation approach. RESULTS The meta-analysis identified 9423 studies, of which 43 were used in the final analysis. Overall, no association of selenium alone or antioxidants was seen with CVD and all-cause mortality. However, a decreased risk with antioxidant mixtures was seen for CVD mortality when selenium was part of the mix (RR: 0.77; 95% CI: 0.62, 0.97; P = 0.02), with no association when selenium was absent. Similarly, when selenium was part of the antioxidant mixture, a decreased risk was seen for all-cause mortality (RR: 0.90; 95% CI: 0.82, 0.98; P = 0.02) as opposed to an increased risk when selenium was absent (RR: 1.09; 95% CI: 1.04, 1.13; P = 0.0002). CONCLUSION The addition of selenium should be considered for supplements containing antioxidant mixtures if they are to be associated with CVD and all-cause mortality risk reduction. This trial was registered at https://www.crd.york.ac.uk/PROSPERO/ as CRD42019138268.
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Inflammaging and Oxidative Stress in Human Diseases: From Molecular Mechanisms to Novel Treatments.
Zuo, L, Prather, ER, Stetskiv, M, Garrison, DE, Meade, JR, Peace, TI, Zhou, T
International journal of molecular sciences. 2019;20(18)
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Reactive oxygen species (ROS) are produced during normal metabolic processes or can be induced by environmental factors. High levels of ROS in the cell can lead to oxidation causing cellular damage and a subsequent increase in inflammation, which is a significant contributor to disease. Age-associated increases in such chronic, low-grade inflammation is also referred to as inflammaging. This review summarizes how inflammaging plays a role in various age-related health conditions. Described are the mechanisms of how ROS and the age-related decline in cellular turn-over and immune activation contribute to the pathology of cardiovascular disease, cancer, neurodegeneration concerning Alzheimer’s and Parkinson’s disease, diabetes and rheumatoid arthritis. Furthermore, the authors discuss potential treatments that could assist in the management of such inflammaging-related diseases. These include vaccines to stimulate immune activity, stem cell intervention, drugs like metformin, nutritional and nutraceutical supplements like zinc, vitamin E, vitamins C, D, carotenoids, polyphenols and flavonoids like resveratrol, red algae extract and melatonin. Addressed are also general dietary concepts like calorie restriction, the benefits of the Mediterranean diet or a whole foods diet, and the potential of specific plant derived compounds like baicalin and sulforaphanes. The authors also briefly highlight the importance of the gut microbiome, as a poor gut microbiota has been associated with unfavourable age-related immune alterations and overall inflammaging. This review provides a comprehensive resource, detailing the effects and mechanisms of oxidative damage and its contribution to age-related diseases, including a list of interventions to consider when navigating the impact and risks associated with inflammaging.
Abstract
It has been proposed that a chronic state of inflammation correlated with aging known as inflammaging, is implicated in multiple disease states commonly observed in the elderly population. Inflammaging is associated with over-abundance of reactive oxygen species in the cell, which can lead to oxidation and damage of cellular components, increased inflammation, and activation of cell death pathways. This review focuses on inflammaging and its contribution to various age-related diseases such as cardiovascular disease, cancer, neurodegenerative diseases, chronic obstructive pulmonary disease, diabetes, and rheumatoid arthritis. Recently published mechanistic details of the roles of reactive oxygen species in inflammaging and various diseases will also be discussed. Advancements in potential treatments to ameliorate inflammaging, oxidative stress, and consequently, reduce the morbidity of multiple disease states will be explored.
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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
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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.
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Metabolic stress-dependent regulation of the mitochondrial biogenic molecular response to high-intensity exercise in human skeletal muscle.
Fiorenza, M, Gunnarsson, TP, Hostrup, M, Iaia, FM, Schena, F, Pilegaard, H, Bangsbo, J
The Journal of physiology. 2018;596(14):2823-2840
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Endurance exercise stimulates mitochondrial biogenesis in skeletal muscles, a crucial adaptive protective mechanism against various metabolic disorders. Mitochondrial biogenesis is a process that involves the expansion of mitochondrial volume and changes in mitochondrial composition. Continuous moderate‐intensity exercise (CM) may lead to mild but prolonged metabolic disturbances, and low‐volume intense intermittent exercise regimes such as repeated‐sprint (RE) and speed endurance (SE) exercises may lead to a distinct degree of metabolic stress. This randomised counter-balanced crossover trial included 12 healthy trained men to investigate the effect of RE and SE exercise and high‐volume CM on metabolic perturbations and its impact on the regulation of molecular response stimulating mitochondrial biogenesis in human skeletal muscle. Compared to CM, PGC‐1α mRNA (Peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PGC‐1α) mRNA) showed elevation in response to RS and SE exercises in well-trained subjects, and this was associated with high accumulation of muscle lactate, greater decline in muscle pH and elevated plasma adrenaline levels. Elevated metabolic perturbations lead to enhanced mitochondrial biogenesis-related mRNA responses. SE was associated with a greater increase in the PGC‐1α mRNA and severe metabolic stress. SE and CM elevated exercise-induced signalling and mRNA content of genes controlling mtDNA. Further robust research is required to elucidate the role of metabolic stress in initiating mitochondrial biogenesis in skeletal muscles in response to acute exercise, regulating genes modulating mtDNA transcription and mitochondrial remodelling dynamics. However, healthcare professionals can use the results of this study to understand that low-volume high-intensity exercise programmes can promote mitochondrial biogenesis in skeletal muscles in healthy trained men and have a similar effect to that of high-volume moderate-intensity exercise programmes.
Abstract
KEY POINTS Low-volume high-intensity exercise training promotes muscle mitochondrial adaptations that resemble those associated with high-volume moderate-intensity exercise training. These training-induced mitochondrial adaptations stem from the cumulative effects of transient transcriptional responses to each acute exercise bout. However, whether metabolic stress is a key mediator of the acute molecular responses to high-intensity exercise is still incompletely understood. Here we show that, by comparing different work-matched low-volume high-intensity exercise protocols, more marked metabolic perturbations were associated with enhanced mitochondrial biogenesis-related muscle mRNA responses. Furthermore, when compared with high-volume moderate-intensity exercise, only the low-volume high-intensity exercise eliciting severe metabolic stress compensated for reduced exercise volume in the induction of mitochondrial biogenic mRNA responses. The present results, besides improving our understanding of the mechanisms mediating exercise-induced mitochondrial biogenesis, may have implications for applied and clinical research that adopts exercise as a means to increase muscle mitochondrial content and function in healthy or diseased individuals. ABSTRACT The aim of the present study was to examine the impact of exercise-induced metabolic stress on regulation of the molecular responses promoting skeletal muscle mitochondrial biogenesis. Twelve endurance-trained men performed three cycling exercise protocols characterized by different metabolic profiles in a randomized, counter-balanced order. Specifically, two work-matched low-volume supramaximal-intensity intermittent regimes, consisting of repeated-sprint (RS) and speed endurance (SE) exercise, were employed and compared with a high-volume continuous moderate-intensity exercise (CM) protocol. Vastus lateralis muscle samples were obtained before, immediately after, and 3 h after exercise. SE produced the most marked metabolic perturbations as evidenced by the greatest changes in muscle lactate and pH, concomitantly with higher post-exercise plasma adrenaline levels in comparison with RS and CM. Exercise-induced phosphorylation of CaMKII and p38 MAPK was greater in SE than in RS and CM. The exercise-induced PGC-1α mRNA response was higher in SE and CM than in RS, with no difference between SE and CM. Muscle NRF-2, TFAM, MFN2, DRP1 and SOD2 mRNA content was elevated to the same extent by SE and CM, while RS had no effect on these mRNAs. The exercise-induced HSP72 mRNA response was larger in SE than in RS and CM. Thus, the present results suggest that, for a given exercise volume, the initial events associated with mitochondrial biogenesis are modulated by metabolic stress. In addition, high-intensity exercise seems to compensate for reduced exercise volume in the induction of mitochondrial biogenic molecular responses only when the intense exercise elicits marked metabolic perturbations.
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Changes in LDL Oxidative Status and Oxidative and Inflammatory Gene Expression after Red Wine Intake in Healthy People: A Randomized Trial.
Di Renzo, L, Marsella, LT, Carraro, A, Valente, R, Gualtieri, P, Gratteri, S, Tomasi, D, Gaiotti, F, De Lorenzo, A
Mediators of inflammation. 2015;2015:317348
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It is recognised that inflammation and oxidative stress may play a role in the development of heart disease. Red wine has previously been shown to lower inflammation and improve antioxidant status. This small, randomised, crossover trial aims to investigate if resveratrol in red wine causes these effects. The trial involved twenty-four healthy adults who took part in the four intervention arms, with a three week washout period in between. Blood markers and genomic information were measured at (1) baseline and after each intervention: (2) a high-fat McDonald’s meal (McDM), (3) McDM + red wine and (4) just red wine. While eating McDM alone raised markers of oxidative stress, having red wine with McDM lowered markers. The authors concluded that having red wine with a meal could reduce the levels of inflammation and oxidative stress normally seen after eating. It was suggested that moderate red wine consumption (2 drinks a day for men and 1 drink a day for women) could potentially lower the risk of heart disease, but longer term studies are needed before definite conclusions can be drawn.
Abstract
Postprandial oxidative stress is characterized by an increased susceptibility of the organism towards oxidative damage after consumption of a meal rich in lipids and/or carbohydrates. Micronutrients modulate immune system and exert a protective action by reducing low density lipoproteins (LDL) oxidation via induction of antioxidant enzymes. We evaluated the gene expression of oxidative stress (HOSp), inflammasome (HIp), and human drug metabolism pathways (HDM) and ox-LDL level at baseline and after the intake of red wine naturally enriched with resveratrol (NPVRW), in association with or without a McDonald's meal (McDM). The ox-LDL levels significantly increase comparing baseline (B) versus McDM and decreased comparing McDM versus McDM + NPVRW (P ≤ 0.05). Percentages of significant genes expressed after each nutritional intervention were the following: (1) B versus McDM, 2.88% HOSp, 2.40% of HIp, and 3.37% of HDMp; (2) B versus McDM + NPVRW, 1.44% of HOSp, 4.81% of HIp, and 0.96% of HDMp; (3) McDM versus McDM + NPVRW, 2.40% of HOSp, 2.40% of HIp, and 5.77% of HDMp; (4) B versus NPVRW, 4.80% HOSp, 3.85% HIp, and 3.85% HDMp. NPVRW intake reduced postprandial ox-LDL and the expression of inflammation and oxidative stress related genes. Chronic studies on larger population are necessary before definitive conclusions.