OBJECTIVES:To explore the interrelationship and mediating effect of factors that are beneficial (i.e., antioxidants) and harmful (i.e., inflammation and oxidative stress) to the relationship between sleep and cardiometabolic health.

DESIGN:Cross-sectional data from the 2005-2006 National Health and Nutrition Examination Survey.

SETTING:Nationally representative population sample from the US.

PARTICIPANTS:Age≥ 20 y with sleep data; final analytical sample of N = 2,079.

INTERVENTIONS:N/A.

MEASUREMENTS AND RESULTS:Metabolic syndrome was classified according to the Joint Interim Statement, and sleep duration was categorized as very short, short, adequate, and long sleepers (≤4, 5-6, 7-8, and ≥9 h per night, respectively). The indirect mediation effect was quantified as large (≥ 0.25), moderate (≥ 0.09), modest (≥ 0.01), and weak (<0.01). In general, inflammation was above the current clinical reference range across all sleep duration categories, whereas oxidative stress was elevated among short and very short sleepers. Select sleep duration-cardiometabolic health relationships were mediated by C-reactive protein (CRP),γ-glutamyl transferase (GGT), carotenoids, uric acid, and vitamins C and D, and were moderated by sex. Specifically, moderate-to-large indirect mediation by GGT, carotenoids, uric acid, and vitamin D were found for sleep duration-waist circumference and systolic blood pressure relationships, whereas vitamin C was a moderate mediator of the sleep duration-diastolic blood pressure relationship.

CONCLUSIONS:Several factors related to inflammation, oxidative stress, and antioxidant status were found to lie on the casual pathway of the sleep duration-cardiometabolic health relationship. Further longitudinal studies are needed to confirm our results.

The antiperoxidative effect of coriander seeds (Coriandrum sativum) was studied in rats administered high fat diet. Significant decrease in the levels of lipid peroxides, free fatty acids and glutathione was observed when compared to control group whereas the activity of antioxidant enzymes showed increase.

This article summarizes the likely benefits of melatonin in the attenuation of COVID-19 based on its putative pathogenesis. The recent outbreak of COVID-19 has become a pandemic with tens of thousands of infected patients. Based on clinical features, pathology, the pathogenesis of acute respiratory disorder induced by either highly homogenous coronaviruses or other pathogens, the evidence suggests that excessive inflammation, oxidation, and an exaggerated immune response very likely contribute to COVID-19 pathology. This leads to a cytokine storm and subsequent progression to acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) and often death. Melatonin, a well-known anti-inflammatory and anti-oxidative molecule, is protective against ALI/ARDS caused by viral and other pathogens. Melatonin is effective in critical care patients by reducing vessel permeability, anxiety, sedation use, and improving sleeping quality, which might also be beneficial for better clinical outcomes for COVID-19 patients. Notably, melatonin has a high safety profile. There is significant data showing that melatonin limits virus-related diseases and would also likely be beneficial in COVID-19 patients. Additional experiments and clinical studies are required to confirm this speculation.

OBJECTIVE:Mushroom crude polysaccharides offer a complete package of various medicinal activities. In this context, the present study aimed to unveil structural and biomedical properties of crude polysaccharide (MLHWP) obtained from an edible wild mushroom Macrocybe lobayensis (R. Heim) Pegler&Lodge.

METHOD:Chemical characterization was accomplished with the help of spectrophotometry, Fourier-transform infrared spectroscopy, HPTLC and GC-MS. Immunomodulatory activity of the crude polysaccharide and its signalling mechanism was assessed using RAW 264.7 cells. Furthermore, antioxidant activity was analysed based on radical scavenging, metal ion chelating and reducing effect.

KEY FINDINGS:Compositional study revealed that MLHWP possessed triple helical structure and its backbone consisted ofβ-linked glucan along with xylose, rhamnose, mannose and galactose. Investigation on bioactive potency revealed that MLHWP augmented macrophage activity in terms of viability, phagocytosis, NO and ROS generation. Gene expression studies indicated that MLHWP signalled through TLR and modulated expression of immunomodulation-related genes including NF-κB, COX-2, IFN-γ, TNF-α, iNOS and Iκ-βα. Besides, MLHWP displayed noticeable antioxidant potential as reflected in all investigating assays.

CONCLUSIONS:Overall, the results portrayed possibility of MLHWP as pharmaceutical agent with multidimensional application.

When exercises are done in intense or exhaustive modes, several acute biochemical mechanisms are triggered. The use of cryotherapy as cold-water immersion is largely used to accelerate the process of muscular recovery based on its anti-inflammatory and analgesic properties. The present study aimed to study the biochemical effects of cold-water immersion treatment in mice submitted to exercise-induced exhaustion. Swiss albino mice were divided into 4 treatment groups: control, cold-water immersion (CWI), swimming exhaustive protocol (SEP), and SEP+CWI. Treatment groups were subdivided into times of analysis: 0, 1, 3, and 5 days. Exhaustion groups were submitted to one SEP session, and the CWI groups submitted to one immersion session (12 min at 12°C) every 24 h. Reactive species production, inflammatory, cell viability, and antioxidant status were assessed. The SEP+CWI group showed a decrease in inflammatory damage biomarkers, and reactive species production, and presented increased cell viability compared to the SEP group. Furthermore, CWIincreased acetylcholinesterase activity in the first two sessions. The present study showed that CWI was an effective treatment after exercise-induced muscle damage. It enhanced anti-inflammatory response, decreased reactive species production, increased cell viability, and promoted redox balance,which could decrease the time for the recovery process.

Dietary curcumin was studied for its potential to decrease adiposity and reverse obesity- associated cognitive impairment in a mouse model of midlife sedentary obesity. We hypothesized that curcumin intake, by decreasing adiposity, would improve cognitive function in a manner comparable to caloric restriction (CR), a weight loss regimen. 15-month-old male C57BL/6 mice were assigned in groups to receive the following dietary regimens for 12 weeks: (i) a base diet (Ain93M) fed ad libitum (AL), (ii) the base diet restricted to 70% of ad libitum (CR) or (iii) the base diet containing curcumin fed AL (1000 mg/kg diet, CURAL). Blood markers of inflammation, interleukin 6 (IL-6) and C-reactive protein (CRP), as well as an indicator of redox stress (GSH: GSSG ratio), were determined at different time points during the treatments, and visceral and subcutaneous adipose tissue were measured upon completion of the experiment. After 8 weeks of dietary treatment, the mice were tested for spatial cognition (Morris water maze) and cognitive flexibility (discriminated active avoidance). The CR group showed significant weight loss and reduced adiposity, whereas CURAL mice had stable weight throughout the experiment, consumed more food than the AL group, with no reduction of adiposity. However, both CR and CURAL groups took fewer trials than AL to reach criterion during the reversal sessions of the active avoidance task, suggesting an improvement in cognitive flexibility. The AL mice had higher levels of CRP compared to CURAL and CR, and GSH as well as the GSH: GSSG ratio were increased during curcumin intake, suggesting a reducing shift in the redox state. The results suggest that, independent of their effects on adiposity; dietary curcumin and caloric restriction have positive effects on frontal cortical functions that could be linked to anti-inflammatory or antioxidant actions.

Huntington's disease (HD) is a progressive, dominantly inherited neurological disorder caused by an abnormal expansion of polyglutamine (polyQ) repeat within the Huntingtin (Htt) protein with no disease modifying treatments. In a Drosophila model of HD, expression of mutant Huntingtin (Htt) protein with expanded polyQ leads to formation of inclusion bodies (IBs), increase in cellular toxicity, progression of motor disabilities and reduced viability. Multiple cellular events such as oxidative stress, mitochondrial dysfunction, inflammation and transcriptional dysregulation are reported to contribute to pathology, however, till date there are no disease-modifying treatments with least side effects. Therefore, we investigated effect of the phytochemical curcumin on HD pathogenesis. Curcumin, a phytochemical and commonly used ingredient in Asian food has a wide spectrum of anti-oxidant, anti-inflammatory and anti-fibrilogenic properties. In this study, we provide evidence that curcumin significantly ameliorates disease symptoms in a Drosophila model of HD by suppressing cell death and can be a key to halting the progression of Huntington's disease with least side effects.

The bioassay-guided isolation and purification of the hexane extract of the cultured mycelia of Grifola frondosa led to the characterization of a fatty acid fraction and three compounds, ergosterol (1), ergostra-4,6,8(14),22-tetraen-3-one (2), and 1-oleoyl-2-linoleoyl-3-palmitoylglycerol (3). The composition of fatty acid fraction was confirmed as palmitic, oleic, and linoleic acids by GC-MS and by comparison with the retention values of authentic samples. The structures of compounds 1-3 were established by spectroscopic methods. The fatty acid fraction and compounds 1-3 showed cyclooxygenase (COX) enzyme inhibitory and antioxidant activities. The inhibition of COX-1 enzyme by the fatty acid fraction and compounds 1-3 at 250 microg/mL were 98, 37, 55, and 67%, respectively. Similarly, COX-2 enzyme activity was reduced by fatty acid fraction and compounds 1-3 at 250 microg/mL by 99, 37, 70, and 4%, respectively. The inhibitions of liposome peroxidation by the fatty acid fraction and compounds 1 and 2 at 100 microg/mL were 79, 48, and 42%, respectively. This is the first report of compounds 2 and 3 from the cultured mycelia of G. frondosa. The COX inhibitory activities of compounds 1-3 are reported here for the first time.

Vitamin C, available in its reduced form (ascorbic acid; AA) and in its oxidized form (dehydroascorbic acid; DHA), may act in physiological conditions as an antioxidant or pro-oxidant. The aim of this study is to evaluate the cytotoxic effects of pharmacological doses of AA in a human colorectal adenocarcinoma cell line (WiDr) in vitro, through spectrophotometry, clonogenic assays and flow cytometry, and in vivo with xenotransplanted Balb/c nu/nu mice. The results show that the reduced form of vitamin C induces an anti-proliferative and cytotoxic effect in adenocarcinoma colorectal cells under study. The results obtained in vivo after treatment with AA showed a large reduction in the rate of tumor growth. Such understanding can guide decisions about which colorectal cancer patients might potentially benefit from vitamin C pharmacologic therapy.

BACKGROUND:Mushrooms have been valued for their nutritive content and as traditional medicines; several important medicinal properties of mushrooms have been recognized worldwide.

OBJECTIVE:The purpose of this study was to elucidate the cell growth inhibitory potential of four edible mushrooms; Coprinus comatus (O.F. Mull.) Pers. (Agaricaceae), Tricholoma fracticum (Britzelm.) Kreisel (Tricholomataceae), Rhizopogon luteolus Fr. and Nordholm (Rhizopogonaceae), Lentinus tigrinus (Bull.) Fr. (Polyporaceae) on hepatocellular carcinoma (HepG2) cells in conjunction with their antioxidant and antibacterial capacities.

MATERIALS AND METHODS:Five different extracts of edible mushrooms were obtained using water, methanol, acetone, n-hexane and chloroform as solvent systems for cytotoxic, antioxidant and antibacterial properties.

RESULTS:C. comatus showed substantial in vitro cytotoxic activity against HepG2 cell lines with all extracts especially with chloroform 50% inhibition (IC50 value of 0.086 mg/ml) and acetone (IC50 value of 0.420 mg/ml). Chloroform extract of C. comatus had maximum amount ofβ-carotene (25.94 μg/mg), total phenolic content (76.32 μg/mg) and lycopene (12.00 μg/mg), and n-hexane extract of L. tigrinus had maximum amount of flavonoid (3.67 μg/mg). While chloroform extract of C. comatus showed the highest 2, 2-diphenyl-1-picrylhydrazyl (DPPH) capturing activity (1.579mg/ml), the best result for metal chelating activity was obtained from methanolic extract (0.842 mg/ml). Moreover, all tested mushrooms demonstrated antibacterial activity and n-hexane extract of L. tigrinus and acetone extracts of T. fracticum were the most active against tested microorganism.

CONCLUSION:These results indicate that different extracts of investigated mushroom have considerable cytotoxic, antioxidant and antibacterial properties and may be utilized as a promising source of therapeutics.

Regular exercise is essential to a healthy lifestyle but evokes an oxidative and inflammatory stress. Depending upon its intensity and duration this can result in either beneficial adaptive changes or underlying tissue damage that impacts upon long-term health and individual sporting training schedules. Functional foods containing plant bioactives have potential to support exercise through management of the detrimental aspects of exercise and complement ergonomic adaptive benefits.Previously we reported that a single consumption of a 3.2 mg/kg New Zealand blackcurrant anthocyanin-rich extract (BAE) 1 h before a 30 min rowing exercise attenuated moderate exercise-mediated oxidative stress and supported innate immunity. Here we evaluate whether the efficacy of a single consumption of BAE 1 h prior to exercise is changed after extended daily BAE consumption for 5 weeks.On week 1, a single consumption of BAE 1 h before a 30 min row mediated a significant (<0.05) 46% reduction in post-exercise-induced malondialdehyde (MDA) by 2 h compared to a 30% reduction in the placebo group. Similar efficacy was observed 5 weeks later after daily consumption of BAE. In addition, daily BAE consumption for 5 weeks improved the efficacy to (a) resolve acute inflammation, and (b) increased plasma IL-10, salivary beta-defensin 2 (BD2) and secretory IgA. Although no change in plasma antioxidant capacity was detected, a significant (<0.009) positive correlation between plasma IL-10 and plasma antioxidant capacity (= 0.35) was observed on week 6 after 5 week BAE consumption suggesting IL-10 influences antioxidant properties. Using a differentiated myotubule cell-line revealed that whilst IL-10 had no direct antioxidant neutralizing action, longer-term exposure (24 h) attenuated 2,2'-Azobis(2-amidinopropane) dihydrochloride (AAPH)-induced myotubule oxidative stress, supporting a putative role for IL-10 in the modulation of cellular antioxidant systems.Daily consumption of BAE for 5 weeks serves to enhance the exercise recovery effectiveness of a single consumption of BAE and promotes beneficial/protective antioxidant/anti-inflammatory cellular events that facilitate exercise recovery.

Flavonoids and coumaric acid derivatives were identified from dandelion flower (Taraxacum officinale). Characteristics of chain-breaking antioxidants, such as extended lag phase and reduced propagation rate, were observed in oxidation of linoleic acid emulsion with the addition of dandelion flower extract (DFE). DFE suppressed both superoxide and hydroxyl radical, while the latter was further distinguished by both site-specific and non-specific hydroxyl radical inhibition. DPPH-radical-scavenging activity and a synergistic effect with alpha-tocopherol were attributed to the reducing activity derived from phenolic content of DFE. A significant (p < 0.05) and concentration-dependent, reduced nitric oxide production from acterial-lipopolysaccharide-stimulated mouse macrophage RAW264.7 cells was observed with the addition of DFE. Moreover, peroxyl-radical-induced intracellular oxidation of RAW264.7 cells was inhibited significantly (p < 0.05) by the addition of DFE over a range of concentrations. These results showed that the DFE possessed marked antioxidant activity in both biological and chemical models. Furthermore, the efficacy of DFE in inhibiting both reactive oxygen species and nitric oxide were attributed to its phenolic content.

Objective:The aim of the study was to estimate the impact of whole-body cryotherapy (WBC) and subsequent kinesiotherapy on oxidative stress and lipid profile when performed in a closed cryochamber on healthy subjects.

Material and Methods:The effect of ten WBC procedures lasting 3 minutes a day followed by a 60-minute session kinesiotherapy on oxidative stress and lipid profile in healthy subjects (WBC group,= 16) was investigated. The WBC group was compared to the kinesiotherapy only (KT;= 16) group. The routine parameters of oxidative stress (antioxidant enzymatic and nonenzymatic antioxidant status, lipid peroxidation products, total oxidative status (TOS), and oxidative stress index (OSI)) and lipid profile were estimated one day before the beginning and one day after the completion of the research program.

Results:After treatment, in the WBC group, a significant decrease of oxidative stress markers (TOS and OSI) and a significant increase of total antioxidant capacity were observed. The activity of plasma SOD-Mn and erythrocyte total SOD increased significantly in the WBC group. In the KT group, the erythrocyte activity of total SOD, CAT, and GR decreased significantly after the treatment. The levels of T-Chol and LDL-Chol decreased significantly after treatment in both groups, but the observed decrease of these lipid parameters in the WBC group was higher in comparison to the KT group. The level of TG decreased significantly after treatment in the WBC group only.

Conclusion:WBC performed in a closed cryochamber followed by kinesiotherapy improves lipid profile and decreases oxidative stress in healthy subjects.

Antioxidants may protect against oxidative stress, which is associated with tuberculosis disease. However, direct evidence for the protective association between dietary antioxidants and tuberculosis incidence in humans has been lacking. The relation between intake of antioxidant vitamins (A, C, D, E) and individual carotenoids (α-carotene, β-carotene, β-cryptoxanthin, lycopene, lutein) and tuberculosis incidence was examined in the Singapore Chinese Health Study, a prospective cohort of 63,257 adults 45-74 years old enrolled during 1993-1998. Baseline intake of these antioxidants was estimated using a validated semi-quantitative food-frequency questionnaire including use of dietary supplements. After an average of 16.9 years follow-up, 1,186 incident active tuberculosis cases were identified among cohort participants. Compared to the lowest quartile, reduced active tuberculosis risk was observed for the highest quartile of vitamin A (hazard ratio = 0.71, 95% confidence interval: 0.59-0.85; P-trend < 0.01) and β-carotene (hazard ratio = 0.76, 95% confidence interval: 0.63-0.91; P-trend < 0.01), regardless of smoking status. Lower tuberculosis risk was seen for vitamin C among current smokers only. Other vitamins and carotenoids were not associated with tuberculosis risk. These results suggest vitamin C may reduce tuberculosis risk among current smokers by ameliorating oxidative stress, while vitamin A and β-carotene may have additional anti-mycobacterial properties.

Resveratrol, a polyphenol found in red wine, peanuts, soy beans, and pomegranates, possesses a wide range of biological effects. Since resveratrol's properties seem ideal for treating neurodegenerative diseases, its ability to diminish amyloid plaques was tested. Mice were fed clinically feasible dosages of resveratrol for forty-five days. Neither resveratrol nor its conjugated metabolites were detectable in brain. Nevertheless, resveratrol diminished plaque formation in a region specific manner. The largest reductions in the percent area occupied by plaques were observed in medial cortex (-48%), striatum (-89%) and hypothalamus (-90%). The changes occurred without detectable activation of SIRT-1 or alterations in APP processing. However, brain glutathione declined 21% and brain cysteine increased 54%. The increased cysteine and decreased glutathione may be linked to the diminished plaque formation. This study supports the concept that onset of neurodegenerative disease may be delayed or mitigated with use of dietary chemo-preventive agents that protect against beta-amyloid plaque formation and oxidative stress.

Despite growing interest in the protective role that dietary antioxidant vitamins may have in the development of type 2 diabetes (T2D), little epidemiological evidence is available in non-Western populations especially about the possible mediators underlying in this role. The present study aimed to investigate the association of vitamin C and vitamin E intakes with T2D risk in Chinese adults and examine the potential mediators. 178 incident T2D cases among 3483 participants in the Harbin People Health Study (HPHS), and 522 newly diagnosed T2D among 7595 participants in the Harbin Cohort Study on Diet, Nutrition and Chronic Non-communicable Diseases (HDNNCDS) were studied. In the multivariable-adjusted logistics regression model, the relative risks (RRs) were 1.00, 0.75, and 0.76 (Ptrend = 0.003) across tertiles of vitamin C intake in the HDNNCDS, and this association was validated in the HPHS with RRs of 1.00, 0.47, and 0.46 (Ptrend = 0.002). The RRs were 1.00, 0.72, and 0.76 (Ptrend = 0.039) when T2D diagnosed by haemoglobin A1c in the HDNNCDS. The mediation analysis discovered that insulin resistance (indicated by homeostasis model assessment) and oxidative stress (indicated by plasma total antioxidative capacity) partly mediated this association. But no association was evident between vitamin E intake and T2D. In conclusion, our research adds further support to the role of vitamin C intake in reducing the development of T2D in the broader population studied. The results also suggested that this association was partly mediated by inhibiting or ameliorating oxidative stress and insulin resistance.

The racemic mixture of the antioxidant alpha-lipoic acid (ALA) enhances insulin-stimulated glucose metabolism in insulin-resistant humans and animals. We determined the individual effects of the pure R-(+) and S-(-) enantiomers of ALA on glucose metabolism in skeletal muscle of an animal model of insulin resistance, hyperinsulinemia, and dyslipidemia: the obese Zucker (fa/fa) rat. Obese rats were treated intraperitoneally acutely (100 mg/kg body wt for 1 h) or chronically [10 days with 30 mg/kg of R-(+)-ALA or 50 mg/kg of S-(-)-ALA]. Glucose transport [2-deoxyglucose (2-DG) uptake], glycogen synthesis, and glucose oxidation were determined in the epitrochlearis muscles in the absence or presence of insulin (13.3 nM). Acutely, R-(+)-ALA increased insulin-mediated 2-DG-uptake by 64% (P<0.05), whereas S-(-)-ALA had no significant effect. Although chronic R-(+)-ALA treatment significantly reduced plasma insulin (17%) and free fatty acids (FFA; 35%) relative to vehicle-treated obese animals, S-(-)-ALA treatment further increased insulin (15%) and had no effect on FFA. Insulin-stimulated 2-DG uptake was increased by 65% by chronic R-(+)-ALA treatment, whereas S-(-)-ALA administration resulted in only a 29% improvement. Chronic R-(+)-ALA treatment elicited a 26% increase in insulin-stimulated glycogen synthesis and a 33% enhancement of insulin-stimulated glucose oxidation. No significant increase in these parameters was observed after S-(-)-ALA treatment. Glucose transporter (GLUT-4) protein was unchanged after chronic R-(+)-ALA treatment but was reduced to 81 +/- 6% of obese control with S-(-)-ALA treatment. Therefore, chronic parenteral treatment with the antioxidant ALA enhances insulin-stimulated glucose transport and non-oxidative and oxidative glucose metabolism in insulin-resistant rat skeletal muscle, with the R-(+) enantiomer being much more effective than the S-(-) enantiomer.

The aim of this study was to determine the influence of long-term docosahexaenoic acid (DHA) dietary supplementation on the erythrocyte fatty acid profile and oxidative balance in soccer players after training and acute exercise. Fifteen volunteer male athletes (age 20.0± 0.5 years) were randomly assigned to a placebo group that consumed an almond-based beverage (n = 6), or to an experimental group that consumed the same beverage enriched with DHA (n = 9) for 8 weeks. Blood samples were taken in resting conditions at the beginning and after 8 weeks of nutritionalintervention and training in resting and in post-exercise conditions. Oxidative damage markers (malonyldialdehyde, carbonyl and nitrotyrosine indexes) and the activity and protein level of antioxidant enzymes (catalase, superoxide dismutase, glutathione reductase and peroxidase) were assessed. The results showed that training increased antioxidant enzyme activities in erythrocytes. The experimental beverage increased DHA from 34.0 ± 3.6 to 43.0 ± 3.6 nmol/10(9) erythrocytes. DHA supplementation increased the catalytic activity of superoxide dismutase from 1.48 ± 0.40 to 10.5 ± 0.35 pkat/10(9) erythrocytes, and brought about a reduction in peroxidative damage induced by training or exercise. In conclusion, dietary supplementation with DHA changed the erythrocyte membrane composition, provided antioxidant defense and reduced protein peroxidative damage in the red blood cells of professional athletes after an 8-week training season and acute exercise.

The neurodegeneration in colchicine induced AD rats (cAD) is mediated by cox-2 linked neuroinflammation. The importance of ROS in the inflammatory process in cAD has not been identified, which may be deciphered by blocking oxidative stress in this model by a well-known anti-oxidant vitamin C. Therefore, the present study was designed to investigate the role of vitamin C on colchicine induced oxidative stress linked neuroinflammation mediated neurodegeneration and memory impairments along with peripheral immune responses in cAD. The impairments of working and reference memory were associated with neuroinflammation and neurodegeneration in the hippocampus of cAD. Administration of vitamin C (200 and 400 mg/kg BW) in cAD resulted in recovery of memory impairments, with prevention of neurodegeneration and neuroinflammation in the hippocampus. The neuroinflammation in the hippocampus also influenced the peripheral immune responses and inflammation in the serum of cAD and all of these parameters werealso recovered at 200 and 400 mg dose of vitamin C. However, cAD treated with 600 mg dose did not recover but resulted in increase of memory impairments, neurodegeneration and neuroinflammation in hippocampus along with alteration of peripheral immune responses in comparison to cAD of the presentstudy. Therefore, the present study showed that ROS played an important role in the colchicine induced neuroinflammation linked neurodegeneration and memory impairments along with alteration of peripheral immune responses. It also appears from the results that vitamin C at lower doses showed anti-oxidant effect and at higher dose resulted in pro-oxidant effects in cAD.

OBJECTIVE To assess the effect of yoga on anthropometry, blood pressure, glycemic control, and oxidative stress in type 2 diabetic patients on standard care in comparison with standard care alone. RESEARCH DESIGN AND METHODS The study involved 123 patients stratified according to groups with microvascular complications, macrovascular complications, and peripheral neuropathy and without complications and assigned to receive either standard care or standard care along with additional yoga for 3 months. RESULTS In comparison with standard care alone, yoga resulted in significant reduction in BMI, glycemic control, and malondialdehyde and increase in glutathione and vitamin C. There were no differences in waist circumference, waist-to-hip ratio, blood pressure, vitamin E, or superoxide dismutase in the yoga group at follow-up. CONCLUSIONS Yoga can be used as an effective therapy in reducing oxidative stress in type 2 diabetes. Yoga in addition to standard care helps reduce BMI and improve glycemic control in type 2 diabetic patients.