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Astaxanthin Improves Endurance in Older AdultsAstaxanthin and heart health -
The HRQoL was evaluated by the Short Form SF -8 TM consisting of 8 questionnaires. The Japanese version of SF-8 was validated 14 , There are eight subscales, such as physical functioning, role limitations due to physical problems role-physical , bodily pain, general health perception, vitality, social functioning, role limitations due to emotional problems role-emotional , and mental health.
Two aggregate scores, the physical component summary PCS and mental component summary MCS scores, were computed from the eight subscales. These scores were computed by weighing each subscale Scoring was based on the Japanese standards; the possible scores range from 0 to , with higher scores representing a better HRQoL Patients took astaxanthin supplement containing 12 mg of astaxanthin with 40 mg of tocotrienol vitamin E and 30 mg of L-ascorbic acid 2-glucoside vitamin C orally AstaReal ACT, AstaReal Co.
No changes in other medications were allowed in the study periods. The measurements of body weight, systolic and diastolic BP, and HR were obtained at baseline and follow-up clinic visit. Blood sampling, LVEF assessment, and questionnaires SAS and SF-8 were repeated at 3 months after starting astaxanthin supplementation.
Because no data regarding the effects of astaxanthin supplement in patients with HF were available, we did not compute the specific sample size and conduct the present study as a pilot study.
Values are expressed as mean±SD unless indicated otherwise. The differences between the baseline and follow-up measurements were compared using the paired t-test for normally distributed data and the Wilcoxon signed-rank test for non-normally distributed data.
Changes in parameters from baseline to 3 months i. A P value less than 0. Analyses were performed by SPSS Nineteen eligible patients were enrolled, all of whom had been diagnosed as HF and treated for at least 6 months at enrollment.
However, 2 patients were excluded because of lost to follow-up. Thus, data of 17 patients 14 males, 3 females who completed oxidative stress and inflammatory marker and LVEF assessments and questionnaires were analyzed.
All other medications remained unchanged during the study period. Although 1 patient had worsening of spinal stenosis at follow-up, which was determined not to be related to astaxanthin supplementation, no other complaints or adverse events were observed. The baseline characteristics of these 17 patients are shown in Table 1.
From the baseline to the follow-up, the plasma astaxanthin concentration increased significantly from 0 0 to Following 3-month astaxanthin supplementation, LVEF increased, and dROM decreased significantly Table 2. However, there were no changes in other parameters Table 2.
The SAS score significantly increased following 3-month astaxanthin supplementation Figure 1. In addition, both PCS and MCS scores in SF-8 significantly increased following 3-month astaxanthin supplementation Figures 2 and 3. The specific findings of this sub-study also provide some novel insights into the associations of astaxanthin supplement with the self-reported physical activity and HRQoL in patients with HF.
First, improvements of the self-reported physical activity, SAS score, and HRQoL assessed by SF-8 summary scores were observe following 3-month astaxanthin supplementation.
Second, patients with increased baseline HR or low baseline MCS score were likely to have an improvement of the SAS score.
Third, patients with ischemic etiology were likely to have an improvement of the PCS score. Finally, the improvement of the SAS score was correlated directly with the improvement of the MCS score.
Taken together, in patients with HF with LV systolic dysfunction, following 3-month astaxanthin supplementation, improvements of the self-reported physical activity and HRQoL scores were observed and such improvements in the physical activity and HRQoL could be more prominent in patients with rapid HR, ischemic etiology, or HRQoL.
In previous studies in animal models and human subjects, astaxanthin supplementation was shown to have direct and indirect effects through the suppression of oxidative stress on the myocardium and skeletal muscles and consequently may have potential to improve exercise performance in HF patients.
Indeed, in our main study, we have shown that the 6-min walk distance increased significantly in patients with HF. In this sub-study, we found that the SAS score, which can allow the expression of the extent of submaximal physical activities, also increased significantly following 3-month astaxanthin supplementation.
It is of great interest that patients with greater baseline HR were likely to have more improvement of the SAS score. This is supported by the facts that increased resting HR was associated with increased levels of several surrogate markers and poor clinical outcomes in patients with HF 16 and the reduction of resting HR in patients with HF by beta blockers or ivabradine improved exercise tolerance 17 , In addition, it should be noted that lower baseline MCS score s could also be a predictor for greater improvement of the SAS score in patients.
There is a growing body of scientific evidence supporting the benefits of astaxanthin for heart health, including reduced oxidative stress and inflammation, improved lipid profiles, and better blood flow.
Cardiovascular diseases CVDs have become one of the primary health concerns worldwide. Every year, disorders of the heart and blood vessels take the lives of CVDs are equally alarming when it comes to their financial burden.
Given these sobering statistics, it is not surprising that cardiovascular health is an important topic for consumers of dietary supplements. In the past three consumer surveys measuring consumer attitudes towards dietary supplements conducted by the Council for Responsible Nutrition CRN; Washington, DC , heart health ranked number six or higher among the reasons why Americans take supplements.
A powerful antioxidant that is attracting a lot of interest in the heart health category is astaxanthin, a naturally occurring carotenoid organic pigment sourced from the microalgae Haematococcus pluvialis.
In nature, astaxanthin is produced by microalgae as a defense mechanism against harsh environmental conditions.
For humans, astaxanthin is a powerful dietary supplement that can provide a superior nutritional advantage. Due to its unique chemical properties, astaxanthin is regarded as one of the most powerful natural antioxidants known. It is 6, times more powerful than vitamin C, times more powerful than vitamin E, and five times more powerful than beta-carotene in its ability to trap energy from singlet oxygen.
In practice, this means that a higher dosage of these other antioxidants is required per serving-around mg of vitamin C, and mg of lutein, for example-to equal the antioxidant capacity of astaxanthin. Antioxidants like astaxanthin help to counteract the damaging effects of reactive oxygen species ROS , promoting a healthy oxidative balance.
Simply put, an antioxidant is a molecule stable enough to donate an electron to a ROS and neutralize it, thus reducing its capacity for damage. Due to its ability to combat ROS, astaxanthin can play an important role in support of cardiovascular health. The overproduction of ROS can have harmful effects on many important cells and tissues in the body.
It is estimated that each cell in the body forms more than 20 trillion of ROS per day through normal metabolism, and each cell in the body is believed to be attacked by these reactive molecules 10, times per day.
The damage caused by ROS is called oxidative stress and it is a key contributor to CVD. Atherosclerotic plaque rupture is a common reason for CVDs such as stroke and myocardial infarction.
Supplementation with astaxanthin has been shown to support a healthy oxidative balance in groups at elevated risk of CVD. A study with postmenopausal women 13 , for example, concluded that this group could benefit from supplementing with astaxanthin. Additionally, research has demonstrated the benefits of astaxanthin in fighting obesity-induced oxidative stress in overweight young adults 14 and in women with an increased oxidative stress burden.
Like oxidation, inflammation is an established process contributing to CVD. Astaxanthin has been shown to help support a healthy lipid profile. A human study on the effect of astaxanthin on dyslipidemia an excess of LDL and other lipids in the blood found that supplementation decreased levels of triglycerides, a lipid that has been shown to increase the risk of CVD.
The same study also demonstrated that astaxanthin significantly increased levels of HDL cholesterol. Astaxanthin also offers additional support for cardiovascular health.
For example, its antioxidative and anti-inflammatory properties can significantly shorten blood transit times. As populations continue to live longer, new strategies to support healthy aging become increasingly important. from X. dendrorhous have also been positively evaluated by the EFSA Panel on Additives and Products or Substances used in Animal Feed FEEDAP for the same use.
At the same time, it is worth mentioning that until now, only astaxanthin from H. pluvialis either in dried form or extracted with ethanol or supercritical CO 2 has been authorized for direct human consumption in form of dietary supplements both by the FDA notifications filed at dosages up to 12 mg per die and up to 24 mg per die for no more than 30 days as well as by EFSA, with FDA having received also a notification for a new dietary ingredient derived from Paracoccus carotinifaciens at a dose of 6 mg per die.
Regarding the possible use of astaxanthin in conventional foods, FDA had no questions for different GRAS Generally Recognized as Safe notifications made with astaxanthin extracted from H.
pluvialis at the proposed level of use up to a maximum level of 0. In contrast, the EFSA has recently rejected the market authorization at the requested use levels for one product intended to be incorporated into yogurts. Moreover, well-designed studies are urgently required to discern the activity profile of natural and synthetic astaxanthin and their constituents here especially the relative contribution of the different optical and geometrical isomers but also of non-astaxanthin nature in order to establish areas of application in consumer health care.
Finally, aging — as the main risk factor for CVD — should move more into the center of attention. There is now good experimental in vivo evidence that oxidative stress — although intimately linked to several aging-related pathologies — is probably not a key driver of the aging process. In conclusion, the pitfalls afflicting many experimental studies and gaps in our understanding regarding the effects of astaxanthin on cardiovascular health and disease leave plenty of room for discovery with regards to this promising bioactive molecule, which is both bioavailable and safe for human consumption.
View PDF Version Previous Article Next Article. DOI: Received 27th November , Accepted 1st December Abstract Cardiovascular disease is the main contributor to morbidity and mortality worldwide.
Table 1 Natural sources of astaxanthin in animals 22,27—29, Table 2 Natural and synthetic sources of astaxanthin 22,27,28, Table 3 Studies reporting plasma values and distribution of astaxanthin isomers in humans. Østerlie et al. Table 4 Antioxidant activity of astaxanthin in test-tube systems.
pluvialis Astaxanthin-P and —CO 2 vs. Table 5 Effects of astaxanthin on Nrf2-ARE signaling pathway and oxidative stress parameters in un-stressed cell cultures.
sc Li et al. Table 6 Anti-hypertensive activity of astaxanthin in animal models. Negative numbers indicate a blood-pressure lowering effect of astaxanthin. Hussein et al. Data were taken from Uchiyama et al.
Fasting glucose levels were significantly lower in HFFD-fed animals treated orally with 6 mg per kg BW of astaxanthin obtained from Sigma. Data were taken from Arunkumar et al. Data were taken from Ravi Kumar et al.
Table 7 Animal studies of astaxanthin effects related to the reduction of atherosclerosis and CVD events.
Upon oral ingestion, it is hydrolyzed in the intestine, yielding free astaxanthin for absorption and systemic distribution. b Studies reporting effects of the formerly available astaxanthin derivate DDA disodium disuccinate astaxanthin have been reviewed elsewhere.
pluvialis Fuji Chemicals 60 days No effect on atherosclerotic lesion formation in the aorta Shen et al. Table 8 List of knowledge gaps and potential pitfalls in astaxanthin research.
Considering that aging, however, is the most important risk factor for CVD, the question arises whether astaxanthin, touted as a superior antioxidant in vivo , can have a significant impact on cardiovascular health and disease.
in the gastro-intestinal tract and blood , like for most natural compounds, have been poorly investigated.
As previously shown for other antioxidants, significant effects of astaxanthin on the MTT signal need to be considered when interpreting MTT data as a measure of astaxanthin's antioxidant potential in vitro.
are often underappreciated. Coral-Hinostroza et al. Rüfer et al. Okada et al. Park et al. Miki Lim et al. Scavenging of peroxyl radical generated by lipid-soluble radical generator.
High antioxidant conc. Jørgensen and Skibsted Shimidzu et al. Iwamoto et al. Goto et al. Nishida et al. Hama et al. Hydroxyl radical scavenging in aqueous solutions with liposome-encapsulated antioxidants. Sueishi et al. Chang et al. Hydroxyl radical scavenging in a CuSO 4 -Phen-Vc-H 2 O 2 system.
Hydrogen peroxide scavenging in a luminol-H 2 O 2 system. Régnier et al. Natural astaxanthin from H. synthetic form Astaxanthin-S.
Ben-Dor et al. Ye et al. Saw et al. Li et al. Franceschelli et al.
Astaxanthin, is a red-orange xanthophyll carotenoid that Astaxanthin and heart health Ataxanthin Astaxanthin and heart health by microalgae Haematococcus Astaxnathin and neart in many marine Astaxantthin such as salmon, trout, Astaxanthin and heart health, and lobster. Previous research suggests Nutrient timing for endurance astaxanthin has health-promoting benefits which may Astaxantihn the risk of developing various diseases and support their treatment, such as chronic inflammatory diseases, metabolic syndrome, diabetes, cardiovascular disease, neurodegenerative diseasesand exercise-induced fatigue. According to a study published in June in Nutrients, researchers investigated the effects of astaxanthin supplementation in patients with heart failure. Oxidative stress accelerates the progression of heart failure and is considered a target for treatment. This investigation was a small, prospective pilot study that included 16 patients with heart failure taking 12 mg of astaxanthin supplementation daily for three months.Astaxanthin, is Asgaxanthin red-orange xanthophyll Astaxanthin and heart health that is produced primarily by anv Haematococcus Astacanthin and accumulates Caloric needs for seniors many marine organisms such as Gut health and performance optimization, trout, shrimp, and lobster.
Previous research suggests that astaxanthin Astaxanthin and heart health health-promoting benefits which Astaxanthin and heart health lower the risk of Self-care plans for diabetes management various diseases and support their heeart, such as chronic inflammatory diseases, metabolic syndrome, Astaxxanthin, cardiovascular disease, neurodegenerative Fat burner for stubborn fatAstaxanthin and heart health exercise-induced fatigue.
According to a study annd in June in Astaxanthin and heart health, researchers investigated the Asttaxanthin of astaxanthin supplementation hearr patients with hdalth failure. Znd stress Roasted cauliflower ideas Astaxanthin and heart health progression of heart hearf and is considered a target for treatment.
This investigation Astaxabthin a small, prospective pilot study that included 16 patients with heart failure taking 12 mg of Astaxanthij supplementation daily for anx months. Researchers assessed body mass index Healrhblood pressure, heart rate, left Astaxanthin and heart health ejection fraction LVEFAstaxanthih 6-minute walk heaet, and numerous Astaxajthin stress markers including Diacron reactive oxygen metabolite Hfalthhezlth antioxidant potential BAPAstaxanthin and heart health healtj 8-hydroxydeoxyguanosine 8-OHdG.
Additional laboratory assessments included estimated glomerular filtration rate eGFRcreatinine, C-reactive Astaxanthin and heart health, tumor Astaxsnthin factor-α, B-type Astaxanthin and heart health hear BNPand plasma astaxanthin levels.
The above laboratory assessments, echocardiography, and 6-minute walk test were repeated at the end of the study. Throughout the study, plasma astaxanthin levels increased significantly.
As a result, astaxanthin supplementation decreased oxidative stress levels demonstrated by a decrease in dROM levels. As researchers anticipated, a more significant reduction in oxidative stress markers was observed in patients whole baseline oxidation levels were highest.
In addition to reducing oxidative stress, this study demonstrated improved cardiac contractility and exercise tolerance in heart failure patients with left ventricular systolic dysfunction. There were no changes in inflammatory markers after supplementation. This study is the first of its kind to investigate the effects of astaxanthin supplementation on oxidative stress, systemic inflammation, cardiac function, and exercise tolerance in patients with heart failure.
As astaxanthin is a fat-soluble carotenoid, its bioavailability is enhanced when taken with dietary fats or fish oil. Other nutrients to consider to support the treatment of patients with heart failure include CoQ10, D-ribose, carnitine, magnesium, delta and gamma tocotrienols, and melatonin.
By Michael Jurgelewicz, DC, DACBN, DCBCN, CNS. Source: Kato T, Kasai T, et al. Effects of 3-Month Astaxanthin Supplementation on Cardiac Function in Heart Failure Patients with Left Ventricular Systolic Dysfunction-A Pilot Study.
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Science Update. New Study Investigates the Effects of Astaxanthin on Cardiac Function in Patients with Heart Failure. July 1, - facebook twitter linkedin. By Michael Jurgelewicz, DC, DACBN, DCBCN, CNS Source: Kato T, Kasai T, et al.
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| Astaxanthin: The Super Nutrient Revolutionising Heart Health | Jekell A, Hossain A, Alehagen U, Dahlström U and Rosén A: Elevated circulating levels of thioredoxin and stress in chronic heart failure. Eur J Heart Fail. Aviram M: Introduction to the serial review on paraoxonases, oxidative stress, and cardiovascular diseases. Augusti PR, Quatrin A, Somacal S, Conterato GM, Sobieski R, Ruviaro AR, Maurer LH, Duarte MM, Roehrs M and Emanuelli T: Astaxanthin prevents changes in the activities of thioredoxin reductase and paraoxonase in hypercholesterolemic rabbits. Cui G, Li L, Xu W, Wang M, Jiao D, Yao B, Xu K, Chen Y, Yang S, Long M, et al: Astaxanthin protects ochratoxin a-induced oxidative stress and apoptosis in the heart via the Nrf2 pathway. Naunyn Schmiedebergs Arch Pharmacol. Wu Q, Zhang XS, Wang HD, Zhang X, Yu Q, Li W, Zhou ML and Wang XL: Astaxanthin activates nuclear factor erythroid-related factor 2 and the antioxidant responsive element Nrf2-ARE pathway in the brain after subarachnoid hemorrhage in rats and attenuates early brain injury. Kavitha K, Thiyagarajan P, Rathna Nandhini J, Mishra R and Nagini S: Chemopreventive effects of diverse dietary phyto-chemicals against DMBA-induced hamster buccal pouch carcinogenesis via the induction of Nrf2-mediated cytoprotective antioxidant, detoxification, and DNA repair enzymes. Tripathi DN and Jena GB: Astaxanthin intervention ameliorates cyclophosphamide-induced oxidative stress, DNA damage and early hepatocarcinogenesis in rat: Role of Nrf2, p53, p38 and phase-II enzymes. Mutat Res. Saw CL, Yang AY, Guo Y and Kong AN: Astaxanthin and omega-3 fatty acids individually and in combination protect against oxidative stress via the Nrf2-ARE pathway. Food Chem Toxicol. Visioli F and Artaria C: Astaxanthin in cardiovascular health and disease: Mechanisms of action, therapeutic merits, and knowledge gaps. Food Funct. BMC Gastroenterol. Yasui Y, Hosokawa M, Mikami N, Miyashita K and Tanaka T: Dietary astaxanthin inhibits colitis and colitis-associated colon carcinogenesis in mice via modulation of the inflammatory cyto-kines. Chem Biol Interact. Nagendraprabhu P and Sudhandiran G: Astaxanthin inhibits tumor invasion by decreasing extracellular matrix production and induces apoptosis in experimental rat colon carcinogenesis by modulating the expressions of ERK-2, NFkB and COX Invest New Drugs. Moroni F, Ammirati E, Norata GD, Magnoni M and Camici PG: The role of monocytes and macrophages in human atherosclerosis, plaque neoangiogenesis, and atherothrombosis. Mediators Inflamm. Hashizume M and Mihara M: Blockade of IL-6 and TNF-α inhibited oxLDL-induced production of MCP-1 via scavenger receptor induction. Eur J Pharmacol. Zou TB, Zhu SS, Luo F, Li WQ, Sun XR and Wu HF: Effects of astaxanthin on reverse cholesterol transport and atherosclerosis in mice. Biomed Res Int. Kishimoto Y, Tani M, Uto-Kondo H, Iizuka M, Saita E, Sone H, Kurata H and Kondo K: Astaxanthin suppresses scavenger receptor expression and matrix metalloproteinase activity in macrophages. Eur J Nutr. Santos SD, Cahú TB, Firmino GO, de Castro CC, Carvalho LB Jr, Bezerra RS and Filho JL: Shrimp waste extract and astaxanthin: Rat alveolar macrophage, oxidative stress and inflammation. J Food Sci. Lee SJ, Bai SK, Lee KS, Namkoong S, Na HJ, Ha KS, Han JA, Yim SV, Chang K, Kwon YG, et al: Astaxanthin inhibits nitric oxide production and inflammatory gene expression by suppressing I kappa B kinase-dependent NF-kappaB activation. Mol Cells. Franceschelli S, Pesce M, Ferrone A, De Lutiis MA, Patruno A, Grilli A, Felaco M and Speranza L: Astaxanthin treatment confers protection against oxidative stress in U cells stimulated with lipopolysaccharide reducing O 2 -production. PLoS One. Macedo RC, Bolin AP, Marin DP and Otton R: Astaxanthin addition improves human neutrophils function: In vitro study. Choi SK, Park YS, Choi DK and Chang HI: Effects of astaxanthin on the production of NO and the expression of COX-2 and iNOS in LPS-stimulated BV2 microglial cells. J Microbiol Biotechnol. Kim YJ, Kim YA and Yokozawa T: Protection against oxidative stress, inflammation, and apoptosis of high-glucose-exposed proximal tubular epithelial cells by astaxanthin. J Agric Food Chem. Abdelzaher LA, Imaizumi T, Suzuki T, Tomita K, Takashina M and Hattori Y: Astaxanthin alleviates oxidative stress insults-related derangements in human vascular endothelial cells exposed to glucose fluctuations. Life Sci. Speranza L, Pesce M, Patruno A, Franceschelli S, de Lutiis MA, Grilli A and Felaco M: Astaxanthin treatment reduced oxidative induced pro-inflammatory cytokines secretion in U SHP-1 as a novel biological target. Jones WK, Brown M, Wilhide M, He S and Ren X: NF-kappaB in cardiovascular disease: Diverse and specific effects of a 'general' transcription factor? Cardiovasc Toxicol. Pashkow FJ, Watumull DG and Campbell CL: Astaxanthin: A novel potential treatment for oxidative stress and inflammation in cardiovascular disease. Am J Cardiol. Ghosh S, May MJ and Kopp EB: NF-kappa B and Rel proteins: Evolutionarily conserved mediators of immune responses. Annu Rev Immunol. Woronicz JD, Gao X, Cao Z, Rothe M and Goeddel DV: IkappaB kinase-beta: NF-kappaB activation and complex formation with IkappaB kinase-alpha and NIK. Mercurio F, Zhu H, Murray BW, Shevchenko A, Bennett BL, Li J, Young DB, Barbosa M, Mann M, Manning A and Rao A: IKK-1 and IKK Cytokine-activated IkappaB kinases essential for NF-kappaB activation. Zandi E, Rothwarf DM, Delhase M, Hayakawa M and Karin M: The IkappaB kinase complex IKK contains two kinase subunits, IKKalpha and IKKbeta, necessary for IkappaB phosphorylation and NF-kappaB activation. DiDonato JA, Hayakawa M, Rothwarf DM, Zandi E and Karin M: A cytokine-responsive IkappaB kinase that activates the transcription factor NF-kappaB. Ghosh S and Karin M: Missing pieces in the NF-kappaB puzzle. Wang HH, Garruti G, Liu M, Portincasa P and Wang DQ: Cholesterol and lipoprotein metabolism and atherosclerosis: Recent advances in reverse cholesterol transport. Ann Hepatol. Khera AV and Rader DJ: Future therapeutic directions in reverse cholesterol transport. Tall AR and Yvan-Charvet L: Cholesterol, inflammation and innate immunity. Nat Rev Immunol. Shao B, Tang C, Sinha A, Mayer PS, Davenport GD, Brot N, Oda MN, Zhao XQ and Heinecke JW: Humans with atherosclerosis have impaired ABCA1 cholesterol efflux and enhanced high-density lipoprotein oxidation by myeloperoxidase. Clarke MC and Bennett MR: Cause or consequence: What does macrophage apoptosis do in atherosclerosis? Monteiro R and Azevedo I: Chronic inflammation in obesity and the metabolic syndrome. Int Rev Cell Mol Biol. Sanderson TH, Reynolds CA, Kumar R, Przyklenk K and Hüttemann M: Molecular mechanisms of ischemia-reperfusion injury in brain: Pivotal role of the mitochondrial membrane potential in reactive oxygen species generation. Mol Neurobiol. Am J Transl Res. J Pharmacol Exp Ther. Ni Y, Nagashimada M, Zhuge F, Zhan L, Nagata N, Tsutsui A, Nakanuma Y, Kaneko S and Ota T: Astaxanthin prevents and reverses diet-induced insulin resistance and steatohepatitis in mice: A comparison with vitamin E. Sci Rep. Liu H, Liu M, Fu X, Zhang Z, Zhu L, Zheng X and Liu J: Astaxanthin prevents alcoholic fatty liver disease by modulating mouse gut microbiota. Lyu Y, Wu L, Wang F, Shen X and Lin D: Carotenoid supple-mentation and retinoic acid in immunoglobulin A regulation of the gut microbiota dysbiosis. Exp Biol Med Maywood. Tang WH, Kitai T and Hazen SL: Gut microbiota in cardiovascular health and disease. Saad MJ, Santos A and Prada PO: Linking gut microbiota and inflammation to obesity and insulin resistance. Physiology Bethesda. Wu L, Lyu Y, Srinivasagan R, Wu J, Ojo B, Tang M, El-Rassi GD, Metzinger K, Smith BJ, Lucas EA, et al: Astaxanthin-shifted gut microbiota is associated with inflammation and metabolic homeostasis in mice. J Nutr. Ou W, Liao Z, Yu G, Xu H, Liang M, Mai K and Zhang Y: The effects of dietary astaxanthin on intestinal health of juvenile tiger puffer takifugu rubripes in terms of antioxidative status, inflammatory response and microbiota. Aquaculture Nutrition. Zhang L, Cao W, Gao Y, Yang R, Zhang X, Xu J and Tang Q: Astaxanthin ATX enhances the intestinal mucosal functions in immunodeficient mice. Gao Y, Yang L, Chin Y, Liu F, Li RW, Yuan S, Xue C, Xu J and Tang Q: Astaxanthin n-octanoic acid diester ameliorates insulin resistance and modulates gut microbiota in high-fat and high-sucrose dietfed mice. Int J Mol Sci. Wang J, Liu S, Wang H, Xiao S, Li C, Li Y and Liu B: Xanthophyllomyces dendrorhous-derived astaxanthin regulates lipid metabolism and gut microbiota in obese mice induced by a high-fat diet. Linton MRF, Yancey PG, Davies SS, Jerome WG, Linton EF, Song WL, Doran AC and Vickers KC: The role of lipids and lipoproteins in atherosclerosis. Endotext Feingold KR, Anawalt B, Boyce A, Chrousos G, Dungan K, Grossman A, Hershman JM, Kaltsas G, Koch C, Kopp P, et al: MDText Com, Inc; South Dartmouth, MA: Strassheim D, Dempsey EC, Gerasimovskaya E, Stenmark K and Karoor V: Role of inflammatory cell subtypes in heart failure. J Immunol Res. Gröschel C, Sasse A, Röhrborn C, Monecke S, Didié M, Elsner L, Kruse V, Bunt G, Lichtman AH, Toischer K, et al: T helper cells with specificity for an antigen in cardiomyocytes promote pressure overload-induced progression from hypertrophy to heart failure. Kallikourdis M, Martini E, Carullo P, Sardi C, Roselli G, Greco CM, Vignali D, Riva F, Ormbostad Berre AM, Stølen TO, et al: T cell costimulation blockade blunts pressure overload-induced heart failure. Nat Commun. Gisterå A and Hansson GK: The immunology of atherosclerosis. Nat Rev Nephrol. Swirski FK and Nahrendorf M: Leukocyte behavior in athero-sclerosis, myocardial infarction, and heart failure. Stemme S, Faber B, Holm J, Wiklund O, Witztum JL and Hansson GK: T lymphocytes from human atherosclerotic plaques recognize oxidized low density lipoprotein. Proc Natl Acad Sci USA. Frostegård J, Ulfgren AK, Nyberg P, Hedin U, Swedenborg J, Andersson U and Hansson GK: Cytokine expression in advanced human atherosclerotic plaques: Dominance of pro-inflammatory Th1 and macrophage-stimulating cytokines. Tripathi DN and Jena GB: Intervention of astaxanthin against cyclophosphamide-induced oxidative stress and DNA damage: A study in mice. Int Immunopharmacol. Bolin AP, Macedo RC, Marin DP, Barros MP and Otton R: Astaxanthin prevents in vitro auto-oxidative injury in human lymphocytes. Cell Biol Toxicol. Campoio TR, Oliveira FA and Otton R: Oxidative stress in human lymphocytes treated with fatty acid mixture: Role of carotenoid astaxanthin. Toxicol In Vitro. Pilinska MA, capital Ka CD, Rushkovsky SR and Dybska OB: Genoprotective properties of astaxanthin revealed by ionizing radiation exposure in vitro on human peripheral blood lymphocytes. Probl Radiac Med Radiobiol. In English, Ukrainian. Otton R, Marin DP, Bolin AP, de Cássia Santos Macedo R, Campoio TR, Fineto C Jr, Guerra BA, Leite JR, Barros MP and Mattei R: Combined fish oil and astaxanthin supplementation modulates rat lymphocyte function. Mahmoud FF, Haines DD, Abul HT, Abal AT, Onadeko BO and Wise JA: In vitro effects of astaxanthin combined with ginkgolide B on T lymphocyte activation in peripheral blood mononuclear cells from asthmatic subjects. J Pharmacol Sci. Lin KH, Lin KC, Lu WJ, Thomas PA, Jayakumar T and Sheu JR: Astaxanthin, a carotenoid, stimulates immune responses by enhancing IFN-γ and IL-2 secretion in primary cultured lymphocytes in vitro and ex vivo. Biochim Biophys Acta Gen Subj. Park JS, Mathison BD, Hayek MG, Massimino S, Reinhart GA and Chew BP: Astaxanthin stimulates cell-mediated and humoral immune responses in cats. Vet Immunol Immunopathol. Chew BP, Wong MW, Park JS and Wong TS: Dietary beta-carotene and astaxanthin but not canthaxanthin stimulate splenocyte function in mice. Anticancer Res. Jyonouchi H, Hill RJ, Tomita Y and Good RA: Studies of immunomodulating actions of carotenoids. Effects of beta-carotene and astaxanthin on murine lymphocyte functions and cell surface marker expression in in vitro culture system. Nutr Cancer. Mahmoud FF, Haines D, Al-Awadhi R, Arifhodzic N, Abal A, Azeamouzi C, Al-Sharah S and Tosaki A: In vitro suppression of lymphocyte activation in patients with seasonal allergic rhinitis and pollen-related asthma by cetirizine or azelastine in combination with ginkgolide B or astaxanthin. Acta Physiol Hung. Jyonouchi H, Zhang L and Tomita Y: Studies of immunomodulating actions of carotenoids. Astaxanthin enhances in vitro antibody production to T-dependent antigens without facilitating polyclonal B-cell activation. January Volume 47 Issue 1. Sign up for eToc alerts. You can change your cookie settings at any time by following the instructions in our Cookie Policy. To find out more, you may read our Privacy Policy. I agree. Home Submit Manuscript My Account. Advanced Search. Register Login. Oncology Letters International Journal of Oncology Molecular and Clinical Oncology Experimental and Therapeutic Medicine International Journal of Molecular Medicine Biomedical Reports Oncology Reports Molecular Medicine Reports World Academy of Sciences Journal International Journal of Functional Nutrition International Journal of Epigenetics Medicine International. International Journal of Molecular Medicine. 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Serum insulin level was measured by commercial kits Monobind, Lake Forest, CA, United States. Serum levels of Sirtuin1 and TNF-α were measured based on ELISA method with kits of Zelbio Co, Germany and LDN Co, Germany, respectively. To determine the sample size, primary data including mean and standard deviation of HDL-C was obtained from Yoshida et al. All statistical data was analyzed using SPSS software version 20 SPSS Inc. The Kolmogorov—Smirnov test was used to assess the normality of data distribution. Rank signed Wilcoxon test and a Paired t-test were utilized to analyze variable changes within-group. U Mann Whitney test and independent sample t-test were conducted to analyze variable changes between group. Analysis of covariance ANCOVA and quantile regression adjusted for confounding factors such as age, baseline values, and mean changes in weight was applied to determine the absolute effects of the therapy. The average of age, weight, and BMI of all subjects were Three participants were excluded from the placebo group, of whom one patient immigrated, and two patients were infected with COVID Additionally, three individuals of the AX group were excluded due to uncontrolled diabetes, required surgery, or refused to continue the study. The intervention was completed by 22 individuals in each treatment group Figure 1. Participants who took AX or placebo supplements did not report any side effects. Distribution of age, BMI, gender, degree of physical activity and consumed drugs were not significantly different between the AX and placebo groups at the beginning of the study Table 1. The comparison of anthropometric parameters of two groups was presented in Table 2. Baseline values of BMI, HC, WC and body composition were not significantly different between AX and placebo groups. However, the changes between the two groups were not significant. Despite the significant reduction in visceral fat in the control group compared to the AX group at the end of the intervention, the between-group difference was not statistically significant. The baseline values of lipid profile and glycemic indices were not statistically different between two groups Table 4. Although, the between-group difference of TC and LDL-C were not statistically significant. The results revealed that there was no significant difference in TG and HDL-C within and between groups. The baseline values of Sirtuin1 and TNF-α were not statistically different between two groups Table 5. TNF-α levels did not change significantly in both groups. In vivo studies have demonstrated that AX intake has cardiovascular protective effects, although the results of human studies regarding the beneficial effects of AX on cardiovascular risk factors are contradictory and limited. To the best of our knowledge, this study was the first randomized, double-blind, placebo controlled, clinical trial investigating the impacts of AX supplementation on metabolic parameters in CAD patients. The findings revealed that AX had no effect on the lipid profile compared to the placebo group, but it should be noted that LDL-C and TC levels decreased significantly in the AX group. However, it had no significant improvements on body composition and other metabolic and anthropometric parameters. The results of a recent meta-analysis conducted in are in line with our findings and demonstrate that body weight and BMI changes were not statistically significant Choi et al. According to the food intake data, the energy intake of the patients in both groups decreased, as a result, BMI and body weight decreased in both groups. Despite of adjusting confounding factors, no substantial between-group changes were found. WC and HC are parameters that were only analyzed in this study, even though the differences between the AX-receiving group and the placebo group are not statistically significant. Alike our results, Roustae Rad et al. Two recent meta-analysis investigated that AX consumption was not associated with TC, LDL-C, TG reduction. However, only Xia reported an overall increase in HDL-C 23 , Tominaga et al. and Saito et al. showed that AX had no impact on lipid profile in healthy individuals regardless of the duration of supplementation and the AX dosage 28 , It is well known that the major causative risk factors for CAD and a definite contributor to accelerated atherosclerosis is dyslipidemia 30 , Statins are used as the first line of treatment in both primary and secondary prevention to lower cholesterol and enhance lipid composition 32 , Therefore, AX might not have affected TC, TG, and LDL-C levels since the majority of the patients were taking statins and lipid profile had improved before the intervention. However, the TC and LDL-C levels were significantly decreased only in the intra-group analysis of AX group. The capacity of AX to upregulate SREBP-2 and therefore boost the gene expression of LDLR and HMGR may have contributed to the ability of AX to reduce cholesterol levels It has been demonstrated that SIRT1 also regulates PPARα expression, which helps to control lipid metabolism 36 , The current study also declared that AX intake did not significantly improve serum levels of insulin, FBS, and HOMA-IR index. A recent meta-analysis revealed that FBS did not decrease after AX supplementation compare with placebo group. According to yang et al. Alike our result, Saito and Tominaga et al. Yoshida et al. also reported the similar result which FBS did not change significantly in subjects with mild hyperlipidemia However, the blood glucose levels have dropped significantly or even slightly in trials on diabetic subjects 16 , SIRT1 play an important role in controlling cellular physiological processes It has been identified as a novel homoeostasis regulator in the human cardiovascular system through protecting against aging and endothelial inflammation, inducing resistance against oxidative stress and hypertrophic, inhibiting apoptosis of cardiomyocytes, and modulating cardiac energy metabolism 39 , Furthermore, transcription factor SIRT1 plays an important role in energy and lipid metabolism, inflammation and insulin sensitivity Nishida et al. reported that AX treatment induced upregulation of the gene expression of the mitochondrial SRIT1 and mitochondrial biogenesis in mice In our investigation no significant change in serum level of SIRT1 following AX supplementation were observed even after adjusting for confounders. Non-significant alterations in lipid profile and glycemic indices may be associated with negligible changes in SIRT1. The impact of AX on SIRT1 levels has not been studied in any RCT. Furthermore, drawing a definite conclusion on the effects of AX on SIRT1 is not feasible due to the insufficient number of studies in this field. TNF-α is a pro-inflammatory cytokine found in atherosclerotic lesions and can have a direct effect on vascular endothelial cells and induce the expression of adhesive molecules in leukocytes and other inflammatory cells In our study the changes of TNF-α levels were not significant and in line with our study. Park et al. Alternatively, the result of non-significant change in TNF-α levels in our study is in line with the hypothesis of the recent meta-analysis about the effect of carotenoids supplementation on inflammation, which suggests that higher baseline levels of pro-inflammatory cytokines indicate a potential for a greater response to carotenoid supplementation such as AX SIRT1 directly can deacetylate the p65 subunit of the NF-κB complex to suppress NF-κB activation. Furthermore, SIRT1 promotes oxidative energy generation by activating of AMP-activated protein kinase AMPK , Peroxisome proliferator-activated receptor α PPARα and Peroxisome proliferator-activated receptor gamma coactivator 1-alpha. These factors concurrently inhibit NF-κB signaling and led to decline inflammation If this pathway is blocked, TNF-α production can also decrease. The small sample size may be the reason for the lack of noticeable changes in the parameters of present study. The follow-up duration in our study was short and extending the duration of the intervention might show potential benefits. Moreover, we were not able to measure the concentration of AX in the plasma in order to evaluate its bioavailability. Future trials may be able to better understand the impacts of AX by assessing certain genes involved in the regulation of metabolic variables. The trial was completely conducted using a double-blind, random allocation approach. Patients who had recovered from COVID even before the intervention were excluded from the study due to prevent disturbances in the measured factors, especially the inflammatory index. However, more clinical trials with various AX supplementation doses and durations are required to obtain a definitive conclusion. The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation. The studies involving human participants were reviewed and approved by Tabriz University of medical science. MH, MA, and MC designed the study. MH, MC, and BS coordinated the collection of the samples and data collection from study participants. MH carried out the statistical analysis and wrote the first draft of the article. MH, MC, MA, BS, and SK participated in revising it critically for important intellectual content. All authors contributed to the article and approved the submitted version. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. Benjamin, EJ, Muntner, P, Alonso, A, Bittencourt, MS, Callaway, CW, Carson, AP, et al. Heart disease and stroke statistics— update: a report from the American Heart Association. doi: CrossRef Full Text Google Scholar. Hansson, GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med. Peluso, I, Morabito, G, Urban, L, Ioannone, F, and Serafi, M. Most of the exercise tests were aiming to assess exercise performance around maximal workloads, but daily activities did not require energy expenditure in the maximal range. In this regard, the SAS allowed the expression of the extent of submaximal physical activities. The HRQoL was evaluated by the Short Form SF -8 TM consisting of 8 questionnaires. The Japanese version of SF-8 was validated 14 , There are eight subscales, such as physical functioning, role limitations due to physical problems role-physical , bodily pain, general health perception, vitality, social functioning, role limitations due to emotional problems role-emotional , and mental health. Two aggregate scores, the physical component summary PCS and mental component summary MCS scores, were computed from the eight subscales. These scores were computed by weighing each subscale Scoring was based on the Japanese standards; the possible scores range from 0 to , with higher scores representing a better HRQoL Patients took astaxanthin supplement containing 12 mg of astaxanthin with 40 mg of tocotrienol vitamin E and 30 mg of L-ascorbic acid 2-glucoside vitamin C orally AstaReal ACT, AstaReal Co. No changes in other medications were allowed in the study periods. The measurements of body weight, systolic and diastolic BP, and HR were obtained at baseline and follow-up clinic visit. Blood sampling, LVEF assessment, and questionnaires SAS and SF-8 were repeated at 3 months after starting astaxanthin supplementation. Because no data regarding the effects of astaxanthin supplement in patients with HF were available, we did not compute the specific sample size and conduct the present study as a pilot study. Values are expressed as mean±SD unless indicated otherwise. The differences between the baseline and follow-up measurements were compared using the paired t-test for normally distributed data and the Wilcoxon signed-rank test for non-normally distributed data. Changes in parameters from baseline to 3 months i. A P value less than 0. Analyses were performed by SPSS Nineteen eligible patients were enrolled, all of whom had been diagnosed as HF and treated for at least 6 months at enrollment. However, 2 patients were excluded because of lost to follow-up. Thus, data of 17 patients 14 males, 3 females who completed oxidative stress and inflammatory marker and LVEF assessments and questionnaires were analyzed. All other medications remained unchanged during the study period. Although 1 patient had worsening of spinal stenosis at follow-up, which was determined not to be related to astaxanthin supplementation, no other complaints or adverse events were observed. The baseline characteristics of these 17 patients are shown in Table 1. From the baseline to the follow-up, the plasma astaxanthin concentration increased significantly from 0 0 to Following 3-month astaxanthin supplementation, LVEF increased, and dROM decreased significantly Table 2. However, there were no changes in other parameters Table 2. The SAS score significantly increased following 3-month astaxanthin supplementation Figure 1. In addition, both PCS and MCS scores in SF-8 significantly increased following 3-month astaxanthin supplementation Figures 2 and 3. The specific findings of this sub-study also provide some novel insights into the associations of astaxanthin supplement with the self-reported physical activity and HRQoL in patients with HF. First, improvements of the self-reported physical activity, SAS score, and HRQoL assessed by SF-8 summary scores were observe following 3-month astaxanthin supplementation. Second, patients with increased baseline HR or low baseline MCS score were likely to have an improvement of the SAS score. Third, patients with ischemic etiology were likely to have an improvement of the PCS score. Finally, the improvement of the SAS score was correlated directly with the improvement of the MCS score. Taken together, in patients with HF with LV systolic dysfunction, following 3-month astaxanthin supplementation, improvements of the self-reported physical activity and HRQoL scores were observed and such improvements in the physical activity and HRQoL could be more prominent in patients with rapid HR, ischemic etiology, or HRQoL. In previous studies in animal models and human subjects, astaxanthin supplementation was shown to have direct and indirect effects through the suppression of oxidative stress on the myocardium and skeletal muscles and consequently may have potential to improve exercise performance in HF patients. Indeed, in our main study, we have shown that the 6-min walk distance increased significantly in patients with HF. In this sub-study, we found that the SAS score, which can allow the expression of the extent of submaximal physical activities, also increased significantly following 3-month astaxanthin supplementation. It is of great interest that patients with greater baseline HR were likely to have more improvement of the SAS score. |
| Related products | However, there were no Asraxanthin in other parameters Table Astaxanthin and heart health. Hashizume M and Mihara M: Blockade Heart health products IL-6 and TNF-α inhibited Astaxanthin and heart health production of MCP-1 via abd receptor Astacanthin. The epitopes generated neart enzymatic or non-enzymatic oxidation of LDL are the main damage-associated molecular patterns recognized by macrophages and are responsible for the onset of the inflammatory cascade, with the release of cytokines and chemokines that recruit more resident vascular macrophages and monocytes from the blood. doi: Woronicz JD, Gao X, Cao Z, Rothe M and Goeddel DV: IkappaB kinase-beta: NF-kappaB activation and complex formation with IkappaB kinase-alpha and NIK. |
| Astaxanthin Is a Heart-Health Ingredient with Growing Science | In agreement with the results obtained in HFFD-fed mice, the astaxanthin effects in L6 cells were associated with an increase in insulin receptor substrate-1 tyrosine and Akt phosphorylation, as well as a decrease in c-Jun N-terminal kinase and insulin receptor substrate-1 serine phosphorylation. Probl Radiac Med Radiobiol. Ron Goedeke, an expert in the domain of functional medicine, dedicates his practice to uncovering the root causes of health issues by focusing on nutrition and supplement-based healing and health optimisation strategies. Leave a comment Name. It is well known that the major causative risk factors for CAD and a definite contributor to accelerated atherosclerosis is dyslipidemia 30 , |
| Astaxanthin: The Super Nutrient Revolutionizing Heart Health | Biosphere Nutrition | In practice, this means that a higher dosage of these other antioxidants is required per serving-around mg of vitamin C, and mg of lutein, for example-to equal the antioxidant capacity of astaxanthin. Antioxidants like astaxanthin help to counteract the damaging effects of reactive oxygen species ROS , promoting a healthy oxidative balance. Simply put, an antioxidant is a molecule stable enough to donate an electron to a ROS and neutralize it, thus reducing its capacity for damage. Due to its ability to combat ROS, astaxanthin can play an important role in support of cardiovascular health. The overproduction of ROS can have harmful effects on many important cells and tissues in the body. It is estimated that each cell in the body forms more than 20 trillion of ROS per day through normal metabolism, and each cell in the body is believed to be attacked by these reactive molecules 10, times per day. The damage caused by ROS is called oxidative stress and it is a key contributor to CVD. Atherosclerotic plaque rupture is a common reason for CVDs such as stroke and myocardial infarction. Supplementation with astaxanthin has been shown to support a healthy oxidative balance in groups at elevated risk of CVD. A study with postmenopausal women 13 , for example, concluded that this group could benefit from supplementing with astaxanthin. Additionally, research has demonstrated the benefits of astaxanthin in fighting obesity-induced oxidative stress in overweight young adults 14 and in women with an increased oxidative stress burden. Like oxidation, inflammation is an established process contributing to CVD. Astaxanthin has been shown to help support a healthy lipid profile. A human study on the effect of astaxanthin on dyslipidemia an excess of LDL and other lipids in the blood found that supplementation decreased levels of triglycerides, a lipid that has been shown to increase the risk of CVD. The same study also demonstrated that astaxanthin significantly increased levels of HDL cholesterol. Astaxanthin also offers additional support for cardiovascular health. For example, its antioxidative and anti-inflammatory properties can significantly shorten blood transit times. As populations continue to live longer, new strategies to support healthy aging become increasingly important. There is a solid scientific foundation supporting the case for astaxanthin as an effective ingredient for heart health supplements. Furthermore, it is safe, natural and can be sustainably produced, adding to its consumer appeal globally. Tryggvi Stefánsson, PhD, is science manager for algae-ingredients supplier Algalif Reykjanesbaer, Iceland. Stefánsson has a PhD in microbiology and genetics from ETH Zurich in Switzerland. The Science Behind Astaxanthin. Algalif Astaxanthin Gains Novel Food Status as Ingredient Gains Traction in Europe, North America, and Asia. First Astaxanthin Product Debuts with Natural Algae Astaxanthin Association Verification Seal. Magnesium is well-established and trusted across multiple categories. Magnesium's trajectory is similar to ashwagandha in that its reach is extending across multiple categories. Ex-vivo study finds potential impact of low-no-calories sweeteners on gut microbiota. Low-no-calories sweeteners may have an impact on gut microbiota and metabolite production. Saw CL, Yang AY, Guo Y and Kong AN: Astaxanthin and omega-3 fatty acids individually and in combination protect against oxidative stress via the Nrf2-ARE pathway. Food Chem Toxicol. Visioli F and Artaria C: Astaxanthin in cardiovascular health and disease: Mechanisms of action, therapeutic merits, and knowledge gaps. Food Funct. BMC Gastroenterol. Yasui Y, Hosokawa M, Mikami N, Miyashita K and Tanaka T: Dietary astaxanthin inhibits colitis and colitis-associated colon carcinogenesis in mice via modulation of the inflammatory cyto-kines. Chem Biol Interact. Nagendraprabhu P and Sudhandiran G: Astaxanthin inhibits tumor invasion by decreasing extracellular matrix production and induces apoptosis in experimental rat colon carcinogenesis by modulating the expressions of ERK-2, NFkB and COX Invest New Drugs. Moroni F, Ammirati E, Norata GD, Magnoni M and Camici PG: The role of monocytes and macrophages in human atherosclerosis, plaque neoangiogenesis, and atherothrombosis. Mediators Inflamm. Hashizume M and Mihara M: Blockade of IL-6 and TNF-α inhibited oxLDL-induced production of MCP-1 via scavenger receptor induction. Eur J Pharmacol. Zou TB, Zhu SS, Luo F, Li WQ, Sun XR and Wu HF: Effects of astaxanthin on reverse cholesterol transport and atherosclerosis in mice. Biomed Res Int. Kishimoto Y, Tani M, Uto-Kondo H, Iizuka M, Saita E, Sone H, Kurata H and Kondo K: Astaxanthin suppresses scavenger receptor expression and matrix metalloproteinase activity in macrophages. Eur J Nutr. Santos SD, Cahú TB, Firmino GO, de Castro CC, Carvalho LB Jr, Bezerra RS and Filho JL: Shrimp waste extract and astaxanthin: Rat alveolar macrophage, oxidative stress and inflammation. J Food Sci. Lee SJ, Bai SK, Lee KS, Namkoong S, Na HJ, Ha KS, Han JA, Yim SV, Chang K, Kwon YG, et al: Astaxanthin inhibits nitric oxide production and inflammatory gene expression by suppressing I kappa B kinase-dependent NF-kappaB activation. Mol Cells. Franceschelli S, Pesce M, Ferrone A, De Lutiis MA, Patruno A, Grilli A, Felaco M and Speranza L: Astaxanthin treatment confers protection against oxidative stress in U cells stimulated with lipopolysaccharide reducing O 2 -production. PLoS One. Macedo RC, Bolin AP, Marin DP and Otton R: Astaxanthin addition improves human neutrophils function: In vitro study. Choi SK, Park YS, Choi DK and Chang HI: Effects of astaxanthin on the production of NO and the expression of COX-2 and iNOS in LPS-stimulated BV2 microglial cells. J Microbiol Biotechnol. Kim YJ, Kim YA and Yokozawa T: Protection against oxidative stress, inflammation, and apoptosis of high-glucose-exposed proximal tubular epithelial cells by astaxanthin. J Agric Food Chem. Abdelzaher LA, Imaizumi T, Suzuki T, Tomita K, Takashina M and Hattori Y: Astaxanthin alleviates oxidative stress insults-related derangements in human vascular endothelial cells exposed to glucose fluctuations. Life Sci. Speranza L, Pesce M, Patruno A, Franceschelli S, de Lutiis MA, Grilli A and Felaco M: Astaxanthin treatment reduced oxidative induced pro-inflammatory cytokines secretion in U SHP-1 as a novel biological target. Jones WK, Brown M, Wilhide M, He S and Ren X: NF-kappaB in cardiovascular disease: Diverse and specific effects of a 'general' transcription factor? Cardiovasc Toxicol. Pashkow FJ, Watumull DG and Campbell CL: Astaxanthin: A novel potential treatment for oxidative stress and inflammation in cardiovascular disease. Am J Cardiol. Ghosh S, May MJ and Kopp EB: NF-kappa B and Rel proteins: Evolutionarily conserved mediators of immune responses. Annu Rev Immunol. Woronicz JD, Gao X, Cao Z, Rothe M and Goeddel DV: IkappaB kinase-beta: NF-kappaB activation and complex formation with IkappaB kinase-alpha and NIK. Mercurio F, Zhu H, Murray BW, Shevchenko A, Bennett BL, Li J, Young DB, Barbosa M, Mann M, Manning A and Rao A: IKK-1 and IKK Cytokine-activated IkappaB kinases essential for NF-kappaB activation. Zandi E, Rothwarf DM, Delhase M, Hayakawa M and Karin M: The IkappaB kinase complex IKK contains two kinase subunits, IKKalpha and IKKbeta, necessary for IkappaB phosphorylation and NF-kappaB activation. DiDonato JA, Hayakawa M, Rothwarf DM, Zandi E and Karin M: A cytokine-responsive IkappaB kinase that activates the transcription factor NF-kappaB. Ghosh S and Karin M: Missing pieces in the NF-kappaB puzzle. Wang HH, Garruti G, Liu M, Portincasa P and Wang DQ: Cholesterol and lipoprotein metabolism and atherosclerosis: Recent advances in reverse cholesterol transport. Ann Hepatol. Khera AV and Rader DJ: Future therapeutic directions in reverse cholesterol transport. Tall AR and Yvan-Charvet L: Cholesterol, inflammation and innate immunity. Nat Rev Immunol. Shao B, Tang C, Sinha A, Mayer PS, Davenport GD, Brot N, Oda MN, Zhao XQ and Heinecke JW: Humans with atherosclerosis have impaired ABCA1 cholesterol efflux and enhanced high-density lipoprotein oxidation by myeloperoxidase. Clarke MC and Bennett MR: Cause or consequence: What does macrophage apoptosis do in atherosclerosis? Monteiro R and Azevedo I: Chronic inflammation in obesity and the metabolic syndrome. Int Rev Cell Mol Biol. Sanderson TH, Reynolds CA, Kumar R, Przyklenk K and Hüttemann M: Molecular mechanisms of ischemia-reperfusion injury in brain: Pivotal role of the mitochondrial membrane potential in reactive oxygen species generation. Mol Neurobiol. Am J Transl Res. J Pharmacol Exp Ther. Ni Y, Nagashimada M, Zhuge F, Zhan L, Nagata N, Tsutsui A, Nakanuma Y, Kaneko S and Ota T: Astaxanthin prevents and reverses diet-induced insulin resistance and steatohepatitis in mice: A comparison with vitamin E. Sci Rep. Liu H, Liu M, Fu X, Zhang Z, Zhu L, Zheng X and Liu J: Astaxanthin prevents alcoholic fatty liver disease by modulating mouse gut microbiota. Lyu Y, Wu L, Wang F, Shen X and Lin D: Carotenoid supple-mentation and retinoic acid in immunoglobulin A regulation of the gut microbiota dysbiosis. Exp Biol Med Maywood. Tang WH, Kitai T and Hazen SL: Gut microbiota in cardiovascular health and disease. Saad MJ, Santos A and Prada PO: Linking gut microbiota and inflammation to obesity and insulin resistance. Physiology Bethesda. Wu L, Lyu Y, Srinivasagan R, Wu J, Ojo B, Tang M, El-Rassi GD, Metzinger K, Smith BJ, Lucas EA, et al: Astaxanthin-shifted gut microbiota is associated with inflammation and metabolic homeostasis in mice. J Nutr. Ou W, Liao Z, Yu G, Xu H, Liang M, Mai K and Zhang Y: The effects of dietary astaxanthin on intestinal health of juvenile tiger puffer takifugu rubripes in terms of antioxidative status, inflammatory response and microbiota. Aquaculture Nutrition. Zhang L, Cao W, Gao Y, Yang R, Zhang X, Xu J and Tang Q: Astaxanthin ATX enhances the intestinal mucosal functions in immunodeficient mice. Gao Y, Yang L, Chin Y, Liu F, Li RW, Yuan S, Xue C, Xu J and Tang Q: Astaxanthin n-octanoic acid diester ameliorates insulin resistance and modulates gut microbiota in high-fat and high-sucrose dietfed mice. Int J Mol Sci. Wang J, Liu S, Wang H, Xiao S, Li C, Li Y and Liu B: Xanthophyllomyces dendrorhous-derived astaxanthin regulates lipid metabolism and gut microbiota in obese mice induced by a high-fat diet. Linton MRF, Yancey PG, Davies SS, Jerome WG, Linton EF, Song WL, Doran AC and Vickers KC: The role of lipids and lipoproteins in atherosclerosis. Endotext Feingold KR, Anawalt B, Boyce A, Chrousos G, Dungan K, Grossman A, Hershman JM, Kaltsas G, Koch C, Kopp P, et al: MDText Com, Inc; South Dartmouth, MA: Strassheim D, Dempsey EC, Gerasimovskaya E, Stenmark K and Karoor V: Role of inflammatory cell subtypes in heart failure. J Immunol Res. Gröschel C, Sasse A, Röhrborn C, Monecke S, Didié M, Elsner L, Kruse V, Bunt G, Lichtman AH, Toischer K, et al: T helper cells with specificity for an antigen in cardiomyocytes promote pressure overload-induced progression from hypertrophy to heart failure. Kallikourdis M, Martini E, Carullo P, Sardi C, Roselli G, Greco CM, Vignali D, Riva F, Ormbostad Berre AM, Stølen TO, et al: T cell costimulation blockade blunts pressure overload-induced heart failure. Nat Commun. Gisterå A and Hansson GK: The immunology of atherosclerosis. Nat Rev Nephrol. Swirski FK and Nahrendorf M: Leukocyte behavior in athero-sclerosis, myocardial infarction, and heart failure. Stemme S, Faber B, Holm J, Wiklund O, Witztum JL and Hansson GK: T lymphocytes from human atherosclerotic plaques recognize oxidized low density lipoprotein. Proc Natl Acad Sci USA. Frostegård J, Ulfgren AK, Nyberg P, Hedin U, Swedenborg J, Andersson U and Hansson GK: Cytokine expression in advanced human atherosclerotic plaques: Dominance of pro-inflammatory Th1 and macrophage-stimulating cytokines. Tripathi DN and Jena GB: Intervention of astaxanthin against cyclophosphamide-induced oxidative stress and DNA damage: A study in mice. Int Immunopharmacol. Bolin AP, Macedo RC, Marin DP, Barros MP and Otton R: Astaxanthin prevents in vitro auto-oxidative injury in human lymphocytes. Cell Biol Toxicol. Campoio TR, Oliveira FA and Otton R: Oxidative stress in human lymphocytes treated with fatty acid mixture: Role of carotenoid astaxanthin. Toxicol In Vitro. Pilinska MA, capital Ka CD, Rushkovsky SR and Dybska OB: Genoprotective properties of astaxanthin revealed by ionizing radiation exposure in vitro on human peripheral blood lymphocytes. Probl Radiac Med Radiobiol. In English, Ukrainian. Otton R, Marin DP, Bolin AP, de Cássia Santos Macedo R, Campoio TR, Fineto C Jr, Guerra BA, Leite JR, Barros MP and Mattei R: Combined fish oil and astaxanthin supplementation modulates rat lymphocyte function. Mahmoud FF, Haines DD, Abul HT, Abal AT, Onadeko BO and Wise JA: In vitro effects of astaxanthin combined with ginkgolide B on T lymphocyte activation in peripheral blood mononuclear cells from asthmatic subjects. J Pharmacol Sci. Lin KH, Lin KC, Lu WJ, Thomas PA, Jayakumar T and Sheu JR: Astaxanthin, a carotenoid, stimulates immune responses by enhancing IFN-γ and IL-2 secretion in primary cultured lymphocytes in vitro and ex vivo. Biochim Biophys Acta Gen Subj. Park JS, Mathison BD, Hayek MG, Massimino S, Reinhart GA and Chew BP: Astaxanthin stimulates cell-mediated and humoral immune responses in cats. Vet Immunol Immunopathol. Chew BP, Wong MW, Park JS and Wong TS: Dietary beta-carotene and astaxanthin but not canthaxanthin stimulate splenocyte function in mice. Anticancer Res. Jyonouchi H, Hill RJ, Tomita Y and Good RA: Studies of immunomodulating actions of carotenoids. Effects of beta-carotene and astaxanthin on murine lymphocyte functions and cell surface marker expression in in vitro culture system. Nutr Cancer. Mahmoud FF, Haines D, Al-Awadhi R, Arifhodzic N, Abal A, Azeamouzi C, Al-Sharah S and Tosaki A: In vitro suppression of lymphocyte activation in patients with seasonal allergic rhinitis and pollen-related asthma by cetirizine or azelastine in combination with ginkgolide B or astaxanthin. Acta Physiol Hung. Jyonouchi H, Zhang L and Tomita Y: Studies of immunomodulating actions of carotenoids. Astaxanthin enhances in vitro antibody production to T-dependent antigens without facilitating polyclonal B-cell activation. January Volume 47 Issue 1. Sign up for eToc alerts. You can change your cookie settings at any time by following the instructions in our Cookie Policy. To find out more, you may read our Privacy Policy. I agree. Home Submit Manuscript My Account. Advanced Search. Register Login. Oncology Letters International Journal of Oncology Molecular and Clinical Oncology Experimental and Therapeutic Medicine International Journal of Molecular Medicine Biomedical Reports Oncology Reports Molecular Medicine Reports World Academy of Sciences Journal International Journal of Functional Nutrition International Journal of Epigenetics Medicine International. International Journal of Molecular Medicine. 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Mechanisms of action of astaxanthin Antioxidant effect Cell membrane systems are particularly vulnerable to RONS attacks due to their content of polyun-saturated fatty acids PUFAs and their metabolic activities, which endogenously generate other oxidizing metabolites Table I Clinical studies that have demonstrated the potential beneficial effects of oral astaxanthin supplementation on cardiovascular physiology. Study type Subjects age Intervention no. of subjects per group Mechanism of action evaluated Main findings Refs. Open-label 24 healthy volunteers mean, b Non-smoking individuals without supplementation. Figure 1 Scheme of the antioxidant and anti-inflammatory mechanisms of action of astaxanthin in cardiovascular diseases. Figure 2 Mechanism of atherosclerotic plaque formation in the subendothelial layer of the vascular wall and the action of astaxanthin adapted from Fig. They also cited existing findings on how astaxanthin could increase mitochondrial respiration, adenosine triphosphate production, and consequently, LV systolic function. Nineteen patients were enrolled in the pilot study. All suffered from heart failure due to ischemic or non-ischemic cardiomyopathy and had treatment for at least six months. Before starting on astaxanthin supplementation, their cardiac function, LVEF, plasma concentration of astaxanthin, and blood serum levels of the inflammatory markers were measured. Once the study commenced, all patients consumed a commercially available astaxanthin supplement containing 12 mg of astaxanthin, 40 mg of tocotrienol, and 30 mg of natural vitamin C L-ascorbic acid 2-glucoside once daily. Their blood and urine sampling, echocardiography, and 6-min walk test were repeated at a follow-up visit 3 months after starting astaxanthin supplementation. This is also accompanied by an improvement in LVEF, which increased from No significant change was seen in other oxidative and inflammatory markers such as CRP, TNF-α levels though. There was also no decrease in urinary oxidative stress as seen from the 8-OHdG results. As for the 6-min walking test, the distance walked increased from As this was an observational study without control groups, the researchers acknowledged that no causal relationship between astaxanthin supplementation and improvements in cardiac function was proven. As such, they also pointed a possibility that the improvement in cardiac function could be due to a mechanism that was independent of oxidative stress suppression. In addition, since the supplement used in the study contained tocotrienol and vitamin C which are antioxidants, these ingredients could also have played a role in reducing oxidative stress and improving cardiac function. |
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