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The #1 Best Remedy to Prevent a Heart Attack for $3.19Astaxanthin and heart health -
In addition, the presence of a series of conjugated bonds in the central non-polar region of astaxanthin enables the molecule to remove free radicals high-energy electrons from the cell interior by transporting them along its own carbon chain, resembling a 'lightning rod' for these electrons, so that these are neutralized by other antioxidants located outside the cell membrane, such as vitamin C The increased susceptibility of membrane lipids and low-density lipoprotein LDL to oxidation may trigger the formation of thrombi and the development of atherosclerosis 5.
The LDL oxidation time in the presence of astaxanthin has been analyzed in vitro and ex vivo. In the in vitro assays, astaxanthin prolonged LDL oxidation in a dose-dependent manner, in addition to being more effective compared with lutein and α-tocopherol. In turn, the blood samples of individuals who were supplemented daily with 1.
Thus, it was demonstrated that the intake of astaxanthin delayed LDL oxidation, one of the key factors involved in the process of atherosclerosis. Clinical studies that have demonstrated the potential beneficial effects of oral astaxanthin supplementation on cardiovascular physiology.
LDL oxidation is also associated with the development of endothelial dysfunction in patients with diabetes mellitus, which increases the risk of cardiovascular complications Endothelial dysfunction consists of impaired vessel relaxation dependent on endothelial factors, such as the production of nitric oxide NO by endothelial NO synthase eNOS One of the pathways responsible for this type of dysfunction is the binding of oxidized LDL to its endothelial receptor, lectin-like ox-LDL receptor 1 LOX-1 , thus favoring oxidative stress, which leads to increased lipid peroxidation and eNOS inactivation The oxidation of erythrocytes is associated with both the formation of atheromas and the occurrence of intraplate hemorrhage during the development of atherosclerosis As regards lipid peroxidation in erythrocytes, daily supplementation with 6 or 12 mg of astaxanthin for 12 weeks in healthy individuals demonstrated that this carotenoid is incorporated and distributed into these blood cells.
When incorporated into erythrocytes, astaxanthin exerted antioxidant effects on the cell membrane by significantly reducing the levels of phospholipid hydroperoxides, which are the primary products of phospholipid oxidation In that study, the two doses of astaxanthin used had similar effects when compared to placebo, suggesting that the intake of 6 mg of this carotenoid is sufficient to inhibit oxidative stress in erythrocytes Table I Blood rheology is important for cardiovascular homeostasis.
Astaxanthin was shown to reduce blood transit time in a hypertensive rat model 35 as well as in humans In the latter study, individuals receiving supplementation with 6 mg astaxanthin for 10 days had a significantly faster blood transit time compared with that before supplementation and with that in the placebo group One hypothesis for the improvement of blood rheology by astaxanthin is its antioxidant effect on the intra- and extracellular environment and the consequent increase in the flexibility of the erythrocyte membrane conferred by the structural arrangement of astaxanthin in the membrane.
Other factors that affect the blood flow velocity, such as plasma viscosity and vasodilation, affect peripheral vascular resistance and may contribute to hypertension and its main cardiac complication, myocardial hypertrophy Studies of spontaneously hypertensive rats SHR reported that astaxanthin supplementation significantly reduced systolic pressure and induced significant histological changes in the aorta associated with decreased vascular stiffness and blood pressure 37 - This response was caused by increased endothelial cell-dependent vasodilation due to the greater bioavailability of NO, as well as the remodeling of the arteries.
The increase in NO was caused by the reduced production of superoxide anion radicals released by NADPH oxidase, which is one of the antioxidant effects of astaxanthin 37 , Chen et al reported that this carotenoid also participated in the remodeling of the smooth muscle cells of the vessels, reducing their proliferation and the damage caused by oxidative stress.
Astaxanthin lowered RONS levels by increasing the activity of antioxidant enzymes and regulating mitochondrial dynamics, mitophagy and mitochondrial biogenesis, which are important for the maintenance of mitochondrial and cellular metabolism The high bioavailability of NO due to lower oxidative stress promoted by astaxanthin was also associated with its antithrombogenic effects.
The observed antithrombogenic effect may have been due to vasodilation and inhibition of platelet aggregation caused by an increased bioavailability of NO The authors suggested that the increase in blood flow was due to vasodilation caused by increased release of NO by endothelial cells and reduced platelet activation triggered by the antioxidant effect Some of the vascular benefits promoted by the antioxidant effect of astaxanthin were reported in an open study of 20 postmenopausal women who had a high rate of oxidative stress After 8 weeks of supplementation with 12 mg astaxanthin, there was a significant reduction of 4.
Reduced vascular resistance in the lower limbs 3. In addition to the protective role of astaxanthin in the lipid oxidation process, this carotenoid affects the activity of antioxidant enzymes involved in lipid metabolism, such as thioredoxin reductase TrxR and paraoxonase TrxR is an antioxidant enzyme involved in the reduction of thioredoxin, lipid hydroperoxides and hydrogen peroxide A previous study demonstrated that thioredoxin in its oxidized form was associated with the degree of severity of chronic heart failure and with the resulting oxidative stress Paraoxonase-1 binds to serum high-density lipoprotein HDL and is responsible for protecting both LDL and HDL from oxidation, as well as for breaking down oxidized lipids The effect of astaxanthin on these two enzymes was evaluated in rabbits fed a cholesterol-rich diet Choi et al 11 , 16 also conducted two randomized and double-blind clinical studies on overweight or obese individuals to demonstrate the antioxidant effects of astaxanthin Table I.
In one study, volunteers who received 5 and 20 mg astaxanthin for 3 weeks exhibited lower oxidative stress biomarkers associated with lipid peroxidation compared with prior to treatment, with a No significant differences were observed between the results obtained with the two doses, indicating that the clinical effects of this carotenoid are not dose-dependent.
Later, the same authors analyzed lipid profile, oxidative stress and antioxidant system parameters After 12 weeks of supplementation with 20 mg astaxanthin, the same results in oxidative stress and the antioxidant system as in the previous study were observed. Regarding the lipid profile, there was a significant reduction of Therefore, these studies demonstrated that astaxanthin reduces oxidative stress and modulates the lipid profile in overweight and obese individuals, mitigating the risk of developing cardiovascular diseases.
Astaxanthin also has potent detoxifying and antioxidant effects in smokers The free radicals induced by smoking have been strongly associated with increased oxidative stress, contributing to the increased susceptibility of smokers to the pathogenesis of cardiovascular diseases.
This group of individuals requires a higher daily intake of antioxidants compared with non-smokers to reduce the consequences of prolonged exposure to toxins present in cigarettes. After 3 weeks, supplementation with different doses of astaxanthin 5, 20 and 40 mg in active smokers prevented oxidative damage by suppressing lipid peroxidation and stimulating the activity of the antioxidant system Table I This effect was confirmed by the significant reduction in serum MDA and ISP levels and the increased SOD activity and total antioxidant capacity in the three astaxanthin groups compared with the indices prior to treatment The authors also observed that the serum concentration of astaxanthin in the groups treated with 20 and 40 mg was similar, showing that there was saturation of its absorption and that smaller doses, such as 5 mg, may have the necessary antioxidant effect for these individuals.
However, placebo-controlled studies with larger groups and longer interventions may help determine the optimal dosage for smokers. Several preclinical studies have demonstrated that astaxanthin also exerts an indirect antioxidant effect by activating transcription factor nuclear factor erythroid 2-related factor 2 Nrf2 , and increasing the expression of its antioxidant target genes, such as phase II biotransformation enzymes 46 - Thus, astaxanthin may accumulate in the blood plasma and, through its antioxidant action, it helps reduce the levels of RONS responsible for LDL oxidation and lipid peroxidation; it increases the bioavailability of NO, enabling its vasodilator and antithrombogenic effects; it increases the activity of antioxidant enzymes; and it ensures the stability of blood rheological properties, thus avoiding the loss of erythrocyte flexibility and the increase in plasma viscosity, factors that affect the blood flow velocity.
These actions of astaxanthin against early events of atherosclerotic plaque formation and arterial dysfunction may delay the progression of cardiovascular diseases Fig. Scheme of the antioxidant and anti-inflammatory mechanisms of action of astaxanthin in cardiovascular diseases.
LDL, low-density lipoprotein; RONS, reactive oxygen and nitrogen species; NF-κB, nuclear factor-κB; MMP, matrix metallopeptidase; MAPK, mitogen-activated protein kinase; NO, nitrogen oxide. Inflammation plays an important role in the development of cardiovascular diseases and other comorbidities, such as hypertension, hypercholesterolemia, type 2 diabetes, chronic kidney disease and obesity Astaxanthin exerts a marked anti-inflammatory effect, which may be interrelated with its antioxidant effect and contributes to physiological changes that benefit cardiovascular function Fig.
Atherosclerosis is a degenerative and chronic disease that affects large- and medium-caliber arteries. Atherogenesis, the initial phase of the atherosclerotic process, is character-ized by the accumulation of LDL in the subendothelial layer of the vascular wall, which is responsible for inflammation mediated by the innate and adaptive immune responses The anti-inflammatory effects promoted by astaxanthin are evidenced in its role in atherosclerosis prevention, as will be detailed below.
The epitopes generated from 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.
Macrophages bind to oxidized LDL via scavenger receptors, such as SR-A, SR-B2 CD36 and LOX-1 The expression of these receptors is controlled by nuclear factor-κB NF-κB , the main mediator of the inflammatory response, which is activated by pattern recognition receptors and pro-inflammatory cytokines In inflammatory states, macrophages produce excessive amounts of pro-inflammatory mediators, such as cytokines, chemokines, NO, cyclooxygenase-2 COX-2 and matrix metalloproteinases MMPs.
MMPs are responsible for the degradation of most extracellular matrix proteins and mediate the tissue remodeling associated with atherosclerosis 5. In vitro and in vivo studies have evaluated the effect of astaxanthin on the formation of atherosclerotic plaques 54 - 58 , 61 - Supplementation with 10 µ M astaxanthin significantly reduced the expression of the SR-A and CD36 scavenger receptors in the THP-1 macrophage line and reduced the total activity of MMPs, as reflected by reduced protein expression of MMP-9 and MMP-2 and of the mRNA levels of five MMPs Astaxanthin at this concentration also reduced the gene expression of pro-inflammatory markers, such as interleukin IL -1β, IL-6, tumor necrosis factor-α TNF-α , inducible nitric oxide synthase iNOS and COX-2 These results corroborate those of other studies indicating that astaxanthin reduces the expression of pro-inflammatory mediators in macrophages 62 - 65 and other cell types, such as microglia, endothelial vascular cells and human neutrophils 66 - The significant decreases in the levels of MMPs and proinflammatory cytokines may result from the suppression of the NF-κB transcription factor by astaxanthin 54 - 58 , 62 , 64 , 68 , 70 , NF-κB is frequently activated at inflammation sites associated with various pathologies, particularly cardiovascular diseases, in the etiology of which the increased expression of its pro-inflammatory target genes plays a key role The inflammatory pathway of NF-κB is, at least in part, regulated by oxidative stress Astaxanthin inhibits the activity of IκB kinase, a complex responsible for the control of NF-κB activation.
This maintains NF-κB inactive in the cell cytoplasm, and its pro-inflammatory target genes, such as TNF-α, IL-1β and iNOS, are downregulated Cholesterol uptake is balanced by the transfer of this molecule from macrophages to free apolipoproteins A1 or to HDL, the latter being responsible for the reverse cholesterol transport process.
When cholesterol uptake exceeds cholesterol efflux in macrophages, lipid droplets accumulate in the cytoplasm, forming foam cells, the main markers of atherosclerosis Fig. The progression of cholesterol accumulation may lead to its precipitation in the form of crystals, which activate the inflammasome, leading to cell death by apoptosis or necrosis The atherosclerotic plaque is separated from the bloodstream by a fibrous layer, which, upon rupture, initiates intraluminal thrombosis, the initial event of stroke and other coronary syndromes Mechanism of atherosclerotic plaque formation in the subendothelial layer of the vascular wall and the action of astaxanthin adapted from Fig.
AST, astaxanthin; LDL, low-density lipoprotein; HDL, high-density lipoprotein; ROS, reactive oxygen species; NF-κB, nuclear factor-κB; MMP, matrix metallopeptidase; ABCA1, ATP-binding cassette A1. Reverse cholesterol transport consists in HDL removing excess cholesterol from peripheral tissues and transporting it to the liver, where it is degraded by bile juice and excreted in the feces, thus preventing the accumulation of cholesterol in macrophages Both the liver and intestine synthesize apolipoprotein A-I apoA-I and apoA-II in the plasma, which incorporate free cholesterol and phospholipids through the ATP-binding cassette A1 ABCA1 hepatic transporter, originating from nascent HDL.
In peripheral tissues, nascent HDL molecules recruit free cholesterol from foam cells via the macrophage ABCA1 transporter Of note, this reverse cholesterol transport was also observed in the lymphatic system, which is largely responsible for the removal of cholesterol from different tissues Finally, mature HDL can transport cholesterol directly to the liver via the SR-B1 scavenger receptor or can transfer cholesteryl esters to very low-density lipoprotein VLDL through the cholesteryl ester transfer protein These lipoproteins are absorbed in the liver by their specific receptors, which is likely the predominant pathway in humans.
Once in the liver, cholesterol is secreted into the bile via the ABCG5 and ABCG8 transporters. Some of these molecules can be reabsorbed by the intestine and reach the bloodstream again, while the rest is excreted in the feces In atherosclerosis, apolipoproteins are oxidized by the enzyme myeloperoxidase, which is expressed in macrophages during the inflammatory process, compromising cholesterol efflux via ABCA1 In individuals with heart disease, elevated levels of apoA-I modified by myeloperoxidase were identified, and their HDL molecules were dysfunctional in performing reverse cholesterol transport.
Thus, the oxidation of apolipoproteins by macrophage myeloperoxidase is a determining factor in HDL dysfunction in cholesterol transport and, therefore, in the risk of cardiovascular diseases. The effects of astaxanthin on reverse cholesterol transport have been demonstrated in vivo.
Thus, astaxanthin may exert antiatherosclerotic effects by increasing the activity of the reverse cholesterol transport pathway, but the molecular mechanisms underlying this action remain elusive In addition to its function in reverse cholesterol transport, astaxanthin is involved in certain lipid metabolism steps, a finding corroborated by a randomized, placebo-controlled clinical study of 61 adult individuals with moderate hyperlipidemia Table I In that study, daily supplementation with 6, 12 or 18 mg astaxanthin for 12 weeks led to an improvement in the lipid profile of the patients.
Triglycerides were reduced by Inflammation is also involved in the pathophysiology of metabolic syndrome, a multifactorial disorder associated with glucose and lipid metabolism disorders.
This disease has risk factors that are also strongly associated with the development of cardiovascular complications, including type 2 diabetes, dyslipidemia, hypertension and abdominal fat deposition In this context, astaxanthin has been found to be promising in the improvement of glucose and lipid metabolism in a randomized, placebo-controlled clinical study with 43 diabetic patients aged years Table I Furthermore, astaxanthin marginally reduced fasting glucose levels 8.
Patients receiving astaxanthin supplementation also exhibited lower visceral fat deposition In mice with non-alcoholic steatohepatitis NASH induced by a high-lipid diet, supplementation with astaxanthin 0.
Additionally, astaxanthin was more effective in preventing and treating NASH and improving liver inflammation and fibrosis compared with vitamin E standard NASH treatment. The effects of astaxanthin on the relief of liver injury was shown to be correlated to its positive effects on the intestinal microbiota and consequent reduction of inflammation In fact, a growing body of evidence indicates that gut microbiota plays a key role in the pathogenesis of inflammatory disorders and cardiovascular diseases, and alterations in its composition dysbiosis have been associated with heart failure, hypertension, atherosclerosis and metabolic syndrome 93 - Several recent in vivo studies revealed that astaxanthin supplementation improved gut microbiota composition, which may contribute to its local and systemic anti-inflammatory and antioxidant effects 92 , 96 - The beneficial effect of astaxanthin on gut microbiota has been shown to be correlated with the mitigation of cardiovascular disease-related pathologies and risk factors, such as obesity , insulin resistance 99 and alcoholic fatty liver disease Astaxanthin improved the immune responses of the participants, as evidenced by the increased cytotoxic activity of natural killer cells 8 mg dose, Although macrophages are the main type of immune cell found in atherosclerotic plaques, T lymphocytes also contribute to the development of the disease In fact, the inflammatory response mediated by T lymphocytes plays a crucial role in the etiology of cardiovascular diseases, contributing to atherosclerosis, heart failure and myocardial infarction - For example, T helper cells can be activated by LDL particles in the arterial wall and trigger inflammation through an autoimmune response, contributing to the development of atherosclerotic plaques , , Similarly, self-reactive T helper cells may target cardiomyocytes, contributing to the development of heart failure Astaxanthin was shown to be effective not only in preventing oxidative stress in T lymphocytes - , but also in modulating their activity - In the aforementioned clinical study on healthy young women 17 , astaxanthin supplementation stimulated mitogen-induced lymphoproliferation and increased the subpopulation of T lymphocytes, without changing the populations of T killer or T helper cells, as well as increased the response to tuberculin, an indicator of T lymphocyte function.
In a mouse model of NASH, astaxanthin reduced T helper and T killer cell recruitment to the liver, contributing to the improvement of inflammation and insulin resistance In in vitro studies with peripheral blood mononuclear cells from patients with asthma and allergic rhinitis, it was demonstrated that astaxanthin significantly suppressed the activation of T lymphocytes induced by phytohemagglutinin , Another in vitro and ex vivo study with cultured lymphocytes demonstrated that astaxanthin stimulated their immune response and increased the production of IL-2 and IFN-γ, without inducing cytotoxicity The administration of astaxanthin in mice prevented renal fibrosis by mechanisms involving stimulation of T killer cell recruitment and increased production of IFN-γ In cats, astaxanthin increased the immune response mediated by total T lymphocytes and T helper cells Therefore, astaxanthin was shown to exert a clear modulatory effect on T lymphocytes, overall improving their immune response or downregulating their potentially pathological immune activation.
However, the role of T lymphocyte modulation by astaxanthin in the risk and progression of cardiovascular diseases remain to be fully elucidated. In summary, inflammation plays a key role in the pathophysiology of cardiovascular diseases and their risk factors, while astaxanthin exerts beneficial anti-inflammatory effects.
The mechanism of action of this carotenoid involves inhibition of the NF-κB and MAPK signaling pathways, which suppresses the inflammatory process and stimulates reverse cholesterol transport, thereby attenuating the formation of foam cells Fig.
The potential beneficial effects of oral astaxanthin supplementation on cardiovascular physiology were evidenced in 11 clinical studies, summarized in Table I. Of these 11 studies, 6 were randomized placebo-controlled studies 11 - 13 , 17 , 19 , 20 , 1 was single-blinded 18 , 2 were open-label 10 , 14 , and 2 were randomized but lacked a placebo group 15 , A total of 6 studies evaluated the metabolic and oxidative changes promoted by astaxanthin in healthy individuals, while 5 investigated individuals who had one element of the metabolic syndrome, namely obesity, dyslipidemia or type 2 diabetes.
In addition, the dose of astaxanthin ranged between 1. Despite encompassing a small population with a total of individuals, the results of those studies indicated that the beneficial effect of astaxanthin on cardiovascular health was mainly due to its antioxidant and anti-inflammatory properties, its ability to modulate lipid and glucose metabolism, and its role in the maintenance of blood rheological properties.
Based on preclinical and clinical evidence, the antioxidant and anti-inflammatory effects of astaxanthin appear to delay the progression of cardiovascular diseases. As an antioxidant, astaxanthin reduces oxidative stress, increases the bioavailability of NO and the activity of antioxidant enzymes, and maintains the rheological properties of the blood.
Its anti-inflammatory properties involve modulating the NF-κB and MAPK signaling pathways, reducing the release of pro-inflammatory cytokines and increasing reverse cholesterol transport by HDL, thereby attenuating the accumulation of cholesterol in foam cells and the formation of atherosclerotic plaques.
CPMP and JJN contributed to the conception of the study and critically reviewed the article. SAS scores are expressed as metabolic equivalent Mets. 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.
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.
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