Astaxanthin

 

• Extended male mice lifespan significantly in ITP (ref).

• Alleviated NASH in humans. (a) Representative H&E-stained liver sections from two subjects with NASH before and after treatment revealed that astaxanthin improved steatohepatitis after 24 weeks of treatment. (b) NAFLD activity score (NAS) in NASH subjects dropped on astaxanthin (AX, n = 7). P < 0.05 vs. pretreatment.

• Lowered HS-CRP by 0.528 mg/l (P < 0.05) and decreased a DNA damage biomarker.

• Increased HDL-C marginally (WMD: 1.473 mg/dl, p = 0.012). 

• Reduced Diastolic BP by 2.77 mmHg (95 %CI: −4.34, −1.19).

• Significantly reduced blood malondialdehyde and IL-6 in T2DM patients.

• Significantly restored skin moisture content (p = 0.03), improved elasticity (p = 0.009) but marginally decreased wrinkle depth (p = 0.11) compared to placebo.

Impact of astaxanthin supplementation on blood pressure: A systematic review and meta-analysis of randomized controlled trials, 2021

This systematic review and meta-analysis on randomized controlled trials (RCTs) evaluated the impact of astaxanthin (AST) supplementation on blood pressure in adults. We conducted a comprehensive search using different electronic databases. Ten RCTs with 493 participants that reported the effect of AST supplementation on blood pressure in adults were included. AST supplementation led to a marginally decline in diastolic blood pressure (DBP) (mean difference (MD) = −1.21; 95 %CI: −2.51, 0.09), but not systolic blood pressure. In patients, AST supplementation reduced DBP by 2.77 mmHg (95 %CI: −4.34, −1.19). Also, assigning ≥ 12 mg of AST to adults resulted in a slight decrease in DBP (MD = −0.89; 95 %CI: −1.82, 0.04). AST supplementation significantly reduced DBP by 2.27 mmHg in participants from Asian countries (95 %CI: −3.71, −0.83). This meta-analysis of RCTs disclosed that AST supplementation could reduce DBP, especially with a dose of ≥ 12 mg/d supplementation, in patient individuals and in participants from Asian countries.

Systematic Review and Meta-Analysis on the Effects of Astaxanthin on Human Skin Ageing, 2021

Context: Astaxanthin (ASX), a xanthophyll carotenoid derived from microalgae Haematococcus pluvialis, mitigating skin photoaging and age-related skin diseases by its antioxidant and anti-inflammatory effects in animal studies.

Objective: The aim was to systematically evaluate if ASX applications have anti-ageing effects in humans.

Methods: A comprehensive search of PubMed, Scopus and Web of Science found a total of eleven studies. Nine randomised, controlled human studies assessed oral ASX effects and two open-label, prospective studies evaluated topical, oral-topical ASX effects on skin ageing. GetData Graph Digitizer was used to extract mean values and standard deviations of baseline and endpoint, and Cochrane Collaboration's tool assessed RoB for all included studies. Review Manager 5.4 was used to conduct meta-analysis of RCTs; the results were reported as effect size ± 95% confidence interval.

Results: Oral ASX supplementation significantly restored moisture content (SMD = 0.53; 95% CI = 0.05, 1.01; I2 = 52%; p = 0.03) and improved elasticity (SMD = 0.77; 95% CI = 0.19, 1.35; I2 = 75%; p = 0.009) but did not significantly decrease wrinkle depth (SMD = -0.26; 95% CI = -0.58, 0.06; I2 = 0%; p = 0.11) compared to placebo. Open-label, prospective studies suggested slightly protective effects of topical and oral-topical ASX applications on skin ageing.

Conclusions: Ingestion and/or topical usages of ASX may be effective in reducing skin ageing and have promising cosmetical potential, as it improves moisture content and elasticity and reduces wrinkles.

Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans, 2010

Astaxanthin modulates immune response, inhibits cancer cell growth, reduces bacterial load and gastric inflammation, and protects against UVA-induced oxidative stress in in vitro and rodent models. Similar clinical studies in humans are unavailable. Our objective is to study the action of dietary astaxanthin in modulating immune response, oxidative status and inflammation in young healthy adult female human subjects.

Methods

Participants (averaged 21.5 yr) received 0, 2, or 8 mg astaxanthin (n = 14/diet) daily for 8 wk in a randomized double-blind, placebo-controlled study. Immune response was assessed on wk 0, 4 and 8, and tuberculin test performed on wk 8.

Results

Plasma astaxanthin increased (P < 0.01) dose-dependently after 4 or 8 wk of supplementation. Astaxanthin decreased a DNA damage biomarker after 4 wk but did not affect lipid peroxidation. Plasma C-reactive protein concentration was lower (P < 0.05) on wk 8 in subjects given 2 mg astaxanthin. Dietary astaxanthin stimulated mitogen-induced lymphoproliferation, increased natural killer cell cytotoxic activity, and increased total T and B cell subpopulations, but did not influence populations of Thelper, Tcytotoxic or natural killer cells. A higher percentage of leukocytes expressed the LFA-1 marker in subjects given 2 mg astaxanthin on wk 8. Subjects fed 2 mg astaxanthin had a higher tuberculin response than unsupplemented subjects. There was no difference in TNF and IL-2 concentrations, but plasma IFN-γ and IL-6 increased on wk 8 in subjects given 8 mg astaxanthin.

Conclusion

Therefore, dietary astaxanthin decreases a DNA damage biomarker and acute phase protein, and enhances immune response in young healthy females.

The effects of astaxanthin supplementation on obesity, blood pressure, CRP, glycemic biomarkers, and lipid profile: A meta-analysis of randomized controlled trials, 2020

Previous studies lack consistent conclusions as to whether astaxanthin is actually linked to various health benefits as claimed. Here, we attempt to unravel the association of astaxanthin consumption with selected health benefits by performing a systematic review and meta-analysis.

Methods

Online literature search databases including Scopus, Web of Science, PubMed/Medline, Embase and Google Scholar were searched to discover relevant articles available up to 17 March 2020. We used mean changes and SD of the outcomes to assess treatment response from baseline and mean difference, and 95 % CI were calculated to combined data and assessment effect sizes in astaxanthin and control groups.

Results

14 eligible articles were included in the final quantitative analysis. Current study revealed that astaxanthin consumption was not associated with FBS, HbA1c, TC, LDL-C, TG, BMI, BW, DBP, and SBP. We did observe an overall increase in HDL-C (WMD: 1.473 mg/dl, 95 % CI: 0.319–2.627, p = 0.012). As for the levels of CRP, only when astaxanthin was administered (i) for relatively long periods (≥ 12 weeks) (WMD: -0.528 mg/l, 95 % CI: -0.990 to -0.066), and (ii) at high dose (> 12 mg/day) (WMD: -0.389 mg/dl, 95 % CI: -0.596 to -0.183), the levels of CRP would decrease.

Conclusion

In summary, our systematic review and meta-analysis revealed that astaxanthin consumption was associated with increase in HDL-C and decrease in CRP. Significant associations were not observed for other outcomes.

Lipid profile and glucose changes after supplementation with astaxanthin: a systematic review and meta-analysis of randomized controlled trials, 2010

Introduction

Many studies have shown that oral supplementation with astaxanthin may be a novel potential treatment for inflammation and oxidative stress in cardiovascular diseases, but evidence of the effects on lipid profile and glucose is still inconclusive. Therefore, we performed a meta-analysis to evaluate the efficacy of astaxanthin supplementation on plasma lipid and glucose concentrations.

Material and methods

The search included PubMed, Cochrane Library, Scopus, and EMBASE (up to November 27, 2014) to identify randomized controlled trials (RCTs) investigating the effects of astaxanthin supplementation on lipid profile and glucose levels. Two independent reviewers extracted data on study characteristics, methods and outcomes.

Results

Seven studies meeting inclusion criteria with 280 participants were selected for this meta-analysis; 163 participants were allocated to the astaxanthin supplementation group and 117 to the control group. A random-effect meta-analysis of data from 7 RCTs (10 treatment arms) did not show any significant effect of supplementation with astaxanthin on plasma concentrations of total cholesterol (weighted mean difference (WMD): –1.52 mg/dl, 95% CI: –8.69 to –5.66, p = 0.679), LDL-C (WMD: +1.25 mg/dl, 95% CI: –6.70 to +9.21, p = 0.758), HDL-C (WMD: +1.75 mg/dl, 95% CI: –0.92 to +4.42, p = 0.199), triglycerides (WMD: –4.76 mg/dl, 95% CI: –21.52 to +12.00, p = 0.578), or glucose (WMD: –2.65 mg/dl, 95% CI: –5.84 to +0.54, p = 0.103). All these effect sizes were robust, and omission of any of the included studies did not significantly change the overall estimate.

Conclusions

This meta-analysis of data from 10 RCT arms did not indicate a significant effect of supplementation with astaxanthin on plasma lipid profile, but a slight glucose-lowering effect was observed. Further, well-designed trials are necessary to validate these results.

Astaxanthin supplementation mildly reduced oxidative stress and inflammation biomarkers: a systematic review and meta-analysis of randomized controlled trials, 2022

Previous in vitro and animal studies showed that astaxanthin improved oxidative stress and inflammation biomarkers. We hypothesized the same effects of astaxanthin in humans and conducted a systematic review and meta-analysis of previous randomized controlled trials to test this hypothesis. The literature search was performed on PubMed, Cochrane Library, and Scopus databases from January 1970 to April 2021. Main eligibility criteria include: intervention using astaxanthin for at least 1 week; inclusion of placebo control; and measuring at least 1 of the common oxidative stress and inflammation biomarkers before and after intervention. Twelve randomized controlled trials including 380 participants were included. Compared with placebo, astaxanthin significantly reduced blood malondialdehyde concentration (standardized mean difference [SMD]: -0.95; 95% CI, -1.67 to -0.23; P = .01). The lowering effect of astaxanthin supplementation on malondialdehyde was particularly significant in type 2 diabetes mellitus (T2DM) patients (SMD: -0.64; 95% CI, -1.26 to -0.01; P < .05). A limited number of trials were available for the effects of astaxanthin on other oxidative stress biomarkers. Astaxanthin supplementation appeared to improve superoxide dismutase activity and reduce serum isoprostane concentration in overweight subjects. Astaxanthin significantly reduced blood interleukin-6 concentration in T2DM patients (weighted mean difference: -0.70 pg/mL; 95% CI, -1.29 to -0.11 pg/mL; P = .02). The effects of astaxanthin on blood C-reactive protein and tumor necrosis factor-α concentrations were not significant. The current work indicated that astaxanthin supplementation may be beneficial for improving oxidative stress and certain inflammation biomarkers, particularly in T2DM patients. Future work should investigate the effects of astaxanthin on T2DM.

Multiple Mechanisms of Anti-Cancer Effects Exerted by Astaxanthin, 2015

Astaxanthin (ATX) is a xanthophyll carotenoid which has been approved by the United States Food and Drug Administration (USFDA) as food colorant in animal and fish feed. It is widely found in algae and aquatic animals and has powerful anti-oxidative activity. Previous studies have revealed that ATX, with its anti-oxidative property, is beneficial as a therapeutic agent for various diseases without any side effects or toxicity. In addition, ATX also shows preclinical anti-tumor efficacy both in vivo and in vitro in various cancer models. Several researches have deciphered that ATX exerts its anti-proliferative, anti-apoptosis and anti-invasion influence via different molecules and pathways including signal transducer and activator of transcription 3 (STAT3), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and peroxisome proliferator-activated receptor gamma (PPARγ). Hence, ATX shows great promise as chemotherapeutic agents in cancer. Here, we review the rapidly advancing field of ATX in cancer therapy as well as some molecular targets of ATX. 

Astaxanthin improves glucose metabolism and reduces blood pressure in patients with type 2 diabetes mellitus, 2018

Background and Objectives: This randomized, placebo-controlled trial was performed for 8 weeks to investigate the potential effects of astaxanthin (AST) supplementation on the adiponectin concentration, lipid peroxidation, glycemic control, insulin sensitivity, and anthropometric indices in participants with type 2 diabetes mellitus. 

Methods and Study Design: We enrolled 44 participants with type 2 diabetes who met our inclusion criteria. Eight milligrams of AST supplementation or a placebo were randomly administered once daily for 8 weeks to these participants. 

Results: The 8-week administration of AST supplementation increased the serum adiponectin concentration and reduced visceral body fat mass (p<0.01), serum triglyceride and very-low-density lipoprotein cholesterol concentrations, and systolic blood pressure (p<0.05). Furthermore, AST significantly reduced the fructosamine concentration (p<0.05) and marginally reduced the plasma glucose concentration (p=0.057). 

Conclusions: We demonstrated that because participants with type 2 diabetes often have hypertriglycemia and uncontrolled glucose metabolism; our findings of dual beneficial effects are clinically valuable. Our results may provide a novel complementary treatment with potential impacts on diabetic complications without adverse effects.

ValAsta Sam Shepherd talks about Diabetes, 2021

NIH selects Cardax compound (ZanthoSyn) for important anti-aging research program, 2017

In March of this year, JABSOM and Cardax jointly announced that CDX-085 showed the ability to significantly activate the FOXO3 gene in mice, which plays a proven role in longevity.

"Out of all the compounds they could have chosen, they chose ours," said David G. Watumull, Cardax CEO. "It's an important validation of the work that we've done here in Hawaii."

Effects of 3-Month Astaxanthin Supplementation on Cardiac Function in Heart Failure Patients with Left Ventricular Systolic Dysfunction-A Pilot Study, 2020

Astaxanthin prevents and reverses diet-induced insulin resistance and steatohepatitis in mice: A comparison with vitamin E, 2015

Astaxanthin Inhibits JAK/STAT-3 Signaling to Abrogate Cell Proliferation, Invasion and Angiogenesis in a Hamster Model of Oral Cancer, 2014

Identifying agents that inhibit STAT-3, a cytosolic transcription factor involved in the activation of various genes implicated in tumour progression is a promising strategy for cancer chemoprevention. In the present study, we investigated the effect of dietary astaxanthin on JAK-2/STAT-3 signaling in the 7,12-dimethylbenz[a]anthracene (DMBA)-induced hamster buccal pouch (HBP) carcinogenesis model by examining the mRNA and protein expression of JAK/STAT-3 and its target genes. Quantitative RT-PCR, immunoblotting and immunohistochemical analyses revealed that astaxanthin supplementation inhibits key events in JAK/STAT signaling especially STAT-3 phosphorylation and subsequent nuclear translocation of STAT-3. Furthermore, astaxanthin downregulated the expression of STAT-3 target genes involved in cell proliferation, invasion and angiogenesis, and reduced microvascular density, thereby preventing tumour progression. Molecular docking analysis confirmed inhibitory effects of astaxanthin on STAT signaling and angiogenesis. Cell culture experiments with the endothelial cell line ECV304 substantiated the role of astaxanthin in suppressing angiogenesis. Taken together, our data provide substantial evidence that dietary astaxanthin prevents the development and progression of HBP carcinomas through the inhibition of JAK-2/STAT-3 signaling and its downstream events. Thus, astaxanthin that functions as a potent inhibitor of tumour development and progression by targeting JAK/STAT signaling may be an ideal candidate for cancer chemoprevention.

Effects of astaxanthin supplementation in healthy and obese dogs (link)

Results: In the healthy dog groups, after 6 weeks, plasma triglyceride (TG) and malondialdehyde concentrations and lactate dehydrogenase (LDH) values significantly decreased in the test group. There was no significant difference in the control group. In clinically obese dogs, plasma TG concentration decreased after 8 weeks of ASX supplementation. Plasma alanine aminotransferase and LDH values clearly decreased in all 5 dogs and 4 dogs out of 5 dogs, respectively.

Conclusion: ASX supplementation (0.3 mg/kg body weight/day) for 6 weeks in healthy dogs and 8 weeks in obese dogs induced the elevation of antioxidant function and of liver function by ameliorating lipid metabolism.