Astaxanthin is used for age-related macular degeneration (AMD), Alzheimer's and Parkinson's diseases, stroke, cancer, and hypercholesterolemia.
Astaxanthin is a reddish carotenoid pigment found in the microalgae Haematococcus pluvialis. It is a powerful antioxidant that is structurally similar to beta-carotene.
Astaxanthin contains the highest relative antioxidant activity when compared with alpha-tocopherol, alpha-carotene, beta-carotene, lutein, and lycopene.
Data suggests astaxanthin may decrease environmentally- chemically-caused oxidative liver damage. It also seems to decrease oxidative consumption of glutathione (GSH) and increase hepatoprotective (liver) antioxidant activity. There is also preliminary data that suggests that astaxanthin might have gastroprotective effects against Helicobacter pylori, possibly by inhibiting inflammation and acting as an antioxidant.
Evidence also suggests that astaxanthin might stimulate immunity. Additional research suggests astaxanthin might protect against mammary cancer, liver cancer, bladder cancer, and oral cancer. It seems to suppress the growth of tumor cells by increasing concentrations of gamma-interferon and increasing the activity of cytotoxic T lymphocytes. It appears that astaxanthin needs to be part of the diet prior to tumor development to inhibit tumor growth, hence protective, not curative.
Published Clinical Studies
Astaxanthin: a novel potential treatment for oxidative stress and inflammation in cardiovascular disease. Pashkow FJ, Watumull DG, Campbell CL.
John A. Burns School of Medicine, University of Hawaii, Honolulu, Hawaii, USA.
Oxidative stress and inflammation are implicated in several different manifestations of cardiovascular disease (CVD). They are generated, in part, from the overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) that activate transcriptional messengers, such as nuclear factor-kappaB, tangibly contributing to endothelial dysfunction, the initiation and progression of atherosclerosis, irreversible damage after ischemic reperfusion, and even arrhythmia, such as atrial fibrillation. Despite this connection between oxidative stress and CVD, there are currently no recognized therapeutic interventions to address this important unmet need. Antioxidants that provide a broad, "upstream" approach via ROS/RNS quenching or free radical chain breaking seem an appropriate therapeutic option based on epidemiologic, dietary, and in vivo animal model data. However, human clinical trials with several different well-known agents, such as vitamin E and beta-carotene, have been disappointing. Does this mean antioxidants as a class are ineffective, or rather that the "right" compound(s) have yet to be found, their mechanisms of action understood, and their appropriate targeting and dosages determined? A large class of potent naturally-occurring antioxidants exploited by nature-the oxygenated carotenoids (xanthophylls)-have demonstrated utility in their natural form but have eluded development as successful targeted therapeutic agents up to the present time. This article characterizes the mechanism by which this novel group of antioxidants function and reviews their preclinical development. Results from multiple species support the antioxidant/anti-inflammatory properties of the prototype compound, astaxanthin, establishing it as an appropriate candidate for development as a therapeutic agent for cardiovascular oxidative stress and inflammation.
Astaxanthin inhibits cytotoxic and genotoxic effects of cyclophosphamide in mice germ cells.
Tripathi DN, Jena GB.
Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Sector-67, SAS. Nagar, Punjab 160062, India.
Cyclophosphamide (CP), an alkylating agent used in the treatment of several cancers as well as an immunosuppressant in rheumatoid arthritis. It is used against several cancers due to its broad spectrum efficacy, but at the same time possesses unwanted risks for occupational exposure as well as therapy related toxicities to patients. The present study was aimed to investigate the protective effect of astaxanthin (AST) a red carotenoid pigment on CP induced germ cell toxicity in male mice. CP was administered intraperitoneally (i.p.) at the dose of 50, 100 and 200mg/kg body weight to mice (20-25 g) once in a week for a period of five weeks. AST was given at the dose of 25mg/kg per oral (p.o.) for five consecutive days in a week for five weeks. The animals were sacrificed one week after the last injection of CP. The protective effect of AST against CP induced male germ cell toxicity was evaluated using body weight, testes and epididymis weight, sperm count, sperm head morphology, sperm comet assay, histology of testes and TUNEL assay. AST treatment significantly improved the testes weight, sperm count and sperm head morphology as compared to only CP treated animals. The result of comet assay showed that AST treatment significantly restored the sperm DNA damage induced by CP. Further, AST treatment showed protection against CP induced testicular toxicity as evident from testes histology and TUNEL assay. The present results indicate the chemoprotective potential of AST against CP induced germ cell toxicity in mice.
Efficacy of the natural antioxidant astaxanthin in the treatment of functional dyspepsia in patients with or without Helicobacter pylori infection: A prospective, randomized, double blind, and placebo-controlled study.
Kupcinskas L, Lafolie P, Lignell A, Kiudelis G, Jonaitis L, Adamonis K, Andersen LP, Wadström T.
Kaunas University of Medicine, 50009 Kaunas, Lithuania.
OBJECTIVES: The aim of this study was to evaluate the efficacy of the natural antioxidant astaxanthin in functional dyspepsia in different doses and compared with placebo. DESIGN: The study was a controlled, prospective, randomized, and double blind trial. PARTICIPANTS: Patients with functional dyspepsia, divided into three groups with 44 individuals in each group (placebo, 16mg, or 40mg astaxanthin, respectively). INTERVENTIONS: Participants were asked to accept gastroscopy before treatment, together with questionnaires: GSRS and SF-36. Urea breath test (UBT) was done before the treatment. MAIN OUTCOME: The primary objective was to test the hypothesis that the antioxidant astaxanthin at two doses regimens compared to placebo should ameliorate gastrointestinal discomfort measured as GSRS in patients with functional dyspepsia, who were either positive or negative for Helicobacter pylori, after 4 weeks of treatment. RESULTS: At the end of therapy (week 4) no difference between the three treatment groups was observed regarding mean Gastrointestinal Symptom Rating Scale (GSRS) scores of abdominal pain, indigestion and reflux syndromes. The same results were observed at the end of follow-up. However reduction of reflux syndrome before treatment to week 4 was significantly pronounced in the higher (40mg) dose compared to the other treatment groups (16mg and placebo, p=0.04). CONCLUSION: In general, no curative effect of astaxanthin was found in functional dyspepsia patients. Significantly greater reduction of reflux symptoms were detected in patients treated with the highest dose of the natural antioxidant astaxanthin. The response was more pronounced in H. pylori-infected patients.