- Sulfated alpha-L-fucan
- Mekabu fucoidan
For Patients & Caregivers
Fucoidan has anticancer properties, but this has not yet been studied in humans.
Fucoidan is a complex polysaccharide found in many species of brown seaweed. It has been shown to slow blood clotting. Laboratory studies suggest that it can prevent the growth of cancer cells and has antiviral, neuroprotective, and immune-modulating effects. Studies in humans have not yet been conducted to determine whether these same anticancer effects may occur. One human study suggests fucoidan may help to enable longer courses of chemotherapy, but more studies are needed to confirm safety and effectiveness. Because of its anti-clotting property, fucoidan may increase the side effects of “blood-thinning” drugs.
To boost the immune system
In vitro data suggest a role for fucoidan in boosting host defense mechanisms. Several human studies also suggest it may help stimulate immune functioning and boost antibody production after vaccination.
To reduce inflammation
Several in vitro and animal studies suggest that fucoidan has anti-inflammatory properties. Human studies are needed.
To prevent cancer
Several in vitro and animal studies show that fucoidan has antitumor properties. Clinical trials have not been conducted.
To lower blood pressure
A study in overweight and obese adults suggests that fucoidan use over a sustained period may decrease diastolic blood pressure and as well as “bad” cholesterol levels. Studies to confirm these results are needed.
To prevent blood clots
Laboratory studies suggest that fucoidan has anticoagulant and antithrombotic effects. A study in humans also suggests it slows the production of blood clots. As such, fucoidan may interfere with blood-thinning medication.
To prevent infections
Laboratory and animal studies indicate that fucoidan has antiviral properties.
For Healthcare Professionals
Fucoidan is a sulfated polysaccharide found in the cell walls of many species of brown seaweed. In vitro studies show that fucoidan has antitumor, antiangiogenic (2) (3) (4) (5) (6) (7), antiviral (15) (16), anti-arthritic (18), and immunomodulatory (17) effects. Fucoidan also exhibited neuroprotective (11) (12), radioprotective (13), and antiulcer (14) properties.
In animal models, fucoidan exerts anti-inflammatory effects to protect against various organ injuries (19) (20) (21). Oral administration of fucoidan extracts also improved inflammatory pathology associated with acute colitis (22). Although a high molecular weight fucoidan did not improve outcomes in mice following intracerebral hemorrhage, it is suggested that low-molecular-weight fucoidans have increased therapeutic potential and should be evaluated for this purpose (23).
In humans, dietary fucoidan modulates platelet aggregation via anti-thrombotic effects (24). In overweight or obese adults, fucoidan administration over 3 months decreased diastolic blood pressure and low-density lipoprotein cholesterol concentrations, and increased insulin secretion (25). Fucoidan administration also decreased pro-viral load in a small group of patients with human T-lymphotropic virus type-1-associated neurological disease (26). The consumption of fucoisan for a 1-month period prior to seasonal influenza vaccination may boost antibody production after vaccination in immune-compromised elderly (27).
Preclinical data suggest that fucoidan can help relieve cyclophosphamide-induced intestinal mucosal injury by altering gut flora, resulting in reduced inflammation and increased expression of tight junction proteins (30). Oral ingestion of fucoidan in a small group of volunteers was found to improve mobilization of hematopoietic progenitor stem cells with high levels of CXCR4 expression (28). In advanced stage colorectal cancer patients receiving chemotherapy, fucoidan coadministration enabled patients to continue chemotherapy and regulated fatigue (29); fucoidan also reduced the levels of pro-inflammatory cytokines in another study of advanced cancer patients (31).
In vitro, a low-molecular-weight fucoidan inhibited human rheumatoid arthritis fibroblast synoviocytes and triggered apoptosis via decreased expression and secretion of metalloproteinase (MMP)-1, MMP-3, and MMP-9, as well as suppression of NF-kappaB binding activity, p65 nuclear translocation, and IkappaB-alpha degradation (18). In animal models fucoidan treatment protected against liver injury via suppression of the inflammatory signaling pathway, inflammatory mediators, and inflammatory cell infiltration (20). It also reduced production of cyclooygenase-2 and nitric oxide, while increasing the expression of the hepatoprotective enzyme hemeoxygenase-1 on murine liver and HepG2 cells (21). Fucoidan suppressed inflammation in an ultraviolet B-irradiated mouse model as evidenced by decreased thickness of the prickle cell layer and decreased MMP-1 (19).
In humans, dietary fucoisan shortens lysis time of the thrombus by elevating prostacyclin (PGI2) secretion caused by increased H2O2 production in the blood (24). Various antitumor, antiviral and immune-modulating effects of fucoidan are attributed to the stimulation of natural killer (NK) cells, downregulation of transcription factor AP-I involved in cellular proliferation, and to the downregulation of IGF-IR signaling through the main IRS-1/PI3K/AKT pathway (2) (3) (32). In melanoma cells, fucoidan increased the antitumor effects of lapatinib via inhibition of ERBB3, known to promote melanoma metastasis (33). It was also shown to reduce tumor-promoting M2 macrophages and in combination with etoposide, to prevent HCT116 tumorigenicity in human colorectal cells (34). Neuroprotective effects are attributed to suppression of tumor necrosis factor-alpha (TNF-alpha)- and interferon-gamma (IFN-gamma)-induced nitric oxide production in C6 glioma cells (11) and to its antioxidative effects (12). Fucoidan inhibits metastasis by preventing adhesion of tumor cells to the extracellular matrix. This is achieved by blocking the fibronectin cell-binding domain, necessary for formation of adhesion complexes (4). It also induced apoptosis of human T-cell leukemia virus type I (HTLV-1) that causes adult T-cell leukemia by inactivating NF-kB, which regulates antiapoptotic proteins (3). In a murine model, fucoidan suppressed angiogenesis induced by sarcoma 180 cells (5).