- Sulfated alpha-L-fucan
- Mekabu fucoidan
For Patients & Caregivers
How It Works
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
Several human studies suggest it may stimulate immune functioning and boost antibody production after vaccination.
To reduce inflammation
Lab studies suggest that fucoidan has anti-inflammatory properties. Human studies are needed.
To prevent cancer
Lab 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 used over a sustained period may decrease blood pressure and “bad” cholesterol levels. Confirming studies are needed.
To prevent blood clots
A study in humans suggests it slows the production of blood clots. It may also increase bleeding risk with blood-thinning medications.
Do Not Take If
For Healthcare Professionals
Fucoidan is a sulfated polysaccharide found in the cell walls of many species of brown seaweed. In vitro studies show that it has antitumor, antiangiogenic (2) (3) (4) (5) (6) (7), antiviral (15) (16), antiarthritic (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) and improved inflammatory pathology of 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 over 3 months decreased diastolic blood pressure and LDL cholesterol, and increased insulin secretion (25). Fucoidan also decreased pro-viral load in a small group of patients with human T-lymphotropic virus type-1-associated neurological disease (26). Fucoisan consumption for one month prior to influenza vaccination may boost post-vaccination antibody production 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 (30). Oral fucoidan in a small group of volunteers improved mobilization of hematopoietic progenitor stem cells with high levels of CXCR4 expression (28). In advanced cancer patients, fucoidan coadministration enabled patients to continue chemotherapy, regulated fatigue (29), and reduced levels of pro-inflammatory cytokines (31).
Because fucoidan demonstrates anticoagulant (8) (9) and antithrombotic (10) activities, it may have additive effects when taken with anticoagulants. In a small study of breast cancer patients, co-administration of fucoidan with either of two hormonal therapies, letrozole or tamoxifen, was well tolerated and did not result in any clinically significant interactions (35).
Mechanism of Action
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 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 NO, while increasing expression of the hepatoprotective enzyme hemeoxygenase-1 on murine liver and HepG2 cells (21). Fucoidan suppressed inflammation in an ultraviolet B-irradiated mouse model, decreasing thickness of the prickle cell layer and MMP-1 (19).
In humans, dietary fucoisan shortens lysis time of the thrombus by elevating prostacyclin secretion caused by increased H2O2 production in the blood (24). Various antitumor, antiviral and immune-modulating effects are attributed to NK cell stimulation, and downregulation of transcription factor AP-I, and IGF-IR signaling (2) (3) (32). In melanoma cells, it increased lapatinib effects via ERBB3 inhibition (33). In human colorectal cells, it reduced tumor-promoting M2 macrophages and in combination with etoposide, prevented HCT116 tumorigenicity (34). Neuroprotective effects are attributed to suppression of TNF-alpha- and IFNγ-induced NO production in C6 glioma cells (11) and to antioxidative effects (12). Fucoidan inhibits metastasis by preventing adhesion of tumor cells to the extracellular matrix (4). It induced apoptosis of human T-cell leukemia virus type I 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).