Fucoxanthin, a bioactive carotenoid pigment, C40H60O6, present in edible brown seaweeds, such as Undaria
pinnatifida (Wakame), Hijikia fusiformis (Hijiki), Laminaria japonica (Ma-Kombu) and Sargassum fulvellum.. Fucoxanthin
has a unique structure including an unusual allenic bond and 5, 6-monoepoxide in its molecule.  The increasing
popularity of fucoxanthin is certainly due to its anti-obesity effect, primarily detected by murine studies. These works
revealed fucoxanthin mediated induction of uncoupling protein-1 (UCP-1) in abdominal white adipose tissue (WAT)
mitochondria, leading to the oxidation of fatty acids and heat production in WAT. Beyond this important role, in recent
studies fucoxanthin has shown a great antioxidant activity, anti-cancer, anti-diabetic and anti-photoaging properties.
The aim of this review is to highlight the main effects, possible health benefits of fucoxanthin on human health. 
NOTE: Thermogenin (uncoupling protein 1, or UCP1) is an uncoupling protein found in the mitochondria of brown
adipose tissue (BAT). It is used to generate heat by non-shivering thermogenesis.
Health Benefits - Scientific Evidence
Body Weight Management
Researchers found that abdominal white adipose tissue (WAT) weights of rats and mice fed with fucoxanthin were
significantly lower than those fed a control diet. The daily intake of fucoxanthin in mice caused a significant reductions
in body weight. Fucoxanthin intake leads to oxidation of fatty acids and heat production in WAT mitochondria. Substrate
oxidation can directly reduce WAT in animals.  Thus, fucoxanthin may benefit people at risk of overweight.
Fucoxanthin may benefit people at risk of certain cancers. In studies, fucoxanthin and its metabolite fucoxanthinol
inhibited the cell viability of osteosarcoma cell lines. Researchers have tried to find out the mechanism. Fucoxanthinol
induced G1 cell cycle arrest. The G1 phase is the first of four phases of the cell cycle that takes place in eukaryotic cell
division. The arrest is via the reduction of the expression of cyclin-dependent kinase 4, cyclin-dependent kinase 6 and
cyclin E. Cyclin-dependent kinases (CDKs) are protein kinases regulating the cell cycle. Apoptosis is also involved.
Apoptosis is the process of programmed cell death involving blebbing, cell shrinkage, nuclear fragmentation, chromatin
condensation, and chromosomal DNA fragmentation. Fucoxanthinol also inhibited the cell migration and invasion of
osteosarcoma cells.  Again in another study, Fucoxanthin reduced the proliferation of melanoma cell lines B16F10
cells in a dose-dependent manner accompanied by the induction of cell cycle arrest during the G(0)/G(1) phase and
apoptosis.  In another study, both fucoxanthin and fucoxanthinol reduced the viability of malignant B cells, such as
Burkitt's lymphoma, Hodgkin's lymphoma and Epstein-Barr virus-immortalized B cells, in a dose-dependent manner
accompanied by the induction of cell cycle arrest during G1 phase and caspase-dependent apoptosis. Fucoxanthinol
was approximately twice more potent than fucoxanthin in these activities. 
Cisplain, a platinum-containing anticancer drug, has been shown to enhance DNA repair and to inhibit cell apoptosis,
leading to drug resistance. However, fucoxanthin pretreatment significantly attenuated cisplatin-induced excision repair
cross complementation 1 and thymidine phosphorylase mRNA expression, leading to improvement of chemotherapeutic
efficacy of cisplatin.  Excision repair cross complementation group 1 (ERCC-1) is a DNA repair gene that is essential
for life, and it appears to be a marker gene for nucleotide excision repair activity. Overexpression of ERCC-1 during
cisplatin-based chemotherapy is associated with clinical and cellular drug resistance. While, thymidine phosphorylase is
often induced in the tumour microenvironment by physiological and chemical stress. Its induction protects cells from
apoptosis and helps cell survival by stimulating nucleoside metabolism and angiogenesis. Thus, fucoxanthin may
benefit people on chemotherapy, but more studies are needed to confirm the argument.
In a study, rats were fed with normal fat diet (NF, 7% fat) group, high fat diet group (HF, 20% fat), and "high fat with
0.2% fucoxanthin diet group" for 4 weeks. Fucoxanthin supplements significantly increased plasma high density
lipoprotein (HDL) concentration. The hepatic total lipids, total cholesterols, and triglycerides were significantly
decreased while the fecal excretions of total lipids, cholesterol, and triglycerides were significantly increased in "high fat
with 0.2% fucoxanthin diet group". The researchers further found that the mRNA expression of hepatic acetyl-CoA
carboxylase (ACC) and fatty acid synthase (FAS) were significantly lower in the "high fat with 0.2% fucoxanthin diet
group" compared to the HF group. The function of the ACC is fatty acid synthesis, while fatty acid synthase catalyzes
the fatty acid synthesis. The hepatic mRNA expression of hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) and Acyl-
CoA cholesterol acyltransferase (ACAT) were also significantly low in the high fat with 0.2% fucoxanthin diet group. 
In another study, diabetic/obese KK-A(y) mice were fed a diet containing 0.2% fucoxanthin for 4 weeks. Dietary
fucoxanthin significantly increased serum HDL and non-HDL cholesterol levels, and reduced hepatic cholesterol
content.  Thus, it is reasonable to believe that supplementation of fucoxanthin may benefit people at risk of high
Fucoxanthin intake also significantly reduced blood glucose and plasma insulin. Furthermore, intake of fucoxanthin
significantly increased the level of hepatic docosahexaenoic acid (DHA), DHA is an important n-3 functional
polyunsaturated fatty acid in biological systems.  Thus, fucoxanthin may benefit people at risk of overweight.
Fucoxanthin related compounds isolated from Sargassum siliquastrum were found to have anti-inflammatory properties,
possibly related to inhibition of iNOS/NO pathway which associated with the attenuation of TNF-α and IL-6 formation. 
Thus, fucoxanthin may benefit people at risk of certain kinds of inflammatory-related conditions.
An in vitro study demonstrated an attenuation of CCl(4)-induced hepatotoxicity with fucoxanthin. This effect was dose-
dependent; 25 µM was more effective than 10 µM of fucoxanthin for attenuating the hepatotoxicity. Acute CCl(4)-
hepatotoxicity in rats, with numerous cells positive for the terminal deoxynucleotidyl - transferase (TdT) -mediated
deoxyuridine triphosphate-digoxigenin (dUTP) nick-end labeling (TUNEL) stain were seen in the pericentral area of the
hepatic lobule. TUNEL (Terminal deoxynucleotide transferase dUTP Nick End Labeling) is an assay for labeling DNA
breaks to detect apoptotic cells. Oral pretreatment of CCl(4)- injected rats with fucoxanthin significantly reduced
hepatocyte apoptosis.  Thus, fucoxanthin may benefit people at risk of liver injury.
Definitely, fucoxanthin may have many benefits. But, almost of the studies were conducted either in vitro or in animals, it
is not clear if the same effects can be repeated in human body.
Brown Seaweed - Health Benefits and Side Effects
Bladderwrack - Side Effects, Health Benefits and Weight Loss
Uses, Benefits of Kelp, side effects
Chlorella Benefits, Side Effects and Dosage
Seaweed Health Benefits - Reviews
 Maeda H et al, Seaweed carotenoid, fucoxanthin, as a multi-functional nutrient. Asia Pac J Clin Nutr. 2008;17 Suppl
1:196-9  Ha AW, Kim WK. The effect of fucoxanthin rich power on the lipid metabolism in rats with a high fat diet. Nutr
Res Pract. 2013 Aug;7(4):287-93.  Rokkaku T et al, Anticancer effects of marine carotenoids, fucoxanthin and its
deacetylated product, fucoxanthinol, on osteosarcoma. Int J Oncol. 2013 Oct;43(4):1176-86.  Kaneko M et al, The
anti-apoptotic effect of fucoxanthin on carbon tetrachloride-induced hepatotoxicity. J Toxicol Sci. 2013 Feb;38(1):115-
26.  Liu CL et al, Fucoxanthin enhances cisplatin-induced cytotoxicity via NFκB-mediated pathway and
downregulates DNA repair gene expression in human hepatoma HepG2 cells. Mar Drugs. 2013 Jan 8;11(1):50-66. 
Kim KN et al, Inhibition of tumor growth in vitro and in vivo by fucoxanthin against melanoma B16F10 cells. Environ
Toxicol Pharmacol. 2013 Jan;35(1):39-46.  Beppu F et al, Effects of dietary fucoxanthin on cholesterol metabolism in
diabetic/obese KK-A(y) mice. Lipids Health Dis. 2012 Sep 10;11:112  Tafuku S et al, Anti-neoplastic effects of
fucoxanthin and its deacetylated product, fucoxanthinol, on Burkitt's and Hodgkin's lymphoma cells. Oncol Rep. 2012
Oct;28(4):1512-8.  Heo SJ et al, Anti-inflammatory effect of fucoxanthin derivatives isolated from Sargassum
siliquastrum in lipopolysaccharide-stimulated RAW 264.7 macrophage. Food Chem Toxicol. 2012 Sep;50(9):3336-42.
 D'Orazio N, et al, Fucoxantin: a treasure from the sea. Mar Drugs. 2012 Mar;10(3):604-16
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