CCRES FUCUS

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Fucus vesiculosus, may be an effective alternative treatment for hypothyroidism for some people as it contains iodine found naturally in the sea. Hypothyroidism, also called underactive thyroid, is a condition where the thyroid gland fails to produce enough thyroid hormone. This results in one’s metabolism falling outside of the desired range. There are a wide range of thyroid medications available, both natural and pharmaceutical. As with all medicines, Fucus can occasionally cause side effects, so always consult your healthcare practitioner before starting treatment.

#Hypothyroidism

Hashimoto’s thyroiditis is the most common form of hypothyroidism. It is considered to be an autoimmune disease as the body mistakes the thyroid gland for a foreign body and sends antibodies to attack it which eventually destroy it over time. This leaves the body without essential thyroid hormones that are required for controlling body temperature, appetite and rate of metabolism. If left untreated, hypothyroidism can lead to serious health disorders that could prove fatal.

Symptoms

Symptoms of an underactive thyroid include tiredness, reduced heart rate and pulse, weight gain, dry skin and hair, hair loss, sensitivity to cold, confusion, anxiety, depression, joint pain, headaches, numbness in the extremities and menstrual problems. However, as these symptoms can be attributed to any number of health problems they are often overlooked. If you are experiencing a combination of the aforementioned symptoms without any obvious cause, contact your doctor immediately for a check-up.

#Iodine

According to the University of Maryland Medical Center, those who experience hypothyroidism due to a iodine deficiency may be able to treat their condition with kelp. Iodine, found naturally in kelp, is required to enable the thyroid gland to function correctly. The majority of people in the western world use iodized salt and therefore do not need to supplement with iodine unless they suffer from hypothyroidism.

#Fucus

Fucus is rich in iodine and is available in many different forms including tinctures and standardized extracts. According to the NYU Langone Medical Center, fucus is often referred to as kelp as it is present in a large number of kelp tablets. However, kelp is not considered to be the same as fucus as it is actually a different form of seaweed. The University of Maryland Medical Center recommends a dose of 600mg fucus one to three times per day to stimulate thyroid activity. It is not recommended to self-treat hypothyroidism with fucus.

#CCRES #ALGAE TEAM

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2015年の総市場規模は16億ドルを超える見通し

CCRES ALGAE TEAM
㈱グローバル インフォメーションは、米国の市場調査会社SBI Energy (aka Specialist In Business Information)が発行した報告書「藻類バイオ燃料技術:世界市場および製品動向(2010年~2015年)」の販売を開始しました。

2005年から2007年までの藻類バイオ燃料産業への企業の参入は、原油の高値および環境上の懸念から拍車がかかり、550%と記録的に跳ね上がりました。しかしそれ以来、原油価格は下落し、先頃の金融危機が多くの産業の障害となっています。同レポートによれば、「藻類バイオ燃料への関心は現在も維持されています。しかし同時に、産業は期待の先走りに苦しめられてもいます。」と報告されています。藻類によるバイオ燃料製造技術の現在の市場は、相当量の開発活動と規模を縮小した試験で構成されています。今後はデモンストレーションと商業利用が進められ、藻類によるバイオ燃料製造の各種新技術が2015年には総市場の3分の1を占めるに至るでしょう。

なぜ 藻類なのか?

藻類は原料油としての使用が可能です。つまり、藻類はバイオディーゼル、再生可能ディーゼル、再生可能ジェット燃料、藻油、航空用バイオ燃料、バイオガソリン、エタノール、バイオメタン、ブタノール、水素など、実に多くのバイオ燃料の製造用に加工が可能ということであり、これはすばらしいメリットです。また、藻類によるバイオ燃料製造は、ケイソウ類・ラン藻類・緑ソウ類の遺伝子組み換え、養殖用オープンポンドまたは光バイオリアクター、燃料処理用リファイナリー・ダイジェスター・ファーメンター、抽出用プレスおよび遠心分離機といった幅広い技術を必要とします。

藻類バイオ燃料の製造技術市場の今後の展望とは?

藻類バイオ燃料の製造技術市場は、養殖技術の売上が大半を占めると予測されています。残りの市場は採取、抽出、燃料製造設備の区分が占める見通しですが、これらは2015年には、合計で16億ドルを超える市場規模に成長すると予測されています。同レポートによれば、「2010年には推計2億7,100万ドルとされる同市場のこの成長は飛躍的なもので、約43%との年間成長率の予測もあわせ、この数値は同産業が急速に変化を遂げ、進化する産業であることを明確に示すものです」と報告されています。

市場調査レポート: 藻類バイオ燃料技術:世界市場および製品動向(2010年~2015年)Algae Biofuels Technologies – Global Market and Product Trends 2010-2015

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Merry Christmas

Merry Christmas

As 2014 comes to a close, I’d like to take this opportunity to thank you for supporting our work. It’s because of people like you that countless individuals around the world are now living better life stories. With your support, we’re able to take meaningful and measurable action in a number of ways.
Thank you again for helping to empower individuals and strengthen green communities in Croatia, and around the world. Together, we’re building the kind of world we want all our children and grandchildren to live in.
From everyone at the Croatian Center of Renewable Energy Sources (#CCRES) – Merry Christmas, and have a happy holiday season.

Sincerely,  Željko Serdar

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Palmaria Palmata Fights Ebola

 
 

P A L M A R I A   P A L M A T A

is a cold water algae species that is found in the middle to lower shore in many parts of Europe and the North Atlantic Coasts of America. It can grow in depths of up to 20m on both exposed and sheltered shores. It is found growing on rocks and on the stipes of L. hyperborea and Fucus serratus as an epiphyte.

Palmaria palmata can be eaten raw, roasted, fried, dried, or roasted, or as a thickening agent for soups.

 
CONSTITUENT
Alpha-carotene, beta-carotene, calcium, chromium, cobalt, iodine, iron, lutein, manganese, magnesium, niacin, phosphorous, potassium, riboflavin, selenium, silicon, sodium, tin, vitamin C, zeaxanthin, and zinc.

PARTS USES
The entire plant, dried and cut.

TYPICAL PREPARATIONS
Added to food in the form of dried flakes or powder for a slightly salty flavor, can be drunk as a tea. Also suitable as an extract or capsule.

SUMMARY
Palmaria palmata is an excellent source of phytochemicals and minerals, and a superior source of iodine.
 
PRECAUTIONS
Don’t overdue, and avoid it entirely if you suffer hyperthyroidism. You only need a few flakes, or as little as a quarter-teaspoon a day, to get your mineral needs, and it is best to get your minerals from a variety of whole food and whole herb sources. Don’t use on a daily basis for more than 2 weeks at a time, taking a 2 week break before using again. This will prevent you from overdosing iodine with potential imbalance in thyroid function. For periodic use only and not to be taken for extended periods of time. Not to be used while pregnant.
For educational purposes only.
CCRES ALGAE TEAM 
part of 
Croatian Center of Renewable Energy Sources



This information has not been evaluated by the Food and Drug Administration.
This information is not intended to diagnose, treat, cure, or prevent any disease.
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FUCUS ALGA I ŠTITNJAČA

Štitnjača i Fucus alga

 
Štitnjača, žlijezda smještena u području vrata, s prednje strane dušnika, stvara hormone koji u svom sastavu imaju jod, a uvelike kontroliraju metabolizam našeg organizma. 

Jednostavnije rečeno, hormoni štitnjače kontroliraju brzinu kojom će se zbivati izmjena tvari u našem organizmu, koliko brzo će se tvari uz prisustvo kisika razgraditi, a novonastale strukture ugraditi u stanicu. Jod je neophodan element za normalan rad ove male žlijezde, te svaki nedostatak joda u organizmu vrlo brzo dovodi do nastanka jedne od najraširenijih bolesti „nutritivnog karaktera” – uvećanja štitnjače ili takozvane „guše”.
Treba istaći da je u razvijenim zemljama nedostatak joda u prehrani relativno rijetka pojava, te je najčešće povezan s malom koncentracijom joda u vodi za piće i zemlji na kojoj se voće i povrće uzgaja. Ako se zna da je područje na kojem pojedinac živi siromašno jodom zbog raznih okolišnih čimbenika, onda se tim osobama mora sugerirati uzimanje većih količina joda putem hrane.
Namirnice koje su najbogatije jodom jesu: alge, najviše od svih Fucus, morske ribe, jaja, jogurt, sir, jodirana sol. Pojedine namirnice na neki način brane organizmu pravilno iskorištavanje joda i mogu umanjiti sposobnost organizma da iskoristi jod za sintezu hormona štitnjače. Dobro je znati da u te namirnice ubrajamo: karfiol, kelj, prokulice, repu i kikiriki. Najviše su riziku izloženi strogi vegetarijanci (veganisti) koji takve namirnice svakodnevno koriste u prehrani i to u velikim količinama. U zemljama u razvoju gušavost je vrlo često posljedica jedne autoimune bolesti koja smanjuje funkciju štitnjače, pa nastupa hipotireoza.

HIPOTIREOZA

Hipotireoza, odnosno smanjena funkcija štitnjače, dovodi do usporavanja tjelesnog metabolizma. Bolest se razvija izrazito polako. Uz uvećanje štitnjače i pojave gušavosti (što i nije svaki puta pravilo, jer se štitnjača može povećati i samo s jedne strane), javlja se umor, zaboravljivost, uvećanje tjelesne mase, nepodnošljivost hladnoće, zatvor stolice, suhoća kože i kose. Ako je uzrok autoimune prirode, onda se u organizmu stvaraju protutijela koja napadaju vlastito tkivo štitnjače, a posljedica toga je smanjeni nastanak hormona. Hipotireoza se može javiti u svako životno doba, ali je mnogo raširenija među starijim osobama. Ako se razvije tijekom adolescencije može usporiti rast i razvoj sekundarnih seksualnih osobina, a ako se javi u najranijem djetinjstvu vrlo često i normalni razvoj moždanih funkcija. Stoga se danas redovito nivo hormona štitnjače kontrolira odmah po rođenju djeteta. Slabo aktivna štitnjača kod žena vrlo često dovodi do uvećanja vrijednosti kolesterola u serumu. Terapija se sastoji u davanju sintetskih molekula hormona štitnjače. 

Simptomi hipotireoze proizlaze iz usporenih metaboličkih procesa, smanjene potrošnje kisika, poremećenog metabolizma određenih vitamina, lipida i proteina, a s obzirom da u pravilu nastaju postepeno, često prolaze nezapaženi u ranim fazama bolesti. 

Glavni simptomi su: 
– kroničan umor, malaksalost 
– bolovi u mišićima I zglobovima 
– usporenost, pospanost, otežana koncentracija 
– snižena tjelesna temperature, nepodnošenje hladnoće 
– bezvoljnost, napetost, razdražljivost, promjene raspoloženja 
– opstipacija 
– porast tjelesne težine 
– povišene razine kolesterola, LDL i triglicerida u krvi 
– usporen rad srca, smanjeni minutni volume srca / oslabljena srčana funkcija 
– anemija 
– edemi (oticanje nogu, ruku, lica, jezika, kapaka) 
– smanjeno znojenje 
– suha, ispucala kosa koja pojačano opada 
– suha koža koja se ljuska, sklona crvenilu, svrbežu, aknama i upalama 
– krhki, ispucali nokti 
– promuklost (uslijed otoka glasnica), česte grlobolje 
– nagluhost 
– zamagljen vid 
– poremećaj menstruacijskog ciklusa 
– sterilitet 
– pojava gušavosti 
– miksedemska koma – najteži stupanj bolesti s gubitkom svijesti i hipotermijom 

– usporen / smanjen rast u djece 

 
Hipertireoza
Hipertireoza ili uvećana aktivnost štitnjače dovodi do uvećanog stvaranja aktivnih hormona, te po tome nastupa ubrzanje metabolizma, srce brže kuca, krvni tlak je veći, nastupa gubitak težine, povećanje apetita, znojenje, nepodnošljivost topline, izbočenost očiju. Obično se hipertireoza javlja uslijed prisutnosti protutijela u krvi koja stimuliraju štitne stanice, ali se razlog stvaranja tih protutijela još uvijek ne zna. Hiperaktivnost štitnjače ima i svoj genetski uzrok i mnogo je raširenija bolest u žena u usporedbi s muškom populacijom. Zbog ubrzanog metabolizma osobe koje pate od hipertireoze iskorištavaju prehrambene tvari mnogo brže. Ako gubitak težine počinje predstavljati veliki problem moraju se u prehranu uvesti namirnice bogate bjelančevinama kako bi se nadoknadio gubitak mišićne mase. To su meso, riba, jaja, mlijeko i mliječni proizvodi, ali i dodatne količine vitamina B-skupine su neophodne jer sudjeluju u metabolizmu ugljikohidrata i bjelančevina. U tu svrhu treba konzumirati nemasnu svinjetinu, fermentirane mliječne proizvode ili uzeti nadopune u obliku pivskog kvasca.

Glavni simptomi hipertireoze su: 
– razdražljivost, nemir, nervoza, promjene raspoloženja 
– smanjena sposobnost koncentracije 
– dvoslike, smetnje vida, povlačenje kapaka i izbuljene oči 
– tremor (drhtanje ruku, osjećaj “treperenja” tijela) 
– povišen krvni tlak, tahikardija (ubrzan rad srca) 
– pojačano znojenje, nepodnošenje topline 
– opadanje kose 
– učestale stolice 
– gubitak tjelesne težine 
– poremećaj menstrualnog ciklusa 
– malaksalost 
– nesanica 
– guša (povećana štitnjača), osjećaj “knedle” u grlu, pritisak u vratu
 
Konzumiranje namirnica bogatih jodom je jedan od najboljih načina da imate zdravu štitnjaču. Jod je neophodan za zdravu funkciju štitnjače jer joj pomaže da proizvodi hormon tiroksin. Štitnjača koristi tiroksin da regulira metabolizam. Najbolji prirodni izvor joda je alga fucus

Aloe vera – biljka koju bi svi trebali uzgajati

CROATIAN CENTER of RENEWABLE ENERGY SOURCES:

Aloe Vera se sastoji od vitamina; A, B1, B2, B3, B6, B9, B12, C i E, sadrži i folnu kiselinu i više minerala od kojih najviše ima; magnezija, mangana, cinka, bakra, kroma, kalcija, kalija, željeza i 20 vrsta aminokiselina. Za sada je ustanovljeno da žele Aloe vere ima preko 240 hranjivih i ljekovitih sastojaka.

Originally posted on Matrix World:

Autor: Ljubica Šaran

Matrix World

Aloe veru ne treba posebno predstavljati, čak ni u našoj kulturi koja ne favorizira prirodne lijekove i preparate, svi znaju koliko ekstrakt ovog jednostavnog sukulenta pozitivno utječe na obnavljanje i zaštitu kože, no zapravo to je gotovo sve što javnost zna o biljci koja osim nevjerojatnih nutricionističkih svojstava ima toliko ljekovitog utjecaja na ljude da s pravom zaslužuje prastari naziv „biljka lijek za sve.“

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The Effects of Astaxanthin – Type 2 Diabetes

The Effects of Astaxanthin – Type 2 Diabetes

 

Draining the World Wealth


Diabetes mellitus is a worldwide epidemic that is critically linked to prevalence of obesity. More than 220 million people have diabetes and by the year 2030 the figures are expected to grow to 360 million. The diabetes is aggressively growing in both emerging and developed country. According to WHO, the Asian continent has over 90 million people suffering from diabetes – India (40 million) China (29 million); Indonesia (13 million) and Japan (7 million). The prevalence of diabetic patients remains pervasive in USA (22 million), Brazil (6 million), Pakistan (8 million); Russia (6 million); Italy (5 million) and Turkey (4 million). Even in the African region over 10 million people suffer from diabetes, especially in Nigeria where it is expected to reach 5 million within the year 2030.
Diabetic complications lead to heart disease (approximately 65% of death amongst diabetics), blindness, kidney failure and amputations. As a result, the indirect and direct medical expenditure of diabetics represent almost 5 times that of a non-diabetic.

Type 2 Diabetes: A Preventable Disease

High Blood Sugar 

In most cases, diabetes is treated with medication, although about 20% of diabetics may be managed by lifestyle changes. This means that even if we cannot change the genetic influences, fortunately, for most of us diabetes is preventable; for example, making dietary changes, taking nutritional supplements and exercising. To highlight this, people in high risk groups who achieve a 5-7% cut in body weight will reduce risk of developing diabetes approximately 58% across all age and ethnic groups.
While the debate between the contributory effects of carbohydrate and fat intake continues unabated, research reveals a strong link between foods with high glycemic index and prevalence of type 2 diabetes. Excess blood glucose needs to be converted by insulin (produced by the pancreas ß-cells) into glycogen stores, however, when glycogen stores are full, glucose is converted into fat. Over time, the body’s cells may eventually become desensitized to insulin making it necessary to produce more insulin to achieve the same affect. It is this process that would eventually lead to a state known as hyperinsulinaemic state. As a result, the body looses its ability to control high blood glucose levels (hyperglycemia) that could result in toxic conditions and promote further complications such as kidney failure.

New Evidences Emerging from Human Studies

In an anti-aging study conducted by Iwabayashi et al., (2009), 20 female volunteers with increased oxidative stress burden ingested 12 mg/day of astaxanthin for 8 weeks. Results evidenced a significant decrease of diabetes-related parameters that collectively predict trends in diabetes development. Firstly, astaxanthin reduced cortisol by 23 percent.

Astaxanthin Retards Glucose Toxicity and Kidney Damage

Astaxanthin displayed positive effects in a type 2 diabetic mouse model in that it reduced the disease progression by retarding glucose toxicity and kidney damage. This has profound implications for people who belong to high risk groups, display pre-diabetic conditions (impaired fasting glucose or impaired glucose tolerance) or want to manage advanced diabetic kidney problems (nephropathy).
Studies suggested that reactive oxygen species (ROS) induced by hyperglycemia contributes to the onset of Diabetes mellitus and its complications. Non-enzymatic glycosylation of proteins and mitochondria, prevalent in diabetic conditions, is a major source of ROS. For example, pancreatic ß-cells kept in high glucose concentrations show presence of advanced glycosylation products, a source of ROS, which cause the following: i) reduction of insulin expression and ii) induction of cell death (apoptosis). ß–cells are especially vulnerable to ROS because these cells are inherently low in antioxidant status and therefore, requires long term protection. A recent study demonstrated that antioxidants (N-acetyl-L-cysteine, vitamins C and E) exerted beneficial effects in diabetic conditions such as preservation of ß-cell function, so it is likely that a more potent antioxidant such as astaxanthin can do the same or better.
In another study conducted by Preuss et al. (2009), 12 rats fed with 25mg/kg of astaxanthin show a significant decrease in insulin resistance by 13.5%.

Modulation of Glucose Toxicity

Uchiyama et al., 2002 demonstrated in obese diabetes type 2 mouse model that astaxanthin preserved pancreatic ß -cell dysfunction against oxidative damage. Treated mice received 1 mg astaxanthin/day at 6 weeks of age and then tests performed at 6, 12 and 18 weeks. Observations of astaxanthin treated mice (N=8) included: i) significantly reduced fasting glucose sugar levels at 12.


Figure 1. Astaxanthin improved the glucose levels in the Intraperitoneally Glucose Tolerance Test (IPGT) in diabetic mouse model (Uchiyama et al., 2002) Figure 1. Astaxanthin improved the glucose levels in the Intraperitoneally Glucose Tolerance Test (IPGT) in diabetic mouse model (Uchiyama <em>et al.</em>, 2002)
Figure 2. Astaxanthin preserved insulin sensitivity in the diabetic mouse model (Uchiyama et al., 2002) Figure 2. Astaxanthin preserved insulin sensitivity in the diabetic mouse model (Uchiyama <em>et al.</em>, 2002)
Figure 3. Astaxanthin protected kidney function measured by urinary albumin protein loss (Naito et al., 2004) 
 Figure 3. Astaxanthin protected kidney function measured by urinary albumin protein loss (Naito <em>et al.</em>, 2004)

Prevention of Diabetic Nephropathy

As well as substantiating observations by Uchiyama et al., Naito demonstrated that astaxanthin treated type 2 diabetic mice which normally shows renal insufficiency at 16 weeks of age in fact exhibited 67% less urinary albumin loss.

Figure 4. Astaxanthin reduced the amount of DNA damage indicated by urinary 8-OHdG levels (Naito et al., 2004) 
 Figure 4. Astaxanthin reduced the amount of DNA damage indicated by urinary 8-OHdG levels (Naito <em>et al.</em>, 2004)
Figure 5. Astaxanthin preserved the relative mesangial area.

 Figure 5. Astaxanthin preserved the relative mesangial area. +p<0.05 vs positive control (Naito <em>et al.</em>, 2004)
Earlier it was unclear how astaxanthin could ameliorate the progression of diabetic nephropathy, but new evidence revealed additional information in the mechanism of action. Naito et al., (2006) examined changes in the gene expression profile of glomerular cells in diabetic mouse model during the early phase of diabetic nephropathy. The mitochondrial oxidative phosphorylation pathway was most significantly affected by high-glucose concentration (mediated via reactive oxygen species). Long term treatment with astaxanthin significantly modulated genes associated with oxidative phosphorylation, oxidative stress and the TGF-ß-collagen synthesis system.

Manabe et al., 2007 went further and analyzed normal human mesangial cells (NHMC) exposed to high glucose concentrations. In the presence of astaxanthin, it significantly suppressed ROS production (Figure 6) and inhibited nuclear translocation and activation of NF-ĸB (Figure 7) in the mitochondria of NHMC. Furthermore, this was the first time to detect astaxanthin in the mitochondrial membrane (Table 1) and its presence also suppressed ROS attack on membrane proteins.


Figure 6. Astaxanthin reduced ROS production in NHMC-mitochondria exposed to high glucose (Manabe et al., 2007) 
 Figure 6. Astaxanthin reduced ROS production in NHMC-mitochondria exposed to high glucose (Manabe <em>et al.</em>, 2007)  
 
Top left panel: mitochondria as green fluorescence, Top right panel: ROS as red fluorescence; Bottom right panel: Merged picture as yellow fluorescence.
 
Figure 7. Astaxanthin suppressed high-glucose induced nuclear translocation and activation of NF-ĸB (Manabe et al., 2007) 
 Figure 7. Astaxanthin suppressed high-glucose induced nuclear translocation and activation of NF-ĸB (Manabe <em>et al.</em>, 2007)
Table 1. Astaxanthin content in NHMC mitochondria expressed as percentage of total astaxanthin added. 
 
Mean of 3 samples. (Manabe et al., 2007) Table 1. Astaxanthin content in NHMC mitochondria expressed as percentage of total astaxanthin added. Mean of 3 samples. (Manabe <em>et al.</em>, 2007)

Outlook

Although clinical trials involving antioxidants in humans have only recently begun, these preliminary results concluded that strong antioxidant supplementation may improve type 2 diabetic control and inhibit progressive renal damage by circumventing the effects of glycation-mediated ROS under hyperglycemic conditions. Astaxanthin improved pancreas function, insulin sensitivity, reduced kidney damage and glucose toxicity in diabetic mouse models. New techniques by gene chip analysis and fluorescence imaging revealed further details of mechanism and site of protection by astaxanthin. Further research and clinical studies are still required. However, it is reasonable to suggest that astaxanthin may be useful as part of a nutrigenomic strategy for type 2 diabetes and diabetic nephropathy.

References

  1. Forefront (Summer/Fall) 2005, American Diabetes Association.
  2. Functional Foods & Nutraceuticals June 2004. “The dietary solution to diabetes.”
  3. HSR Health Supplement Retailer July 2004. “Fighting Diabetes the natural way.”
  4. Iwabayashi M, Fujioka N, Nomoto K, Miyazaki R, Takahashi H, Hibino S, Takahashi Y, Nishikawa K, Nishida M, Yonei Y. (2009). Efficacy and safety of eight-week treatment with astaxanthin in individuals screened for increased oxidative stress burden. J. Anti Aging Med., 6 (4):15-21.
  5. Manabe E, Handa O, Naito Y, Mizushima K, Akagiri S, Adachi S, Takagi T, Kokura S, Maoka T, Yoshikawa T. (2008). Astaxanthin protects mesangial cells from hyperglycemia-induced oxidative signaling. J. Cellular Biochem. 103 (6):1925-37.
  6. Naito Y, Uchiyama K, Aoi W, Hasegawa G, Nakamura N, Yoshida N, Maoka T, Takahashi J, Yoshikawa T. (2004) Prevention of diabetic nephropathy by treatment with astaxanthin in diabetic db/db mice. BioFactors 20:49-59. Nutritional Outlook April. “Fighting Diabetes”
  7. Naito Y, Uchiyama K, Mizushima K, Kuroda M, Akagiri S, Takagi T, Handa O, Kokura S, Yoshida N, Ichikawa H, Takahashi J, Yoshikawa T. (2006). Microarray profiling of gene expression patterns in glomerular cells of astaxanthin-treated diabetic mice: a nutrigenomic approach. Int. J. Mol. Med.,18:685-695.
  8. Preuss H, Echard B, Bagchi D, Perricone VN, Yamashita E. (2009). Astaxanthin lowers blood pressure and lessens the activity of the renin-angiotensin system in Zucker Fatty Rats. J. Funct. Foods, I:13-22.
  9. The Global Diabetes Community. http://www.diabetes.co.uk. Article retrieved on June 8th, 2010.
  10. Uchiyama K, Naito Y, Hasegawa G, Nakamura N, Takahashi J, Yoshikawa T. (2002). Astaxanthin Protects β–cells against glucose toxicity in diabetic db/db mice. Redox Rep., 7(5):290-293.


CCRES special thanks to 


  Mr. Mitsunori Nishida, 


 
President of Corporate Fuji Chemical Industry Co., Ltd.

Croatian Center of Renewable Energy Sources (CCRES) 

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The Effects of Astaxanthin – Hypertension

The Effects of Astaxanthin – Hypertension

 

 

Astaxanthin Reduces Hypertension

Astaxanthin Reduces Hypertension 

Epidemiological and clinical data suggest that dietary carotenoids such as astaxanthin may protect against cardiovascular disease (CVD) which includes hypertension. This condition is associated with blood vessel dysfunction, altered contractility and tone; mediated by relaxant (nitric oxide NO; prostacyclin) and constrictor factors (thromboxane; endothelin) in the blood. Furthermore, blood flow properties serve an important role in the pathological complications seen in atherosclerosis and coronary heart disease. Research presented here suggests that astaxanthin may be useful as part of an antioxidant therapy to alleviate hypertension (Figure 1).

Figure 1. Mechanisms by which Astaxanthin reduces hypertension Figure 1. Mechanisms by which Astaxanthin reduces hypertension

Reduction of Arterial Blood Pressure

An early study involving a composition of carotenoids have been used against hypertension or high blood pressure (BP), but Hussein et al., (2005a) published the first study involving astaxanthin with spontaneously hypertensive rats (SHR) and stroke prone (SHR-SP). This study investigated the effects of astaxanthin on the aortic vessel blood pressure (BP) in relation to endothelium and nitric oxide (NO) to elucidate mechanism and response.

Figure 2. Astaxanthin (5mg/kg/day) treated SHR reduced mean blood pressure. Hussein et al., 2005b. Figure 2. Astaxanthin (5mg/kg/day) treated SHR reduced mean blood pressure. Hussein <em>et al.</em>, 2005b.

In a double blind controlled placebo study conducted in Japan, 20 healthy postmenopausal women, who ingested 12 mg everyday for 4 weeks, reduced their systolic and diastolic blood pressure by 7% and 4%
In another study, 15 healthy subjects, between 27-50 of age, who received 9mg/day of astaxanthin for 12 weeks had their diastolic blood pressure decreased by 6% (Matsuyama et al., 2010).
A series of animal studies have largely replicated the effects of astaxanthin found in human studies (Ruiz et al., 2010; Preuss, 2009; Preuss, 2011).

Figure 3. Open Label Clinical Study. 73 subjects between 20-60 years of age received 4mg of astaxanthin x day for 4 weeks (Sato et al 2009) Figure 3. Open Label Clinical Study. 73 subjects between 20-60 years of age received 4mg of astaxanthin x day for 4 weeks (Sato et al 2009)

Mechanism of Anti-hypertension

The antihypertensive mechanism may be in part explained by the changes of vascular reactivity and hemorheology.
Microchannel Array Flow Analysis (MC-FAN) measured a significant increase of blood flow of 11% (Figure 3) in the astaxanthin treated group.

Figure 4. Open Label Clinical Study 35 healthy postmenopausal women (BMI 22.1) were included in the study, treated with astaxanthin daily dose of 12 mg for 8 weeks Figure 4. Open Label Clinical Study 35 healthy postmenopausal women (BMI 22.1) were included in the study, treated with astaxanthin daily dose of 12 mg for 8 weeks

In a human study conducted by Iwabayashi et.al., (2009) , 20 healthy women who ingested 6mg / day for 8 weeks increased ABI (ankle brachial pressure index) by 4% suggesting a reduction of lower limb vascular resistance. Another human study also prove that oral administration of 6 mg/day of astaxanthin for 10 days enhanced capillary blood flow by 10%.

Figure 5. Astaxanthin (6 mg/day) supplementation for 10 days improves blood flow in humans as tested by MC-FAN. Miyawaki et al., 2005. Figure 5. Astaxanthin (6 mg/day) supplementation for 10 days improves blood flow in humans as tested by MC-FAN. Miyawaki <em>et al.</em>, 2005.
Figure 6. Astaxanthin increases relaxant and reduces constrictor mechanisms to help reduce blood pressure in SHR.
  Figure 6. Astaxanthin increases relaxant and reduces constrictor mechanisms to help reduce blood pressure in SHR.

Indeed, Hussein et al., (2006b) demonstrated that 5 mg/day of astaxanthin for 7 weeks decreased vascular wall thickness by 47%.

Figure 7. A) Coronary artery wall is thinner and lumen is wider in astaxanthin treated rats. B) Elastin bands are also fewer in number and less elastic compared to the control groups which also show intense and branched elastine feature (C). Hussein et al., (2006a). Figure 7. A) Coronary artery wall is thinner and lumen is wider in astaxanthin treated rats. B) Elastin bands are also fewer in number and less elastic compared to the control groups which also show intense and branched elastine feature (C). Hussein <em>et al.</em>, (2006a).

Outlook

The oxidative status and physiological condition during hypertension are successfully mediated by astaxanthin. The mechanisms of action include improved blood rheology, modulation of constrictor and dilator factors and blood vessel remodelling. Although, these findings are based on spontaneous hypertensive rat models, these serve as a solid basis for extending the hypothesis to human clinical trials.

References

  1. Hussein G, Nakamura M, Zhao Q, Iguchi T, Goto H, Sankawa U, Watanabe H. (2005)a. Antihypertensive and neuroprotective effects of astaxanthin in experimental animals. Biol. Pharm. Bull., 28(1):47-52.
  2. Hussein G, Goto H, Oda S, Iguchi T, Sankawa U, Matsumoto K, Watanabe H. (2005)b. Antihypertensive potential and mechanism of action of astaxanthin II. Vascular reactivity and hemorheology in spontaneously hypertensive rats. Biol. Pharm. Bull., 28(6):967-971.
  3. Hussein G, Goto H, Oda S, Sankawa U, Matsumoto K, Watanabe H. (2006)a. Antihypertensive potential and mechanism of action of astaxanthin: III. Antioxidant and histopathological effects in spontaneously hypertensive rats. Biol. Pharm. Bull. 29(4):684-688.
  4. Hussein G, Sankawa U, Goto H, Matsumoto K, Watanabe H. (2006)b. Astaxanthin, a Carotenoid with Potential in Human Health and Nutrition. J. Nat. Prod., 69(3):443 – 449.
  5. Iwabayashi M, Fujioka N, Nomoto K, Miyazaki R, Takahashi H, Hibino S, Takahashi Y, Nishikawa K, Nishida M, Yonei Y. (2009). Efficacy and safety of eight-week treatment with astaxanthin in individuals screened for increased oxidative stress burden. J. Anti Aging Med., 6 (4):15-21.
  6. Kudo Y, Nakajima R, Matsumoto N. (2002). Effects of astaxanthin on brain damages due to ischemia. Carotenoid Science (5):25.
  7. Li W, Hellsten A, Jacobsson LS, Blomqvist HM, Olsson AG, Yuan XM. (2004). Alpha-tocopherol and astaxanthin decrease macrophage infiltration, apoptosis and vulnerability in atheroma of hyperlipidaemic rabbits. J. Mol. Cell. Cardio., 37(5):969-978.
  8. Miyawaki H, Takahashi J, Tsukahara H, Takehara I. (2005). Effects of astaxanthin on human blood rheology. J. Clin. Thera. Med., 21(4):421-429.
  9. Preuss H, Echard B, Bagchi D, Perricone VN, Yamashita E. (2009). Astaxanthin lowers blood pressure and lessens the activity of the renin-angiotensin system in Zucker Fatty Rats. J. Funct. Foods, I:13-22.


CCRES special thanks to 
  Mr. Mitsunori Nishida, 
 
President of Corporate Fuji Chemical Industry Co., Ltd.

Croatian Center of Renewable Energy Sources (CCRES) 

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The Effects of Astaxanthin – Gastric Health

The Effects of Astaxanthin – Gastric Health

 

 

Astaxanthin for Dyspepsia and Helicobacter pylori

Helicobacter pylori 

Dyspepsia is the general term given to a variety of digestive problems localized in the upper abdominal region. Typical symptoms for example include stomach pain, gas, acid-reflux or bloating. Dyspepsia is like the stomach version of the irritable bowel syndrome and its symptoms may appear at any age or to any gender. The medical approach to dyspepsia involves looking for treatable causes and addressing them if identified. Failing that, doctors suggest treatments by trial-and-error. The problem associated with this non-standardized approach involves drugs that may not work, may cause side effects and exacerbate the patient’s condition brought on by stressful attempts to cure symptoms.
To understand the benefits of astaxanthin in dyspepsia, it is necessary to categorize specific types; most common forms are either non-ulcer dyspepsia or gastric dyspepsia. Non-ulcer dyspepsia problems usually do not have an identifiable cause, but fortunately, for most cases it is non-disease related and therefore temporary. On the other hand, gastric type dyspepsia is more severe and linked to identifiable causes. For example, the bacterial infection of Helicobacter pylori is a commonly known cause. Pathological symptoms of H. pylori infection include high levels of oxidative stress and inflammation in the stomach lining and symptoms like gastric pain and acid reflux., H. pylori can contribute to mild and severe kinds of symptoms, but on the other hand, people who are H. pylori positive can remain asymptomatic whereas others may develop into clinical problems. It is still unclear what triggers the severe form of infection and how the bacteria is passed on, but scientists suggested using strong antioxidants like astaxanthin for therapy and better long term protection.

Helicobacter pylori in Gastric Dyspepsia

This Gram-negative bacterium is present in approximately half of the world population, and typically resides in the human gastric epithelium (stomach lining). H. pylori infection is generally acknowledged as the main cause for type B gastritis, peptic ulcer disease and gastric cancer. The pathogenesis of this infection is partly due to the immunological response as shown by Bennedsen et al., (1999). Astaxanthin (200 mg/kg body weight) fed to H. pylori infected mice for 10 days exhibited signs of improved immune system. Normally, the T-helper1 (Th1) response exacerbates inflammation and epithelial cell damage due to infection, but the astaxanthin treated mice responded with a mixed Th1/Th2-response (Figure 1), which lowered gastric inflammation (Figure 2) and bacterial loads (Figure 3). Furthermore, the findings by Wang et al., (2000) also supported the idea that a diet supplemented with astaxanthin or vitamin C in mice lowered inflammation after 10-days of treatment (in vivo), and also inhibit H. pylori growth (in vitro). The mice treated with astaxanthin (10 mg/kg body weight) had the same effect as vitamin C (400 mg/Kg) which significantly lowered gastric inflammation and lipid peroxidation (Figure 4) compared to infected control mice; which continued to develop severe gastritis.

Figure 1. IL-4 release of splenocytes after restimulation with H. pylori sonicate (Bennedsen et al., 1999) Figure 1. IL-4 release of splenocytes after restimulation with H. pylori sonicate (Bennedsen <em>et al.</em>, 1999)  
Astaxanthin improved the cytokine IL-4 response (Th2 T-cell) to the presence of H. pylori (in vitro).
Figure 2. Gastric inflammation (antrum + corpus) (Bennedsen et al., 1999)
  Figure 2. Gastric inflammation (antrum + corpus) (Bennedsen <em>et al.</em>, 1999)  
Astaxanthin reduced gastric inflammation in Helicobacter pylori infected mice.
Figure 3. Bacterial load (antrum + corpus) (Bennedsen et al., 1999) Figure 3. Bacterial load (antrum + corpus) (Bennedsen <em>et al.</em>, 1999)  
Astaxanthin reduced Helicobacter pylori colonization of the stomach of infected mice.
Figure 4. Amount of lipid peroxidation products (MDA and 4-hydroxyalkenals) during H. pylori infection (Wang et al., 2000) 
Figure 4. Amount of lipid peroxidation products (MDA and 4-hydroxyalkenals) during H. pylori infection (Wang <em>et al.</em>, 2000)  
Lipid peroxidation levels lowered in H. pylori infected mice after treatment with astaxanthin or Vitamin C.

The success of astaxanthin in dyspepsia animal models prompted further prospective human studies. In 1999, the first clinical study performed in collaboration with the Centre for Digestive Diseases, Australia, involved 10 H. pylori positive subjects (non-ulcer) with typical dyspeptic symptoms such as heartburn and gastric pain, were each treated with 40 mg daily dose of astaxanthin for 21 days. 10 clinical parameters assessed the efficacy before and after the treatment period. The gastric pain, heartburn and total clinical symptoms results showed a significant drop of 66%, 78% and 52% drop respectively (Figure 5). Furthermore, follow-up checks 27 days after the cessation of astaxanthin intake (a total of 49 days from day 0), showed that the dyspeptic symptoms remained low (Lignell et al., 1999). In summary, astaxanthin effectively controlled the dyspepsia symptoms, and H. pylori eradication trend was observed, but not significant.

Figure 5. Total Clinical Symptoms (Lignell et al., 1999) Figure 5. Total Clinical Symptoms (Lignell <em>et al.</em>, 1999)  
Astaxanthin reduced total grade of clinical symptoms in H. pylori positive non-ulcer dyspeptic subjects after 21 days. Low symptom score continued even up to 28 days after treatment ceased.

Reflux in Non-Ulcer Dyspepsia

Helicobacter pylori 

Approximately one in four people experience dyspepsia at some time that are linked to common causes such as food types, stress, stomach ulcers, or acid reflux (stomach acid backs-up into the esophagus). If the exact causes of non-ulcer dyspepsia are unknown, there are no standardized treatments that exist to effectively treat the patient. The usual procedure involves the problematic remedies of acid blocking medicines, painkillers or antibiotics. However, drug treatment faces problems with increasing antibiotic resistant bacteria and carries increased risk of damage to the stomach. Therefore, clinically proven non-drug treatments are becoming more attractive to physicians and patients.
Astaxanthin efficacy in non-ulcer dyspepsia was demonstrated in a randomized double-blind placebo controlled study involving 131 patients complaining of non-ulcer dyspepsia. This collaborative trial conducted by the Kaunas University Hospital, Lithuania; Rigshospitalet, Copenhagen; University of Lund and the Karolinska Institute, Sweden demonstrated that 40 mg astaxanthin treatment up to 4 weeks significantly reduced reflux compared to the 16 mg.

Figure 6. Reflux-syndrome 
 Figure 6. Reflux-syndrome  
Reduced reflux-syndrome score of non-ulcer dyspepsia patients treated with 16 mg and 40 mg astaxanthin.

Outlook

There are considerable overlaps in a number of gastrointestinal disorders that may be treatable with conventional medicine, but what if it does not work? In that case, astaxanthin may be useful, particularly against H. pylori positive gastritis and non-ulcer dyspepsia acid reflux. The mechanisms of action include the following: decreasing oxidative stress by astaxanthin’s potent antioxidant property; controlling bacterial infection by shifting the immune response; and alleviating dyspeptic symptoms by retarding inflammation. Furthermore, these results infer that acid reflux in connection with either H. pylori positive or negative conditions can still expect improvements with astaxanthin.

References

  1. Bennedsen M, Wang X, Willen R. Treatment of H. pylori infected mice with antioxidant astaxanthin reduces gastric inflammation, bacterial load and modulates cytokine release by splenocytes. Immunol Lett. 1999. 70: 185-189.
  2. Kupcinskas L, Lafolie P, Lignell A, Kiudelis G, Jonaitis L, Adamonis K, Andersen LP, Wadstrom T. 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. Phytomedicine 2008. 15: 391–399.
  3. Lignell A, Surace R, Bottiger P, Borody TJ. Symptom improvement in Helicobacter pylori positive non-ulcer dyspeptic patient after treatment with the carotenoid astaxanthin. In: 12th International Carotenoid Symposium, Cairns, Australia, 18-23 July 1999.
  4. Wang X, Willen R, Wadstrom T. Astaxanthin rich algal meal and vitamin C inhibit Helicobacter pylori infection in BALB/cA mice. Antimicrob Agents Chemother. 2000. 44: 2452-2457.


CCRES special thanks to 
  Mr. Mitsunori Nishida, 
 
President of Corporate Fuji Chemical Industry Co., Ltd.

Croatian Center of Renewable Energy Sources (CCRES)

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The Effects of Astaxanthin – Weight Control

The Effects of Astaxanthin – Weight Control

 

 

Physical Endurance and Muscle Recovery

Physical Endurance and Muscle Recovery 

Work, Sport, Leisure – in fact all physical activity will generate reactive oxygen species (ROS); the more intense the activity the greater number of free radicals. ROS are shown to have damaging effects on muscle performance and recovery. Published and on-going research, focused on improving endurance and reducing recovery time, are showing dramatic benefits linked to the potent carotenoid – astaxanthin. These findings are bringing astaxanthin to the forefront as a dietary supplement for professional athletes and physically active people.

Important to physical activity are our mitochondrial cells, often referred to as the “power stations of the cell” , which provide as much as 95% of our body’s pure energy (primarily by the burning of muscle glycogen and fatty acids). Unfortunately, a portion of this energy produces highly reactive and damaging ROS. ROS damage cells by triggering peroxidation of the cell membrane components, and oxidation of DNA and proteins. Furthermore, ROS continue to affect muscles even after the strenuous exercise has ceased. ROS activate the inflammation response whereby monocytes migrate into the muscle tissue causing additional cell damage. Often we will notice the onset of muscle damage during recovery in the form of tiredness and soreness. In addition to improving muscle performance through devised exercise regime, the sports research community is looking at other methods, such as nutrition to fuel and protect the body under extreme physical conditions. In the past, Vitamins E and C helped make the use of antioxidants a popular tool against oxidative damage during intense physical activity. Today, informed by current research we can point to astaxanthin as the antioxidant of choice for sports performance. Astaxanthin demonstrated 3 important physical benefits in clinical trials and supporting studies. Astaxanthin increased endurance, reduced muscle damage and improved lipid metabolism.

Did you know?

Astaxanthin Boosts Endurance

In a randomized, double-blind, placebo controlled study on healthy men supplemented with 4 mg astaxanthin per day for up to 6 months at Karolinska Institute, Sweden, standardized exercise tests demonstrated that the average number of knee bends performed increased only in the astaxanthin treated group at 3 months, and by the 6 month significant improvements were observed (Figure 1) (Malmsten & Lignell, 2008).

Figure 1. Increase in strength/endurance (Malmsten & Lignell, 2008)
  Figure 1. Increase in strength/endurance (Malmsten & Lignell, 2008)  
Astaxanthin improved strength/endurance at 3 and 6 months determined by the average number of knee bends per person.
Figure 2. Effect of astaxanthin on swimming time (Ikeuchi et al., 2006) Figure 2. Effect of astaxanthin on swimming time (Ikeuchi <em>et al.</em>, 2006)  
Astaxanthin improves endurance in a dose-dependant manner.

Astaxanthin Boosts EnduranceIn another study, Aoi et al., (2008) demonstrated that astaxanthin may modify muscle metabolism by its antioxidant property and result in improved muscle performance and weight loss benefits. After 4 weeks the mice running time to exhaustion had significantly improved by up to 20 % , (2002) of Juntendo University, Japan, demonstrated by using 1200 meter track athletes, that a daily dose of 6 mg per day for 4 weeks resulted in their bodies accumulating lower levels of lactic acid (Figure 3). Ikeuchi et al., (2006) also reported the same findings and furthermore, astaxanthin efficacy had a dose-dependent response (Figure 4).

Figure 3. Reduction of lactic acid build-up after astaxanthin supplementation in track subjects (Sawaki et al., 2002) 
Figure 3. Reduction of lactic acid build-up after astaxanthin supplementation in track subjects (Sawaki <em>et al.</em>, 2002)
Figure 4. Effect of astaxanthin on blood lactate during swimming for 15 minutes (Ikeuchi et al., 2006) Figure 4. Effect of astaxanthin on blood lactate during swimming for 15 minutes (Ikeuchi <em>et al.</em>, 2006)  
Astaxanthin reduced build-up of lactic acid in a dose-dependant manner.

In a double blind controlled placebo study, healthy women (n= 32; age-23-60) who ingested 12 mg of astaxanthin for 6 weeks significantly reduced their body fat (4%) when conducting routine walking exercise, compared to a placebo group. In addition, while control group increased their lactic acid by 31% compared to the astaxanthin group – only 13%

The Mechanism

The mechanism behind muscle endurance is based on several findings. Generally, astaxanthin protected the skeletal muscle from the increased damage of oxidative stress generated by physical activity. Furthermore, astaxanthin increased the metabolism of lipids as the main source of energy production by protecting the carnitine palmitoyltransferase I (CPT I) involved in fatty acid transport into mitochondria. Aoi et al., (2003) of Kyoto Prefecture University used mice models that may partially explain the efficacy of astaxanthin; they compared control, exercise placebo, and astaxanthin treated exercise groups after intense physical activity. 4-hydroxy-2-nonenal-modified-protein (4-HNE) stain analyses of the calf (gastrocnemius) muscles revealed significantly lower peroxidation damage (Figure 5).

Figure 5. Effect of astaxanthin on 4-HNE-modifed proteins in leg muscle before and after exercise (Aoi et al., 2003) Figure 5. Effect of astaxanthin on 4-HNE-modifed proteins in leg muscle before and after exercise (Aoi <em>et al.</em>, 2003)

Other biochemical markers for oxidative damage and inflammation such as DNA, (2003) also explained that astaxanthin directly modulates inflammation caused by the release of the pro-inflammatory cytokines and mediators. In vivo and in vitro tests demonstrate that astaxanthin inhibits the IκB Kinase (IKK) dependant activation of the Nuclear Factor-kB (NF-κB) pathway, a key step in the production of pro-inflammatory cytokines and mediators. Aoi et al., 2008 also demonstrated increased lipid metabolism compared to carbohydrate as the main source of energy during strenuous activity (Figure 6). Furthermore, analysis of the mitochondrial lipid transport enzyme known as carnitine palmitoyltransferase I (CPT I) revealed increased fat localization (Figure 7) and reduction of oxidative damage in the presence of astaxanthin (Figure 8). CPT I is important because it regulates fatty acyl-CoA entry into the mitochondria in the oxidation of fatty acids in muscle. Exercise-induced ROS may partly limit utilization of fatty acid via diminishing CPT I activity.

Figure 6. Fat substrate utilization increased with astaxanthin (Aoi et al., 2008)
  Figure 6. Fat substrate utilization increased with astaxanthin (Aoi <em>et al.</em>, 2008)  

 Calculated from the respiratory exchange ratio (RER) and oxygen consumption. Values are means ± SE obtained from 8 mice.

Figure 7. Increased amount of FAT/CD36 that coimmunoprecipitated with CPT I skeletal muscle after a single session of exercise at 30 m/min for 30 min (Aoi et al., 2008) Figure 7. Increased amount of FAT/CD36 that coimmunoprecipitated with CPT I skeletal muscle after a single session of exercise at 30 m/min for 30 min (Aoi <em>et al.</em>, 2008)  
Values are means ± SE obtained from 6 mice.
Figure 8. Astaxanthin reduced the amount of HEL-modified CPT1 in skeletal muscle after a single session of exercise at 30m/min for 30min (Aoi et al., 2008) Figure 8. Astaxanthin reduced the amount of HEL-modified CPT1 in skeletal muscle after a single session of exercise at 30m/min for 30min (Aoi <em>et al.</em>, 2008)  
Values are means ± SE obtained from 6 mice.

Outlook

Outlook 

Strenuous physical activity generates high levels of ROS which affect muscle performance and metabolism of lipids. New research shows that astaxanthin can modify muscle metabolism via its antioxidant effect, resulting in the improvement of muscle function during exercise. Therefore, astaxanthin is expected to be useful for physically active people as well as athletes.

References

  1. Aoi W, Naito Y, Sakuma K, Kuchide M, Tokuda H, Maoka T, Toyokuni S, Oka S, Yasuhara M, Yoshikawa T. (2003). Astaxanthin limits exercise-induced skeletal and cardiac muscle damage in mice. Antioxid Redox Signal, 5(1):139-144.
  2. Aoi W, Naito Y, Takanami Y, Ishii T, Kawai Y, Akagiri S, Kato Y, Osawa T, Yoshikawa T. (2008). Astaxanthin improves muscle lipid metabolism in exercise via inhibitory effect of oxidative CPT I modification. Biochem. Biophys. Res. Com., 366:892–897.
  3. Fukamauchi, M. (2007). Food Functionality of astaxanthin-10: Synergistic effects of astaxanthin-10 intake and aerobic exercise. Food Style 21, 11(10). [In Japanese]
  4. Ikeuchi M, Koyama T, Takahashi J, Yazawa K. (2006). Effects of astaxanthin supplementation on exercise-induced fatigue in mice. Bio. Pharm. Bull., 29(10):2106-2110.
  5. Lee SJ, Bai SK, Lee KS, Namkoong S, Na HJ, Ha KS, Han JA, Yim SV, Chang K, Kwon YG, Lee SK, Kim YM. (2003). Astaxanthin Inhibits Nitric Oxide Production and Inflammatory Gene Expression by Suppressing IκB Kinase-dependent NF-κB Activation. Mol. Cells, 16(1):97-105.
  6. Malmsten C, Lignell A. (2008). Dietary supplementation with astaxanthin rich algal meal improves muscle endurance – a double blind study on male students. Carotenoid Science 13:20-22.
  7. Sawaki K, Yoshigi H, Aoki K, Koikawa N, Azumane A, Kaneko K, Yamaguchi M. (2002). Sports performance benefits from taking natural astaxanthin characterized by visual activity and muscle fatigue improvements in humans. J Clin.Therap. Med., 18(9):73- 88.


CCRES special thanks to 
  Mr. Mitsunori Nishida, 
 
President of Corporate Fuji Chemical Industry Co., Ltd.

Croatian Center of Renewable Energy Sources (CCRES) 

Tagged , , , , ,
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