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) 

Tagged

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 , , , , ,

The Effects of Astaxanthin – Skin Health

The Effects of Astaxanthin – Skin Health

 

 

Brighter Skin and Well-Being Goes Hand-in-Hand

Brighter Skin and Well-Being Goes Hand-in-Hand 

The multibillion dollar beauty industry continues to flourish, spurred by consumers’ desire to look and feel forever-young. Several categories exist within the beauty industry, but none more vibrant than the anti-aging segment which includes products to reduce or reverse visible signs of aging such as wrinkles, age spots, and freckles. While aging is natural and cannot be avoided, there are factors such as solar radiation and physical and mechanical damage that accelerate the propensity of visible aging. Today, humans face increasing exposure to chemical pollution, ultraviolet radiation and ozone levels, all of which can damage the skin’s dermal layer causing wrinkles and enhancing the risk of malignant skin cancer. These negative effects are compounded with increasingly poor diets and lifestyle habits which are not conducive to maintaining the skin’s natural repair process and antioxidant network. Clearly, there is opportunity for natural ingredients to help improve long term skin health management through topical application and nutritional supplementation.
In the past, Beta-carotene (provitamin A) and Vitamin E have been extensively studied. Recent focus, however, has switched to other carotenoids such as astaxanthin, (derived from the microalgae Haematococcus pluvialis), which is shown to have potent quenching and anti-lipid-peroxidation properties; a weakness of Beta-carotene and Vitamin E (Miki, 1991). In human trials, astaxanthin has been shown to reduce visible signs of UV-aging through both topical and dietary supplementation within 4 to 6 weeks of use. This data is supported by a number of in-vitro and animal studies. Research suggests potential skin benefits from the use of astaxanthin to maintain a youthful appearance, reverse premature signs of aging and prevent UV induced skin cancer. Naturally, further investigation is necessary to elucidate the mechanism of action and to replicate results using significantly larger clinical trials. To date, the astaxanthin potential is promising.

Table 1. Astaxanthin maintains skin health by several methods Table 1. Astaxanthin maintains skin health by several methods

Protecting the Skin’s Natural Antioxidant Network and DNA

Protecting the Skin's Natural Antioxidant Network and DNA 

Oxygen radicals formed from UV radiation attack skin cells in a variety of ways. As demonstrated by O’Connor & O’Brien (1998), UVA light is capable of producing oxidative stress in living cells in-vitro. By monitoring catalase (CAT), superoxide dismutase (SOD) levels and thiobarbituric acid reactive substances (TBARS), Astaxanthin is capable of reducing oxidative stress, (2002) demonstrate that UVA irradiated skin cells pretreated with astaxanthin (10 μM) suffered significantly less DNA damage. Furthermore, astaxanthin protected the skin’s endogenous antioxidants SOD and glutathione (GSH) from oxygen radical attack. Topical restoration of the skin’s natural antioxidant balance is one method to maintaining healthy skin. UV radiation and air borne pollutants tend to strip away the nutrients essential to maintain the skin’s hydrolipidic barrier. As a result, the skin will become dry and unhealthy in appearance.

Topical Wrinkle Reduction

In a study using hairless mice, Arakane (2002) demonstrates astaxanthin’s ability to suppress the formation of UVB photoinduced wrinkles. UVB doses of 65-95 mJ/cm2 were applied five times per week for 18 weeks on the back skin of the mice. After each UVB treatment, topical application of astaxanthin (350 μM) was coated on the exposed areas. After only 5 weeks, the appearance of new wrinkles were significantly reduced up until the end of the study period, (2001) demonstrates the same anti-wrinkle observations in female human subjects (n=3) using a topical cream containing astaxanthin. A dermatological assessment revealed significant reduction of wrinkles and puffiness on the lower eye and cheeks after 2 weeks of use. In a separate test using female subjects (n=11), instrument analysis recorded significant moisture improvement.
 

Figure 1. Cheek moisture retention after 3 weeks application of astaxanthin cream (0.07% of 5% astaxanthin extract; Seki et al., 2001).

  Figure 1. Cheek moisture retention after 3 weeks application of astaxanthin cream (0.07% of 5% astaxanthin extract; Seki <em>et al.</em>, 2001) 
 Increased moisture content in 8 out of 11 subjects.

Skin Health that can be Swallowed

“Beauty from within” or improved skin condition through nutrition and supplementation is a worldwide trend that is on the increase. The market for beauty supplements is currently worth 800 million dollars, and rapid growth in this segment is expected over the next 10 years. Two human clinical trials established the use of astaxanthin to improve visible signs of premature aging and general skin health. The first, a double-blind placebo controlled study (Yamashita 2002), showed that astaxanthin in combination with tocotrienol, (a superior form of vitamin E), improved several aspects of overall skin condition. Eight female subjects with dry skin conditions (mean age 40 yrs) received daily doses containing 2 mg astaxanthin and 40 mg natural tocotrienols. Several types of data were collected at 2 and 4 weeks and compared to the initial baseline readings. Measurable differences were observed starting just 2 weeks after supplementation. By the 4th week, the treated subjects with dry skin characteristics exhibited the following: increased moisture levels.

Figure 2. Beauty supplement results for the cheek and eye region (Yamashita, 2002) Figure 2. Beauty supplement results for the cheek and eye region (Yamashita, 2002) 
Moisture levels increased in treated groups at 2 and 4 weeks. Control groups got worse.
Figure 3. Magnified Skin Section at start, 2 and 4 weeks (Yamashita, 2002)
  Figure 3. Magnified Skin Section at start, 2 and 4 weeks (Yamashita, 2002)  
Visible reduction of fine wrinkles

In the second study by Yamashita (2006), female subjects with a variety of skin types (n=49, mean age 47 yrs) were given either 4 mg (2 x 2 mg) astaxanthin or placebo in a single-blind, randomized, controlled study. After six weeks of consuming 4mg astaxanthin per day, the results of a standard questionnaire showed that the treated group of women all felt that their skin condition had improved significantly (Figure 4).

Figure 4. Subject response after 6 weeks astaxanthin supplementation (Yamashita, 2006) Figure 4. Subject response after 6 weeks astaxanthin supplementation (Yamashita, 2006)  
Skin improvements seen in all categories after astaxanthin supplementation.

Instrument analysis proved that the treated group had indeed achieved positive results in hydration.

Figure 5. Dermatologist skin analysis of moisture and elasticity at 3 and 6 weeks astaxanthin supplementation (Yamashita, 2006).
  Figure 5. Dermatologist skin analysis of moisture and elasticity at 3 and 6 weeks astaxanthin supplementation (Yamashita, 2006).  
Astaxanthin reduced wrinkles and increase elasticity.

Astaxanthin and Skin Cancer

The risk of skin cancer is increased in skin which is frequently damaged by the sun. Although skin cancer is almost 99% curable if detected early, 1 out of 90 people in the US or 1 out of 150 people in the UK will develop melanomas. Those in the highest risk category are people exposed to frequent short bursts of strong sunlight. Sun screens can block the UV rays, but dietary carotenoids such as astaxanthin can be vital for skin protection as well.
In another study on hairless mice, Black (1998) demonstrates that astaxanthin significantly delays the UV ray formation of skin lesions and tumors. Further support comes from Savoure et al., (1995) which shows that hairless mice (SKH1) deficient in vitamin A, fed 10 mg/kg/feed astaxanthin alone or in combination with retinol, show enhanced skin protection after UVA and UVB irradiation. Astaxanthin significantly inhibited accumulation of putrescine .

Mechanism of Action

Skin is composed of three layers: the epidermis, the dermis, and the subcutaneous fat. The dermis contains collagen, elastin, and other fibers that support the skin’s structure. It is these elements that give skin its smooth and youthful appearance – and these are the parts of the skin that are damaged by UV radiation (UVR).

Anti-wrinkle

The UVR that affects the skin is composed of two types of waves; UVA and UVB. UVB rays are shorter than UVA rays, and are the main cause behind inflammation and melanin production. However, it is the UVA rays, with their longer wavelength, that are responsible for much of the damage associated with photoaging. UVA rays penetrate deep into the dermis, where they damage collagen fibers, leading to wrinkle formation (Figure 6).

Figure 6. Illustration showing effect of UVA, UVB & Ozone on skin

Figure 6. Illustration showing effect of UVA, UVB & Ozone on skin

 
UV rays induce the production of in situ radical oxygen species (ROS) and matrix metalloproteinases (MMP). These factors are the root of wrinkle formation because they destroy the collagen matrix in the dermis. Fortunately, the skin’s repair mechanism will rebuild the damage collagen. However, the hindrance of skin renewal by repeated exposure to uncontrolled levels of ROS and MMP leads to the formation of wrinkles. The presence of astaxanthin attenuates the effects of reactive oxygen and MMP and therefore, it allows the skin to regenerate properly (Figure 7).

Figure 7. Astaxanthin supports skin renewal by attenuating factors which contribute to wrinkle formation Figure 7. Astaxanthin supports skin renewal by attenuating factors which contribute to wrinkle formation

Astaxanthin defends against Reactive Oxygen Species (ROS)

Oxygen present in our cells can form harmful radicals known as ROS or active oxygen when sufficient energy from UV rays is applied. ROS include singlet oxygen, superoxides and hydroxyl radicals (leading to peroxyl radicals) and they attempt to steal electrons from neighboring molecules such as DNA, phospholipids, enzymes and protein in order to stabilize. Fortunately, astaxanthin is able to quench singlet oxygen reactions and supress lipid peroxidation much more effectively than other well known antioxidants and thus control the presence of ROS. In vitro singlet oxygen quenching activity of Astaxanthin was found to be superior when compared to Catechin, Vitamin C, Alpha Lipoic Acid, Coenzyme Q10, Tocopherol, Lutein and Beta Carotene (Nishida et al., 2007).

Astaxanthin Dominance against Singlet-Oxygen compared to other antioxidants

Singlet oxygen depletes the antioxidant defense system of fibroblasts, especially CAT and SOD. Fibroblasts secrete collagen, a main component of extracellular matrix which provides structural support to the cells. Exposing fibroblasts to singlet oxygen is a widely used technique to model ageing and UV oxidative stress. Furthermore, viability of the fibroblasts remains vital to the maintenance of healthy skin appearance. Tominaga et al (2009a) showed evidence on the ability of Astaxanthin to protect human dermal fibroblasts through in-vitro study. Human dermal fibroblasts were pre-incubated with Astaxanthin and other antioxidants and then exposed to singlet oxygen (Figure 8). Cell viability was restored to more than 80% when the cells were treated with Astaxanthin.
In another study, Camera et al. (2008) compared the photoprotective properties of astaxanthin to other antioxidants on human dermal fibroblasts. After a physiological dose of UVA was applied, roughly equal to a UV dose accumulated within 1-2 hours on a sunny day. Astaxanthin was considerably superior at preventing cell death (reduction of caspase-3 activity at protein level) compared to Canthaxanthin and Beta Carotene (Figure 9).

Figure 8. Astaxanthin’s cell protection ability comparison with other anti-oxidants (Tominaga 2009a) Figure 8. Astaxanthin's cell protection ability comparison with other anti-oxidants (Tominaga 2009a)  
Study showed that astaxanthin had the highest ability to protect cells.
Figure 9. UVA-induced activation of caspase-3, detected by annexin V staining, 24h after irradiation (Camela et al., 2008) 
 Figure 9. UVA-induced activation of caspase-3, detected by annexin V staining, 24h after irradiation (Camela <em>et al.</em>, 2008)

Gaining Customers’ Hearts with Tangible Results – Astaxanthin Inner and Outer Treatment

Complementing astaxanthin oral administration with astaxanthin topical treatment (dual treatment) can have enhanced synergistic effects against premature skin aging since astaxanthin is effective at all layers of skin, the skin surface, epidermis and dermis.
According to studies conducted by Tominaga et al. (2009b), astaxanthin “dual treatment” was found to be effective in all layers of skin. In a study with 28 subjects aged 20-55 years, astaxanthin effectively reduced wrinkles as well as improved skin elasticity. Replica analysis after 6 mg of astaxanthin supplementation combined with topical application for 8 weeks showed a reduction in the overall average wrinkle depth.
Furthermore, a reduction in wrinkle width by 9%.

Figure 10. Effects of Astaxanthin on skin elasticity after extended intake/external application (Tominaga 2009b)

  Figure 10. Effects of Astaxanthin on skin elasticity after extended intake/external application (Tominaga 2009b)

Figure 11. Stimulatory effects of Astaxanthin on collagen production and maintenance (Tominaga 2009b) Figure 11. Stimulatory effects of Astaxanthin on collagen production and maintenance (Tominaga 2009b)

Anti-inflammatory Action

Inflammation that normally follows sun exposure can be modulated by a powerful antioxidant. Yamashita (1995) shows in healthy male subjects (n=7), that topical natural astaxanthin significantly reduces burn level (erythema) by 60% at 98 hours after UVB exposure. We now know that astaxanthin works by suppressing the proinflammatory mediators and cytokines via the IκB kinase dependant NF-κB activation pathway (Lee et al., 2003).

Safety for Topical & Nutritional Use

Natural astaxanthin is determined safe for topical and nutritional use. A total of forty-five subjects (males and females) were exposed to the Standard Japanese Patch test and results were reported 24 and 48 hours after application. Dermatitis was only induced by the adhesive plaster and not astaxanthin itself (Seki et al., 2002). Furthermore, Koura (2005) reports no adverse topical reactions in animal sensitization models. Astaxanthin is listed in the JP Cosmetics and INCI name as astaxanthin.

Outlook

Naturally, the best way to avoid photo-aging is through prevention of the solar effects on skin by applying sunscreen to areas vulnerable to increased exposure. However, recent surveys reveal that people in general are not doing enough to protect their skin. The use of powerful carotenoids like astaxanthin in topical and nutritional skin products can help deliver the benefits against the risk of accelerated photo-aging and skin cancer.

References

  1. www.skincancer.org
  2. www.skincancerfacts.org.uk/facts.asp
  3. Yamashita(2006). The Effects of a Dietary Supplement Containing Astaxanthin on Skin Condition. Carotenoid Science, 10:91-95.
  4. Koura(2005). Skin sensitization study of Astaxanthin in Guinea Pigs. Study No. 05035. New Drug Research Center Inc., Hokkaido Japan.
  5. Lee et al., (2003). Astaxanthin Inhibits Nitric Oxide Production and Inflammatory Gene Expression by Suppressing IκB Kinase-dependent NF-κB Activation. Molecules and Cells, 16(1):97-105.
  6. Arakane (2002), Superior Skin Protection via Astaxanthin. Carotenoid Sci., 5:21-24.
  7. Lyons & O’Brien et al., (2002). Modulatory effects of an algal extract containing astaxanthin on UVA-irradiated cells in culture. Journal of Derma. Sci., 30(1):73-84.
  8. Yamashita (2002). Cosmetic benefit of the supplement health food combined astaxanthin and tocotrienol on human skin. Food Style 21, 6(6):112-117.
  9. Seki et al., (2001). Effects of astaxanthin from haematococcus pluvialis on human skin. Fragrance J., 12:98-103.
  10. Black (1998). Radical Interception by carotenoids and effects on UV carcinogenesis. Nutrition Cancer., 31(3):212-217.
  11. O’Connor & O’Brien (1998). Modulation of UVA light induced oxidative stress by beta-carotene, lutein and astaxanthin in cultured fibroblasts. J. Derma. Sci., 16(3):226-230.
  12. Savoure et al., (1995). Vitamin A status and metabolism of cutaneous polyamines in the hairless mouse after UV irradiation: action of beta-carotene and astaxanthin. International J Vit. and Nutr. Res., 65(2):79-86.
  13. Yamashita (1995). Suppression of post UVB hyperpigmentation by topical astaxanthin from krill. Fragrance J., 14:180-185.
  14. Miki (1991). Biological functions and activities of animal carotenoids. Pure & Appl. Chem., 63(1):141-146.
  15. Camera et al., (2009). Astaxanthin, canthaxanthin and beta carotene differently affect UVA-induced oxidative damage and expression of oxidative stress-responsive enzymes. Experimental Dermatology. Vol. 18 (3), Pages 222 – 231 .
  16. Tominaga et al., (2009a). Protective effects of astaxanthin against single oxgyen induced damage in human dermal fibroblasts in-vitro Food Style 21, 13(1):84-86.
  17. Tominaga et al., (2009b). Cosmetic effects of astaxanthin for all layers of skin. Food Style 21, 13(10):25-29.
  18. Nishida et al. (2007). Carotenoid Science. Vol.11:16-20.
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 – Eye Health

The Effects of Astaxanthin – Eye Health

 

Astaxanthin for Eye Health

Astaxanthin for Eye Health 
The advances of information technology, software and electronics have led to the widespread use of screen based equipment or Visual Display Terminals (VDT) for both work and leisure. According to The National Center for Education Statistics, about 90 percent of children and adolescents in developed countries, ages 5 to 17, use computers at school or at home. About 50 percent of 9-year-olds use the Internet and at least 75 percent by ages 15 to 17.
This phenomenon often lead to asthenopia or eye fatigue. The symptoms include sensitivity to glare, headaches, sore eyes and blurred vision. A recent study conducted by the National Institute of Occupational Safety and Health in USA found that over 90 percent of habitual users of VDT reported eyestrain and other visual problems associated with computer use. The American Optometric Association supported this in a survey reporting that between 50 and 75 percent of all VDT workers report eye problems. In another study conducted in Sweden, 23 percent of schoolchildren, aged 6-15 suffered from asthenopia-related symptoms (Anshel, 2009).
Asthenopia prompted a large number of occupational safety studies. For example, epidemiological studies over the last decade revealed significant factors that contribute to eye fatigue. These studies, sometimes involving up to 6,000 sufferers identified the following causes: insufficient lighting, poor ergonomics and uncorrected vision. Despite the new information, follow-up studies later showed that the implemented improvements were only effective in 50% of sufferers. The possible explanations for this observation could be that other factors remained undiscovered, poor implementation of improvements, or visual work had become even more visually demanding. It is likely to be a combination of these factors so that current solutions are insufficient to reduce asthenopia.

Definition  

Standardized questionnaires that assessed subjective eye fatigue symptoms are in most cases mild, but symptoms get progressively worse if the causes are not rectified. Furthermore, certain ophthalmological tests can also detect eye problems, for example accommodation amplitudes, rate of accommodative reaction (positive and negative directions), critical flicker fusion (CFF) and pattern visual evoked potential (PVEP). So far, 10 Japanese clinical studies conducted by 9 independent ophthalmological establishments were able to conclude the efficacy of astaxanthin to alleviate visual asthenopia by observed improvements in the accommodation function and recovery of the ciliary body (Figure 1); retinal blood flow and inflammation markers.

Figure 1. Location of the ciliary body in the human eye

  Figure 1. Location of the ciliary body in the human eye

Astaxanthin Reduces Eye Fatigue

Asthenopia (eye fatigue) occurs on a daily cycle, in that the visual performance generally decreases naturally from morning until night. This problem exacerbates with a daily VDT load that lasts between 4 to 7 hours by affecting the accommodation performance of the ciliary body, which controls lens refraction. A couple of randomized double blind placebo controlled pilot studies demonstrated the positive effects of astaxanthin supplementation on visual function. For example, a study by Nagaki et al., (2002), demonstrated that subjects (n=13) who received 5 mg astaxanthin per day for one month showed a 54% reduction of eye fatigue complaints (Figure 2). In a sports vision study led by Sawaki et al., (2002), they demonstrated that depth perception and critical flicker fusion had improved by 46% and 5% respectively on a daily dose of 6 mg (n=9). The effect of astaxanthin on visual performance prompted a number of other clinical studies to evaluate the optimum dose and identify the mechanism of action.

Figure 2. VDT Subjects with Eye Strain Symptoms before and after astaxanthin supplementation  

  Figure 2. VDT Subjects with Eye Strain Symptoms before and after astaxanthin supplementation (Nagaki <em>et al.</em>,2002)  

 Overall, the 6 mg group improved significantly better at week 2 and 4 of the test period. Furthermore, questionnaire results obtained by Shiratori et al., (2005) and Nagaki et al., (2006), also confirmed the previous findings that astaxanthin supplementation at 6 mg for 4 weeks improved symptoms associated with tiredness, soreness, dryness and blurry vision. Another study by Takahashi & Kajita (2005), also demonstrated that astaxanthin attenuates induced-eye fatigue, as opposed to treating eye fatigue, which suggests prevention rather than treatment. Astaxanthin treated groups (asthenopia negative) were able to recover quicker than the control group after heavy visual stimulus. Later, Iwasaki & Tawara (2006) also confirmed the same tendencies of subjective eye fatigue complaints in a randomized double-blind placebo controlled double-crossover study.
In addition to questionnaires, direct measurement associated with asthenopia is also strong indicators for understanding astaxanthin efficacy. These include accommodation amplitude (Figure 3); rate of accommodation reaction (positive and negative directions); CFF (critical flicker fusion) and PVEP (pattern visual evoked potential).
Based on the quantitative information, the accommodation related measurements consistently improved after the treatment period (Nagaki et al., 2002, 2006; Nakamura et al., 2004; Takahashi & Kajita, 2005; Shiratori et al., 2005; Nitta et al., 2005; Iwasaki & Tawara, 2006) whereas the CFF and PVEP remained inconclusive (Sawaki et al., 2002; Nagaki et al., 2002; Nakamura et al., 2004). Therefore, the mechanism by which astaxanthin improved eye fatigue strongly indicates accommodation.

Figure 3. Objective accommodation (Nitta et al., 2005) Figure 3. Objective accommodation (Nitta <em>et al.</em>, 2005)  
Objective accommodation amplitude improves with 6mg astaxanthin.

Delaying Progression of Presbyopia

In a questionnaire survey study conducted by Kajita et al. (2009), 77 percent of 22 elderly males (age 46-65), after ingested 6 mg of astaxanthin daily for 4 weeks, felt better about the subjective symptoms related to presbyopia – a reduced ability to focus on near objects caused by loss of elasticity of the crystalline lens after age 45. In more detail, participants felt an improvement when seeing nearby objects and a decrease in blurred vision. This was followed by alleviation of eye strain and shoulder stiffness. In addition, the pupillary constriction ratio, used to assess the accommodative function of the eye, showed an overall improvement of 19 percent after supplementation of astaxanthin. Therefore, Kajita et al. (2009) concluded that astaxanthin may slow down the progression of presbyopia in middle-aged and elderly people.

Mechanism of Action

Accommodation Improvement

Accommodation Improvement 

Accommodation measures the lens refractive property and it corresponds to the ciliary body function. This small ocular muscle controls the lens thickness in order to focus the light on the retina. In heavy visual workloads, the eye is focused on a fixed object distance for extended periods that will cause muscle spasms or develop fatigue detectable by accommodation tests. These tests are interrelated and include the following: accommodation amplitude; accommodation reaction (positive or negative) and high frequency component (HFC). Each clinical study used a combination of accommodation tests to indicate the amount of fatigue present. For example, increased accommodation amplitude in all treated subjects indicated improved reaction on near and far objects (Nagaki et al., 2002, 2006; Nakamura et al., 2004). Figure 4, Figure 5 and Table 1 reveal the higher rate of accommodation reactions measured in astaxanthin treated groups. These indicate the speed at which the ciliary body reacted to the direction change of focus (negative accommodation means from a near object at 35 centimeters to distant object at 5 meters or vice versa); (Nitta et al., 2005; Shiratori et al., 2005; Nakamura et al., 2005; Iwasaki & Tawara, 2006). The effects of astaxanthin are significant from 2 weeks.

Table 1. Improvement of negative accommodation time with astaxanthin (Iwasaki & Tawara, 2006)

  Table 1. Improvement of negative accommodation time with astaxanthin (Iwasaki & Tawara, 2006) 

 
Figure 4. Positive accommodation change (Shiratori et al., 2005)

  Figure 4. Positive accommodation change (Shiratori <em>et al.</em>, 2005)  

Rate of positive accommodation improves with 6 mg astaxanthin
Figure 5. Negative accommodation (Shiratori et al., 2005)

  Figure 5. Negative accommodation (Shiratori <em>et al.</em>, 2005)  

Rate of negative accommodation improves with 6 mg astaxanthin

Another technique called HFC directly measured the microfluctuations in the lens during the accommodation response and typical values exist between 50 and 60 for normal eyes. Asthenopia sufferers (values greater than 60) experienced faster rates of recovery (Figure 6) in that their HFC results decrease towards normal values in less time compared to control groups (Takahashi & Kajita, 2005).

Figure 6. Accommodative Recovery observing difference of HFC (Takahashi & Kajita, 2005) Figure 6. Accommodative Recovery observing difference of HFC (Takahashi & Kajita, 2005)  
Astaxanthin improves HFC accommodation recovery during rest periods after visual work.

Increased Blood-flow


Figure 7. Increase of retinal blood flow (Nagaki et al., 2005) Figure 7. Increase of retinal blood flow (Nagaki <em>et al.</em>, 2005) 
 Retinal blood flow increases with astaxanthin after 4 weeks.

Anti-inflammation

Lastly, a top Japanese ophthalmology research collaboration between Hokkaido, Yokohama and Tokyo concluded anti-inflammatory properties of astaxanthin in endotoxin-induced uveitis (EIU or eye inflammation) both in vivo and in vitro models.
In another study, Suzuki et al., (2006) confirmed the same effects while they carefully studied the anti-inflammatory effect of astaxanthin in the iris-ciliary body of rat eyes. This was also the first study to prove that astaxanthin suppressed NF-kB activation by free radicals in the EIU rat model (Figure 8). The result is a lower pro-inflammatory response that would otherwise perpetuate local sites of inflammation that may also help explain why astaxanthin worked to alleviate eye fatigue in numerous clinical trials.

Figure 8. Number of NF-κB positive cells in eye ciliary body during inflammation (Suzuki et al., 2006)

  Figure 8. Number of NF-κB positive cells in eye ciliary body during inflammation (Suzuki <em>et al.</em>, 2006)  

Astaxanthin reduced the number of inflamed cells in the ciliary body.

Outlook

Outlook 

Eye fatigue or asthenopia is a common problem that occurs with the regular use of VDTs and may be resolved with findings from many worldwide epidemiological studies. However, if current improvements tend to be only 50% successful and other factors are likely to be involved, therefore, based on the current clinical evidence, astaxanthin offers a complementary alternative by reducing inflammation, improving accommodation and increasing blood flow.

References

  1. Anshel D. J. (2009). Healthy Eyes Better Vision, Summerlin Publishing Group, USA.
  2. Fukuda M, Takahashi J, Nishida Y, Sasaki H. (2008). Intraocular penetration of astaxanthin in rabbit eyes. Atarashii Ganka, 25(10):1461-1464. [In Japanese]
  3. Hashimoto H, Arai K, Takahashi J, Chikuda M, Obara Y. (2009). Effect of Astaxanthin Consumption on Superoxidize Scavenging Activity in Aqueous Humor. Atarashii Ganka, 26(2): 229-234. [In Japanese]
  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. Iwasaki T, Tawara A. (2006). Effects of Astaxanthin on Eyestrain Induced by Accommodative Dysfunction. Atarashii Ganka, (6):829-834. [In Japanese]
  6. Kajita M, Tsukahara H, Kato M. (2009). The Effects of a Dietary Supplement Containing Astaxanthin on the Accommodation Function of the Eye in Middle-aged and Older People. Medical Consultation & New Remedies, 46(3). [In Japanese]
  7. Miyawaki H, Takahashi J, Tsukahara H, Takehara I. (2005). Effects of astaxanthin on human blood rheology. J. Clin. Thera. Med., 21(4):421-429.
  8. Nagaki Y, Hayasaka S, Yamada T, Hayasaka Y, Sanada M, Uonomi T. (2002). Effects of astaxanthin on accommodation, critical flicker fusions, and pattern evoked potential in visual display terminal workers. J. Trad. Med., 19(5):170-173.
  9. Nagaki Y, Mihara M, Tsukuhara H, Ohno S. (2006). The supplementation effect of astaxanthin on accommodation and asthenopia. J. Clin. Therap. Med., 22(1):41-54.
  10. Nagaki Y, Miharu M, Jiro T, Akitoshi K, Yoshiharu H, Yuri S, Hiroki T. (2005). The effects of astaxanthin on retinal capillary blood flow in normal volunteers. J. Clin. Therap. Med., 21(5):537-542.
  11. Nakamura A, Isobe R, Otaka Y, Abematsu Y, Nakata D, Honma C, Sakurai S, Shimada Y, Horiguchi M. (2004). Changes in Visual Function Following Peroral Astaxanthin. Japan J. Clin. Opthal., 58(6):1051-1054.
  12. Nitta T, Ohgami K, Shiratori K, Shinmei Y, Chin S, Yoshida K, Tsukuhara H, Ohno S. (2005). Effects of astaxanthin on accommodation and asthenopia – Dose finding study in healthy volunteers. J. Clin. Therap. Med., 21(6):637-650.
  13. Ohgami K, Shiratori K, Kotake S, Nishida T, Mizuki N, Yazawa K, Ohno S. (2003). Effects of astaxanthin on lipopolysaccharide-induced inflammation in vitro and in vivo. Invest. Ophthal. Vis. Sci., 44(6):2694-2701.
  14. 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. Ther. Med., 18(9):73-88.
  15. Shiratori K, Ohgami K, Nitta T, Shinmei Y, Chin S, Yoshida K, Tsukahara H, Takehara I, Ohno S. (2005). Effect of astaxanthin on accommodation and asthenopia – Efficacy identification study in healthy volunteers. J. Clin. Therap. Med., 21(5):543-556. Sussman M. (2001) Total Health At The Computer, Station Hill, New York.
  16. Suzuki Y, Ohgami K, Shiratori K, Jin XH, Ilieva I, Koyama Y, Yazawa K, Yoshida K, Kase S, Ohno S. (2006). Suppressive effects of astaxanthin against rat endotoxin-induced uveitis by inhibiting the NF-kB signaling pathway. Exp. Eye Res., 82:275-281.
  17. Takahashi N, Kajita M. (2005). Effects of astaxanthin on accommodative recovery. J. Clin. Therap. Med., 21(4):431-436.

 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 – Cardiovascular Health

 

The Effects of Astaxanthin – Cardiovascular Health

 

Atherosclerosis: 

A Silent Cardiovascular Condition that Kills 1 Person Every 3 Seconds

Atherosclerosis: A Silent Cardiovascular Condition that Kill 1 Person every 3 SecondsHigh blood pressure, high levels of triglycerides, oxidation of Low Density Lipoprotein (LDL) cholesterol and lowering levels of High Density Lipoprotein (HDL) cholesterol are the primary cause that leads to oxidative stress and chronic inflammation in the vessels. This condition emerges at early age and gradually compromises vascular integrity leading to atherosclerosis at a later stage of a person lifespan. Atherosclerosis is a cardiovascular condition in which fat deposits and become oxidized along the inner lining of the artery walls. This silent yet deadly build up progressively thickens, hardens and eventually blocks the arteries leading to sudden and severe circulatory complications including vascular ischemia, stroke or heart attack. Cardiovascular and circulatory deaths related to atherosclerosis accounts for 29% of all deaths globally; the primary cause of death in EU (42%), Eastern Europe (48%), UK (39%), North America (49%), China (34%), South America (31%); Middle East (31%) and India (29%) – World Health Report, 2010.

Salmon Consumption and Lower Incidence of Cardiovascular Diseases Among Japanese. Just a Coincidence?

Salmon Consumption and Lower Incidence of Cardiovascular Diseases Among Japanese. Just a Coincidence?The cardiovascular and circulatory benefits of natural astaxanthin are evident among Japanese who are the uppermost consumers of food containing astaxanthin (AX) in the world and have the lowest incidences of heart diseases amongst developed countries. As the French paradox of cardiovascular health is connected to “sipping red-wine” and Italians longevity to “olive oil dressed” salads, Japanese cardiovascular resilience can be associated with consumption of “astaxanthin-soaked” salmon. In fact, a growing number of scientific evidence points to a robust link between natural astaxanthin and cardiovascular health – 30 cardiovascular specific research publications including 10 clinical studies. Research suggests that oral supplementation of astaxanthin may reduce the risks of cardiovascular diseases by reducing hypertension while enhancing blood rheology, capillary circulation and vascular resilience.

The Effects of Astaxanthin on Atherosclerosis Prevention and Development

The Effects of Astaxanthin on Atherosclerosis Prevention and Development

Astaxanthin Increase HDL Cholesterol and Decrease Serum Triglycerides

For every 1 mg/dl increase in good cholesterol HDL, the risk of cardiovascular diseases drops by 3%. In fact, baby boomers with low-HDL (> 40mg/dL) increase their chances of experiencing coronary events by 50%. Recent studies suggest that individuals with low HDL cholesterol who also have high triglycerides levels are 11 times more likely to develop cardiovascular diseases. Achieving a significant increase of HDL is notoriously hard because it requires drastic lifestyle changes, so often ending with modest results or sudden relapses.
Recent research suggests that astaxanthin supplementation can support lifestyle changers by synergizing HDL increasing effect with decreased level of serum triglycerides. Two recent studies demonstrated that astaxanthin consumption can steadily increase HDL cholesterol in both healthy and less healthy individuals -both as preventive and therapeutic use. Yoshida et al., (2009) conducted the first ever randomized, placebo-controlled human study to evaluate astaxanthin effect on dyslipidemia and metabolic syndrome. Sixty-one hyper-triglyceride subjects between 42-47 years old (BMI 24 mg/kg), received 0 (placebo), 6 mg, 12mg, 18mg of astaxanthin daily for 12 weeks. While the placebo group did not change their existing condition, the astaxanthin groups increased their HDL cholesterol by 11%, 15% and 7% respectively and decreased their serum triglycerides level by 17%, 25% and 24% respectively (figure 1).

Figure 1. Astaxanthin increase HDL cholesterol and decrease Serum Triglycerides (STR). Subjects with lower levels of HDL and higher levels of STR are 11 times more likely to develop cardiovascular diseases (Yoshida et al., 2009) Figure 1. Astaxanthin increase HDL cholesterol and decrease Serum Triglycerides (STR). Subjects with lower levels of HDL and higher levels of STR are 11 times more likely to develop cardiovascular diseases (Yonei et al, 2010) 61 hyper- triglyceride subjects between 42-47 yo; (BMI 24 mg/kg), received 0 (placebo), 6 mg, 12mg, 18mg of astaxanthin per day for 12 weeks

In a recent clinical study, 73 subjects between 20-60 years of age who received 4mg of natural astaxanthin per day for 4 weeks had their serum triglycerides level decreased by 25 %(Satoh et al., 2009). In another study conducted in Japan, 15 healthy adults increased their HDL by 6% after ingesting 9mg/daily of astaxanthin for 8 weeks (Matsumaya et al., 2010). In 2007, Hussein et al., has shown that astaxanthin reduced the size of fat cells in rats, which lead to a lower risk of cardiovascular complications and chronic inflammation (figure 2).

Figure 2. Astaxanthin reduced the size of fat cells. Large cells usually indicate higher risk of fat-oxidation chronic inflammation and oxidative stress, which are the leading causes of cardiovascular diseases (x10) (Hussein et al., 2006) Figure 2. Astaxanthin reduced the size of fat cells. Large cells usually indicate higher risk of fat-oxidation chronic inflammation and oxidative stress, which are the leading causes of cardiovascular diseases (x10) (Hussein <em>et al.</em>, 2006)

Astaxanthin Decrease Red Blood Cells Oxidation and Lipid-Peroxidation

Astaxanthin Decrease Red Blood Cells Oxidation and Lipid-PeroxidationHigh levels of triglycerides and low levels of HDL also increase the likelihood of fat-oxidation in vessels and formation of “wounds” in the inner lining of artery walls (endothelium) leading to chronic inflammation and oxidative stress; this situation causes degradation, narrowing and thickening of arteries. Three recent clinical studies have robustly pointed to astaxanthin ability to reduce fat peroxidation in blood plasma. In a randomized-double-blind placebo study, 33 overweight subjects received 5mg or 20mg astaxanthin daily for 3 weeks. Their lipid peroxidation markers plasma MDA Level (mmol) and plasma ISP (ng/mL) decreased by 30% and 60% in average (Choi et al., 2011).
In another randomized double blind placebo controlled study, 30 subjects between 50 and 69 years of age received 0 (placebo), 6 or 12mg astaxanthin daily for 12 weeks (Nakagawa et al., 2011). The amount of oxidized red blood cells (PLOOH um0l/ml) decreased by 17% and 24% respectively(figure 3).

Figure 3. Astaxanthin reduces red blood cells oxidation (RBCO) in senior subjects. RBCO cells has high correlation with neuro-degenerative (eg. dementia) and cardiovascular diseases (eg. heart attack) (Nakagawa et al., 2011) Figure 3. Astaxanthin reduces red blood cells oxidation (RBCO) in senior subjects. RBCO cells has high correlation with neuro-degenerative (eg. dementia) and cardiovascular diseases (eg. heart attack) (Nakagawa <em>et al.</em>, 2011) 30 subjects (15 F and 15 M) between 50 and 69 years of age , BMI 27·5 kg/m2 received 0 (placebo), 6 or 12mg astaxanthin per day for 12 weeks

In 2007, Karppi et al., conducted a randomized double blind conducted placebo controlled study with 40 non-smoking subjects between 19-33 years of age who received 0 (placebo) or 8mg of astaxanthin daily for 12 weeks. Their lipid peroxidation markers -plasma-15-hydroxy fatty acidsdecreased by 60% and plasma-12-hydroxy fatty acids by 36%. In 2000, Iwamoto et al., has also shown that astaxanthin inhibited LDL oxidation in human subjects. Professor Aoi from Kyoto Prefectural University, has shown that astaxanthin limits exercise-induced cardiac oxidation damage in mice.

Astaxanthin Enhance Biomarkers of Anti-oxidant Healthiness in the Blood Plasma

Low antioxidant activity in the blood correlates with high incidences of stroke, neurological impairment in stroke patients and cardiovascular diseases. Therefore, it is crucial to monitor the biomarkers of antioxidant capacity in the blood when assessing the efficacy of an active ingredient. In a randomized double blind study, 33 overweight subjects received 5mg or 20mg astaxanthin daily for 3 weeks. Their plasma Superoxide Dismutase Level (SOD) (U/mL) and Plasma Total Antioxidant Capacity (TAC) Level (mmol) increased 45% and 19% respectively. (Choi et al., 2011) (figure 4).
Other studies have produced similar results using different assessment methods. In an open label clinical study, 35 postmenopausal women were treated with astaxanthin daily dose of 12 mg for 8 weeks (Yonei et al., 2009). Astaxanthin supplementation increased biological antioxidant potential in the blood plasma by 5% in 8 weeks. In addition, Camera et al., suggested that astaxanthin protects and synergize with our endogenous antioxidant systems (superoxide dismutase, catalase and glutathione) from early degradation when subjected to oxidative stress (Camera et al., 2008).

Figure 4. Astaxanthin increases Plasma SOD Level and Plasma TAC level. Low levels of SOD and TAC correlates with higher incidences of stroke, neurological impairment and cardiovascular diseases (Choi et al., 2011) fig4 33 subjects received 5mg or 20mg astaxanthin x day for 3 weeks; BMI (25.0 -30.0 kg/m2) – aged 25.Normal Body Subjects – 10 non-intervention subjects (20.0 < BMI≤24.9 kg/m2) age 26

Astaxanthin Decrease Chronic Inflammation that comprise Blood Vessels Integrity

In the presence of oxidized cells in the endothelial lesions, macrophages white blood cells infiltrate in affected areas to clear away pathogens and dead cells. Yet, in the attempt to clean up the oxidized areas, macrophages may get overweighed with excessive lipoproteins and unable to leave the artery walls. This peculiar but common situation triggers a cascade of chronic inflammatory responses and pro-oxidant activities that degraded the structural integrity of the vessels. Therefore, up-regulated activity of oxidized LDL via macrophage induced inflammation is central to the initiation and progression of atherosclerosis. They are closely associated with plaque development, aggravation and ruptures.
A recent study shows that astaxanthin decreased macrophage occupied lesion areas and therefore inflammation in the vessels of rabbits by 40% compared to control group (figure 5). Furthermore, rabbits that ingested 4mg astaxanthin everyday for 24 weeks decreased programmed cell death (apoptosis) by 42% and cell death (necrosis) by 17% in the aorta (Li et al., 2004).

Figure 5. Astaxanthin decrease chronic inflammation and cell death in the inner lining of the vessels. Chronic inflammation and apoptosis in the endothelium dramatically accelerates vascular degradation and atherosclerotic plaque formation. (Li et al., 2004) Figure 5. Astaxanthin decrease chronic inflammation and cell death in the inner lining of the vessels. Chronic inflammation and apoptosis in the endothelium dramatically accelerates vascular degradation and atherosclerotic plaque formation. (Li <em>et al.</em>, 2004) Rabbits ingested 4mg of placebo, Vitamin E or astaxanthin everyday for 24 weeks.

In-vitro study provides further evidences that astaxanthin (5-10uM) decreases macrophages related activation (SR-A and CD36) by 48% and 58% respectively (Kishimoto et al., 2009). A recent animal studies show that astaxanthin could ameliorate endothelial dysfunction by significantly improving the level of substances important for the regulation of vascular integrity. In more details, treatment with astaxanthin for 42 days decreased serum oxidized LDL cholesterol, aortic MDA levels, attenuated endothelium-dependent vasodilatory to acetylcholine, up-regulate eNOS expression and decreased LDL cholesterol receptor expression (figure 6).

Figure 6. Astaxanthin treatment improved markers of endothelial dysfunction by reducing oxidation of LDL cholesterol and MDA. Higher levels of LDL oxidation and MDA expression highly correlates with structural damages in blood vessels and impairment of blood flow. (Zhao et al., 2011) Figure 6. Astaxanthin treatment improved markers of endothelial dysfunction by reducing oxidation of LDL cholesterol and MDA. Higher levels of LDL oxidation and MDA expression highly correlates with structural damages in blood vessels and impairment of blood flow. (Zhao <em>et al.</em>, 2011) Diabetic rats were treated with 10 mg/kg of astaxanthin or olive oil for 42 days.

Animal studies have also shown that astaxanthin ameliorated structural changes in the blood vessels – reduction in wall thickness by 47% and improved vascular tone by 36% in spontaneously hypertensive rats (Hussein et al., 2006). Such structural changes was observed in the reduction of the number of branched elastin bands and improved vessel wall to lumen thickness ratio.
In another study, 24 weeks supplementation of natural astaxanthin reduced levels of MMP3 expression in the aorta of rabbits – a crucial factor that lead to a degradation of elastin and collagen structures which determines the mechanical properties of connective tissues in the vessels (figure 7). In the experiment, astaxanthin enhanced plaque stability leading to a significant reduction of plaque ruptures (Li et al., 2004).

Figure 7. Astaxanthin inhibit MMP over-expression in the thoracic aorta. Over-expression of MMP is a crucial factor that leads to the degradation of vascular integrity and escalation of atherosclerotic plaque ruptures (Li et al., 2004) Figure 7. Astaxanthin inhibit MMP over-expression in the thoracic aorta. Over-expression of MMP is a crucial factor that leads to the degradation of vascular integrity and escalation of atherosclerotic plaque ruptures (Li <em>et al.</em>, 2004) Animal Study – Rabbits ingested AX 4mg/ Kg of body weight daily x 24weeks

Astaxanthin Improving Vascular Resilience and Capillary Blood Flow

Astaxanthin Improving Vascular Resilience and Capillary Blood FlowGood circulation, quality of blood and resilient vessels are the key features required to fight development and progression of atherosclerosis. Blood rich in antioxidants bring nutrients and oxygen to organs while removing waste through a smooth vascular resilience and capillary flow.
Recent human studies suggest that 6mg daily of astaxanthin can enhance blood flow by 10% in terms of capillary transit time -how fast the blood runs through the vessels (Miyawaki et al., 2008). Another complementary study showed that astaxanthin decreased lower limb vascular resistance by 17% – the degree to which the blood vessels impede the flow of blood (Iwabayashi et al., 2009).(figure 8) High resistance causes an increase in blood pressure, which increases the workload of the heart. In 2005, Nagaki et al., conducted another randomized double-blind study in which 36 subjects who received oral astaxanthin, 6mg/day for 4 weeks experienced a 4% improvement in capillary blood flow (Nagaki et al., 2005).

Figure 8. astaxanthin decreased lower limb vascular resistance (LLVR) – the degree to which the vessels impede the flow of blood. LLVR increase blood pressure and circulatory complications that lead to peripheral vascular diseases, venous thrombosis and painful claudication (Yonei et al., 2009) Figure 8. astaxanthin decreased lower limb vascular resistance (LLVR) – the degree to which the vessels impede the flow of blood. LLVR increase blood pressure and circulatory complications that lead to peripheral vascular diseases, venous thrombosis and painful claudication (Yonei <em>et al.</em>, 2009) 35 healthy postmenopausal women (BMI 22.1) were included in the study, treated with astaxanthin daily dose of 12 mg for 8 weeks.

Astaxanthin Reduces Hypertension

A series of human studies suggest that astaxanthin decreases blood pressure by improving blood flow and vascular tone. In a recent clinical study, 73 subjects, between 20-60 years of age, who received 4mg of astaxanthin for day for 4 weeks showed a significant decrease in systolic blood pressure (Satoh et al., 2009). 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 significantly (Matsuyama et al., 2010).
A series of animal studies have largely replicated the effects of astaxanthin found in human studies (e.g. Ruiz et al., 2010; Preuss, 2011).

Outlook

Clinical studies suggests that oral supplementation of natural astaxanthin (4mg-12mg) may reduce the risk cardiovascular complications by enhancing blood rheology, lipid-metabolism, capillary circulation, vascular resilience and the endogenous antioxidant defense. Other clinical studies have also shown that astaxanthin reduce lipid-peroxidation, LDL cholesterol, blood pressure and DNA damage. Mechanism of action includes inhibition of macrophage-induced inflammation in the endothelium, oxidative stress-induced apoptosis and MPP-induced-structural degradation of the vessels. Furthermore, recent studies have also outlined that astaxanthin ameliorates nitric oxide dependent vessels dilation and reduce sensitivity to the angiotensin.

References

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 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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