Showing posts with label CCRES ALGAE PROJECT. Show all posts
Showing posts with label CCRES ALGAE PROJECT. Show all posts

Thursday, June 2, 2016

Gracilaria Lemaneiformis






Edible seaweed are low-calorie and packed with nutrients. Now scientists have found that a type of commercial red macroalgae could help counteract food allergies. They report their findings, using mice, in ACS’ Journal of Agricultural and Food Chemistry (May 17, 2016).
Food allergies are a major global health issue that can be life threatening. A 2014 study by researchers at Mount Sinai Hospital estimated that the condition affects about 8 percent of children and 5 percent of adults worldwide. In people who are allergic, certain compounds in food trigger a cascade of immune system reactions that lead to symptoms such as hives, wheezing and dizziness — and in the worst cases, anaphylactic shock.



Previous research has suggested that certain seaweed varieties contain polysaccharides with anti-asthmatic and anti-allergy effects. But no one had investigated whether similar molecules in #Gracilaria #lemaneiformis, a commercial variety of red algae, might have similar properties.
Guang-Ming Liu and colleagues wanted to find out. The researchers isolated polysaccharides from G. lemaneiformis and fed them to a group of mice sensitive to tropomyosin, a protein that is a major shellfish allergen. Another group of mice, also sensitive to tropomyosin, did not get the polysaccharides. After both groups were given the allergen, allergy symptoms in the treated mice were reduced compared to the untreated animals. 

CCRES ALGAE TEAM part of Croatian Center of Renewable Energy Sources ( #CCRES )

Thursday, September 24, 2015

CCRES ALGAE Research Programme




Researchers at CCRES ALGAE have been investigating lipids from a variety of seaweed species for their heart-health properties.


Seaweed species of commercial interest in Croatia include Laminaria Digitata and Fucus species (Fucus vesiculosus, Fucus serratus, and Fucus spiralis), which are harvested primarily for their valuable carbohydrates, Laminarin and Fucoidan, respectively. The value-added sector of the seaweed industry in Croatia has emerged to produce attractive, high-quality products for use as functional body care products and cosmetics. However, there is, to date, limited activity aimed at exploiting seaweed resources as materials for functional food ingredients with enhanced health benefits that go beyond basic nutrition for the consumer. The CCRES ALGAE Research Programme is currently working on developing the area of marine-origin functional foods in Croatia.

Seaweeds are known to contain a number of heart-health compounds, including ACE inhibitors, antioxidants, and essential fatty acids (lipids).

As part of a research collaboration with the University of Zagreb, Zeljko Serdar, and Branka Kalle developed methods for the isolation of total lipids from a number of seaweed species.
"Seaweeds are a known source of essential fatty acids, which are thought to reduce thrombosis and atherosclerosis -- factors important in the reduction of the risk of heart disease," explains Serdar.

Of the eight seaweed species used in this study, Fucus vesiculosus had the highest percentage of total lipids per dry weight.

CCRES ALGAE TEAM
part of
Croatian Center of Renewable Energy Sources (CCRES)

Tuesday, May 26, 2015

CCRES Microalgae Process Design



 Microalgae Process Design


    The waters of the world house a tremendous variety of microorganisms able to use light as the only source of energy to fuel metabolism. These unicellular organisms, microalgae and cyanobacteria, have the potential to produce energy sources and biofuels, and many other products. To make economical large-scale production of such bulk products possible, the optimal design of bioreactors and cultivation strategies are essential.
    Target group
    The course is aimed at PhD students, postgraduate and postdoctoral researchers, as well as professionals, that would like to acquire a thorough understanding of microalgal metabolism and photobioreactor design. An MSc level in bioprocess technology, or similar, is recommended.
    Course contents
    This course provides the essential skills for designing optimal microalgae-based production processes, for both research and commercial purposes.
    Through lectures, digital cases and a photobioreactor practical session, the participants will learn:
    1) how to describe microalgal metabolism quantitatively;
    2) how to apply basic design principles and set up mass/energy balances for photobioreactors;
    3) how to cultivate microalgae in fully controlled photobioreactors; and
    4) how to integrate all acquired knowledge into optimal production strategies for microalgae biomass or secondary metabolites.
    The daily programme is divided into approximately 5.5 hours of lectures and digital cases, and 2.5 hours of practical work. On Saturday and Sunday, 1.5 hours will be spent on practical work (microalgae do not stop growing at the weekends...). Saturday will also feature an excursion to the CCRES research facility, Zadar, Zaton, followed by a barbecue.
    The course will be conducted in English and Croatian.
    Course coordinators
    Mr. Zeljko Serdar, President of CCRES
    Mrs. Branka Kalle, President of Council CCRES
    The course will be conducted in English and Croatian.
    Location & accommodation
    Lectures and practicals will be given at Croatian Center of Renewable Energy. Participants have to book their own hotel room.
    Contact information
    More information concerning the course content can be obtained from Mr. Zeljko Serdar (solarserdar@gmail.com).
    For organisational matters please contact Mrs. Aleksandra Maradin, phone: +385-91-5475049.
    Registration
    To be able to fill in the registration form, you need to create an account, please contact solarserdar@gmail.com
    The number of participants to the course is limited.
    The final registration date is 9 June 2014.
    Applicants will receive a confirmation of their registration within one week and will be informed about their acceptance to the course 1 May 2015 at the latest. When accepted to the course they will receive instructions for further course details.
    The course is free for all CCRES members (which includes materials, coffee/tea during breaks, lunches one dinner and one BBQ but does not cover accommodation).


    We look forward to collaborating with you.

    Sunday, May 10, 2015

    FUCOSE




    #Fucose is an essential hexose deoxy sugar the human body needs to optimally communicate from cell to cell. Simply put, it plays an important role in transmitting information in the brain. Research studies show that this sugar stimulates brain development and can also influence the brain to be able to create long-term memories. This is further supported by studies in which doctors inhibited protein containing fucose; amnesia was the result.

    Fucose is found in a number of places in the human body. Its location in the male testes suggests that it may play an important role during reproduction. Also found in the epidermis, it may help in maintaining skin hydration. Beyond these locations, this sugar is found at the articulation between each nerve, in the tubules of the human kidney, and in significant quantities in human breast milk.

    It's important not to confuse this with the similar sounding fructose. While both are sugars that can be commonly found in the body, fructose is a simple monosaccharide sugar found in many foods. For example, you can find a high amount of fructose in baby food, salad dressing, blackberries, tree fruits, honey and even some root vegetables. On the other hand, fucose, as previously stated, can be found in the human body naturally.

    Studies also show that fucose may play a role in certain diseases, such as cancer and its infection method. Though research is not yet conclusive, there is promise shown for using fucose to inhibit both breast cancer and leukemia, in addition to tumor growth, in general. Some studies have even gone as far as to conclude that this hexose deoxy sugar seems to be among the most effective sugars at attempting to prevent cancer cells from growing.

    Research indicates that even taking in fucose in extremely high amounts does not seem to present any real ill side effects, though recommendations are that the average 150-pound (68.2 kg) human adult can safely handle 34 grams of this sugar on a daily basis. During urination, fucose leaves the body, so people who urinate frequently can experience a deficiency in fucose. People with rheumatoid arthritis also generally are deficient in this kind of sugar. Many people opt to take supplements to ensure they have the right amount in their body. Seaweeds such as kelp, beer yeast, and medicinal mushrooms are also a good alternative to supplements and for people who have difficulty taking pills.

    #CCRES #ALGAE TEAM

    Friday, March 20, 2015

    CCRES FUCUS




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

    #Hypothyroidism

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

    Symptoms

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

    #Iodine

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

    #Fucus

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

    #CCRES #ALGAE TEAM

    Tuesday, September 23, 2014

    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.

    Sunday, May 4, 2014

    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) 

    Friday, May 2, 2014

    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)

    Wednesday, April 30, 2014

    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) 

    Friday, December 28, 2012

    Nutrient data for Spirulina

     



    CCRES Spirulina, raw
    Nutrient Unit
    Value per 100.0g
    Proximates
    Water g 90.67
    Energy kcal 26
    Protein g 5.92
    Total lipid (fat) g 0.39
    Carbohydrate, by difference g 2.42
    Fiber, total dietary g 0.4
    Sugars, total g 0.30
    Minerals
    Calcium, Ca mg 12
    Iron, Fe mg 2.79
    Magnesium, Mg mg 19
    Phosphorus, P mg 11
    Potassium, K mg 127
    Sodium, Na mg 98
    Zinc, Zn mg 0.20
    Vitamins
    Vitamin C, total ascorbic acid mg 0.9
    Thiamin mg 0.222
    Riboflavin mg 0.342
    Niacin mg 1.196
    Vitamin B-6 mg 0.034
    Folate, DFE µg 9
    Vitamin B-12 µg 0.00
    Vitamin A, RAE µg 3
    Vitamin A, IU IU 56
    Vitamin E (alpha-tocopherol) mg 0.49
    Vitamin D (D2 + D3) µg 0.0
    Vitamin D IU 0
    Vitamin K (phylloquinone) µg 2.5
    Lipids
    Fatty acids, total saturated g 0.135
    Fatty acids, total monounsaturated g 0.034
    Fatty acids, total polyunsaturated g 0.106




    CCRES Spirulina, dried




    Nutrient Unit
    Value per 100.0g

    cup
    112g

    tablespoon
    7g
    Proximates
    Water g 4.68 5.24 0.33
    Energy kcal 290 325 20
    Protein g 57.47 64.37 4.02
    Total lipid (fat) g 7.72 8.65 0.54
    Carbohydrate, by difference g 23.90 26.77 1.67
    Fiber, total dietary g 3.6 4.0 0.3
    Sugars, total g 3.10 3.47 0.22
    Minerals
    Calcium, Ca mg 120 134 8
    Iron, Fe mg 28.50 31.92 2.00
    Magnesium, Mg mg 195 218 14
    Phosphorus, P mg 118 132 8
    Potassium, K mg 1363 1527 95
    Sodium, Na mg 1048 1174 73
    Zinc, Zn mg 2.00 2.24 0.14
    Vitamins
    Vitamin C, total ascorbic acid mg 10.1 11.3 0.7
    Thiamin mg 2.380 2.666 0.167
    Riboflavin mg 3.670 4.110 0.257
    Niacin mg 12.820 14.358 0.897
    Vitamin B-6 mg 0.364 0.408 0.025
    Folate, DFE µg 94 105 7
    Vitamin B-12 µg 0.00 0.00 0.00
    Vitamin A, RAE µg 29 32 2
    Vitamin A, IU IU 570 638 40
    Vitamin E (alpha-tocopherol) mg 5.00 5.60 0.35
    Vitamin D (D2 + D3) µg 0.0 0.0 0.0
    Vitamin D IU 0 0 0
    Vitamin K (phylloquinone) µg 25.5 28.6 1.8
    Lipids
    Fatty acids, total saturated g 2.650 2.968 0.186
    Fatty acids, total monounsaturated g 0.675 0.756 0.047
    Fatty acids, total polyunsaturated g 2.080 2.330 0.146
    Cholesterol mg 0 0 0

    CCRES special thanks to US National Nutrient Database for Standard Reference

    CCRES ALGAE PROJECT
    part of
    Croatian Center of Renewable Energy Sources (CCRES)