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

 

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 2. Astaxanthin preserved insulin sensitivity in the diabetic mouse model (Uchiyama et al., 2002)

Figure 3. Astaxanthin protected kidney function measured by urinary albumin protein loss (Naito et al., 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 5. Astaxanthin preserved the relative mesangial area.

 
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-?B (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) 

   

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-?B (Manabe et al., 2007) 

 

Table 1. Astaxanthin content in NHMC mitochondria expressed as percentage of total astaxanthin added. 

Mean of 3 samples. (Manabe et al., 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 ?–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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CO2 Capture and Storage CCS

  

 

Everything you wanted to know about
CO2 Capture and Storage (CCS), but had no one to ask .

 

 

1. What is CCS?

CO2 Capture and Storage (CCS) describes a technological process by which the carbon dioxide (CO2) generated by large stationary sources - such as coal- fired power plants, steel plants and oil refineries - is prevented from entering the atmosphere.

That’s because it enables at least 90% of these CO2 emissions to be captured, then stored in geological formations – safely and permanently – deep underground (at least 800m). In fact, it uses the same natural trapping mechanisms which have already kept huge volumes of oil, gas and CO2 underground for millions of years.

Currently, all of the CO2 produced by these large stationary sources is released into the atmosphere – directly contributing to global warming.

2. Why is it a critical technology for combating climate change?

CCS is the single biggest lever to combat climate change (compared to, for example, energy efficiency which requires many different actions). In fact, CCS has the potential to address almost half of the world’s current CO2 emissions.

Experts estimate that by 2050, CCS could reduce annual CO2 emissions by 0.6 to 1.7 billion tonnes in the EU and by 9 to 16 billion tonnes worldwide. The upper end of this range would require its application to all fossil fuel power plants and to almost all other large industrial emitters – with the large volumes of hydrogen produced used for transport fuel.

3. What other benefits will CCS provide?

In addition to its potential to reduce CO2 emissions on a massive scale, CCS will also provide greater energy security – by making the burning of Europe’s abundant coal reserves more environmentally acceptable and reducing its dependency on imported natural gas. CCS could also facilitate the transition to a hydrogen economy through the production of large volumes of clean hydrogen which that could be used for electricity or transport fuel.

EU demonstration efforts on CCS will not only demonstrate the EU’s commitment to delivering on its own CO2 reduction targets, but spur other countries to do the same – especially large CO2 emitters, such as China, India and the US. As a global solution to combating climate change, CCS could therefore also give a major boost to the European economy – promoting technology leadership, European competitiveness and creating jobs.

4. How does CCS work?

CCS consists of three stages:
i. Capture: CO2 is captured and compressed at the emissions site.
ii. Transport: The CO2 is then transported to a storage location.
iii. Storage: The CO2 is permanently stored in geological formations, deep underground.

Each of these stages – capture, transport and storage – can be accomplished in different ways.

i. Capture processes:

    Post-combustion: CO2 is removed from the exhaust gas through absorption by selective solvents.
    Pre-combustion: The fuel is pre- treated and converted into a mix of CO2 and hydrogen, from which the CO2 is separated. The hydrogen is then used as fuel, or burnt to produce electricity.
    Oxy-fuel combustion: The fuel is burned with oxygen instead of air, producing a flue stream of CO2 and water vapour without nitrogen; the CO2 is relatively easily removed from this stream.

ii. Transport options:
Pipelines are the main option for large-scale CO2 transportation, but shipping and road transport are also possibilities.

iii. Storage options:

    Deep saline aquifers (saltwater-bearing rocks unsuitable for human consumption)
    Depleted oil and gas fields (with the potential for Enhanced Oil Recovery)

5. How long has CCS been in existence?

Although there are currently no fully integrated, commercial-scale CCS projects for power plants in operation, many of the technologies that make up CCS have been around for decades:

    CO2 capture is already practised on a small scale, based on technology that has been used in the chemical and refining industries for decades.
    Transportation is also well understood: it has been shipped regionally for over 17 years, while a 5,000km network has been operating in the USA for over 30 years for Enhanced Oil Recovery.
    Small-scale CO2 storage projects have been operating successfully for over a decade, e.g. at Sleipner (Norway), Weyburn (Canada) and In Salah (Algeria). The industry can also build on knowledge obtained through the geological storage of natural gas, which has also been practised for decades.

6. What’s the next step?

CCS technology now needs to be scaled up – including full process integration and optimisation – with demonstration projects of a size large enough to allow subsequent projects to be at commercial scale. This will also build public confidence in CCS as more and more people see that CO2 storage is safe and reliable.

7. Why should we use CCS, given its link to fossil fuels?

Scientists have confirmed that unless we stabilise CO2- equivalent concentrations at their current level of 450 parts per million (ppm), average global temperature is likely to rise by 2.4ºC to 6.4ºC by 2100. If we fail to keep below 2ºC, devastating – and irreversible – climate changes will occur.

This means reducing CO2-equivalent emissions by 50% by 2030. But with world energy demand expected to double by 2030 and renewable energies to make up ~30% of the energy mix by this date, only a portfolio of solutions will achieve this goal. This includes energy efficiency, a vast increase in renewable energy – and CCS.

Around 750 new coal power plants are already planned for the period 2005–2018, totaling more than 350 Gigawatt (GW), of which 50 will be in Europe, almost 300 in China, 200 in India and 50 in the US.

8. Why is it so important to deploy CCS as soon as possible?

Time is of the essence. Any delay in the roll-out of CCS could not only lead to unnecessary CO2 emissions but additional costs, as instead of being able to apply it to the current pipeline of coal plants, a retrofit would be required, increasing the cost of achieving the same emissions reduction. With decisions on the building of new power plants being made now in Europe, it is vital that we are not locked into an infrastructure that is not optimised for CCS.

Indeed, every year that CCS is delayed is a missed opportunity to reduce CO2 emissions. Today, we have ~450 parts per million (ppm) CO2 equivalent in the atmosphere, with concentration rising at over 2 ppm per annum. The Intergovernmental Panel on Climate Change states that if we are to avoid major climate change effects, we must not exceed this 450 ppm. Delaying the implementation of CCS by just 6 years would mean CO2 concentrations increasing by around 10 ppm by 2020.

9. If we are at such a critical phase, why isn’t it already being deployed?

The incremental costs of the first large-scale CCS demonstration projects will be exceptionally high – too high to be fully justifiable to company shareholders.

That’s because all ‘First Movers’ will incur:

    Unrecoverable costs from making accelerated investments in scaling up the technology.
    Market risk due to uncertainty over:
    a) which CCS technologies will prove the most successful
    b) the future CO2 price and
    c) construction and operational costs.

Based on an independent study recently undertaken by McKinsey and Company, it is estimated that the total incremental costs of 10-12 CCS demonstration projects would be €7 billion - €12 billion.

Industry has already declared its willingness to cover both the base costs of the power plant (without CCS) and a major portion of the risks of implementing these CCS demonstration activities. Given that it will bring incalculable benefits to both the public and European industry and that these projects are inherently loss-making, public funding has therefore been provided to support 12 industrial-scale CCS projects. Without this, commercialisation will be severely delayed – until at least 2030 in Europe.

10. Why are public funds needed for CCS demonstration projects?

Currently, a CCS demonstration project would be a loss-making enterprise for industry, given the current price of implementing and using the technology; the current price of carbon; and uncertainty surrounding long-term viability and profitability. No shareholder can therefore be expected to fund it fully at this stage.

The typical cost of a demonstration project is likely to be in the range €60-90 per tonne of CO2 abated. Recent analyst estimates for Phase II of the European Union Emissions Trading Scheme (EU ETS) range from €30 to €48 per tonne of CO2 and, at this stage, similar levels are assumed beyond Phase II (up to 2030). In this range, the carbon price is insufficient for demonstration projects to be “stand-alone”, commercially viable.

Assuming that CCS demonstration projects would cost between €60 and €90 per tonne of CO2, and projecting a median carbon price of €35 per tonne of CO2, there is an “economic gap” of €25-€55 per tonne of CO2 per project. This corresponds to around €500 million - €1.1 billion, expressed as a Net Present Value (NPV) over the lifespan of a 300MW size power plant. The range depends on variations in specific project variables, such as capture technology and capex, transport distance and storage solutions.

11. The UK and the Netherlands are well on their way to implementing CCS demonstration projects – won’t these be enough to make the technology commercially viable?

As it is not yet known which CCS technologies will prove the most successful, it is vital that the full range is tested – including higher-risk technologies – optimised across projects and locations. As each region has its own challenges, local demonstration is also important in order to maximise public and political support.

As importantly, EU CCS demonstration efforts will ensure that cross-border projects – where CO2 is stored in a different country or region to where it is captured – are not excluded. As capture and storage locations are unevenly distributed throughout Europe, cross-border pipelines will play a crucial role in the wide-scale deployment of CCS and the development of clusters in major industrial areas as the next key step.

12. How much will it cost to retrofit CCS technology to existing power plants?

In general, retrofitting an existing power plant would lead to a higher cost for CCS, but these are highly dependent on specific site characteristics, including plant specifications, remaining economic life and overall site layout. For this reason, no generalisation or “reference case” would be meaningful.

There are four main factors likely to drive the cost increase for retrofits:

    The higher capex (capital costs) of the capture facility: the existing plant configuration and space constraints could make adaption to CCS more difficult than for a new build.
    The installation’s shorter lifespan: the power plant is already operating so where (for example) a new plant with CCS may run for 40 years, the capture facility of a 20 year-old plant is likely to have only a 20 year life, reducing the “efficiency” of the initial capex.
    There is a higher efficiency penalty, leading to a higher fuel cost when compared to a fully integrated, newly-built CCS plant.
    There is the “opportunity cost” of lost generating time, because the plant would be taken out of operation for a period to install the capture facility.

13. How can we accelerate the building of CCS projects?

Building a CCS project is a lengthy process: a fully integrated project can take 6.5-10 years before it becomes operational. However, Final Investment Decision can only be made once permits have been awarded across the entire value chain. In the case of CO2 storage, this can take as long as 6.5 years. In such a scenario, even a commercial project started as early as 2016 would not itself become operational until 2024.

Ideally, 10-12 CCS demonstration projects should be operational by 2015. The first early commercial projects should be operational by 2020, with the remaining demonstration projects sufficiently advanced for early commercial projects to be ordered from 2020 onwards. Some 80-120 large- scale CCS projects could therefore be operational in Europe by 2030.

There are several ways we can fast-track the building of CCS projects:

    Starting a commercial project as early as possible during the building of the demonstration project so that – for example – build can start after just one year of the demo being in operation.
    Accelerating feasibility studies etc.
    Making faster investment decisions
    Shortening the tender process
    Introducing special measures to shorten the permitting process.

Some projects, by their very nature, will of course be quicker to build than others, e.g. retrofitting existing power plants with CCS; using well-known oil and gas fields with infrastructure and seismic data already available; those with only a short distance from the power plant to the storage site, etc.

14. How much CO2 can be captured using CCS?

One 900 MW CCS coal-fired power plant can abate around 5 million tonnes of CO2 a year. If, as projected, 80-120 commercial CCS projects are operating in Europe by 2030, they would abate some 400 million tonnes of CO2 per year.

By 2050, CCS could reduce annual CO2 emissions by 0.6 to 1.7 billion tonnes in the EU and by 9 to 16 billion tonnes worldwide. The upper end of this range would require its application to all fossil fuel power plants and to almost all other large industrial emitters – with the large volumes of hydrogen produced used for transport fuel.

15. Isn’t more energy utilised where CCS is implemented?

The absolute efficiency penalty, estimated at around 10% for the reference case (meaning plant efficiency drops from 50% to around 40%), drives an increase in fuel consumption and does require an over- sizing of the plant to ensure the same net electricity output.

However, next-generation technology - such as ultra-supercritical 700°C technology for boilers, coupled with drying in the case of lignite - will achieve a 50% level of overall plant efficiency. While this technology is not currently available, it is expected to be when early commercial CCS projects are built around 2020.

16. Where will CO2 be stored?

The regional distribution and cost of storage in Europe will play an important role in any roll-out of CCS. Most experts agree that depleted oil and gas fields and deep saline aquifers have the largest storage potential.

Depleted oil and gas fields
Depleted oil and gas fields are well understood and around a third of total oil and gas field capacity in Europe is estimated to be economically useable for CO2 storage. With an estimated capacity for 10 to 15 billion tonnes of CO2, this is sufficient for the lifetime of around 50 to 60 CCS projects. However, most of these fields are located offshore in northern Europe and the transportation to and storage of CO2 in these fields (excluding capture) is around twice as costly as onshore fields.

Deep saline aquifers
While much less work has been done to map and define deep saline aquifers, most sources indicate that their capacity should be sufficient for European needs overall. Preliminary conservative estimates by EU GeoCapacity indicate that Europe can store some 136 billion tonnes of CO2 - equivalent to around 70 years of current CO2 emissions from the EU’s power plants and heavy industry. At the higher end of these estimations, EU GeoCapacity estimates some 380 billion tonnes of CO2 could be stored in Europe alone.

17. Storing enormous quantities of CO2 underground must present some risk?

The geological formations that would be used to store CO2 diffuse it, making massive releases extremely unlikely. Indeed, because the CO2 becomes trapped in the tiny pores of rocks, any leakage through the geological layers would be extremely slow, allowing plenty of time for it to be detected and dealt with. In fact, it would not raise local CO2 concentrations much above normal atmospheric levels.

Higher concentration leaks could come from man-made wells, but the oil and gas industry already has decades of experience in monitoring wells and keeping them secure. Storage sites will not, of course, be located in volcanic areas.

18. But won’t CO2 storage increase the likelihood of seismic activity?

A detailed survey takes place to identify any potential leakage pathways before a CO2 storage site is selected. If these are discovered, then the site will not be selected. In areas where some natural seismic activity is already taking place, we can ensure that the pressure on the CO2 does not exceed the strength of the rock by making the volume of CO2 stored relative to that of the storage site. CO2 storage has even proved to be robust in volcanic areas: in 2004, a storage site in Japan endured a 6.8 magnitude earthquake with no damage to its boreholes and no CO2 leakage. But then CO2 has remained undisturbed underground for millions of years – despite thousands of earthquakes.

19. How will we know if the CO2 is leaking?

Before a CO2 storage site is chosen, a detailed survey takes place to identify any potential leakage pathways. If these are found to exist then the site will not be selected. In Europe, underground gas storage (natural gas and hydrogen) has an excellent safety record, with sophisticated monitoring techniques that are easily adaptable to CCS. On the surface, air and soil sampling can be used to detect potential CO2 leakage, whilst changes underground can be monitored by detecting sound (seismic), electromagnetic, gravity or density changes within the geological formations.

The risk of leakage through man-made wells is expected to be minimal because they can easily be monitored and fixed, while CO2 leaking through faults or fractures would be localised and simply withdrawn; and, if necessary, the well closed.

20. Who will be liable for CO2 storage sites over the long-term?

As the CO2 will remain stored underground indefinitely, long-term liability will follow the example set by the petroleum industry, whereby the state assumes liability after a regulated abandonment process. Indeed, EU law governing the safe and permanent storage of CO2 has already been approved and is currently being implemented at national level.

21. Large stationary emitters of CO2 also include refineries, steel and cement plants - how are they linked into what the EC is doing?

The EC encourages the deployment of CCS in other sectors, as 25% of all European CO2 emissions addressable by CCS come from refineries and the cement, iron and steel industries.

 

The European CCS Demonstration Project Network

The EC has established a Network of CCS demonstration projects to generate early benefits from a coordinated European action.
CCS demonstration projects fulfilling minimum qualification criteria are invited to join the Network and benefit from its operations.
The Network allows early-movers to exchange information and experience from large-size industrial demonstration of the use of CCS technologies, to maximise their impact on further R&D and policy making, and optimise costs through shared collective actions.
It is envisaged that, as the Network evolves, its EU-wide, integrating and binding role may be reinforced and complemented by other measures in support of further development of CCS technologies, building towards the establishment of a European Industrial Initiative.

To help fulfil the potential of CO2 Capture and Storage (CCS), the European Commission is sponsoring and coordinating the world’s first network of demonstration projects, all of which are aiming to be operational by 2015. The goal is to create a prominent community of projects united in the goal of achieving commercially viable CCS by 2020.
The CCS Project Network fosters knowledge sharing amongst the demonstration projects and leverage this new body of knowledge to raise public understanding of the potential of CCS. This accelerates learning and ensures that we can assist CCS to safely fulfil its potential, both in the EU and in cooperation with global partners.

CCS Project Network Advisory Forum

To guarantee that the Network is valuable to the wider energy community in Europe, an annual Advisory Forum has been established to review progress and specify the knowledge that can most usefully be generated by the CCS Project Network.

• The first Advisory Forum meeting was held in Brussels on 17 September 2010.
  Read more..
• The second Advisory Forum Meeting was held on 16 June 2011 in Brussels. Read more..

CCS World News

• 2012-07-18 - Carbon capture would create substantial challenges, witnesses say at energy ...
• 2012-07-18 - Opinions Divided on Climate Change and CCS in Saskatchewan
• 2012-07-18 - Planned Tees CCS project could be in line for EU cash
• 2012-07-13 - Yorkshire leads race for €1.5bn EU carbon capture funding
• 2012-07-16 - Codexis releases enzyme CO2 capture results
• 2012-07-16 - U.S. DOE advancing Hydrogen Energy plant in California
• 2012-07-16 - Yorkshire leads race for €1.5bn EU carbon capture funding ...
• 2012-07-15 - UK Don Valley project leads EU funding bid
• 2012-07-15 - Alberta projects get funding boost
• 2012-07-13 - Don Valley leads UK CCS charge for €1.5bn EU funds
• 2012-07-13 - EU says up to 1.5 billion euros ready for low-carbon investment
• 2012-07-12 - Anglo mines to become carbon neutral, CCS-aware by 2030
• 2012-07-12 - Clean coal tech is ready, but theres a catch

Membership of the CCS Project Network is open to all European projects that are at a sufficient scale and level of maturity that will generate valuable output and knowledge about industrial-scale CCS demonstration.
The application process for membership of the Network is designed to be as simple and transparent as practicable, but sufficiently robust to ensure that all members are large-scale demonstration projects at a similar level of maturity.
Project developers may submit applications at any time to demonstrate that they fulfil the eligibility criteria, can provide evidence of the maturity of the project, commit to knowledge sharing and agree to the Network organisation and procedures. The qualification criteria and application process are described in the Qualification Criteria document. The Network is open to all qualifying projects and will not distinguish between EU-funded and non-EU funded projects.

Eligibility Criteria

Projects in the Network shall have sound plans to demonstrate the full CCS value chain by 2015 and shall fulfil the following technical criteria:

• The CCS project shall for a fossil fuel-fired power plant have a minimum gross production of 250MWe before CO2 capture and compression
• The CCS project shall for an industrial plant realise a minimum of 500kt per year of stored CO2
• The CO2 capture rate shall not be less than 85% of the treated flue gas stream
• The project, i.e. the plant to which CCS is applied, shall be located within the European Economic Area (EEA)

Knowledge Sharing

Projects in the Network are committed to knowledge sharing with similar projects and other stakeholders in order to help accelerate CCS deployment and raise public engagement, as described in the Knowledge Sharing Protocol document.

Key documents

European CCS Demonstration Project Network Qualification Criteria
European CCS Demonstration Project Network Knowledge Sharing Protocol

Learn more about CCS

To learn more about CCS, please have a look at the following videos, kindly provided by ZEP:

http://www.ccsnetwork.eu/index.php?p=videos

CROATIAN CENTER of RENEWABLE ENERGY SOURCES (CCRES)
special tanks to

Daniel Rennie
Global CCS Institute
Actualis, Level 2
21 & 23 Boulevard Haussmann
PARIS 75009 France

---

Jose Manuel Hernandez
Programme Manager - EU Policies
European Commission

CROATIAN CENTER of RENEWABLE ENERGY SOURCES (CCRES)

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CCRES Algae Astaxanthin

CCRES Algae Astaxanthin

Astaxanthins ability to scavenge free radicals in your body* is up to...

    550 times more powerful than vitamin E
    65 times more powerful than vitamin C
    54 times more powerful than beta-carotene
    5 times more powerful than lutein

CCRES ALGAE

It does this by quenching a molecule called singlet oxygen - a harmful reactive oxygen species formed through normal biological processes occurring in your body.* Singlet oxygen possesses a high amount of excess energy that must be released to keep it from damaging other cells.

CCRES Lab

Astaxanthin absorbs this energy and dissipates it as heat, thereby returning the singlet oxygen to a grounded state.*

Theres another way, too, that astaxanthin helps to protect cells, organs and tissues against oxidative damage from free radicals.*

CCRES Algae Astaxanthin

It traps free radicals at both ends of the molecule.* Once captured, the potentially harmful free radicals pass into cellular fluids where they become neutralized by vitamin C. In this way, astaxanthin is sometimes considered a ‘booster for other antioxidants like vitamins A, C and E.*

Whats more, astaxanthin cant act as a potentially detrimental “pro-oxidant” like some of the other carotenoids such as beta-carotene, lycopene, and zeaxanthin.

CCRES CO2

    Support your joint health, flexibility, and mobility*
    Support a healthy immune response*
    Support your central nervous system*
    Support your cardiovascular system*
    Support your brain and eye health due to its unique ability to cross blood-brain and blood-retina barriers*

CCRES ALGAE PROJECT

part of 

Croatian Center of Renewable Energy Sources (CCRES)

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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

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Merry Christmas!

Merry Christmas!

From everyone at 

Croatian Center of Renewable Energy Sources, we wish you very happy holidays and a prosperous new year.

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Benefits of Astaxanthin

                                                                       Astaxanthin

Astaxanthin is a naturally occurring high-value  ketocarotenoid pigment with excellent antioxidant effects belonging to the  xanthophyll group of carotenoids, or the oxygenated carotenoids.  The hydroxyl and keto functional groups  present in the ending ionone ring of astaxanthin  is responsible for its uniquely powerful  antioxidant activity. They differs from other antioxidants in its ability to  penetrate the blood brain and retina barriers. Therefore, it is believed to  protect the brain and nervous system from neurodegenerative diseases (e.g.  cerebral thrombosis and stroke) and aging. 

Natural astaxanthin production  and commercialization is estimated to be a 1.2 billion dollar annual market.  Today, essentially all commercial astaxanthin for aquaculture is produced  synthetically from petrochemical sources, with an annual turnover of over $200  million, and a selling price of around $2000 per kilogram of pure astaxanthin.  Natural astaxanthin is sold for over $7000 per kg.

Source of Astaxanthin
Astaxanthin is present in many types of seafood, including  salmon, trout, red sea bream, shrimp and lobster, as well as in birds such as  flamingo and quail. As of today, astaxanthin is commercially produced from the  microalga Hematococcus pluvialis.
Benefits of Astaxanthin

• Astaxanthin acts as a chain-breaking  anti-oxidant, and therefore protect lipid-rich cell membranes from degradative  oxidation.
• Natural astaxanthin is a dietary supplement  with extremely powerful antioxidant benefits for human applications.
• Astaxanthin traps more free radicals than any  other antioxidant. 
• Astaxanthin has been proven to cross the human  blood-brain barrier, and therefore has the ability to directly act as a superb  antioxidant in the brain and the eyes.
• Astaxanthin enhances the action of other  antioxidants like Vitamin E and C.
• Astaxanthin protects nucleic acid components  of DNA, avoiding mutations to genetic material due to oxidative stress and  protects muscle cells from damaging effects of active oxygen produced upon  swimming upstream.
• Astaxanthin has been documented to  prevent age-related macular degeneration (AMD) and enhance immune functions.

Applications of Astaxanthin

• Astaxanthin finds application in  the nutraceutical Industry, pharmaceutical  Industry and food coloration application
• Astaxanthin is  used as an animal feed additive to impart  coloration to salmonids (salmon and trout), as well as to red sea bream and  Tai.
• Recent studies revealed the wrinkling  and moisturizing effect of astaxanthin which suggest its potential  cosmeceutical applications in protection against skin aging.

Algae Strains for Astaxanthin Production

The most commonly  used algae strain that is used for Astaxanthin production is Haemotococcus Pluvalis. H  pluvialis is believed to accumulate the highest levels of astaxanthin in  nature. Commercially grown H pluvialis can accumulate more than 40g  of astaxanthin per kilogram of dry biomass. Other strains that could be used  for astaxanthin production include: Chlorella vulgaris, Chlorella zofingiensis,  Coelastrella striolata var. multistriata

Haematocyst of Haemotococcus pluvialis with red pigment astaxanthin.

Astaxanthin

Commerical Production of Astaxathin
Natural astaxanthin is produced in a two-stage culture process and its concentration can reach 1.5% to 4% of the dry weight.



Market Scope
The demand for natural astaxanthin is now emerging in the multi-billion dollar nutraceutical market. Astaxanthin is principally consumed by the salmon feed industry. The annual worldwide aquaculture market of this pigment is estimated at US$ 200 million with an average price of US$ 2500/kg.
The global astaxanthin market is estimated at about $257 million, most of which is used in fish coloration (2009 data; estimates by BCC Research for astaxanthin market size are however lower). The human uses market is growing and estimated at about $27-$40 million. Most astaxanthin is derived from the algae, H pluvialis, which is commonly consumed by fish and crustaceans – like salmon and lobster – and is responsible for their pink coloration.

Market Sectors	Market Size   ( as of 2009) ( Million USD)	Potential Market(2020) ( Million USD)
Animal feed colouring agents	300	800
Antioxidant nutraceuticals	30	300
Pharmaceuticals	Emerging	500
Cosmetics	Emerging	30

Table: Market Sectors and Future Market Potential  of Astaxanthin

Prominent Players in the Astaxanthin Market

Company	Location
Alga Technologies	Israel
Cyanotech	Hawaii
CCRES	Croatia
Algaetech International	Malaysia
Parry Nutraceuticals	India
Mera Pharmaceuticals Inc.,	Hawaii
Fuji Chemicals	Japan, Sweden
Valensa International	Florida

University and Research Efforts
Arizona State University – Recently developed a harvesting system for Astaxanthin production from Hematococcus combining acidification and dissolved air flotation. This system is capable of harvesting more than 95% of the biomass without the need for a coagulant or flocculent, and extracting over 95% of the intracellular astaxanthin from Haematococcus biomass.	Ben-Gurion University of Negev Professor Sammy Boussiba of the Microalgal Biotechnology Laboratory in the Ben Gurion University of Negev has developed the biotechnology of producing astaxanthin-rich Haematococcus pluvialis biomass.

Challenges in Astaxanthin Production

• Although natural sources have long been exploited for astaxanthin production, it is still uncertain if natural astaxanthin can be produced at lower cost than that of synthetic astaxanthin or not.
• One of the major limitations with the H pluvialis production system is that the astaxanthin gets trapped behind thick cells walls, thus complicating the extraction process and the production yields.
• Production capacity of H pluvialis is constrained by its intrinsic slow growth, low cell yield, ease of contamination by bacteria and protozoa, and susceptibility to adverse weather conditions. These challenges are magnified as processes are scaled up, and therefore require advanced technology to control

H pluvialis cannot be efficiently cultivated in dark heterotrophic mode, which requires high levels of irradiance, making the process economically less reasonable.
Astaxanthin - Factoids

• One of the technical challenges to developing Haematococcus algae astaxanthin has been the tough cell wall of the spores, which must be ruptured to allow the cell contents to be effectively digested by animals.  Cyanotech Corporation in Hawaii uses a combination of closed photobioreactors and open culture ponds to successfully mass produce astaxanthin-rich Haematococcus biomass, and proprietary milling technology to crack the cell walls.
• Commercial production of astaxanthin is being carried out in USA, India, Japan and Israel
• Astaxanthin is a carotenoid. Astaxanthin has been shown in studies to have 100-500 times the antioxidant capacity of Vitamin E as well as 10 times beta-carotene’s antioxidant capacity. Astaxanthin is found in many places in nature, but it is usually in small quantities as in salmon or shrimp.  
• By far the most concentrated and natural source of astaxanthin is the Haematococcus pluvialis algae.  These green algae also provide other important carotenoids such as beta-carotene. It accumulate the highest levels of astaxanthin in nature; commercially more than 40g of astaxanthin per kilo of dry biomass.
• Research shows that due to astaxanthins potent antioxidant activity, it may be beneficial in cardiovascular, immune, inflammatory and neurodegenerative diseases. Some sources have demonstrated its potential as an anti-cancer agent. Research supports the assumption that it protects body tissues from oxidative damage. It also crosses the blood-brain barrier, which makes it available to the eye, brain and central nervous system to alleviate oxidative stress that contributes to ocular, and neurodegenerative diseases such as glaucoma and Alzheimers.
• Astaxanthin, as other carotenoids, can act as a quencher of singlet oxygen and other free radicals by absorbing the excited energy of singlet oxygen onto the polyene electron-rich chain, resulting first in the excitation of the carotenoid to a triplet state, and then in the dissipation of the extra energy in the form of heat by relaxation back to the ground state. In this way, it prevents cellular components or tissues from being damaged. The carotenoid structure remains unchanged, and ready to act as a radical quencher.
• Astaxanthin has been shown to protect against free radicals and promote numerous health functions. Astaxanthin offers protection against a broad range of human diseases like neuro-degenerative disorders. The antioxidant of astaxanthin is stronger than ?-carotene and vitamin E by 40x and 1,000x respectively.

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

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CCRES Microalgae Process Design

CCRES Microalgae Process Design

Join the ranks of hundreds of 
Energy Day organisers across Europe for the 
2015 EU Sustainable Energy Week!

CCRES 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).

More info : 

http://www.eusew.eu/component/see_eventview/?view=see_eventdetail&index=2&countryID=55&sort=4&pageNum=0&eventid=4478&mapType=europe&keyword=&city=&organiser=&eventDate=&eventType=-1

We look forward to collaborating with you.

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The Effects of Astaxanthin 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.

 

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

 

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  

   

 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)  

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 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)

   

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

   

Rate of positive accommodation improves with 6 mg astaxanthin

Figure 5. Negative accommodation (Shiratori et al., 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)  

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)  

 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-?B positive cells in eye ciliary body during inflammation (Suzuki et al., 2006)

   

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

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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