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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Environment

Quality of life for the planet

Need for high quality water and other resources

Clean water is the primary pre-requisite to successful aquaculture. A clean environment is therefore critical for its commercial success. Any environmental impact that would compromise the quality of the water used on fish farms must be monitored and minimised through appropriate siting (choice of locations) of farms and production processes.

 In recent years, the development of aquaculture has raised some associated environmental concerns. Like any farming operation on land, fish farm cages produce waste materials. These fall into three categories - uneaten feed, fish faeces and dead fish. Most of the environmental impacts of aquaculture can be managed and minimised through understanding of the processes involved, responsible management and the effective siting of farms.

 Uneaten feed - Should uneaten feed reach the bottom of a cage, processes that break it down can reduce the amount of oxygen in the sediment. In severe cases, oxygen levels in the water above may also decrease, creating "anoxic" conditions in which only a few animal species can survive. Should the feed contain antibiotics used to treat the farmed fish above, bacteria in the sediment and the natural breakdown of waste material might be affected.

In practice, fish farmers do everything they can to prevent such a situation, since the cost of fish feed amounts up to 40 percent of the total production cost. Feed reaching the sediment is lost, and it is in the farmers interest to minimise such waste. On well-managed farms, feeding is carefully regulated to ensure that the maximum amount of food is taken up directly by the fish and farmers aim to ensure that less than 5 percent of the feed is wasted. To improve uptake by fish, feed pellets are manufactured to either float or to sink slowly through the water.

Fish faeces - Unlike land animals, fish do not generally produce compact solid faecal material and more often excrete a loose cloud of faecal material that is easily dispersed by water currents. In still conditions, however, faecal material can build up beneath fish cages. It is, however, not in the farmers interest to let this happen, since the buildup of faecal material can lead to anoxic conditions which affect the fish above. Fish farmers wanting to ensure the health of their fish will frequently check the bottom below their fish cages to ensure that faecal material is not building up. In addition, in many EU Member States, the government employs diving teams to carry out inspections.
If faecal build-up is observed, farmers will be advised to move their cages, allowing the bottom to recuperate for a short period, however full recovery typically takes between three to ten years. In recent years, improved feed formulations have also been introduced that fish digest more efficiently, producing less waste.

Fish farmers generally avoid overly sheltered and stagnant sites, preferring areas that contain a healthy flow of water through the cages. Such flows disperse fish faeces so it can enter the natural food chain.

Dead fish - Dead fish are a loss to the farmer and a potential health hazard to the stock as well as a source of pollution. Fish farmers will, at all times, endeavour to minimise the number of dead fish on their farms and to remove such mortalities where they occur.

Fish farms are required to report significant fish deaths when they occur and are inspected by state agencies at least twice a year.

Shellfish cultivation

Shellfish such as oysters, mussels and clams are filter feeders and take their food directly from the water in which they live. This means that they do not require supplementary food and, if anything, actually improve the quality and clarity of the water. Shellfish farming can only provide the best quality products if practiced in pristine environments with the highest water quality.

Environmental problems can arise on shellfish farms where the animals are held at overly high densities, leading to depletion of food in the water and build-up of faeces below the holding areas. Both effects will harm the outcome for the farmer and hence shellfish farms are generally sited where water exchange is high and the stock is kept at densities that are compatible with the level of water exchange. In many cases, stocking densities on farms are lower than those of clusters of shellfish (e.g. mussels) that occur on natural beds.

Shellfish farms have been thought to disturb wildlife habitats by taking up space on a beach where wading birds feed. It has been shown, however, that wading birds and oyster farms can exist side by side. The fallen oyster or mussel can have a positive impact on a birds feeding pattern.

Other potential impacts include the importation of parasites, pests and diseases onto the shellfish farm which would then spread to other areas. The microscopic oyster parasite Bonamia ostrea, for example, gradually spread through Europe with the spread of oyster farming. Oyster farmers have responded by significantly reducing the density at which their shellfish are farmed.

Some people complain of "visual pollution" caused by large numbers of floating barrels or shellfish trestles in otherwise unspoilt areas. Low-profile and dark-coloured floats have recently been developed to minimise the visual impact.

Pond fish farming

Fish pond systems represent the oldest fish farming activity in Europe, at least dating back to medieval times. Ponds were built in areas where water supply was available and the soil was not suitable for agriculture. The wetlands of Central and Eastern Europe are good examples of this. The total European production from pond farming is approximately 475,000 tonnes. About half of this production is cyprinid fish, such as common carp, silver carp and bighead carp. The main producer countries are the Russian Federation, Poland, Czech Republic, Germany, Ukraine and Hungary.

Typical fish ponds are earthen enclosures in which the fish live in a natural-like environment, feeding on the natural food growing in the pond itself from sunlight and nutrients available in the pond water.

In order to reach higher yields, farmers today introduce nutrients into the pond such as organic manure. This is accompanied by stocking of fingerlings and by water being flushed through the pond. Fish pond production, however, remains ‘extensive or ‘semi-intensive (with supplementary feeding) in most countries, where semi-static freshwater systems play an important role in aquaculture. Chemicals and therapeutics are not usually used in such ponds. Hence the main environmental issue is the use of organic fertilisers, which may cause eutrophication in the surrounding natural waters. The use of organic fertilisers is regulated at national levels.

Extensive fish ponds are usually surrounded by reed belts and natural vegetation, thus providing important habitats for flora and fauna. They play a growing role in rural tourism. Many pond fish farms have been turned into multifunctional fish farms, where various other services are provided for recreation, maintenance of biodiversity and improvement of water management.

In areas where water is scarce, some farm systems recirculate, treat and re-use their water. Such systems are generally self-contained and therefore pose little threat to the environment. Solid waste material produced in such systems is rich in organic compounds and often used as a fertilizer elsewhere. Alternatively, new hydroponic systems have been developed to grow vegetables and other food crops in the nutrient-enriched water. There is much interest in these systems, but their economic viability remains challenging.

Trout farming in flow-through systems

 The most widely-practiced form of inland aquaculture in Europe is trout farming. Water is taken from the river, circulated through the farm and treated before being released downstream. All water in the farm is renewed at least once per day. Where more than one farm exists on the same river, it is in everyones interests that the quality of the outflowing water from one farm is good, as this then becomes the inflowing water for the next farm. Other water sources include spring water or drilled and pumped ground water. In some countries, heated industrial water sources (such as electricity generating plants) are used to increase the water temperature (by heat exchange)
used in the farm, thereby saving energy costs to heat the water. Geothermal water also provides naturally warmed water, thus allowing the farming of new fresh water species (especially eel, sturgeon, perch and tilapia) with low environmental impact.

Recirculation Aquaculture Systems

Recirculation Aquaculture Systems (RAS) are land-based systems in which water is re-used after mechanical and biological treatment so as to reduce the needs for water and energy and the emission of nutrients to the environment. These systems present several advantages such as: water and energy saving, a rigorous control of water quality, low environmental impacts, high biosecurity levels and an easier control of waste production as compared to other production systems. The main disadvantages are high capital costs, high operational costs, requirements for very careful management (and thus highly skilled labour forces) and difficulties in treating disease. RAS is still a
small fraction of Europes aquaculture production and has its main relevance in The Netherlands and Denmark. The main species produced in RAS are catfish and eel but other species are already being produced using this type of technology such as turbot, sea bass, pikeperch, tilapia and sole.

Other environmental impacts of fish farming - the case of escaped fish

It is inevitable that fish farmed in net pens in either fresh or salt water will sometimes escape into the wild. In some cases, there will be a small but steady release of fish. Sometimes, large numbers will escape due to severe damage to the net pen by way of storms, predator attacks or vandalism.

 There has been vigorous debate on the potential impact of escaped farmed fish, in particular salmon, on wild populations. On the one hand, it has been suggested that escaped farmed salmon could compete for living space, breeding partners and food resources, spread disease, or interbreed with wild fish, causing "genetic pollution" and thereby weakening the wild strain and reducing its ability to survive . On the other hand, scientists have argued that farmed salmon, which are bred for fast growth in perfect conditions, are less able to compete for food, territory and mate in the wild than their wild colleagues. Therefore, a limited escape of farmed fish would be unlikely to have a serious effect on wild fish populations. Only if very large numbers of fish escape into a small area, would interbreeding occur and the fitness of the local population potentially be reduced.

 In its Aquaculture Europe 2005 conference, the European Aquaculture Society invited the North Atlantic Salmon Conservation Organisation (NASCO) to hold a special workshop on the interactions between wild and farmed salmon. The summary report of this event "Wild and Farmed Salmon - Working Together" drew the following main conclusions:

Through the use of single bay management, single generation sites and synchronised fallowing, real progress is being made in relation to minimising impacts of diseases and parasites, which are key issues for wild fish interests. The development of third-party audited containment management systems may represent a significant step forward. The liaison group should look more at the possibilities of rearing all-female triploid salmon, which could eliminate genetic interaction with the wild stocks, but which need to be balanced by the production cost of these fish, as well as consumer resistance to what could be seen as genetic manipulation.

Restoration programmes can benefit from fish farmers expertise, but habitat protection and restoration have equal or greater importance in species restoration than stocking programmes alone.

CCRES AQUAPONICS

part of NGO

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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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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The Effects of Astaxanthin Skin Health

 

 

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

 

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

Table 1. Astaxanthin maintains skin health by several methods

Protecting the Skins Natural Antioxidant Network and DNA

 

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

Topical Wrinkle Reduction

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

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

   
 Increased moisture content in 8 out of 11 subjects.

Skin Health that can be Swallowed

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

Figure 2. Beauty supplement results for the cheek and eye region (Yamashita, 2002)  
Moisture levels increased in treated groups at 2 and 4 weeks. Control groups got worse.

Figure 3. Magnified Skin Section at start, 2 and 4 weeks (Yamashita, 2002)
   
Visible reduction of fine wrinkles

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

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

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

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

Astaxanthin and Skin Cancer

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

Mechanism of Action

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

Anti-wrinkle

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

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

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

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

Astaxanthin defends against Reactive Oxygen Species (ROS)

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

Astaxanthin Dominance against Singlet-Oxygen compared to other antioxidants

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

Figure 8. Astaxanthins cell protection ability comparison with other anti-oxidants (Tominaga 2009a)  
Study showed that astaxanthin had the highest ability to protect cells.

Figure 9. UVA-induced activation of caspase-3, detected by annexin V staining, 24h after irradiation (Camela et al., 2008) 
 

Gaining Customers Hearts with Tangible Results - Astaxanthin Inner and Outer Treatment

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

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

 

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

Anti-inflammatory Action

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

Safety for Topical & Nutritional Use

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

Outlook

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

References

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

CCRES special thanks to 

 Mr. Mitsunori Nishida, 

 
President of Corporate Fuji Chemical Industry Co., Ltd.

Croatian Center of Renewable Energy Sources (CCRES) 

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Health and welfare of farmed fish shellfish

CCRES AQUAPONICS

Farmed fish are contained - in ponds, tanks or cages - as with all farmed animals. Just as in land-based farming, farm managers increasingly choose stocking densities and handling practices that optimize growth and health status while avoiding unnecessary suffering.

CCRES AQUAPONICS

Questions are sometimes raised about welfare aspects of aquaculture production. Usually, such questions focus on three issues: stocking densities, the possibility to have ‘free-range aquaculture and the way farmed fish is slaughtered at harvest.

There are many definitions of animal welfare. One definition is based upon the Farm Animal Welfare Councils "five freedoms":

• Freedom from thirst, hunger and malnutrition
• Freedom from discomfort due to environment
• Freedom from pain, injury and disease
• Freedom to express normal behaviour for the species
• Freedom from fear and distress.
  

Scientific studies have identified operating indicators of fish welfare so that producers are able to measure the welfare status of their stock. The Freedom Food certification scheme of the RSPCA in the UK is a very good example of a welfare standard that has been built by on-farm dialogue with producers and which is now available for salmonid species.

Stocking Density

Many species of fish, such as herring and mackerel, live in large shoals in the wild and are therefore used to very high densities. Keeping such fish in high densities on a farm will only become a problem if the water quality deteriorates, or if the fish are deprived of oxygen or exposed to disease. Fish farmers do their best to prevent such conditions since they will reduce production.

Fish farms holding fish at high stocking densities carefully monitor the oxygen in the water and maintain it at the optimum level for fish growth. Every effort is made to ensure that fish are kept in a healthy condition and that disease is prevented wherever possible, or identified and treated should it occur.

Stocking density has often been proposed as an indicator to measure welfare and there is considerable debate about its value. Also, since the 1980s the volume of cages used for salmon culture in Northern Europe has increased considerably - in some cases more than 200 times, reducing densities and enhancing the ability for the fish to show natural behaviour. However, as land animals that are kept within fences, some limits on behaviour are necessary in farmed fish production.

Free-range aquaculture

"Freerange" aquaculture exists in several forms - for example in "ranching" of salmon and lobster, in "organic" salmon production and in shellfish farming.

Photo: Juvenile lobsters reared for restocking Copyright: The AquaReg Lobster Project www.aquareg.com

"Ranching" - is an aquaculture technique whereby fish and shellfish are bred in captivity and then released into the wild to complete their life cycle before being harvested at some time in the future. Ranching has effectively been applied to Atlantic and Pacific salmon production, whereby juvenile fish have been reared from wild-caught eggs and sperm, raised in hatcheries and then released into specific rivers as smolt, allowed to migrate to sea and recaptured on their return to their river of origin.

Lobster ranching has also been tried on a number of commercial lobster beds in the past, with juvenile lobsters being raised in shore-based hatcheries and then placed on the seabed in sheltered rocky habitats where their chance of survival is thought to warrant the expense of production.

"Organic" salmon farming is conducted according to agreed codes of organic production. Rearing takes place in large, open water floating pens where conditions are as close to the open ocean as possible. Stocking densities are reduced to allow the fish to grow and develop in as natural a way as possible and the only feed used comes from sustainable fisheries. Because of lower stocking densities and open water conditions, the fish tend to be less prone to disease and therefore the use of medicines can be kept to a minimum. Increased production cost for "organic" fish is recouped with higher prices on the marketplace.

Shellfish farming, such as the laying of oysters and mussels directly on the seabed or the hanging of mussels on suspended ropes, can be said to be "free range" in so far as it is allowing the shellfish to grow in identical conditions to those they would encounter in the wild.

Slaughter methods

Recent studies suggest that fish, like warm-blooded animals, can experience fear and pain, leading to justifiable concern that codes of practice for the welfare of warm-blooded farm animals should be extended to cover farmed fish.

Accordingly, a four-step process for the humane slaughter of farmed fish has been developed similar to the European Directive covering warm-blooded animals. It covers transport and live storage, restraining, stunning and slaughter.

The process decrees that, to spare fish avoidable trauma, stunning prior to slaughter should induce immediate (within one second) and permanent loss of consciousness or, where loss of consciousness is not immediate, it should be without any avoidable excitement, pain or suffering.

Photo: Electrical stunning of Atlantic Salmon in Tasmania. Systems identical to this are currently being
installed in Norway, so that all farms are equipped by July 2008. Photo courtesy of Bruce Goodrick.

Farmers currently employ any of three ways to reach this goal: electrical stunning (passing a current through the animal); mechanical stunning (a captive needle destroys the brain) or chemical stunning (adding a food-grade substance like eugenol, based on clove oil, to the water in which the fish are held.)

CCRES AQUAPONICS 
part of NGO
Croatian Center of Renewable Energy Sources (CCRES)

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The Effects of Astaxanthin Gastric Health

 

 

Astaxanthin for Dyspepsia and 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)  

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)

   

Astaxanthin reduced gastric inflammation in Helicobacter pylori infected mice.

Figure 3. Bacterial load (antrum + corpus) (Bennedsen et al., 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) 

 

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)  

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

 

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 

   

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) 

Read more