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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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) 

Read more

FUCUS TREATMENTS

Fucus Treatments

Fucus Treatments

Our best source of biological iodine and our best protection against thyroid disruption is to body-load with iodine contained in iodine-rich whole raw seaweeds as regular daily consumption. If our bodies have an ongoing full complement of I-127, we can better resist taking in incidental I-131. This means that eating seaweeds regularly in the diet, especially the big northern kelps, to provide both dietary iodine and protection against the ongoing I-131 hazards.
No land plants are a reliable natural source of iodine. 

Garlic grown near the sea often has relatively high amounts of biological iodine. Besides garlic, root crops, such as turnips, carrots, potatoes, parsnips, and sweet potatoes, are plant sources of iodine. However, the best natural source of biological iodine is seaweed. Any seaweed contains more available dietary iodine than any land plant. The seaweeds with the most available iodine are the giant kelps of the northern hemisphere. The highest concentrations of iodine occurs in Icelandic kelp (8000 ppm), Norwegian kelp (4000 ppm), and Maine and California kelp (1000-2000 ppm). The seaweeds with the least amounts of iodine are nori (about 15ppm) and sargassum (about 30-40 ppm). The amounts of iodine in land plants can be greatly increased by fertilizing food plants with seaweeds applied directly to the soil as topical mulch or tilled into the soil.
The complexity of many thyroid dysfunction cases precludes a simple set of all-purpose formulas. Each thyroid patient has a unique thyroid presentation. I try to compose an individualized functional treatment plan for each, using a few basic methods. Diet and behavior modification also are very important in thyroid case management. What follows are some of my treatment approaches and some general guidelines and notes:

Treatment Guideline 1: Rather uncomplicated seaweed therapy seems to help relieve many of the presenting symptoms of thyroid dysfunction. Some of the results are very likely from whole body remineralization (especially potassium, zinc, calcium, magnesium, manganese, chromium, selenium, and vanadium), in addition to thyroid gland aid from both sustained regular reliable dietary sources of biomolecular iodine and from thyroxin-like molecules present in marine algae, both the large edible seaweeds and their almost ubiquitous epiphytic micro-algae, predominantly the silica-walled diatoms. Seaweeds provide ample supplies of most of the essential trace elements required for adequate enzyme functioning throughout the body but especially in the liver and endocrine glands.

Treatment Guideline 2: Regular biomolecular seaweed iodine consumption is more than just thyroid food: it can also protect the thyroid gland from potential resident I-131-induced molecular disruption and cell death when the thyroid gland is fully iodized with I-127. The fear of eating seaweed that might be contaminated with I-131 is easily mitigated by allowing the seaweed to be stored for 50 days prior to dietary consumption; this will give enough time for most (99%) of any I-131 to decay radioactively.
A simple folk test for iodine deficiency or at least aggressive iodine uptake is to paint a 2-inch diameter round patch of USP Tincture of Iodine (strong or mild) on a soft skin area, such as the inner upper arm, the inside of the elbow, the inner thigh, or the lateral abdomen between the lowest rib and the top of the hip. If you are iodine deficient, the patch will disappear in less than 2 hours, sometimes as quickly as 20 minutes; if it fades in 2 to 4 hours, you may just be momentarily iodine needy. If it persists for more than 4 hours, you are probably iodine sufficient. Iodine deficiency seems to predispose to thyroid malignancy; this could explain the apparent thyroid cancer distribution “fans” downwind of nuclear facilities in previous ‘goiter belt’ areas. This test is of course easier to use with Caucasians and may not offer sufficient color contrast in brown-skinned people.

Treatment Guideline 3: Many patients with underactive thyroid glands complain of a sense of “coldness” or feeling cold all of the time; often they are over-dressed for warmth according to ‘thyronormal’ people’s standards. They may also present a low basal body resting temperature, as measured by taking their armpit temperature before rising in the morning. (Remember to shake down the thermometer the night before). Other symptoms may include sluggishness, gradual weight gain, and mild depression. For these patients, add 5 to 10 grams of several different whole seaweeds to the daily diet; that is, 5 to 10 grams total weight per day, not 5 to 10 grams of each seaweed. I usually suggest a mix of 2 parts brown algae (all kelps, Fucus, Sargassum, Hijiki) to one part red seaweed (Dulse, Nori, Irish moss, Gracillaria). The mixed seaweeds can be eaten in soups and salads or easily powdered and sprinkled onto or into any food. I recommend doing this for at least 60 days, about two lunar cycles or at least two menstrual cycles; watch for any changes in signs and symptoms and any change in average daily basal temperature.
Note that patients can have a normal 98.6°F temperature and still feel cold and also present many of the signs and symptoms of functional hypothyroidism. Do not insist that all hypothyroid patients must have abnormally low basal resting temperatures. If no symptoms improve or the temperature remains low (less than 98.6°F), continue seaweeds and request a TSH and T4 test. If TSH and T4 tests indicate low circulating thyroxin levels, continue seaweeds for another 2 months. It may take the thyroid that long to respond positively to continual regular presentation of adequate dietary iodine. Powdered whole seaweed may be much more effective than flakes, pieces, or granules. The powdered seaweed is best added to food immediately prior to eating; do not cook the seaweed for best results.
All corticosteroids tend to depress thyroid function. Before trying to fix the thyroid, be sure to inquire about both internal and topical steroid use, including Prednisone and topical creams. These, as well as salicylates and anticoagulants, can aggravate existing mild hypothyroidism.

Treatment Guideline 4: Partial thyroidectomy cases can be helped by regular continual dietary consumption of 3-5 grams of whole seaweeds three to four times a week. By whole seaweed I mean untreated raw dried seaweed, in pieces or powder, not reconstructed flakes or granules.

Treatment Guideline 5: Patients with thyroid glands on thyroid replacement hormone (animal or synthetic) can respond favorably to replacing part or all their entire extrinsic hormone requirement by adding dietary Fucus in 3 to 5 gram daily doses, carefully and slowly. Fucus spp. has been the thyroid folk remedy of choice for at least 5000 years. The best candidates are women who seek a less hazardous treatment than synthetic hormone (after reading variously that prolonged use of synthetic thyroid hormone increases risk for heart disease, osteoporosis, and adverse interactions with many prescribed drugs, particularly corticosteroids and antidepressants).
Fucus spp. contains di-iodotyrosine (iodogogoric acid) or DIT. Two DIT molecules are coupled in the follicular lumina of the thyroid gland by a condensing esterification reaction organized by thyroid peroxidase (TPO). This means that Fucus provides easy-to use-prefabricated thyroxine (T4) halves for a boost to weary thyroid glands, almost as good as T4. European thalassotherapists claim that hot Fucus seaweed baths in seawater provide transdermal iodine; perhaps hot Fucus baths also provide transdermal DIT.
The best results with Fucus therapy are obtained with women who were diagnosed with sluggish thyroid glands and who are or were on low or minimal maintenance replacement hormone dosages. They may remark that they miss, forget, or avoid taking their thyroid medication for several days with no obvious negative short-term sequelae; others claim to have just stopped taking their medication. I do not recommend stopping thyroid medication totally at once. Thyroxin is essential for human life and all animal life; it has a long half-life in the body of a week or more, so that a false impression of non-dependency can obtain for up to 2 months before severe or even acute hypothyroidism can manifest, potentially fatal.
Even though I personally do not recommend it, women regularly stop taking their thyroid replacement hormone, even after years of regularly and faithfully taking their medication. In many cases, their respective thyroid glands resume thyroxine production after a 2- to 3-month lag time with many of the signs and symptoms of hypothyroidism presenting while their thyroid glands move out of inactivity. This complete cessation of taking thyroid replacement can only be successful in patients who have a potentially functioning thyroid gland. Those who have had surgical or radiation removal of their thyroid glands must take thyroid hormone medication containing thyroxine to stay alive.
Fucus can be easily added to the diet as small pieces, powdered Fucus in capsules, or freeze-dried powder in capsules. Sources of Fucus in capsules are listed under Seaweed Sources at the end of this paper. The actual Fucus is much more effective than extracts. A nice note is that Fucus spp are the most abundant intertidal brown seaweeds in the northern hemisphere. This is of especial interest to those patients who might be trading one dependency for another, as seems to be the case for some. A year’s supply can be gathered in an hour or less and easily dried in a food dehydrator or in hot sun for 10 to12 hours and then in a food dehydrator until completely crunchy dry. Fucus dries down about 6 to 1 (six pounds of wet Fucus dry down to about one pound). It has a modest storage life of 8 to 12 months in completely airtight containers stored in the dark at 50° F. A year’s supply at 4 grams per day is slightly more than 3 pounds dry. Encapsulated Fucus is available from Naturespirit Herbs, Oregon’s Wild Harvest, and Eclectic Institute.

Treatment Guideline 6: Aggressive attempts to replace thyroid replacement hormone with Fucus involve halving the dose of medication each week for 4 weeks while adding 3 to 5 grams of dried Fucus to the diet daily from the beginning and continuing indefinitely. If low thyroid symptoms appear, return to lowest thyroid hormone maintenance level and try skipping medication every other day for a week, then for every other 2 days, then 3 days, etc. The intent is to establish the lowest possible maintenance dosage by patient self-evaluation and/or to determine if replacement hormones can be eliminated when the patient ingests a regular reliable supply of both biomolecular iodine and DIT. Thoughtful, careful patient self-monitoring is essential for successful treatment.

Treatment Guideline 7: A more conservative replacement schedule is similar to the aggressive approach, except that the time intervals are one month instead of one week, and the Fucus addition is in one gram increments, beginning with one gram of Fucus the first month of attempting to halve the replacement hormone dosage, and increasing the amount of Fucus by a gram each succeeding month to 5 grams per day. The conservative schedule is urged with anxious patients and primary caregivers.
There is some concern that excess (undefined) kelp (species either unknown or not mentioned) consumption may induce hypothyroidism. It seems possible. The likely explanation is an individual’s extreme sensitivity to dietary iodine: Icelandic kelp can contain up to 8000 ppm iodine; Norwegian kelp can contain up to 4000 ppm iodine. Most kelps contain 500 to 1500 ppm iodine.
The only definitive study I have seen is a report from Hokkaido, Japan, where study subjects, at a rate of 8% to 10% of total study participants, presented with iodine-induced goiter from the consumption of large amounts of one or more Laminaria species (Kombu) of large kelps, known to be rich (more than 1000 ppm) in available iodine. Reduction of both total dietary iodine and/or dietary Kombu led to complete remission of all goiters. The apparent iodine-induced goiters did not affect normal thyroid functioning in any participants. Two women in the study did not care if they had goiters and refused to reduce their Kombu intake. Note that the Japanese have the world’s highest known dietary intakes of both sea vegetables and iodine.
Reduction or elimination of seaweeds from the diet is indicated for at least a month in cases of both hyperthyroidism and hypothyroidism, to ascertain if excess dietary iodine is a contributing factor to a disease condition. Other dietary iodine sources, particularly dairy and flour products, should also be reduced and or eliminated during the same time period. Some individuals do seem to be very dietarily iodine-extraction efficient and iodine sensitive simultaneously.

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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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FUCOSE

FUCOSE

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

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

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

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

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

#CCRES #ALGAE TEAM

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The Effects of Astaxanthin Weight Control

 

 

Physical Endurance and Muscle Recovery

 

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

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

Astaxanthin Boosts Endurance

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

Figure 1. Increase in strength/endurance (Malmsten & Lignell, 2008)

   

Astaxanthin improved strength/endurance at 3 and 6 months determined by the average number of knee bends per person.

Figure 2. Effect of astaxanthin on swimming time (Ikeuchi et al., 2006)  

Astaxanthin improves endurance in a dose-dependant manner.

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

Figure 3. Reduction of lactic acid build-up after astaxanthin supplementation in track subjects (Sawaki et al., 2002) 

Figure 4. Effect of astaxanthin on blood lactate during swimming for 15 minutes (Ikeuchi et al., 2006)  

Astaxanthin reduced build-up of lactic acid in a dose-dependant manner.

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

The Mechanism

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

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

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

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

   

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

Figure 7. Increased amount of FAT/CD36 that coimmunoprecipitated with CPT I skeletal muscle after a single session of exercise at 30 m/min for 30 min (Aoi et al., 2008)  

Values are means ± SE obtained from 6 mice.

Figure 8. Astaxanthin reduced the amount of HEL-modified CPT1 in skeletal muscle after a single session of exercise at 30m/min for 30min (Aoi et al., 2008)  

Values are means ± SE obtained from 6 mice.

Outlook

 

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

References

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

CCRES special thanks to 

 Mr. Mitsunori Nishida, 

 
President of Corporate Fuji Chemical Industry Co., Ltd.

Croatian Center of Renewable Energy Sources (CCRES) 

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