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  • Astaxanthin: Could be amazingly good for rosacea or horribly bad...

    Anyone heard of this?

    ---------


    The Worlds Top 5 Superfoods For Silky Smooth Skin

    (NaturalNews) When it comes to healthy-looking skin, nutrition beats cosmetics hands down. Creating radiant, glowing, youthful-looking skin can best be accomplished by focusing on what's inside, not by covering up the skin with artificial colors that try to paint a new face on the outside. But which superfoods, exactly, are best for supporting healthy skin in the first place?

    In this article, I reveal the five best superfoods and health supplements I know of for creating youthful-looking skin with the power of nutrition. All of these supplements are available right now. Below, I'll tell you how and where to get them.


    Superfood #1: Astaxanthin

    What's astaxanthin, you ask? It's a deep-red microalgae that's a fat-soluble antioxidant. That means it can be delivered to the fat molecules of your body, and that includes your skin, of course, which is primarily made of fat and water (by weight).

    Astaxanthin is one of my top nutrients of all time. It even protects the skin from sunburn, eliminating the need to use toxic sunscreen lotions. In addition, astaxanthin protects the brain from Alzheimer's disease, the eyes from UV light damage and the entire nervous system from oxidative damage.

    You can get astaxanthin at www.Nutrex-Hawaii.com or www.Vitacost.com

    Read my article on astaxanthin here: http://www.naturalnews.com/023177.html

    The best way to take astaxanthin is with a dietary source of healthy fats (see below). That's because astaxanthin binds to fats during digestion and is carried with those fats throughout your body where it protects organs and cells from free radical damage. There is probably no stronger fat-soluble antioxidant in the world than astaxanthin.

    FULL ARTICLE HERE

  • #2
    This stuff becomes more and more interesting the more I read...


    Daily supplements of astaxanthin – the pigment that gives salmon its pink colour – may protect DNA from damage and boost the immune response in healthy young women, says a new study.

    The trial is reported to be the first comprehensive human study to investigate if astaxanthin may regulate immune response, oxidative damage and inflammation, state researchers from Washington State University, Inha University in Korea, and La Haye Labs, Inc.

    “Our present study suggests astaxanthin to be a bioactive natural carotenoid that may be important to human health,” they wrote in the open-access journal Nutrition & Metabolism.

    A rosy future for the pink pigment?
    The global astaxanthin market is estimated to be worth about $200 million by 2015, most of which is used as a pigment to enhance the pink coloration of fish such as salmon. The human uses market is growing and estimated at about $35-60 million, according to 2008 data from Frost & Sullivan.

    Its main health benefits are eye and skin health although it has also been linked to joint health and central nervous system health and is said to have an antioxidant payload 500 times that of vitamin E.

    Most astaxanthin is derived from the algae, Haematococcus pluvialis, which is commonly consumed by fish and crustaceans and is responsible for their pink coloration.

    Study details
    Led by Washington State’s Boon Chew, the researchers recruited 42 young women with an average age of 21.5 and randomly assigned them to one of three groups: The first group received placebo capsules, the second and third groups received astaxanthin supplements providing a daily dose of 2 or 8 milligrams. The astaxanthin used in the study was provided astaZanthin by Washington State-based La Haye Laboratories.

    After eight weeks of supplementation, the researchers noted that astaxanthin levels in the blood increased significantly in both astaxanthin groups, but not in the control group. Furthermore, a marker of DNA damage - 8-hydroxy-2'-deoxyguanosine (8-OHdG) – was 32 and 43 per cent lower in the 2 and 8 mg astaxanthin groups, respectively, compared with placebo.

    Reductions in levels of C-reactive protein (CRP), a marker of inflammation, were also significantly lower following supplementation with the carotenoid.

    With regards to the immune system, women who received the astaxanthin supplements experienced increases in the activity of their natural killer cells, without increasing the population of these cells. On the other hand, levels of both T and B cells increased, said the researchers.

    “Therefore, dietary astaxanthin decreases a DNA damage biomarker and acute phase protein, and enhances immune response in young healthy females,” stated the researchers.

    SOURCE

    And one on eye strain.


    Astaxanthin is the latest natural supplement found to improve eye health and visual acuity while reducing eye fatigue, dryness, weakness and irritation.
    The plant nutrient or phytochemical called astaxanthin is a member of the family of carotenoid xanthophylls. Astaxanthin is found naturally in the alga H. pluvialis, which is responsible for the reddish hue found in lobster, shrimp, salmon and other marine life.

    Eye Fatigue
    Eye fatigue is a common problem caused by an increasing dependence on computers. Even with proper ergonomics and lighting, time spent in front of a computer terminal takes its tolls on our eye muscles. In people with autoimmune eye conditions such as thyroid eye disease (TED), uveitis, and Cogan’s disease, astaxanthin has the potential to reduce inflammation and improve visual acuity.

    Symptoms of eye fatigue include poor accommodation (in changes in focus from near to distant vision), poor depth perception, sensitivity to glare, eye dryness and eyestrain. Eye fatigue can exacerbate symptoms in patients with autoimmune eye disorders.

    Astaxanthin to the Rescue
    Several well-controlled clinical trials suggest that astaxanthin can help prevent eyestrain and reduce its effects. In a study of 26 computer workers receiving 5 mg astaxanthin daily for one month, subjects noted a 54 percent reduction of eye fatigue complaints and objective improvements in accommodation ability. Test subjects also showed a significant reduction in subjective symptoms.

    Astaxanthin is shown to reduce inflammation in eye muscles and improve blood flow to the eyes, especially in the capillary vessels that supply blood to the retina. As an antioxidant, astaxanthin protects against free radical damage and oxidative stress. Because it is fat soluble, astaxanthin has a special affinity for cell membranes, particularly the double cell membrane found in eye muscle.

    Astaxanthin and other xanthophylls are also known to reduce the risk of cataract formation and age-related macular degeneration. In patients with uveitis, animals studies showed that astaxanthin had the same anti-inflammatory actions as the steroid prednisolone. Effects include reduced inflammatory markers, including nitric oxide synthase, prostaglandin E2, and tumor necrosis factor alpha. Compared to beta- carotenoids, astaxanthin is twice as likely to be absorbed by retinal cells.

    Athletic Performance
    A similar study in athletes showed that depth perception and critical flicker fusion, an objective measure of visual acuity, improved by 46 percent in subjects taking 6 mg
    astaxanthin daily for 4 weeks. In addition, athletic performance and endurance showed improvement as evidenced in a reduction in lactic acid levels.

    Additional Benefits
    Astaxanthin has also been shown in studies to improve cardiovascular health, including reducing blood pressure. It’s also shown to help in conditions of diabetes and in preventing the development of metabolic syndrome.

    Dosage
    Astaxanthin works well in combination with lutein, zeaxanthin, beta-carotene and other phytonutrients that promote eye health. In clinical trials a dose of 4-12 mg daily has been shown to reduce eyestrain with no apparent side effects.
    Resources;

    Laurie Barclay, Relieve Your Tired Eyes While Guarding Against Common Eye Diseases, Life Extension, January 2009: 37-43.
    W. Aoi, Y. Naito, and T. Ishii, Astaxanthin improves muscle lipid metabolism in exercise via inhibitory effect of oxidative CPT I modification, Biochem Biophys Res Commun. 2008 Feb 22;366(4):892-7. Epub 2007 Dec 1


    SOURCE

    Very exciting this one...


    Abstract
    Astaxanthin, a carotenoid without vitamin A activity, has shown anti-oxidant and anti-inflammatory activities; however, its molecular action and mechanism have not been elucidated. We examined in vitro and in vivo regulatory function of astaxanthin on production of nitric oxide (NO) and prostaglandin E2 (PGE2) as well as expression of inducible NO synthase (iNOS), cyclooxygenase-2, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-1beta). Astaxanthin inhibited the expression or formation production of these proinflammatory mediators and cytokines in both lipopolysaccharide (LPS)-stimulated RAW264.7 cells and primary macrophages. Astaxanthin also suppressed the serum levels of NO, PGE2, TNF-alpha, and IL-1beta in LPS-administrated mice, and inhibited NF-kappaB activation as well as iNOS promoter activity in RAW264.7 cells stimulated with LPS. This compound directly inhibited the intracellular accumulation of reactive oxygen species in LPS-stimulated RAW264.7 cells as well as H2O2-induced NF-kappaB activation and iNOS expression. Moreover, astaxanthin blocked nuclear translocation of NF-kappaB p65 subunit and I(kappa)B(alpha) degradation, which correlated with its inhibitory effect on I(kappa)B kinase (IKK) activity. These results suggest that astaxanthin, probably due to its antioxidant activity, inhibits the production of inflammatory mediators by blocking NF-kappaB activation and as a consequent suppression of IKK activity and I(kappa)B-alpha degradation.

    SOURCE

    'inhibits the production of inflammatory mediators' Hmm, I remember reading somewhere something about this and rosacea...

    ...ah here we go:


    'Recent research has shown an increase of specific proinflammatory cytokines, including tumor necrosis factor (TNF-α) and interleukin (IL-1β), in biopsies of inflammatory lesions from acne patients.9 These cytokines trigger a chain of chemical responses in the body, including the release of certain matrix metalloproteinases (MMPs); specifically, MMP-1, -3, and -9.10,11 These MMPs are involved in collagen matrix degradation and inflammatory damage. The likely result is the development of papulopustular lesions. Owing to the similarities between these lesions in acne and rosacea, this evidence offers insight into the inflammatory nature of rosacea.

    Two additional inflammatory mediators thought to incite the symptoms of rosacea are reactive oxygen species (ROS) and nitric oxide (NO). Clinical trial evidence reports that patients with severe rosacea have a reduced capacity to counter the negative effects of ROS; thus, experiencing an increased inflammatory response.11,12 This may also explain the connection between photodamage and rosacea since sun exposure is known to induce the release of ROS which subsequently activates MMPs.13 The role of NO involves vascular changes and is believed to be partially responsible for the erythema, edema, and telangiectatic symptoms of rosacea.11,13 Vasodilation plausibly results in vascular instability leading to increased vessel permeability, edema, and fixed vessels. This may worsen with increased sun exposure as an increase of NO in the keratinocytes has been linked with UVB rays.9"

    Thus, according to the inflammatory theory of rosacea, since TNF-a (tumor necrosis factor) stimulates many of the other cytokines and enzymes involved in the inflammatory process and also in much of the tissue destruction we see with rosacea, decreasing TNF-a levels should theoretically help minimize the increased symptoms of inflammation we see with rosacea. Studies seem to support claims that low-level light therapy reduces levels of TNF-a.

    Also, according to the inflammatory theory of rosacea, since rosaceans have a reduced capacity to counter the negative effects of reactive oxygen species (ROS), increasing levels of superoxide dismutase (SOD), which is key in the process of clearing ROS, should theoretically help to prevent or even reduce some of the damaging effects ROS has on rosacea affected tissues. Studies so far indicate that low-level light therapy increases levels of SOD. (See the page on GliSODin for more information about the effects of SOD on ROS)'

    And...


    Reactive Oxygen Species (ROS)
    'LLLT was reported to produce a shift in overall cell redox potential in the direction of greater oxidation (Karu 1999) and increased ROS generation and cell redox activity have been demonstrated (Alexandratou et al. 2002; Chen et al. 2009b; Grossman et al. 1998; Lavi et al. 2003; Lubart et al. 2005; Pal et al. 2007; Zhang et al. 2008). These cytosolic responses may in turn induce transcriptional changes. Several transcription factors are regulated by changes in cellular redox state. But the most important one is nuclear factor B (NF-B). Figure 5 illustrates the effect of redox-sensitive transcription factor NF-κB activated after LLLT and is instrumental in causing transcription of protective and stimulatory gene products'

    Excessive ROS
    'As discussed in 2.5 the light mediated generation of reactive oxygen species has been observed in many in vitro studies and has been proposed to account for the cellular changes observed after LLLT via activation of redox sensitive transcription factors (Chen et al. 2009a). The evidence of ROS mediated activation of NF-κB in MEF cells presented in 4.1 provides additional support for this hypothesis (Chen et al. 2009a). It is well-accepted that ROS can have both beneficial and harmful effects (Huang and Zheng 2006). Hydrogen peroxide is often used to kill cells in vitro (Imlay 2008). Other ROS such as singlet oxygen (Klotz et al. 2003) and hydroxyl radicals (Pryor et al. 2006) are thought to be harmful even at low concentrations. The concept of biphasic dose response in fact is well established in the field of oxidative stress (Day and Suzuki 2005). If the generation of ROS can be shown to be dose dependent on the delivered energy fluence this may provide an explanation for the stimulation and inhibition observed with low and high light fluences'

    Nitric Oxide (NO)
    'Light mediated vasodilation was first described in 1968 by R F Furchgott, in his nitric oxide research that lead to his receipt of a Nobel Prize thirty years later in 1998 (Mitka 1998). Later studies conducted by other researchers confirmed and extended Furchgott’s early work and demonstrated the ability of light to influence the localized production or release of NO and stimulate vasodilation through the effect NO on cyclic guanine monophosphate (cGMP). This finding suggested that properly designed illumination devices may be effective, noninvasive therapeutic agents for patients who would benefit from increased localized NO availability'

    Excessive Nitric Oxide
    'The other mechanistic hypothesis that is put forward to explain the cellular effects of LLLT relates to the photolysis of nitrosylated proteins that releases free NO (see section 2.6). Again the literature has many papers that discuss the so-called two-faced or “Janus” molecule NO (Anggard 1994; Lane and Gross 1999). NO can be either protective or harmful depending on the dose and particularly on the cell or tissue type where it is generated (Calabrese 2001a)'

    So I wonder...what does this all mean??

    I also use LLLT (Red Light Therapy) and interesting that works by producing NO and ROS...now, Green Tea has an effect on this in a similar way too I think...


    Recently, we introduced into the conventional catalogue of biological aging a new determinant: ordered interfacial water layers. The discovery of their tunability with skin-tolerated levels of 670 nm light inspired a model, which suggested that the light, by interaction with ordered interfacial water layers in the extracellular matrix, would reverse elastin degeneration.

    We validated the model in a 10 month self-experiment and arrived at an effective facial rejuvenation program. Importantly, during the experimental phase we avoided extreme oxidative stressors, in particular exposure to extensive ultraviolet and infrared radiation as well as air pollution. Here we report on the adaptation of our model to the extreme oxidative stress levels prevalent in numerous polluted megacities.

    The results of the extension comprise a new understanding of the protective function of the skin acid mantle, new predictive insight into effects of reactive oxygen species (ROS) on interfacial water layers, and their implication in processes of biological aging, including depletion of follicular stem cell reservoirs and telomere shortening, and led to the design of an accelerated skin rejuvenation method.
    I'm too tired to try and work it all out now, but maybe someone else has some insight...

    But...one more to throw into the mix:


    There are many properties that make this carotenoid special. Here are the main differences:

    Astaxanthin is by far the most powerful carotenoid antioxidant when it comes to free radical scavenging: it is 65 times more powerful than vitamin C, 54 times more powerful than beta-carotene, and 14 times more powerful than vitamin E.

    Astaxanthin is far more effective than other carotenoids at "singlet oxygen quenching," which is a particular type of oxidation. The damaging effects of sunlight and various organic materials are caused by this less-stable form of oxygen. Astaxanthin is 550 times more powerful than vitamin E and 11 times more powerful than beta-carotene at neutralizing this singlet oxygen.

    Astaxanthin crosses the blood-brain barrier AND the blood-retinal barrier (beta carotene and lycopene do not), which has huge implications for the health of your eyes.
    • It is soluble in lipids, so it incorporates into cell membranes.
    • It is a potent UVB absorber.
    • It reduces DNA damage.
    • It is a very powerful natural anti-inflammatory.
    • No adverse reactions have been found for people taking astaxanthin.
    • It is virtually impossible to obtain the recommended daily amount of astaxanthin from diet alone because there are only two prime sources: microalgae and sea creatures that consume the algae (such as salmon, shellfish, and krill).

      SOURCE

    Comment


    • #3
      Everything you ever wanted to know about astaxanthin (well 148 pages worth anyway)

      http://www.roberthenrikson.com/Spiru...hinCapelli.pdf

      Comment


      • #4
        Some very interesting reads within that link above...I think it is only fair, since I am about to quote lots from their article, that I credit this to Bob Capelli with Dr. Gerald Cysewski from Cyanotech Corporation. Their product is BioAstin® (other products are however available).

        It's a publicly available document simply by googling. Full paper can be found here (as stated in the last post).

        The whole document is well worth a read, but there are the highlights I thought worth mentioning.

        Needless to say, I have now gone out and brought some. The only thing that worries me is it will make me flush. I have absolutely no basis for this assumption other then paranoia :/ Too much of a certain green sweet smelling substance in my youth I feel

        In my usual style I have emailed the company with some questions...

        Anyway, the info:



        Nature’s Ultimate Antioxidant: Astaxanthin!

        Astaxanthin has been shown in two different in-vitro experiments to be the strongest natural antioxidant known to science. There are many different ways to measure antioxidant strength. One popular measurement today is called Oxygen Radical Absorbance Capacity (ORAC, as developed by Brunswick Labs, Norton, Massachusetts, USA). According to Brunswick Labs, the ORAC test is not a good measurement for oil soluble carotenoids like Astaxanthin, so Natural Astaxanthin was examined by two alternative procedures. In the two antioxidant tests that we’ve seen to date, Astaxanthin left all competitors far behind.

        In the first experiment on page 18, Astaxanthin yielded an antioxidant strength 550 times stronger than Vitamin E in singlet oxygen quenching (Shimidzu et al, 1996). Vitamin E has been touted to be a strong antioxidant both internally and in topical uses in cosmetics; yet Astaxanthin’s antioxidant strength completely dwarfed Vitamin E!

        It’s also very interesting to note Astaxanthin’s relationship to the closely related carotenoid beta carotene. Beta carotene is the most widely researched carotenoid and is certainly a wonderful compound with many health benefits. It is a carotenoid with Vitamin A activity—it is converted into Vitamin A in the human body as needed. As we examined in the first chapter, Astaxanthin is very similar chemically to beta carotene. Yet Astaxanthin was 11 times stronger than beta carotene in singlet oxygen quenching!





        Never a “Pro-Oxidant”


        There is a potential for some wonderful antioxidants, under certain condi- tions, to become “pro-oxidants” and actually have a negative effect by causing oxidation in the body. Some of the better-known carotenoid antioxidants that can become pro-oxidants are beta carotene, lycopene and zeaxanthin (Martin, et al, 1999). Even such familiar antioxidants as vitamin C, vitamin E and zinc can become pro-oxidants. This is another important factor separating Astaxanthin from other antioxidants—it never becomes a pro-oxidant (Beutner, et al, 2000). This is one more reason that Astaxanthin is clearly a superior antioxidant to others.

        _______




        Side Effects

        Natural Astaxanthin, on the other hand, has never been shown to have any negative side effect or contraindication. The only poten- tial effect from people taking megadosis far above the recommended 4 – 12 mg per day may be a slight orange color in the palms of the hands and soles of the feet. This is due to the pigment in Astaxanthin depositing in the skin, and as we’ll see later, this is a good thing since it’s what allows Astaxanthin to work as an internal sunscreen.

        _______




        Inflamation

        Astaxanthin works to suppress different inflammatory mediators. Among these mediators are tumor necrosis factor alpha (TNF-a), prostaglandin E-2 (PGE-2), interleukin 1B (IL-1b) and nitric oxide (NO). In one experiment done with mice and also in-vitro, Astaxanthin was shown to suppress TNF-a, PGE-2, IL-1b, NO as well as the Cox-2 enzyme and nuclear factor kappa-B (Lee, et al, 2003).

        Remember this from earlier in this post:



        'Recent research has shown an increase of specific proinflammatory cytokines, including tumor necrosis factor (TNF-α) and interleukin (IL-1β), in biopsies of inflammatory lesions from acne patients.'

        ...

        'Two additional inflammatory mediators thought to incite the symptoms of rosacea are reactive oxygen species (ROS) and nitric oxide (NO).'

        This is one of the reasons that Low Level Light Therapy is said to work so well (and why it often increases symptoms on the short term) - see earlier in this thread.



        Anti-inflamatory

        Due to the multitude of ways in which Astaxanthin combats inflammation, it is a very special anti-inflammatory indeed. Both in-vitro and in-vivo research has been done to uncover Astaxanthin’s mechanism of action. This mechanism has been further demonstrated in several double blind, placebo controlled human clinical trials on various inflammatory conditions.



        Astaxanthin and Skin


        By pre- venting UV damage, skin can be pro- tected from these conditions. And there is evidence that Natural Astaxanthin not only prevents UV damage from occur- ring, but may actually help to reverse these external signs of aging from the inside out.

        ...

        In groundbreaking clinical work for which a patent was awarded, Cyanotech Corporation funded a study to test the potential of Natural Astaxanthin as an internal sunscreen. This study was conducted at an independent consumer research laboratory. Twenty one subjects were tested under a solar simulator, a machine designed to emit ultraviolet radiation that mimics sunlight. A filter was used on the machine to ensure ample amounts of both UVA and UVB light reached the subjects’ skin.
        The skin was tested before supplementation began to see how much UV light was needed to cause erythema (reddening of the skin, a.k.a. sunburn). Then, subjects supplemented with 4 mg of Natural Astaxanthin per day for two weeks. After the two week supplementation period was over, the subjects once again underwent the skin reddening test. The pre-supplementation and post-supple- mentation scores were then compared.

        The result was that in only two weeks at a standard dose of just 4 mg per day, there was a statistically significant increase in the amount of time necessary for UV radiation to redden the skin. This result is particularly promising because Astaxanthin has a cumulative effect in the body—it builds up in the organs over time. Two weeks is a relatively short time for the Astaxanthin to concentrate in the body’s largest organ, the skin. Yet this study proved that in just two weeks Natural Astaxanthin was already working as an internal sunscreen (Lorenz, T, 2002).

        This study did not investigate the mechanism of action for Astaxanthin’s abilities as an internal sunscreen, but the answer may not be as complicated as one might think. Sunburn is actually an inflammatory process. When the skin becomes inflamed by exposure to UV light, the inflammation becomes visible through reddening. This is not too different from some other forms of inflamma- tion where the outward appearance manifests as reddening. Swollen ankles, inflamed cuts and abrasions and arthritic hands can all appear red from inflam- mation. So when our body’s largest organ, the skin, turns red, we know that inflammation has taken place. The exact inflammatory pathway or pathways that are being controlled by Astaxanthin’s prevention of sunburn are not known; yet it is almost certain that Astaxanthin’s anti-inflammatory action is to thank for its action as an internal sunscreen.


        This study examined Astaxanthin’s ability in-vitro to reduce melanin. Astaxanthin was found to decrease melanin production by 40%. This result is superior to three other substances that are commonly included in topical formulas as whitening agents (Arakane, K, 2001).

        Is this a good thing?

        Don't some people (rosacea sufferers) take Melototan to increase melanin in the skin...? My Rosacea has disappeared since I tried Melanotan II

        Melatotan has a lot of negatives...but it seems to do the opposite of astaxanthin in this regard.

        However, just a thought, but isn't melanin present in the skin because the body is reacting to inflammation? i.e. sun exposure? Wouldn't it possible that the skin is producing less melanin because astaxanthin is bringing down inflammation?


        Anti-histermine


        Lastly, in-vitro work to explore a novel approach for the treatment of asth- ma showed favorable results with Astaxanthin. The researchers combined Astaxanthin with ginkgolide B and found that the combination suppressed T-cell activation to a comparable level as two commonly sold anti-histamines (Mahmoud, et al, 2004).


        Safety

        It is refreshing to know that for as long as Natural Astaxanthin has been consumed, there has never been an indication of toxicity, negative interaction with any drug, supplement or food, or any other contraindication. And in the ten years that Natural Astaxanthin has been sold as a dietary supplement, there has not been any documented adverse incident, not even an allergic reaction.

        This information is contrary to the case with other commercial sources of Astaxanthin, such as the Astaxanthin that is chemically synthesized from petrochemicals or the Astaxanthin that is grown on mutated yeast.

        ...

        Many human safety studies in addition to all the human clinical trials and all the animal trials have never shown any adverse effects for Astaxanthin. In addition, extensive acute toxicity work in mice and rats has been completed, including studies where the rodents were fed tremendous doses in comparison with their body weight. In each of these, no mortality or symptoms of toxicity were reported. Additionally, safety research has been completed on many other animal species. In one of these studies, mega-doses fed to pregnant rabbits result- ed in no adverse events to either the mothers or the fetuses. (Extensive safety information can be found at www.cyanotech.com or by contacting the Publisher at 808.326.1353.)

        Dose


        The answer to this question depends on a few things: First of all, for what purpose are you using Astaxanthin? Secondly, are you a 5% absorber or a 90% absorber?
        Let’s talk about the second question first: Different humans have a wide ranging ability to absorb carotenoids. For example, your body might be able to absorb 90% of the carotenoids you eat, while your friend (or even a close rela- tive) may only be able to absorb 5%. This makes it difficult to recommend a spe- cific dosage for all people.

        If your body absorbs 90% of carotenoids and you take only 1 mg of Astaxanthin, you’ll get the same benefit as your friend (who absorbs 5% of carotenoids) when he or she takes 18 mg! This huge disparity makes it dif- ficult for supplement manufacturers to decide what dosage to recommend on their labels.
        The other key question is why you’re taking Astaxanthin. If you’re a man taking it who’s been diagnosed with poor semen quality and you and your wife want to have a baby, you probably should take the full level at which the fertility study was done — 16 mg per day. If you’re just looking for an antioxidant and immune system boost and you’re already eating a good diet, you might get by with only 2 mg per day.

        A major factor that determines how well people will absorb Natural Astaxanthin is when it is taken: It is highly recommended that Natural Astaxanthin supplements are taken with meals, preferably with a meal that has some fat content. This is similar to other carotenoids, all of which are fat solu- ble. These lipophilic (“fat-loving”) nutrients, taken in the absence of fats, are poorly absorbed; when taken with fats, the absorption is maximized. One study centered around this premise tested the bioavailability of Natural Astaxanthin in three different lipid-based formulas, all of which resulted in better absorption than a formula that did not have any additional lipids (Mercke, et al, 2003). The message is clear—be sure to take your Astaxanthin with fats, or at the very least in a gelcap containing oil as a base, in order to maximize the benefits.

        The recommended daily dosage amongst manufacturers has become fairly standardized at a 4 mg per day level for the average person who has no serious concerns (such as low fertility or severe joint or tendon problems). Following is a table of recommended dosages that is provided as a rough guideline for consumers.
        Know how much astaxanthin you get from salmon?




        So that's 4mg of astaxanthin from sockeye salmon, and hardly any from the atlantic salmon.


        The end of the document has many testimonials.

        It does sound like hype, but there are so many studies to back it up that is hard not to believe it all...

        ...I googled rosacea and astaxanthin and got very little back. I am surprised I have not heard about this substance. EVER. It is not mentioned on the rosacea forum sticky about anti-inflamatories nor on many other sites looking at anti-inflamatories or anti-oxidents...you have to specifically search for it.

        Anyway, enough from me. I'll update the board when I start using it.

        Comment


        • #5
          so is salmon the best food for getting Astaxanthin? what other foods are good?
          Doug

          Comment


          • #6
            Originally posted by mrsmoof View Post
            so is salmon the best food for getting Astaxanthin? what other foods are good?
            I pulled this from ehow:


            Fish
            The most regularly consumed sources of astaxanthin, other than in the form of supplements, come from fish such as sockeye salmon, rainbow trout, red sea bream and pink salmon. Fish ingest astaxanthin as a result of feeding on the microalgae that produces it or through the food which they are fed if they are farm raised. A 113g portion of salmon from the wild yields 4.5mg of astaxanthin, while 113g of farmed varieties only give up to 2mg per serving.

            Seafood
            Shellfish and seafood such as lobsters, crab and shrimp, all of which contain astaxanthin, get their reddish-pink color from it and offer a dietary change from fish. Farmed seafood shows lower levels of astaxanthin per gram than seafood caught in the wild.

            Haematococcus Pluvialis Microalgae
            Some fish get their red pigmentation from consuming large amounts of tiny creatures called microalgae. Haematococcus pluvialis microalgae produce astaxanthin as a natural sunscreen to protect themselves from the harmful effects of the sun's rays or the UV radiation when the region they inhabit periodically dries up. Sold in a cracked and dried form like some seaweed products, the algae contains 1.5 to 3.5 percent astaxanthin. Care should be taken to investigate sources of raw algae products to ensure they come from unpolluted waters.

            Red Phaffia Yeast
            Red phaffia yeast contains up to 5,000mg of astaxanthin per kilo. From use as a type of animal feed to coloring eggs, this product is becoming common in North American markets in supplemental form. Technically a synthetic form of astaxanthin, it is often combined with natural forms for production of pills and powders for sale to health food businesses.

            Krill Oil
            This oil is extracted from Krills, which are small shrimp like creatures. It is put into capsules and sold for its high omega 3 content. Krill, like shrimp, also have astaxanthin in them.


            Read more: Foods Containing Astaxanthin | eHow.com http://www.ehow.com/about_5595083_fo...#ixzz1EzpYefSZ

            SOURCE

            Couldn't tell you how much though.

            Unless you are consuming Sockeye Salmon you'll be getting sod all astaxanthin. I think you have to eat 1KG of Atlantic salmon to equal Sockeye Salmon. See the table above.
            Last edited by findingaway; 25 February 2011, 06:28 PM.

            Comment


            • #7
              Hi,

              thanks for the interesting thread! Just wondering, I read in the trial results that this astaxanhin is found to raise the natural killer cells in the trial persons... I am wondering if this is a good thing. I have auto-immune issues, and implantation and early miscarriage issues, and I have understood from my RE that those natural killer cells are not something you want to have in my situation (can be the cause of infertility). Not sure though if those NK cells are troublesome in healthy individuals? It came across to me, reading your article, that they think here that they are linked to raised immunity?
              I am wondering, as some and perhaps many rosaceans seem to have some auto-immune issue, if this raise of NK cells would be actually beneficial for us rosaceans?

              Best wishes Natalja
              My rosacea related blog: http://scarletnat.blogspot.com/2012/...edication.html

              Comment


              • #8
                In my experience, anti-inflammatory substances rarely improve rosacea symptoms, and this stuff increases blood flow and decreases blood pressure (generally increasing vessel size, if I recall correctly from my... um, zero years of med school).

                Not to be a pessimist, but I'm betting the adverse effects on circulation (adverse for rosaceans, anyway) will outweigh any anti-inflammatory benefit, and will make you flush.

                1,000mg Solgar MSM
                25mg diphenhydramine
                Rosacea Care moisturizer, tinted ZincO
                I avoid multi-vitamins and most other high-dose vitamins and supplements, oil-based supplements (like omega 3/6, A, and E), nitrite preservatives, sugar, fruit, milk, exercising in a warm room

                Less is more!

                Comment


                • #9
                  Haven't read anywhere that it increases circulation...be interested to know where you read it. Must have missed it!

                  I have read this on some sites, which absolutely crazes me. It cannot be both statements surely or how could you say it COULD do all those things?


                  'No side effects of astaxanthin have been reported'

                  'Common astaxanthin side effects include increased pigmentation, hair growth, shifts in hormone levels and low blood pressure. Reduced calcium levels, decreased libido and breast enlargement in men have also been observed, but these astaxanthin side effects are rarer. Allergic reactions also are possible and can be quite dangerous. Astaxanthin and astaxanthin-fed foods should be avoided by anyone with a known allergy to the substance.'

                  The research document I read and a couple of others say there is no side effects...but it has to be considered that this research document is a sales pitch for their product...

                  How would one know if one was to flush more? (if note sure how I ended up sounding like the queen there :/) Is there another substance that I can use to 'test' if I may have this reaction?

                  Now my BIG worry would be that this stuff is fat soluble. So once its in your system, it is there to stay for a while. So if I have an adverse reaction, well you know where I am going with this...

                  How come increased circulation and decreased blood flow causes flushing?
                  Last edited by findingaway; 25 February 2011, 07:17 PM.

                  Comment


                  • #10
                    I think there is a definitely a link between antioxients ability to decrease ROS (which is shown to be high in rosaceans.

                    See here (note this is talking about papulopustular rosacea):


                    ABSTRACT

                    Background
                    Recent evidence suggests that inflammation in rosacea is associated with generation of reactive oxygen species (ROS) that are released by inflammatory cells. The efficacy of current therapeutic agents for rosacea such as tetracyclines and metronidazole has also been attributed to their antioxidant properties. Recently, a macrolide antibiotic, azithromycin, has been found to be an effective alternative in the treatment of rosacea.

                    Objectives
                    We planned a study to evaluate the antioxidant effects of azithromycin on ROS in rosacea. We compared basal ROS concentrations measured in the facial skin of patients with rosacea with the post-treatment levels and with those of healthy controls.

                    Methods
                    Facial skin biopsies of 17 papulopustular patients with rosacea and 25 healthy controls were taken. Rosacea patients were assigned to receive oral azithromycin 500 mg on three consecutive days each week for 4 weeks. The total number of inflammatory lesions (the sum of papules and pustules) on the face of each patient with rosacea was counted at each visit. The luminol- and lucigenin-enhanced chemiluminescence (CL) levels of patients with rosacea were measured before and after 4 weeks of treatment and compared with those of healthy controls.

                    Results
                    Rosacea patients had higher ROS levels than healthy controls (P < 0.001). A statistically significant decrease of both luminol- and lucigenin-enhanced CL levels were observed in patients with rosacea after treatment with azithromycin (t = 4.602, P < 0.001; vs. t = 4.634, P < 0.001, respectively).

                    Conclusions
                    Rosacea patients have higher ROS levels than healthy controls. The Results of our study support the antioxidant properties of azithromycin in rosacea.

                    SOURCE

                    I wonder if it is because other anti-oxidents simply are not powerful enough to make a difference.


                    Originally posted by nataljaoo View Post
                    Hi,

                    thanks for the interesting thread! Just wondering, I read in the trial results that this astaxanhin is found to raise the natural killer cells in the trial persons... I am wondering if this is a good thing. I have auto-immune issues, and implantation and early miscarriage issues, and I have understood from my RE that those natural killer cells are not something you want to have in my situation (can be the cause of infertility). Not sure though if those NK cells are troublesome in healthy individuals? It came across to me, reading your article, that they think here that they are linked to raised immunity?
                    I am wondering, as some and perhaps many rosaceans seem to have some auto-immune issue, if this raise of NK cells would be actually beneficial for us rosaceans?

                    Best wishes Natalja

                    Sorry, I never answered your question Natalja.

                    I have no idea...but you could email them...info@cyanotech.com
                    Last edited by findingaway; 25 February 2011, 07:37 PM.

                    Comment


                    • #11
                      Originally posted by nataljaoo View Post
                      Hi,

                      I have auto-immune issues, and implantation and early miscarriage issues, and I have understood from my RE that those natural killer cells are not something you want to have in my situation (can be the cause of infertility).
                      Sorry Nataljaoo,

                      I skim read your post the first time. Thats awful. It's enough to just deal with the rosacea!

                      The last bit about anti-histerime might interest you. I have allergies (never had them before the rosacea) which is the body attacking, essentially itself I understand.

                      Need to be clearer on it as the article says it both strengths Killer Cells, but also suppresses them when combined with ginkgolide B. Why you would add a substance that increases T-Cell activation to the mix (astaxanthin) to reduce T-Cell activation is an answer that alludes me...

                      I would definitely email them.

                      Comment


                      • #12
                        Originally posted by findingaway View Post

                        How come increased circulation and decreased blood flow causes flushing?

                        Well, I think what driven was getting at was that if you are going to decrease blood pressure... you would think this would correspond with the dilation of blood vessels... Since pressure and volume are so related... And then just common sense would tell us that having dilated blood vessels and increased circulation probably wouldnt be so great for rosacea... which is after all a direct result of dilated blood vessels!

                        But what I dont understand is why the low blood pressure meds work then (chlondine ,proponol)... ??? I suppose that even if the lowering of blood pressure means the dilation of your vessels... it also means less pressure pumping the blood into your face... maybe that benefit just outweighs the dilation aspect?

                        Well, this astaxanthin super antioxidant sounds interesting enough... Are you going to give it a try findingaway? Keep us updated if you do...

                        Comment


                        • #13
                          Originally posted by evolved View Post
                          But what I dont understand is why the low blood pressure meds work then (chlondine ,proponol)... ??? I suppose that even if the lowering of blood pressure means the dilation of your vessels... it also means less pressure pumping the blood into your face... maybe that benefit just outweighs the dilation aspect?
                          Good question. One I'd love to know the answer too.

                          I did a bit of googling and the only correlation between flushing and blood pressure is high blood pressure. But I think I get what you and Driven are saying. Have you a link?

                          Originally posted by evolved View Post
                          Well, this astaxanthin super antioxidant sounds interesting enough... Are you going to give it a try findingaway? Keep us updated if you do...
                          Yeah, think I'm gonna make the plunge. I have emailed the company mentioned in the research above, so will see what they say...

                          Comment


                          • #14
                            Nataljaoo,

                            I found this on another website:

                            In addition to oxidation, inflammation is another invisible cause of disease and premature aging. AstaXanthin has potent anti-inflammatory activity through inhibition of mast cell degranulation, and inflammatory proteins such as C-reactive protein and COX-2 enzymes.

                            SOURCE

                            And this from Wiki:


                            Autoimmunity
                            Mast cells are implicated in the pathology associated with the autoimmune disorders rheumatoid arthritis, bullous pemphigoid, and multiple sclerosis. They have been shown to be involved in the recruitment of inflammatory cells to the joints (e.g. rheumatoid arthritis) and skin (e.g. bullous pemphigoid) and this activity is dependent on antibodies and complement components. [8]

                            SOURCE

                            So it appears that astaxanthin would beneficial for those with autoimmune disorders...


                            I found this to do with T-Cells, which I understand astaxanthin is said to strengthen!


                            Autoimmune attack of central nervous system (CNS) components is associated with devastating neurodegenerative diseases such as multiple sclerosis. Although autoimmune T cells are usually viewed as detrimental, Schwartz and colleagues report on page 49 of this issue the unexpected finding that they also can be neuroprotective. They administered T cells specific for myelin basic protein (MBP) to rats in which the optic nerve had been injured and, to their surprise, found that the immune cells protected the injured neurons from further damage.

                            "We were somewhat worried because all of these results are against the conventional wisdom of generations of immunologists," says Schwartz. "We have all been taught that the immune system is designed to be kept out of the CNS. These results prompt us to consider the possibility that T cell-mediated immune activity against self CNS components can do good for the immune system as well."

                            CNS injury is accompanied by changes in the concentration of extracellular ions, free radicals, and neurotransmitters, resulting in the gradual secondary loss of adjacent undamaged neurons. The photograph shows a whole-mounted retina excised after partial injury to the optic nerve. Each retrogradely labeled cell (green) represents a neuron that escaped the primary lesion and has not yet undergone secondary degeneration. Schwartz and co-workers demonstrate that MBP-specific T cells inhibit the eventual secondary degeneration of these neurons after the primary injury. These results are particularly interesting given their previous observation that macrophage-induced inflammation can promote neuron re-growth after axonal transection (Nature Med. 4, 814−821; 1998).

                            But how does the immune response help to preserve these neurons? The authors suggest that MBP-specific T cells cause a transient reduction in the electrophysiological activity of damaged neurons, which may prevent depletion of their energy supplies keeping them alive longer.

                            Although their recent investigation into 'benign autoimmunity' has caused them to diverge from their initial goal—to determine the potential of infiltrating T cells to deliver gene therapy vectors to the CNS—the Schwartz team still intends to pursue the notion of T cells as gene therapy vehicles. "At areas in which there is no lesion, T cells don't accumulate. Self-reactive T cells are the perfect gene delivery vehicle because of their specificity for CNS lesion sites," says Schwartz.


                            SOURCE

                            I really don't know enough about autoimmune disorders to comment on this though...

                            I found this on Wiki and it went pretty much over my head, but it seems to imply that B Cells are the issue, not T-Cells and it doesn't even mention mast cells in this bit!


                            Aberrant B cell receptor-mediated feedback - A feature of human autoimmune disease is that it is largely restricted to a small group of antigens, several of which have known signaling roles in the immune response (DNA, C1q, IgGFc, Ro, Con. A receptor, Peanut agglutinin receptor(PNAR)). This fact gave rise to the idea that spontaneous autoimmunity may result when the binding of antibody to certain antigens leads to aberrant signals being fed back to parent B cells through membrane bound ligands. These ligands include B cell receptor (for antigen), IgG Fc receptors, CD21, which binds complement C3d, Toll-like receptors 9 and 7 (which can bind DNA and nucleoproteins) and PNAR. More indirect aberrant activation of B cells can also be envisaged with autoantibodies to acetyl choline receptor (on thymic myoid cells) and hormone and hormone binding proteins. Together with the concept of T-cell-B-cell discordance this idea forms the basis of the hypothesis of self-perpetuating autoreactive B cells.[14] Autoreactive B cells in spontaneous autoimmunity are seen as surviving because of subversion both of the T cell help pathway and of the feedback signal through B cell receptor, thereby overcoming the negative signals responsible for B cell self-tolerance without necessarily requiring loss of T cell self-tolerance.

                            SOURCE


                            Finally, I found this specifically about astaxanthin and autoimmune disorders. They were treating these disorers with astaxanthin so that shows promise


                            The present invention relates to the use and method of treatment concerning utilization of xanthophylls, e.g. astaxantin for suppression of excessive Th1 cell mediated immune responses and stimulation of Th2 cell mediated immune responses in a patient during ongoing infection and/or inflammation in said patient.

                            BACKGROUND OF THE INVENTION

                            CD4 T lymphocytes can be subdivided into two major subsets--Th1 cells and Th2 cells. These cells release different sets of cytokines that define their distinct actions in immunity. Th1 cells secrete interferon-gamma (IFN-γ) and are mainly involved in activating macrophages and CD8 cytotoxic T-lymphocytes. Th2 cells secrete the interleukins Il-4, Il-5 and Il-10 and are mainly involved in stimulating B cells to produce antibodies.

                            There is a balance between the activities of the Th1 and Th2 cells in a normal human body. An excess of Th1 cell activity may be the result of an autoimmune disease, or the result of an ongoing infection. In the normal case, the Th1 cell activity diminishes when the physiological need thereof is reduced. An excess activity is thus seen when the normal reduced level of Th1 cell activity is not achieved as a response to the diminishing presence of the agent that induced the reaction, e.g. the starting point of an autoimmune disease.

                            Immune modulation aims at altering the balance between different subsets of responding T cells so that damaging responses are suppressed In many cases autoimmune diseases and intracellular infections are associated with the activation of Th1 cells, which activate macrophages and drive an inflammatory immune response. The drugs currently used to suppress the immune system can be divided into three categories:

                            1) Powerful anti-inflammatory drugs of the corticosteroid family such as prednisone. Glucocorticoids influence virtually every cellular and humoral mechanism related to inflammation and immune response. However, there are also many adverse effects, including fluid retention, weight gain, diabetes, bone mineral loss and thinning of the skin.

                            2) Cytotoxic drugs such as azthioprine and cyclophosphamide. Cytotoxic drugs cause immunosuppression by killing dividing cells and they have serious side-effects. The use of these compounds is limited due to a range of toxic effects on tissues that have continuous cell dividing, such as the bone marrow.

                            3) Cyclosporin A, tacromycin and rapamycin are powerful immunosuppressive agents that interfere with T-cell signaling.

                            All of these drugs are very broad in their action and inhibit protective functions of the immune system as well as pathological responses that cause tissue injury. Opportunistic infection is therefore a common complication of immune suppressive drugs.

                            It would be desirable to have an immunosuppressive agent that targets the specific part of the immune response that causes tissue injury. In particular, it would be desirable to obtain a medicament for suppression of harmful, i.e. excessive, Th1 cell mediated immune responses and simulation of Th2 cell mediated immune responses in a patient during ongoing infection and/or inflammation in said patient.

                            DESCRIPTION OF THE INVENTION

                            The present invention provides a medicament for suppression of excessive Th1 cell mediated immune responses and stimulation of Th2 cell mediated immune responses in a patient during ongoing infection and/or inflammation in said patient.

                            One aspect of the invention is directed to the use of at least one type of xanthophylls for the production of a medicament for suppression of excessive Th1 cell mediated immune responses and stimulation of Th2 cell mediated immune responses in a patient during ongoing infection and/or inflammation in said patient.

                            In a preferred embodiment of the invention the excessive Th1 cell mediated immune responses are caused by at least one disease from the group of autoimmune diseases and chronic viral and intracellular bacterial infections.

                            Examples of diseases that cause excessive Th1 cell mediated immune responses are Psoriasis vulgaris, Multiple sclerosis (MS), Reumatoid arthritis, Crohn's disease, Insulin-dependant diabetes mellitus, Tubercolosis (TB), Acute graft-versus-host disease (transplant rejection) and HIV virus infection

                            Xanthophylles, including astaxanthin, is a large group of carotenoids containing oxygen in the molecule in addition to carbon and hydrogen. The carotenoids are produced de novo by plants, fungi and some bacteria [Johnson E. A. and Schroeder W. A., 1995, Adv In Biochem Engin. Biotechn 53: 119-178].

                            In a preferred embodiment of the invention, the type of xanthophyll is astaxanthin, preferably in a form esterified with fatty acids.

                            In a particularly preferred embodiment the astaxanthin is derived from a natural source, such as a culture of the algae Haematococcus sp., e.g. Haemotococcus pluvialis.

                            The medicament in the invention is preferably an oral preparation, which optionally comprises an oil of food grade and it is suitably presented in separate unit doses.

                            The medicament may comprise a mixture of different types of xanthophylls or different forms of the same xanthophyll, such as a mixture of synthetic astaxanthin and naturally produced astaxanthin.

                            The oral preparation may comprise in addition to the xanthophylls auxiliary ingredients that are pharmacologically acceptable inactive or active ingredients, such as flavoring agents, fillers, emulsifiers, etc.

                            Examples of separate unit doses are tablets, gelatin capsules and predetermined amounts of solutions, e.g. oil solutions, or emulsions, e.g. water-in- oil or oil-in-water emulsions.

                            Another aspect of the invention is directed to a method of suppressing excessive Th1 cell mediated immune responses and stimulating Th2 cell mediated immune responses in a patient during ongoing infection and/or inflammation in said patient comprising administration of an Th1 cell response suppressing and Th2 cell response stimulating amount of at least one type of xanthophylls to said patient.

                            The examples and preferred embodiments described for the use aspect of the invention also apply for this method aspect of the invention.

                            In particular, excessive Th1 cell mediated immune responses are caused by at least one disease from the group of autoimmune diseases and chronic viral and intracellular bacterial infections, such as Psoriasis vulgaris, Multiple sclerosis (MS), Reumatoid arthritis, Crohn's disease, Insulin-dependent diabetes mellitus, Tubercolosis (TB), Acute graft-versus-host disease (transplant resection) and HIV virus infection, and the type of xanthophyll is preferably astaxanthin, particularly in a form esterified with fatty acids, e.g. from a natural source, such as a culture of the algae Haematococcus sp.

                            The daily doses of the active ingredient of the invention will normally be in the range of 0.01 to 10 mg per kg body weight for a human calculated on the amount of astaxanthin, but the actual dose will depend on the immune response of the individual human patient, the reason for suppression of the excessive Th1 cell mediated immune response, such as the type of disease causing the enhanced pathological Th1 cell response, and the recommendations of the manufacturer.

                            The xanthophyll astaxanthin is commercially produced via culturing of the algae Haematococcus sp. by AstaCarotene AB, Gustavsberg, Sweden. It is marketed and sold in Sweden as a dietary supplement

                            Astaxanthin from other sources, and other xanthophylls as well, are expected to be similarly useful for the purposes of the invention. An advantage of using astaxanthin from algae is, however, that the astaxanthin exists in a form esterified with fatty acids [Renstrom B. et al, 1981, Phytochem 20(11) :2561-2564], which esterified astaxanthin thereby is more stable during handling and storage than free astaxantin.

                            The naturally produced astaxanthin can be obtained also from fungi and crustaceans, in addition to from algae [Johnson E. A. and Schroeder W. A., ibid].

                            Case Studies

                            During the last five years reports have been received from patients taking the commercial dietary supplement capsules of the algal meal of Haematococcus pluvialis, Astaxin.RTM., containing 4 mg astaxanthin. The daily doses recommended as an antioxidant is one capsule per day. However, 2-6 times that dose has been used by some patients without adverse effects. On the contrary, the higher doses have been experienced as beneficial in alleviating symptoms associated with some chronic diseases.

                            Six patient histories are disclosed more in detail below.

                            Chron's Disease

                            Patient 1. Boy, 17 years old, who had suffered from Crohn's disease for at least four years. He has been treated with anti-inflammatory agents, such as cortisone. He started to take the commercial product Astaxin (two capsules, each containing 4 mg of astaxanthin, per day). In about two months the cortisone treatment was phased out and later on stopped altogether. The patient was asymptomatic for more than a year when he experienced a relapse. He was then received a short-term treatment with cortisone in combination with Astaxin, and the cortisone treatment was again phased out.

                            Patient 2. Woman, about 50 years of age, who had suffered from Crohn's disease for a long time. She received treatment with cortisone. Now she has started to take Astaxin in parallel with her steroid medication and she reports that she feels considerably better.

                            Patient 3. Man, 48 years old, who has suffered from Crohn's disease for the last 20 years. He has been operated on several times and he has been treated with cortisone. Directly after the last operation he started taking Astaxin (6 capsules per day) and no cortisone. With regard to the circumstances, he has been asymptomatic. He has compared his clinical status after the operation with the status of two other patients who were operated on at the same time and who received conventional treatment with cortisone. In comparison with these two other patients his recovery has been fully equal with theirs, with the positive exception that edema in his colon diminished more quickly than in the two other patients.

                            Lichen Ruber Planus

                            Patient 4. Woman, more than 70 years of age, who had suffered from the disease for several years. The symptoms of the disease were inter alia open wounds which had not healed She had been treated with anti-inflammatory agents, such as cortisone, for several years, orally and also by injection directly to the local inflammation areas. The treatment has not led to any result. She started to take 4 capsules of Astaxin per day, and after some weeks visible alleviation of the symptoms started to show up. The wounds were healed in slightly more than one month. During this period, the patient herself phased out the cortisone treatment. The dose of Astaxin was lowered to 2 capsules per day when she was asymtomatic. However, the symptoms returned in connection with a common cold. The dose was then increased to 4 capsules per day and the wounds healed again. She says herself that she now feels considerably better.

                            Psoriasis

                            Patient 5. Male, 40 years, who suffers from psoriasis and mainly shows itself in rough skin on the elbows. After treatment with a skin cream enriched with alga meal/astaxanthin (100 mg astaxanthin/kg cream) twice a day for three weeks, the symptoms diminished.

                            Patient 6. Woman, 45 years old, who suffers from psoriasis and mainly shows itself in rough skin on the elbows. After treatment with a skin cream enriched with algal meal/astaxanthin (100 mg astaxanthin/kg cream) twice a day for three weeks, the symptoms diminished.

                            Thus, positive reports have been received from several patients suffering from Crohn's disease, rheumatoid arthritis, psoriasis and lichen planus. All of these diseases are autoimmune diseases which are known to be Th1 cell mediated diseases.

                            Therefore it is likely that the Th1 mediated response in the patients has been suppressed and that there is a shift of the Th1/Th2 balance of the immune response towards the Th2 response. Further, it is likely that patients suffering from other predominantly Th1 cell mediated diseases would benefit from suppression of excessive Th1 cell responses and stimulation of Th2 cell mediated immune responses during ongoing infection and/or inflammation.

                            SOURCE
                            Maybe someone knows a little more about this who can help?
                            Last edited by findingaway; 27 February 2011, 05:58 PM.

                            Comment


                            • #15
                              Originally posted by findingaway View Post
                              Haven't read anywhere that it increases circulation...be interested to know where you read it. Must have missed it!
                              I was just going by this part:

                              Astaxanthin to the Rescue
                              Several well-controlled clinical trials suggest that astaxanthin can help prevent eyestrain and reduce its effects. In a study of 26 computer workers receiving 5 mg astaxanthin daily for one month, subjects noted a 54 percent reduction of eye fatigue complaints and objective improvements in accommodation ability. Test subjects also showed a significant reduction in subjective symptoms.

                              Astaxanthin is shown to reduce inflammation in eye muscles and improve blood flow to the eyes, especially in the capillary vessels that supply blood to the retina. As an antioxidant, astaxanthin protects against free radical damage and oxidative stress. Because it is fat soluble, astaxanthin has a special affinity for cell membranes, particularly the double cell membrane found in eye muscle.


                              ...and making a wild assumption that if it increases blood flow to one part of the body, it will do the same to others. I hope I'm wrong!

                              1,000mg Solgar MSM
                              25mg diphenhydramine
                              Rosacea Care moisturizer, tinted ZincO
                              I avoid multi-vitamins and most other high-dose vitamins and supplements, oil-based supplements (like omega 3/6, A, and E), nitrite preservatives, sugar, fruit, milk, exercising in a warm room

                              Less is more!

                              Comment

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