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

  1. #11
    Senior Member findingaway's Avatar
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    Quote 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.

  2. #12
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    Quote 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...

  3. #13
    Senior Member findingaway's Avatar
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    Quote 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?

    Quote 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...

  4. #14
    Senior Member findingaway's Avatar
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    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?

  5. #15
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    Quote 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!

    1,000 IU D3
    50mg zinc
    50mg magnesium chelate
    25mg diphenhydramine HCI
    Psyllium fiber
    Pure Protein bar
    Drink filtered/bottled water only, wash with tepid water/moisturizing soap, filtered shower head, 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, probiotics, sugar, fruit, alcohol, caffeine, exercising in a warm room

    Less is more!

  6. #16
    Senior Member findingaway's Avatar
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    Default So I heard back...

    This is what the firm that produce a brand of astaxanthin said to my questions about astaxanthin and rosacea:


    Please first understand that I am not an expert in the area of rosacea. In contrast, your emails demonstrate that you have a vast amount of knowledge about rosacea.

    Your concerns about astaxanthin possibly aggravating rosacea (to do with) astaxanthin’s ability to reduce melanin in the skin and improve capillary vessel blood flow are very valid concerns.

    I feel the basic question is: will astaxanthin, due to its anti-inflammatory properties, alleviate the root cause of rosacea as a chronic skin inflammatory disease, or will astaxanthin, due to melanin lowering and improved capillary blood flow, aggravate the symptoms of rosacea? I do not know the answer to this question. However, do to the potential negative effects of astaxanthin on symptoms of rosacea, any use of astaxanthin by patients with rosacea should be monitored very closely and only small and slowly increasing doses should be used.
    What to do, what to do?

    It could be the best decision I ever made, or it could be the worst...I hate decisions like this.

    So lets assume the worse and it causes huge unprecedented tiger wave flushing where my face is so purple passes-by are dialling 999 and asking for an ambulance... (a little melodramatic I agree - will I recover back to where I am now or will I have done irreparable damage?

    Opinions very welcome...

  7. #17
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    well its a progressive disease....


    my understanding is that each new flush progresses the amount of infrastructure in your face further...and the severity of that flush would also have an impact i assume.

    that being said... one flush does not progress the disease that noticeable of an amount i dont think...

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    haha good luck!

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    Default keep us posted

    keep us posted

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