Benfotiamine

Discussion in 'Health and medical' started by Bill Van Antwer, Feb 10, 2004.

  1. There has been a lot of discussion of the potential benefits of Benfotiamine for reducing
    complications, particularly neuropathic pain. Does anyone here have any anecdotal information on the
    use of benfotiamine. Mike Brownlee is very well respected and he is the author of the original data
    on benfotiamine and has proposed a mechanism for its action. Any data will be appreciated.

    thanks BVA
     
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  2. Jon Kaplan

    Jon Kaplan Guest

    I take the stuff. I really can't tell if it does anything.

    Jon
     
  3. Cheri

    Cheri Guest

    Me too, and same here.

    --
    Cheri
    Type 2, no meds for now.

    Jon Kaplan wrote in message <[email protected]>...
    >I take the stuff. I really can't tell if it does anything.
    >
    >Jon
     
  4. Frank Roy

    Frank Roy Guest

    Bill Van Antwerp wrote:

    > There has been a lot of discussion of the potential benefits of Benfotiamine for reducing
    > complications, particularly neuropathic pain. Does anyone here have any anecdotal information on
    > the use of benfotiamine. Mike Brownlee is very well respected and he is the author of the original
    > data on benfotiamine and has proposed a mechanism for its action. Any data will be appreciated.
    >
    > thanks BVA

    I suppose that the article that appeared in Nature or the following that you have reference to
    concerning Dr. Brownlee.

    Benfotiamine Inhibits Intracellular Formation of Advanced Glycation End Products in vivo http://www.uniklinikum-
    giessen.de/med3/poster/publ_pdf/060.pdf JIHONG LIN, ALEX ALT, JUTTA LIERSCH, REINHARD G. BRETZEL,
    MICHAEL BROWNLEE*, HANS-PETER HAMMES Third Medical Department, Justus-Liebig-University Giessen,
    Germany *Albert-Einstein College, New York, NY, USA

    The results with T1 diabetic were impressive in the above article. The blood serum before and after
    24 days of treatment with 600 mg/d were very significant for the intermediates to AGE products that
    cause a lot of kidney problems for diabetics.

    "While treatment with benfotiamin did not affect HbA1c levels, levels of N-epsilon-(carboxymethyl)-
    lysine (CML) decreased by 40 %. The levels of intracellular methylglyoxal-derived AGE were reduced
    by almost 70 %. The data indicate that thiamine derivatives are effective inhibitors of both
    intracellular glycoxidation and AGE formation."

    I took benfotiamine at about 200 mg/day for 2 months and switched to 600 mg/day for six weeks. I had
    a minor amount of symptoms like neuropathy on the bottom of my left big toe. At the end of about 5
    weeks of the higher dosage, this toe became sensitive to the point were I discontinued walking as an
    exercise. I discontinued on 01/18/04. The sensitivity has subsided and the symptoms are less
    pronounced than when I first began treatment. Subsequently, I have gone to a podiatrist and he
    suggested that this was not diabetic neuropathy since such neuropathy usually occurs in the same
    area(s) on the opposite side as well. I have also had gout in the same toe for at least 41 years and
    the symptoms may be due to nerves getting pinched. I had some x-rays taken and the diagnosis will
    follow next week. I also had pain in the area of the heart and the cardiologist suggested that it
    was not a heart problem. I had a echocardiogram and a leaky valve was found. The results of a
    nuclear stress test and diagnosis are in waiting.

    I decided to resume the benfotiamine a 200 mg/day a few days after I had the stress test.

    The way I see it, without appropriate lab work, benfotiamine therapy is sort of blind flying
    especially if it is dose dependent. Consequently, while I do this myself, I don't necessarily
    advocate this for someone else. I am already 68 and who knows how long I have to live even though
    I have reasonably good health and quality of life. Benfotiamine may cleanup some of the results
    of elevated postprandial BGs, but is not considered a cross link breaker of glycated proteins
    such as collagen.

    Frank
     
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