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Ascorbic acid supplementation does not lower plasma lipoprotein(a) concentrations

  • Jennifer L Jenner
    Correspondence
    Corresponding author. Tel.: +1-617-5563228; fax: +1-617-5563103
    Affiliations
    Lipid Metabolism Laboratory (JLJ, LJS, EJS) and the Epidemiology Program (PFJ), Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston, MA 02111, USA
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  • Paul F Jacques
    Affiliations
    Lipid Metabolism Laboratory (JLJ, LJS, EJS) and the Epidemiology Program (PFJ), Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston, MA 02111, USA
    Search for articles by this author
  • Leo J Seman
    Affiliations
    Lipid Metabolism Laboratory (JLJ, LJS, EJS) and the Epidemiology Program (PFJ), Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston, MA 02111, USA
    Search for articles by this author
  • Ernst J Schaefer
    Affiliations
    Lipid Metabolism Laboratory (JLJ, LJS, EJS) and the Epidemiology Program (PFJ), Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston, MA 02111, USA
    Search for articles by this author

      Abstract

      Elevated plasma concentrations of lipoprotein(a) (Lp[a]) are associated with premature coronary heart disease (CHD). Lp(a) is a lipoprotein particle consisting of low-density lipoprotein (LDL) with apolipoprotein (apo) (a) attached to the apo B-100 component of LDL. It has been hypothesized that ascorbic acid supplementation may reduce plasma levels of Lp(a). The purpose of this study was to determine whether ascorbic acid supplementation at a dose of 1 g/day would lower plasma concentrations of Lp(a) when studied in a randomized, placebo-controlled, blinded fashion. One hundred and one healthy men and women ranging in age from 20 to 69 years were studied for 8 months. Lp(a) values at baseline for the placebo group (n=52) and the ascorbic acid supplemented group (n=49) were 0.026 and 0.033 g/l, respectively. The 8-month concentrations were 0.027 g/l (placebo) and 0.038 g/l (supplemented group). None of these values were significantly different from each other. In addition, no difference in plasma Lp(a) concentration was seen between the placebo and supplemented groups when only subjects with an initial Lp(a) value of ≥0.050 g/l were analyzed. Our data indicate that plasma Lp(a) concentrations are not significantly affected by ascorbic acid supplementation in healthy human subjects.

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