Contribution of Metabolic Syndrome Components to Cognition in Older Individuals

  1. Miranda G. Dik, PHD1,
  2. Cees Jonker, MD, PHD12,
  3. Hannie C. Comijs, PHD12,
  4. Dorly J.H. Deeg, PHD1,
  5. Astrid Kok, MSC3,
  6. Kristine Yaffe, MD4 and
  7. Brenda W. Penninx, PHD12
  1. 1EMGO Institute, VU University Medical Center, Amsterdam, the Netherlands
  2. 2Psychiatry, VU University Medical Center, Amsterdam, the Netherlands
  3. 3Clinical Chemistry, VU University Medical Center, Amsterdam, the Netherlands
  4. 4Departments of Psychiatry, Neurology, and Epidemiology, University of California, San Francisco, California
  1. Address correspondence and reprint requests to Dr. Miranda G. Dik, VU University Medical Center, Room B-542, Van der Boechorststraat 7, 1081 BT Amsterdam, Netherlands. E-mail: mg.dik{at}vumc.nl

Abstract

OBJECTIVE— Recent evidence suggests that the metabolic syndrome and inflammation affect cognitive decline in old age and that they reinforce each other. However, it is not known what the roles of the individual components of the metabolic syndrome on cognition are.

RESEARCH DESIGN AND METHODS— The sample consisted of 1,183 participants in the Longitudinal Aging Study Amsterdam who were aged 65–88 years. Metabolic syndrome (U.S. National Cholesterol Education Program definition) and its individual components and the inflammatory markers C-reactive protein (CRP) and α1-antichymotrypsin (ACT) were assessed. Cognitive assessments included general cognition (Mini-Mental State Examination), memory (verbal learning test), fluid intelligence (Raven's Matrices), and information processing speed (coding task).

RESULTS— Of the sample, 36.3% had metabolic syndrome. Metabolic syndrome was significantly associated with all cognitive measures (P < 0.05). Of the individual components, hyperglycemia was most strongly and significantly associated with cognitive function (multivariate adjusted models; B values, indicating differences in scores between both groups, ranging from −0.38 to −1.21). There was a significant interaction between metabolic syndrome and inflammation on cognition (P < 0.01–0.09). Metabolic syndrome was negatively associated with cognition in subjects with high inflammation (highest tertile for both CRP and ACT; B values ranging from −0.86 to −1.94, P < 0.05), whereas an association was absent in subjects with low inflammation (B values ranging from −0.10 to −0.70).

CONCLUSIONS— Subjects with metabolic syndrome showed poorer cognitive performance than subjects without metabolic syndrome, especially those with high levels of inflammation. Hyperglycemia was the main contributor of the association of metabolic syndrome with cognition.

Footnotes

  • Published ahead of print at http://care.diabetesjournals.org on 11 June 2007. DOI: 10.2337/dc06-1190.

    A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.

    The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C Section 1734 solely to indicate this fact.

    • Accepted June 2, 2007.
    • Received June 8, 2006.
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  1. Diabetes Care vol. 30 no. 10 2655-2660
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