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Nonfasting Plasma Total Homocysteine Level and Mortality in Middle-Aged and Elderly Men and Women in Jerusalem

Jeremy D. Kark, MD, PhD; Jacob Selhub, PhD; Bella Adler, MA; Jaime Gofin, MD, MPH; Joseph H. Abramson, MB, BCh; Gideon Friedman, MD; and Irwin H. Rosenberg, MD
[+] Article and Author Information

From Hadassah University Hospital and Hebrew University-Hadassah School of Public Health and Community Medicine, Ein Kerem, Jerusalem; and Tufts University, Boston, Massachusetts.


Grant Support: In part by the U.S. Department of Agriculture, Agricultural Research Service (contract 53-3K06-5-10); by the Ridgefield Foundation (Ridgefield, Connecticut); and by the German Federal Ministry of Education and Research (BMBF) and the Israeli Ministry of Science under the aegis of the GSF- Forschungszentrum fuer Umwelt und Gesundheit GmbH, Neuherberg, Germany.

Requests for Reprints: Jeremy D. Kark, MD, PhD, Department of Social Medicine, Hadassah University Hospital, POB 12000, Ein Kerem 91120, Jerusalem; e-mail, jeremy1@vms.huji.ac.il.

Current Author Addresses: Drs. Kark, Abramson, and Gofin and Ms. Adler: Department of Social Medicine, Hadassah University Hospital, POB 12000, Ein Kerem 91120, Jerusalem.

Drs. Selhub and Rosenberg: The Jean Mayer USDA Human Nutrition Center on Aging at Tufts University, 711 Washington Street, Boston, MA 02111.

Dr. Friedman: Geriatric Unit, Hadassah University Hospital, POB 12000, Ein Kerem 91120, Jerusalem.


Ann Intern Med. 1999;131(5):321-330. doi:10.7326/0003-4819-131-5-199909070-00002
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The metabolism of homocysteine, a sulfur amino acid, is at the intersection of two metabolic pathways: transsulfuration and remethylation (1). McCully (2) first proposed that severe hyperhomocysteinemia is related to both atherosclerosis and vascular thrombosis. Recent evidence (35) has shown an association between mildly to moderately elevated blood concentrations of total homocysteine and vascular disease (including its coronary, cerebral, and peripheral manifestations). Much of the supporting evidence for this association has been obtained from case–control studies; reports of prospective studies of cardiovascular disease, however, are inconsistent (612). It remains to be established whether this relation is causal and whether reduction of plasma homocysteine level will decrease risk. Most studies have been done in Europe and North America. Only two recent reports—one from the Framingham Study (13) and one on patients with coronary heart disease in Norway (14)—have used total mortality as an end point with which to assess health outcomes associated with a modestly elevated homocysteine level.

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Grahic Jump Location
Figure.
Kaplan-Meier survival probabilities by age-adjusted plasma homocysteine level for men (top) and women (bottom).

The top line indicates persons with homocysteine levels less than 8.58 µmol/L (bottom quintile), the middle line indicates persons with homocysteine levels of 8.58 to 14.89 µmol/L (three middle quintiles), and the bottom line indicates persons with homocysteine levels greater than 14.89 µmol/L (top quintile). The numbers of male participants who were present at the initial examination, alive after 5 years of follow-up, and alive at the end of the 9- to 11-year follow-up, respectively, are as follows: bottom quintile, 108, 106, and 101; middle quintiles, 507, 458, and 402; top quintile, 193, 142, and 113. The numbers of female participants who were present at the initial examination, alive after 5 years of follow-up, and alive at the end of the 9- to 11-year follow-up, respectively, are as follows: bottom quintile, 249, 242, and 219; middle quintiles, 567, 517, and 449; top quintile, 164, 137, and 99.

Grahic Jump Location

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