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Hypoandrogenism in Middle Age Men Predicts Metabolic Syndrome, Diabetes Show Comments PDF Print E-mail
Wednesday, 19 May 2004
NEW YORK (Reuters Health) - Middle-age men with low levels of testosterone or sex hormone-binding globulin, or both, are at risk for the development of the metabolic syndrome and diabetes, according to a new study.

NEW YORK (Reuters Health) - Middle-age men with low levels of testosterone or sex hormone-binding globulin, or both, are at risk for the development of the metabolic syndrome and diabetes, according to a new study.

In the May issue of Diabetes Care, a multicenter team led by Dr. David E. Laaksonen of Kuopio University Hospital in Kuopio, Finland reports on its long-term follow-up of 702 middle-age men who were participating in a population-based cohort study. At the start of the study, none of the men had diabetes or the metabolic syndrome. After 11 years, however, 147 men had the metabolic syndrome and 57 had diabetes.

Low levels of total testosterone and sex hormone binding globulin were independent predictors of the metabolic syndrome and diabetes, the authors said.

Specifically, after adjustment for age, the odds ratios for development of the metabolic syndrome for men with lowest-quartile hormone levels were 2.3 (for low testosterone), 1.7 (for low calculated free testosterone), and 2.8 (for low sex hormone-binding globulin).

Odds ratios for development of diabetes for men with lowest-quartile hormone levels were 2.3 (for low testosterone), 1.7 (for low calculated free testosterone), and 4.3 (for low sex hormone-binding globulin).

The associations were not altered by cardiovascular disease, smoking, alcohol intake, or socioeconomic status. After adjustment for factors related to insulin resistance, the associations "remained significant, except for free testosterone," according to the study.

The researchers conclude: "Hypoandrogenism is an early marker for disturbances in insulin and glucose metabolism that may progress to the metabolic syndrome or frank diabetes and may contribute to their pathogenesis."

Diabetes Care 2004;27:1036-1041.


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