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The Journal of Clinical Endocrinology & Metabolism Vol. 90, No. 8 4979
Copyright © 2005 by The Endocrine Society

Letter to the Editor

Letter re: Endogenous Sex Hormones and Metabolic Syndrome in Aging Men

Paul G. Cohen

Department of Pharmaceutical Sciences, Southern School of Pharmacy, Mercer University, Atlanta, Georgia 31119

Address correspondence to: Paul G. Cohen, M.D., Adjunct Professor, Department of Pharmaceutical Sciences, Southern School of Pharmacy, Mercer University, P.O. Box 191405, Atlanta, Georgia 31119. E-mail: cohenpg{at}bellsouth.net.

To the editor:

In their paper, Muller et al. (1) conclude that higher testosterone levels in aging men are associated with a lesser risk of having the metabolic syndrome. This interpretation of their data confounds a complex and contentious concept: the hypogonadal-metabolic-atherogenic disease and aging connection (2), thereby undervaluing the relationship between testosterone and the metabolic syndrome in elderly men.

The male hypogonadal state plays a central role in the development of the metabolic syndrome in younger as well as elderly males. Continued positive energy balance results in the accumulation of adipose mass and increased aromatase activity, which further leads to the hypogonadal state (the hypogonadal-obesity cycle). Decreased testosterone causes an adverse partitioning of both lean and fat tissue mass. The hypotestosteronemia facilitates the deposition of visceral-abdominal fat, which ultimately leads to a progressive increase of insulin resistance and eventuates in the various features of the metabolic syndrome.

The difference in correlation between the various component risk factors and the hypogonadal state probably reflects dissonant intrinsic sensitivities of each facet of the metabolic syndrome, as expressed over varying periods of time, and should not diminish the significance of reduced testosterone concentrations. Furthermore, it has become apparent that the male hypogonadal state should be considered as a risk factor for developing the metabolic syndrome for several reasons. First, it participates in the development of "male distribution" of fat, which is important in the generation of insulin resistance. Second, the progressive increase of total body fat is associated with increased aromatase activity that leads to a progressive hypogonadal state. Additionally, diminished testosterone levels, which can be measured, provide a quantitative value that can be helpful as a criterion for the metabolic syndrome and as a therapeutic goal.

Finally, male hypogonadism responds to aromatase inhibition which normalizes both testosterone and estradiol levels (3) and raises the issue regarding optimal therapy. Therefore, prospective studies will be necessary to determine the ultimate value in normalizing the sex hormones, as well as, their effect on the metabolic syndrome.

Received April 26, 2005.

References

  1. Muller M, Grobbee DE, den Tonkelaar I, Lamberts SWJ, van der Schouw YT 2005 Endogenous sex hormones and metabolic syndrome in aging men. J Clin Endocrinol Metab 90:2618–2623[Abstract/Free Full Text]
  2. Cohen PG 2001 Aromatase, adiposity, aging and disease. The hypogonadal-metabolic-atherogenic-disease and aging connection. Med Hypotheses 56:702–708[CrossRef][Medline]
  3. Leder BZ, Rohrer JL, Rubin SD, Gallo J, Longcope C 2004 Effects of aromatase inhibition in elderly men with low or borderline-low serum testosterone levels. J Clin Endocrinol Metab 89:1174–1180[Abstract/Free Full Text]




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