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Metabolic Factors Associated with Benign Prostatic Hyperplasia

The James Buchanan Brady Urological Institute (J.K.P., H.B.C., A.W.P., P.L., E.A.P.), The Johns Hopkins Medical Institutions, Baltimore, Maryland 21287; The National Institute of Aging, Clinical Research Branch (B.G.W., E.J.M., L.F.), Harbor Hospital, Baltimore, Maryland 21225; and The Department of Epidemiology (E.A.P.), The Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21205

Address all correspondence and requests for reprints to: J. Kellogg Parsons, M.D., M.H.S., Division of Urology, University of California San Diego, 200 West Arbor Drive, San Diego, California 21287. E-mail: k0parsons{at}ucsd.edu.

Context: Benign prostatic hyperplasia poses a significant public health problem, but its etiology remains unclear. Obesity and associated abnormalities in glucose homeostasis may play a role in benign prostatic hyperplasia development by influencing prostate growth.

Objective: The objective of this study was to determine whether obesity, fasting plasma glucose concentration, and diabetes are associated with radiologically determined prostate enlargement, an objective measure of benign prostatic hyperplasia.

Design: This study was a cross-sectional analysis with robust variance estimates to account for multiple measures over time in the same individuals.

Setting: This prospective cohort study was composed of community volunteers.

Patients: Patients studied were 422 adult men enrolled in The Baltimore Longitudinal Study of Aging.

Main Outcome Measurements: Total prostate volume as determined by pelvic magnetic resonance imaging was measured.

Results: Among 422 participants, 91 (21.6%) had prostate enlargement (defined as total prostate volume 40 cc) at first visit. Compared with men of normal weight [body mass index (BMI) < 25 kg/m²], the age-adjusted odds ratio (OR) for prostate enlargement for overweight men (BMI, 25–29.9 kg/m²) was 1.41 (95% CI, 0.84–2.37), for obese men (BMI, 30–34 kg/m²) was 1.27 (95% CI, 0.68–2.39), and for severely obese men (BMI 35 kg/m²) was 3.52 (95% CI, 1.45–8.56) (P = 0.01). Men with elevated fasting glucose (>110 mg/dl) were more likely to have an enlarged prostate than men with normal fasting glucose (110 mg/dl) (OR, 2.98; 95% CI, 1.70–5.23), as were men with a diagnosis of diabetes (OR, 2.25; 95% CI, 1.23–4.11).

Conclusions: Obesity, elevated fasting plasma glucose, and diabetes are risk factors for benign prostatic hyperplasia.