Abstract
Increasing evidence recently has pointed toward a relationship between lower urinary tract symptoms (LUTS) and the presence of metabolic syndrome. This relationship has been supported by recent epidemiologic findings. Possible pathophysiologic links also have been proposed to explain the relationship between these two syndromes. The increasing prevalence of obesity in the United States makes this an increasingly relevant problem. Animal studies support a link between autonomic nervous system (ANS) overactivity and the development of urinary symptoms, low bladder compliance, compensatory prostatic hyperplasia, and blockage of the same using α-blockade. There appears to be a significant link between ANS overactivity as part of the metabolic syndrome and LUTS secondary to benign prostatic hyperplasia (BPH). However, it is unlikely that ANS overactivity could be responsible for the development of LUTS. Rather, ANS overactivity plays a key role in increasing the severity of LUTS above an intrinsic basal intensity that is determined by the genitourinary anatomic/pathophysiologic characteristics of each BPH patient. This paper defines metabolic syndrome as a collection of abnormalities, including being overweight (visceral abdominal fat distribution), dyslipidemia, hypertension, impaired glucose metabolism, elevated C-reactive protein (chronic inflammation), and autonomic-sympathetic overactivity, with insulin resistance as the hypothesized underlying pathogenic mechanisms.
Similar content being viewed by others
References and Recommended Reading
Hammarsten J, Hogstedt B: Hyperinsulinaemia as a risk factor for developing benign prostatic hyperplasia. Eur Urol 2001, 39:151–158.
Lakka TA, Laaksonen DE, Lakka HM, et al.: Sedentary lifestyle, poor cardiorespiratory fitness, and the metabolic syndrome. Med Sci Sports Exerc 2003, 35:1279–1286.
Ford ES, Giles WH, Dietz WH: Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA 2002, 287:356–359. Excellent summary of the MSx epidemic in the United States.
Malik S, Wong ND, Franklin S, et al.: Cardiovascular disease in U.S. patients with metabolic syndrome, diabetes, and elevated C-reactive protein. Diabetes Care 2005, 28:690–693.
Haffner SM: The metabolic syndrome: inflammation, diabetes mellitus, and cardiovascular disease. Am J Cardiol 2006, 97:3A-11A.
Grassi G, Dell’Oro R, Quarti-Trevano F, et al.: Neuroadrenergic and reflex abnormalities in patients with metabolic syndrome. Diabetologia 2005, 48:1359–1365.
Reaven GM, Lithell H, Landsberg L: Hypertension and associated metabolic abnormalities: the role of insulin resistance and the sympathoadrenal system. N Engl J Med 1996, 334:374–381.
Landsberg L: Insulin-mediated sympathetic stimulation: role in the pathogenesis of obesity-related hypertension (or, how insulin affects blood pressure, and why). J Hypertens 2001, 19:523–528. A clear description of the etiology of sympathetic hyperactivity in metabolic syndrome.
McVary KT, Rademaker A, Lloyd GL, Gann P: Autonomic nervous system overactivity in men with lower urinary tract symptoms secondary to benign prostatic hyperplasia. J Urol 2005, 174:1327–1433. Clear demonstration of the relationship between MSx and LUTS/BPH.
McVary KT, Razzaq A, Lee C, et al.: Growth of the rat prostate gland is facilitated by the autonomic nervous system. Biol Reprod 1994, 51:99–107.
Golomb E, Rosenzweig N, Eilam R, Abramovici A: Spontaneous hyperplasia of the ventral lobe of the prostate in aging genetically hypertensive rats. J Androl 2000, 21:58–64.
Glynn RJ, Campion EW, Bouchard GR, Silbert JE: The development of benign prostatic hyperplasia among volunteers in the Normative Aging Study. Am J Epidemiol 1985, 121:78–90.
Hammarsten J, Hogstedt B: Clinical, anthropometric, metabolic and insulin profile of men with fast annual growth rates of benign prostatic hyperplasia. Blood Press 1999, 8:29–36.
Steers WD, Clemow DB, Persson K, et al.: The spontaneously hypertensive rat: insight into the pathogenesis of irritative symptoms in benign prostatic hyperplasia and young anxious males. Exp Physiol 1999, 84:137–147.
Meigs JB, Mohr B, Barry MJ, et al.: Risk factors for clinical benign prostatic hyperplasia in a community-based population of healthy aging men. J Clin Epidemiol 2001, 54:935–944.
McConnell JD, Roehrborn CG, Bautista OM, et al.: Medical Therapy of Prostatic Symptoms (MTOPS) Research Group. The long-term effects of doxazosin, finasteride, and the combination on the clinical progression of BPH. N Engl J Med 2003, 349:2387–2398.
Roehrborn CG, McConnell JD, Kusek J, et al.: Impact of baseline PSA and TRUS volume on longitudinal changes in IPSS and maximum flow rate in MTOPS [Abstract 910]. J Urol 2004, 171:241.
Hammarsten J, Hogstedt B, Holthuis N, Mellstrom D:Components of the metabolic syndrome-risk factors for the development of benign prostatic hyperplasia. Prostate Cancer Prostatic Dis 1998, 1:157–162.
Gann PH, Hennekens CH, Longcope C, et al.: A prospective study of plasma hormone levels, nonhormonal factors, and development of benign prostatic hyperplasia. Prostate 1995, 26:40–49.
Maso LD, Zucchetto A, Tavani A, et al.: Lifetime occupational and recreational physical activity and risk of benign prostatic hyperplasia. Int J Cancer 2006, 118:2632–2635.
Lacey JVJr, Deng J, Dosemeci M, et al.: Prostate cancer, benign prostatic hyperplasia, and physical activity in Shanghai, China. Int J Epidemiol 2001, 30:341–349.
Platz EA, Kawachi I, Rimm EB, et al.: Physical activity and benign prostatic hyperplasia. Arch Intern Med 1998, 158:2349–2356. Excellent paper detailing the risk of physical inactivity and the development of LUTS.
Hammarsten J, Hogstedt B: Hyperinsulinaemia: a prospective risk factor for lethal clinical prostate cancer. Eur J Can 2005, 41:2887–2895.
Rohrmann S, De Marzo AM, Smit E, et al.: Serum Creactive protein concentration and lower urinary tract symptoms in older men in the Third National Health and Nutrition Examination Survey (NHANES III). Prostate 2005, 62:27–33.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Kasturi, S., Russell, S. & McVary, K.T. Metabolic syndrome and lower urinary tract symptoms secondary to benign prostatic hyperplasia. Curr Urol Rep 7, 288–292 (2006). https://doi.org/10.1007/s11934-996-0008-y
Issue Date:
DOI: https://doi.org/10.1007/s11934-996-0008-y