In this study we report the prevalence and growth rate of human benign prostatic hyperplasia with age by combining and analyzing data from 10 independent studies containing more than 1,000 prostates. The normal prostate reaches 20 plus or minus 6 gm. in men between 21 and 30 years old, and this weight remains essentially constant with increasing age unless benign prostatic hyperplasia develops. The prevalence of pathological benign prostatic hyperplasia is only 8 per cent at the fourth decade; however, 50 per cent of the male population has pathological benign prostatic hyperplasia when they are 51 to 60 years old. The average weight of a prostate that is recognized at autopsy to contain benign prostatic hyperplasia is 33 plus or minus 16 gm. Only 4 per cent of the prostates in men more than 70 years old reach sizes greater than 100 gm. An analysis of a logistic growth curve of benign prostatic hyperplasia lesions removed at prostatectomy indicates that the growth of benign prostatic hyperplasia is initiated probably before the patient is 30 years old. The early phase of benign prostatic hyperplasia growth (men between 31 and 50 years old) is characterized by a doubling time for the tumor weight of 4.5 years. In the mid phase of benign prostatic hyperplasia growth (men between 51 and 70 years old) the doubling time is 10 years, and increases to more than 100 years in patients beyond 70 years old.

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The natural history of benign prostatic hyperplasia (BPH) involves two phases. The first, or pathological phase of BPH, involves two stages, termed microscopic and macroscopic BPH, neither of which produces symptomatic clinical dysuria. Nearly all men throughout the world will eventually develop microscopic BPH if they live long enough. In only about one‐half of the men with microscopic BPH, however, will microscopic BPH grow to produce a macroscopic enlargement of the gland (i. e., macroscopic BPH), suggesting that additional factors are required for the progression of microscopic to macroscopic BPH. Several theories have been proposed to explain the etiology of the pathological phase of BPH. The major theories include the hypotheses that pathological BPH is due to 1) a shift in prostatic androgen metabolism that occurs with aging, which leads to an abnormal accumulation of dihydrotestosterone, thus producing the enlarged prostate (i. e., DHT hypothesis), 2) a change in the prostatic stromal‐epithelial interact that occurs with aging, which leads to an inductive effect on prostatic growth (i. e., embryonic reawakening theory), or 3) an increase in the total prostatic stem cell number and/or an increase in the clonal expanding of the stem cells into amplifying and transit cells that occurs with aging (i. e., stem cell theory). The second, or clinical phase of BPH, involves the progression of pathologic BPH to clinical BPH in which the patient develops symptomatic dysuria. Only about one‐half the men with macroscopic BPH progress to clinical BPH. Although the macroscopic enlargement of the prostate is a necessary condition for the development of clinical BPH, this enlargement is usually not sufficient by itself for the progression of pathologic BPH to clinical BPH. The etiology of the progression of pathological BPH to clinical BPH requires additional factors (e. g., prostatitis, vascular infarct, tensile strength of the glandular capsule, etc.). A successful treatment for clinical BPH, therefore, does not necessarily require either the prevention or elimination of all degrees of pathologic BPH. Instead, what is needed is a therapy to prevent or reverse the progression of pathologic BPH to the clinical disease.