The prevention of benign prostatic hyperplasia (bph)

Abstract

Barry Marshall and Robin Warren were the first to show that the chronic diseases (gastric ulcer and chronic gastritis) were caused by an infection (Helicobacter pylori).The chronic disease benign prostatic hyperplasia belongs to the same ilk, except that the infection process is much more subtle and complex.The enzyme Phospholipase D (PLD) which is attached to the outer membrane of Escherichia coli (E. coli) has now been almost completely proven to be the basic cause of BPH. The evidence for this process is now extremely strong and compelling.PLD obtained from the organism Streptomyces chromofuscus has been used in past research because of its PLD content. It is commercially available.In vitro, on a culture of prostatic smooth muscle, PLD stimulated the production of lysophosphatidic acid (LPA) which acted on and caused substantial growth of that muscle in accordance with the quantity of PLD/ LPA generated.It has been asserted that repeated colonization by E. coli of the transitional zone of the prostate gland and the release of PLD following repeated destruction of these colonized bacteria, is the basic cause of BPH. The evidence for colonizing and re-colonizing infection is now overwhelming.PLD is a simple lipid consisting of a phosphate, glycerol and a fatty acid.After absorption into the prostatic stroma (which consists of connective tissue and of smooth muscle), it stimulates the production of LPA which, in turn, apart from directly stimulating prostatic smooth muscle, also acts on the connective tissue in the prostate and induces a complex mixture of growth regulatory proteins, which include members of the fibroblast, insulin-like and growth transforming factor families and implicates autocrine hormones acting on the stroma and paracrine hormones acting on epithelium.Also involved, are a variety of interleukins and other inflammatory cell cytokines, secreted by the stroma, which may further promote autocrine/paracrine proliferation of BPH cells.Cadherins involved in cell adhesion and possibly chalone which exerts negative effects, must also be considered.Overall, the degree of BPH that any older male develops is governed largely by:1.His level of serum testosterone (T) and dihydrotestosterone (DHT).2.The number of receptors for E. coli which he possesses. This is at least partly genetically determined. This is the major and by far the most common factor influencing incidence and degree of severity of this disease.3.The number of times he sexually ejaculates after the age of approximately 40years.Apart from providing the existing huge evidence for infection in BPH, this manuscript explains the production, release and absorption of PLD into the prostate gland where it is converted to LPA. This is a growth factor and acts within the prostate both on smooth muscle (research proof given) and on prostatic connective tissue, resulting in BPH.This manuscript indicates the vital research, including the requisite materials, which would readily provide irrefutable and final etiological proof of all of the hormones involved.It explains how, to a large extent, the use of a vaccine which is now being developed, would likely allow the ultimate prevention of this ubiquitous disease.