Background: A strong association between levator expansion, pelvic organ prolapse (POP) and lower urinary tract symptoms (LUTS). Aim: To test the hypothesis that anatomical damage at childbirth is the underlying cause for excessive hiatal dilatation, prolapse and LUTS. Methods: Anatomy and biomechanics of the levator hiatus (LH), pelvic muscles and effects thereof of labour were analysed. Results: LH is a space between horizontally oriented pubococcygeus muscles containing urethra, vagina, and anorectum. These muscles turn vertically downwards into a “tunnel” surrounded by vertically oriented puborectalis muscle, inserting into anal sphincters and perineum. Hiatal expansion is not necessarily pathogenic. A calculated 45sqcm expansion is required for evacuation of larger stools. Co-occurrence of over-expanded LH, prolapse and LUTS are explained as follows: pre-labour depolymerization of collagen “plasticizes” connective tissues, allowing stretch without rupture. Failure to regain normal length post-delivery may cause nerve damage and extended entheses; both may cause hiatal muscle to sag, resulting in LH expansion; also, causing loose or weakened cardinal/uterosacral ligaments which may cause prolapse and weakened muscle forces which cannot open, close or stretch, leading to bladder/bowel incontinence and evacuation problems. A 79% recurrence of POP after successful surgical confinement of LH by puborectalis mesh sling invalidated the expansion hypothesis. However, data showing 80% cure of OAB, SUI and prolapse by TFS (Tissue Fixation system) minisling ligament repair indicated these ligaments caused the conditions associated with LH expansion, not the expansion per se. Conclusions: Association is not causation. Muscle, nerve, ligament damage by head descent down the birth canal adequately explains LH/prolapse association. Birth damage simultaneously causes levator hiatus overexpansion, prolapse and LUTS.