The symptoms can be socially debilitating without treatment, but it is rarely life-threatening.The true incidence of rectal prolapse is unknown, but it is thought to be uncommon. As most affected people are elderly, the condition is generally under-reported. It may occur at any age, even in children, but there is peak onset in the fourth and seventh decades. Women over 50 are six times more likely to develop rectal prolapse than men. It is rare in men over 45 and in women under 20. When males are affected, they tend to be young and report significant bowel function symptoms, especially obstructed defecation, or have a predisposing disorder (e.g., congenital anal atresia). When children are affected, they are usually under the age of 3. 35% of women with rectal prolapse have never had children, suggesting that pregnancy and labour are not significant factors. Anatomical differences such as the wider pelvic outlet in females may explain the skewed gender distribution.Associated conditions, especially in younger patients include autism, developmental delay syndromes and psychiatric conditions requiring several medications. Signs and symptoms
Signs and symptoms include:

history of a protruding mass. degrees of fecal incontinence, (50-80% of patients) which may simply present as a mucous discharge. constipation (20-50% of patients) also described as tenesmus (a sensation of incomplete evacuation of stool) and obstructed defecation. a feeling of bearing down. rectal bleeding
diarrhea and erratic bowel habits.Initially, the mass may protrude through the anal canal only during defecation and straining, and spontaneously return afterwards.
AHH is an acquired form of the disease often occurring after sexual maturation and is not related to genetic defects. Pathogenesis
CHH is a type of HH resulting from the abnormal migration of GnRH neurons during embryonic development. GnRH neurons are derived from the olfactory placode and migrate into the central nervous system (CNS) during embryonic development. Embryonic migration can be affected by several gene mutations including but not limited to, KAL1, fibroblast growth factor (FGF8), sex determining region Y-Box 10 (SOX10), GNRHR, GNRH1 and KISS1R. Kallmann syndrome results in a loss of smell (anosmia) and is associated with KAL1 mutations. The KAL1 gene encodes anosmin-1, an extracellular adhesion molecule that plays a role in GnRH neuronal migration and adhesion. Mutated KAL1 genes leads to ill GnRH neuronal migration as well as olfactory neuron disorder causing anosmia and non-functional GnRH releasing neurons. Mutations of KAL1 are mostly nucleotide insertion or deletion causing frame shifts in the translation of anosmin-1 resulting in a faulty protein. Inactivating mutations in the genes encoding GNRH1 or its receptor will result in the failure of the HPG axis and give rise to normosmic CHH. Inactivating mutations of KISS1 or KISS1R causes normosmic CHH in humans. This is because KISS1 is the mediator for the feedback loop in the HPG axis allowing low levels of sex steroid to stimulate GnRH secretion from the hypothalamus.CHH is a genetically heterogenous disorder with cases reported as being X-linked, recessive and autosomally inherited.