Hemorrhoids are normal vascular cushions of the anal canal. Hemorrhoidal disease develops when the connective tissue anchoring these cushions deteriorates and the underlying arteriovenous plexuses become engorged, causing bleeding and prolapse.^[1][2] No single cause has been identified. Disease reflects risk factors acting through two linked mechanisms: degeneration of the supporting tissue, and increased anorectal or intra-abdominal venous pressure.^[3][4] The best-supported associations are:

• Disordered defecation, including constipation, straining, and prolonged toilet sitting
• Increasing age
• Pregnancy and parity
• Smoking and hypertension, which are small but independent correlates in large screening data^[5]

The roles of obesity, diet, physical activity, diarrhea, and portal hypertension remain inconsistent. Anatomic hemorrhoids are common and often asymptomatic. Associations derived from endoscopic prevalence studies therefore may not apply directly to symptomatic disease.^[6]

• Connective-tissue degeneration (sliding-cushion model): Age, chronic straining, and pregnancy weaken the anchoring connective tissue, so the cushions bulge and descend. During defecation, stool pushes the prolapsing tissue through the sphincter, which impairs venous return and causes cyclical swelling, trauma, and bleeding.^[3][2] This model has replaced the older view of hemorrhoids as simple varicose veins.^[1]
• Increased venous and intra-abdominal pressure: Sustained pressure (straining, pregnancy, raised intra-abdominal pressure) dilates the submucosal vascular plexus and stretches its fibroelastic support.^[4]
• Anal sphincter tone: Basal anal pressures are higher in patients with hemorrhoids than in controls across manometric studies. Whether this is a cause or a consequence remains uncertain.^[7]
• Anatomic vs symptomatic disease: In a colorectal cancer screening population, 38.9% of 976 adults had hemorrhoids at colonoscopy, but only 44.7% of these reported symptoms.^[6] Why some anatomic hemorrhoids become symptomatic is not well understood.^[3]

• Obesity: Findings conflict across studies.
  • In an Austrian screening cohort, each 1-unit increase in body mass index raised hemorrhoid risk by 3.5%.^[6]
  • In a Korean cohort, overweight was associated with hemorrhoids, but the effect of adiposity differed by sex and parity.^[5]
  • In a US colonoscopy cohort, neither overweight nor obesity was associated with hemorrhoids.^[8]
• Dietary fiber: Among fiber subtypes, only high grain-fiber intake was associated with lower prevalence (quartile 4 vs 1: OR 0.78; 95% CI 0.62–0.98).^[8] Direct evidence that low dietary fiber causes hemorrhoids is limited.
• Spicy food: Spicy food did not worsen hemorrhoidal symptoms in a randomized trial, contrary to common teaching.^[3]
• Physical activity and sedentary behavior: Sedentary behavior was paradoxically associated with lower risk (OR 0.80; 95% CI 0.65–0.98). Physical activity showed no significant association.^[8]
• Diarrhea and bowel frequency: An older case-control study suggested that diarrhea, rather than constipation, was associated with hemorrhoids.^[9] Frequent bowel movements were not associated with hemorrhoids in a later colonoscopy cohort.^[8] Constipation is therefore not the only relevant bowel disturbance, but no single bowel pattern is clearly causal.^[1]
• Direction of the constipation association: Constipation is more common in patients with hemorrhoids. However, hemorrhoids were not significantly more prevalent in constipated patients than in controls (OR 2.37; 95% CI 0.67–8.44). This suggests shared mechanisms, such as dyssynergic defecation and straining, rather than a simple one-way causal relationship.^[7]
• Straining: Straining was not independently associated with endoscopic hemorrhoids after adjustment in the smartphone cohort.^[10] This conflicts with traditional teaching.
• Portal hypertension and cirrhosis:
  • One review reports higher hemorrhoid prevalence in cirrhosis with portal hypertension (59%) than without it (19%).^[4] An older case-control study found no association with cirrhosis.^[9]
  • Clinically significant portal hypertension can produce anorectal varices. These are portosystemic collaterals, distinct from hemorrhoids, and must be distinguished before bleeding is attributed to hemorrhoids.^[4][11]

The following conditions are traditionally listed because they plausibly raise intra-abdominal or pelvic venous pressure:^[12]

• Chronic cough
• Heavy lifting
• Ascites
• Pelvic space-occupying lesions
• Straining related to bladder outlet obstruction

These factors have not been validated as independent risk factors in controlled epidemiologic studies.