Causes of Colonic Diverticula
Primary Mechanism
Colonic diverticula form when the mucosa and submucosa herniate through weak points in the circular muscle layer at sites where blood vessels (vasa recta) penetrate the colonic wall, driven by excessive intraluminal pressure. 1
This herniation creates pseudodiverticula (outpouchings that lack a complete muscular wall), which are the hallmark of diverticular disease. 2
Major Causative Factors
Dietary Factors
- Low dietary fiber intake is the dominant etiological factor, reducing stool bulk and requiring higher propulsive pressures to move colonic contents. 1
- The fiber-deficiency theory, originally proposed by Painter and Burkitt in the 1970s, remains the most widely accepted explanation for diverticular disease in Western populations. 1
- High meat consumption is an additional dietary risk factor. 3
Structural Changes in the Colonic Wall
- Altered connective tissue composition weakens the colonic wall, specifically changes in collagen and elastin content that reduce wall flexibility and strength. 1, 2
- These degenerative changes create preformed weak points where diverticula preferentially develop. 3, 4
- Enteric myopathy with muscular thickening, deranged architecture, and altered myofilament composition contributes to abnormal wall mechanics. 2
Functional and Motility Disorders
- Abnormal colonic motility patterns generate increased intraluminal pressure, which is the fundamental mechanical force driving mucosal herniation. 1, 2
- Intestinal innervation disorders and enteric neuropathy (including hypoganglionosis and neurotransmitter imbalance) induce these abnormal contractile patterns. 3, 2
- In vivo studies demonstrate increased motility index and high-amplitude propagated contractions in patients with diverticular disease. 2
Contributing Risk Factors
Lifestyle Factors
- Obesity, particularly central obesity, increases risk through mechanisms that may include elevated intra-abdominal pressure. 5, 1
- Smoking is an independent risk factor for diverticula formation. 5, 1
- Physical inactivity contributes to disease development. 5
Medications
- NSAIDs, corticosteroids, and opiates increase risk, potentially through effects on colonic motility, tissue integrity, and inflammatory responses. 5, 1
- Non-aspirin NSAIDs carry greater risk than aspirin. 5
Genetic Predisposition
- Approximately 40-50% of diverticular disease risk is attributable to genetic factors, as demonstrated by twin and sibling studies showing three-fold increased risk in siblings of affected individuals. 5, 1
- Genome-wide association studies have identified over 30 susceptibility loci affecting genes important for connective tissue integrity, smooth muscle function, cell adhesion, and immunity. 5, 1
- Specific genes with stronger effects include PHGR1, FAM155A, CALCB, and S100A10. 5
Age-Related Factors
- Aging is a key factor, with prevalence increasing from 32.6% in patients aged 50-59 years to 71.4% in those aged 80 years. 5
- Age-related degenerative changes in collagen and elastin accelerate wall weakening. 4
Multifactorial Nature
The pathogenesis cannot be attributed to a single factor but represents a complex interaction between dietary habits, structural wall changes, functional motility disorders, genetic predisposition, and aging. 3, 6, 7 All these elements contribute to varying degrees in individual patients, with the final common pathway being elevated intraluminal pressure forcing mucosa through weakened points in the colonic wall. 1, 2