Diverticulitis: History and Discovery

The story of diverticular disease is, in a real sense, the story of the modern Western diet. The small out-pouchings of the bowel wall called diverticula were first described by anatomists in the eighteenth and nineteenth centuries — Alexis Littré noted them around 1700, and the great Parisian pathologist Jean Cruveilhier gave the first detailed account of them around 1849 — yet the condition was regarded as a pathological curiosity, genuinely rare, for most of recorded medicine. The term diverticulitis, for inflammation of these pouches, only entered the literature near the turn of the twentieth century, usually credited to Graser in 1899. Then, over the course of the 1900s, diverticular disease went from a footnote to one of the most common structural disorders of the gut in the industrialized world. In 1971 the surgeons Neil Painter and Denis Burkitt advanced the influential idea that this rise was driven by the loss of dietary fibre — that diverticular disease was “a deficiency disease of Western civilization.” That hypothesis reshaped how a generation of doctors and patients thought about the bowel; later research has complicated and partly revised it, and it is presented here as the landmark hypothesis it was, not as settled fact.

Table of Contents

  1. Early Anatomical Description: Littré and Cruveilhier
  2. Naming the Inflammation: The Term “Diverticulitis”
  3. From Rarity to Epidemic: A Twentieth-Century Disease
  4. Painter and the Mechanism: Segmentation and Pressure
  5. The Fibre Hypothesis: Painter and Burkitt, 1971
  6. Revisiting the Fibre Hypothesis
  7. Surgery: Hartmann’s Procedure and Beyond
  8. Modern Understanding and Management
  9. Research Papers and References
  10. Connections

Early Anatomical Description: Littré and Cruveilhier

A colonic diverticulum is a small sac or pouch that balloons outward from the wall of the large intestine. Most are not true diverticula containing all layers of the bowel wall but pseudodiverticula (false diverticula): the inner lining, the mucosa, herniates outward through gaps in the muscular coat, typically at the weak points where blood vessels pierce the wall. These structures were first noticed not by physicians treating sick patients but by anatomists examining the dead. The French surgeon and anatomist Alexis Littré is generally credited with the earliest recorded observation of colonic diverticula, around the year 1700, though his attention was more on hernias than on the bowel itself.

The figure most often named as the first to describe colonic diverticula in clear pathological detail is Jean Cruveilhier (1791–1874), an eminent professor of pathological anatomy in Paris, whose great illustrated atlas of morbid anatomy appeared in installments across the 1830s and 1840s. Around 1849 Cruveilhier described the herniations of mucosa through the muscular layer of the sigmoid colon, picturing them as a row of small, dark, pear-shaped out-pouchings, and he recognized that these pouches could become a site of inflammation and even perforation. Earlier still, the German term Divertikel is attributed to Fleischman in 1815, and the broader concept of an intestinal diverticulum was already familiar to anatomists of the period.

For most of the nineteenth century, however, these pouches remained a curiosity of the dissecting room. They were noted, drawn, and catalogued, but they were not understood as a common cause of human illness, because in that era they genuinely were uncommon. The clinical significance of diverticula — the realization that they could inflame, bleed, obstruct, and kill — belongs to the decades that followed, as the disease itself became dramatically more frequent.

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Naming the Inflammation: The Term “Diverticulitis”

It is worth being precise about what was described when, because the history conflates three distinct things: the anatomical pouch (a diverticulum), the state of having many pouches (diverticulosis), and the inflammation of those pouches (diverticulitis). The anatomy came first, in the work of Littré and Cruveilhier. The recognition of the inflammatory complication, and the coining of a word for it, came near the close of the nineteenth century. The German surgeon Graser is usually credited with describing the inflammation of diverticula and introducing the term diverticulitis in 1899 — placing the birth of the modern clinical concept right at the threshold of the twentieth century.

Other figures filled in the surrounding picture. In 1869 Klebs was among the first to link the formation of diverticula to constipation, an association that would echo through the next century and a half of theorizing about cause. In 1904 Beer correlated the clinical and the microscopic (histologic) findings of the disorder, helping to establish diverticulitis as a genuine disease entity rather than an incidental anatomical finding. A landmark early synthesis came in 1917, when Telling and Gruner published an extensive review of acquired diverticula, diverticulitis, and the surrounding tissue inflammation (peridiverticulitis) of the large intestine in the British Journal of Surgery, drawing together scores of cases — some studied with the then-new tool of radiology — into a clear clinical portrait.

By the 1920s the disease had its own dedicated literature. The English physicians Spriggs and Marxer produced influential accounts of intestinal and colonic diverticula (in the mid-1920s, in the Quarterly Journal of Medicine and The Lancet), and were among the early voices to connect the apparently rising frequency of the condition with the changing diet of industrialized societies. In the space of roughly a generation, then, diverticulitis had gone from an unnamed rarity to a named, illustrated, X-ray-documented, and actively debated clinical problem.

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From Rarity to Epidemic: A Twentieth-Century Disease

The single most striking fact in the history of diverticular disease is how recent it is as a common condition. Reviews of the literature note that diverticular disease was scarcely mentioned in medical writing before the twentieth century, and that for the first decade or two of the 1900s it remained genuinely uncommon. Over the following decades its reported prevalence in Western, industrialized countries rose steeply, until by the later twentieth century diverticulosis had become one of the most common structural abnormalities of the colon in those populations — present in a large fraction of older adults, and the reason for hundreds of thousands of hospital admissions a year.

Equally striking was the geographic pattern. The disease was common in North America, Britain, and Western Europe but conspicuously rare in rural populations of sub-Saharan Africa and parts of Asia. Within migrant communities, the frequency of the disease tended to climb as people adopted a Western lifestyle and diet, and the colonic site most affected differed by region — predominantly the left-sided sigmoid colon in Western countries, but more often the right colon in parts of Asia, a distinction that persists and points to both dietary and genetic contributions. This combination of a sharp historical rise and a sharp geographic gradient is exactly the kind of pattern epidemiologists associate with environment and diet rather than with an unchanging quirk of human anatomy.

That framing — diverticular disease as something the modern world had done to itself — set the stage for the most famous hypothesis in the field. If the pouches were rare when diets were coarse and unrefined, and common once diets became soft and processed, then perhaps something that had been removed from the food supply was to blame. The leading candidate was dietary fibre, and the scientists who made that case were Neil Painter and Denis Burkitt.

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Painter and the Mechanism: Segmentation and Pressure

Before the fibre hypothesis could be persuasive, there had to be a plausible mechanism — a physical explanation for how a low-residue diet might actually push the bowel lining out through its own muscular wall. That mechanism was supplied largely by the British surgeon Neil Stamford Painter, working in the early and mid-1960s, often with colleagues at Oxford. Using pressure-measuring studies of the living human colon, Painter demonstrated that the colon does not move its contents along as a single open tube. Instead it pinches itself into short, closed-off compartments by contracting at intervals — a process called segmentation.

Painter's key insight was that when the colon segments, each isolated little chamber can generate surprisingly high internal pressures, because the contracting muscle is squeezing a sealed pocket of contents rather than propelling an open column. He proposed that these bursts of localized high pressure, repeated over years, drive the mucosa outward through the weak spots in the wall where blood vessels penetrate — producing the characteristic pulsion (push-out) pseudodiverticula. A 1965 study by Painter and colleagues, Segmentation and the Localization of Intraluminal Pressures in the Human Colon, laid out this picture in detail and became a foundational reference for the field.

This work mattered because it joined diet to anatomy. A bulky, fibre-rich stool, Painter reasoned, keeps the colon comfortably distended and reduces the need for the powerful segmenting contractions that spike the pressure; a small, firm, low-fibre stool forces the colon to work harder against a narrow lumen, raising pressure and, over decades, herniating the wall. The segmentation-and-pressure model gave the coming fibre hypothesis its physiological backbone. (It should be said that, like the fibre hypothesis it supported, parts of this mechanistic story have been questioned by later research; it is presented here as the historically pivotal model it was.)

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The Fibre Hypothesis: Painter and Burkitt, 1971

In 1971, Neil Painter joined forces with Denis Parsons Burkitt — the Irish surgeon already famous for describing Burkitt's lymphoma and for championing the broader idea that many “Western” diseases trace to refined, low-fibre food — to publish what became the landmark paper in the field: Diverticular disease of the colon: a deficiency disease of Western civilization, in the British Medical Journal. Its very title was an argument. Painter and Burkitt proposed that diverticular disease is not an inevitable consequence of aging but a deficiency disease — the predictable result of a diet stripped of its fibre by the milling of grain and the rise of refined, processed, low-residue food in industrialized societies.

Their case rested on the convergence of several lines of evidence: the disease had been rare before the twentieth century, its rise tracked the spread of refined flour and processed food, it was common in fibre-poor Western diets and rare where unrefined high-fibre diets prevailed, and Painter's pressure studies offered a mechanism by which low fibre could generate the wall-herniating pressures. The logic was elegant and the conclusion was practical and hopeful: if too little fibre caused the disease, then more fibre — whole grains, bran, fruit, and vegetables — ought to prevent it, and perhaps relieve it.

The influence of this single idea is hard to overstate. For decades afterward, “eat more fibre” became the standard medical advice for preventing and managing diverticular disease, and the older, fearful instruction to avoid nuts, seeds, popcorn, and corn (lest the fragments lodge in a diverticulum and ignite inflammation) coexisted alongside it in clinical lore. The Painter–Burkitt fibre hypothesis became one of the most widely taught explanations in all of gastroenterology — an example, like Burkitt's wider work, of epidemiology shaping everyday dietary advice across the world.

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Revisiting the Fibre Hypothesis

Influential hypotheses invite testing, and as better-designed studies accumulated, the simple version of the fibre story did not hold up cleanly. The most-cited challenge came in 2012, when Anne Peery and colleagues reported a large cross-sectional study of people undergoing screening colonoscopy and found, contrary to expectation, that a high-fibre diet did not protect against asymptomatic diverticulosis — if anything, higher fibre intake and more frequent bowel movements were associated with a greater, not lesser, prevalence of diverticula. Other careful studies likewise found that constipation and a low-fibre diet were not the straightforward causes of diverticulosis that the classic hypothesis assumed. A growing review literature, with titles such as Diverticular Disease: Reconsidering Conventional Wisdom, urged the field to revisit its long-held beliefs.

Two distinctions help make sense of this revision, and both matter for patients. First, the science increasingly separates diverticulosis (merely having the pouches, which is extremely common and usually silent) from diverticulitis (the painful inflammatory complication that only a minority of people with diverticula ever develop). Evidence that fibre does not prevent the pouches from forming is not the same as evidence that fibre is useless against flares. Second, the old advice to avoid nuts, seeds, and popcorn has been specifically overturned: a large prospective study found these foods were not associated with a higher risk of diverticulitis or bleeding, and that fear is no longer considered evidence-based.

So where does fibre stand today? The honest answer is “more nuanced than 1971, and still genuinely useful.” A high-fibre dietary pattern, especially fibre from fruits and vegetables, is associated in cohort studies with a lower risk of developing diverticulitis and its complications, and a fibre-rich diet remains a sensible, mainstream recommendation for people with diverticular disease once an acute attack has settled. What has changed is the certainty and the simplicity: diverticular disease is now understood as multifactorial — involving genetics (heritability is substantial), the colonic muscle and nerves, the gut microbiome, low-grade inflammation, body weight, physical activity, certain medications, and diet together — rather than as a pure fibre-deficiency disease. The Painter–Burkitt hypothesis was a landmark that organized decades of research and dietary advice; like many landmarks, it has been refined rather than simply confirmed.

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Surgery: Hartmann’s Procedure and Beyond

While physicians debated cause and diet, surgeons faced the disease's emergencies: a diverticulum that perforates can spill bowel contents into the abdomen, causing life-threatening peritonitis. The operation that came to dominate the surgical management of these crises was devised for a different problem entirely. In 1921, the French surgeon Henri Albert Hartmann (1860–1952) described, at the 30th Congress of the French Surgical Association, a technique for resecting cancer of the sigmoid colon and upper rectum: remove the diseased segment, bring the healthy upstream colon out to the skin as a temporary colostomy, and close off the rectal stump, deferring any reconnection of the bowel to a later, safer operation.

This Hartmann's procedure proved ideally suited to the contaminated, inflamed conditions of perforated diverticulitis, where sewing the bowel back together immediately would be dangerous. For much of the twentieth century it was the workhorse emergency operation for complicated diverticular disease, saving many lives by separating the urgent task (removing the source of infection) from the elective one (restoring intestinal continuity). A century on, the procedure is still performed, though it is now used more selectively as anesthesia, antibiotics, imaging, and critical care have improved and as surgeons have gained alternatives.

Surgical practice has continued to evolve well beyond Hartmann. Improvements in CT imaging allowed accurate grading of severity (the Hinchey classification of perforated diverticulitis dates from 1978) and made it possible to drain an abscess through the skin rather than operate. Minimally invasive laparoscopic resection, primary anastomosis with or without a protective stoma in selected cases, and a marked shift toward managing uncomplicated diverticulitis without surgery — and increasingly without routine antibiotics for mild cases — all reflect a modern, less aggressive philosophy. The arc from Cruveilhier's autopsy drawings to today's image-guided, often non-operative care spans less than two centuries.

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Modern Understanding and Management

Today diverticular disease is understood as a spectrum rather than a single illness. At one end is diverticulosis: the mere presence of pouches, found incidentally in a very large share of older adults in Western countries and, in most people, causing no symptoms at all for a lifetime. A subset develop symptomatic uncomplicated diverticular disease (recurrent abdominal discomfort without overt inflammation), and a minority go on to acute diverticulitis — the inflammatory complication, ranging from a mild, antibiotic-free outpatient illness to perforation, abscess, fistula, obstruction, or bleeding requiring hospital care or surgery.

Management has shifted decisively toward the conservative. Many cases of mild, uncomplicated acute diverticulitis are now treated with observation and supportive care, with selective rather than automatic use of antibiotics, a reversal of decades of reflexive antibiotic prescribing supported by modern randomized trials. Diet advice has likewise been rewritten: a clear or low-fibre diet during an acute flare, a return to a high-fibre diet for long-term maintenance, and explicit reassurance that nuts, seeds, and popcorn are safe — one of the clearest examples of evidence overturning long-standing medical folklore. Research now actively explores the roles of the gut microbiome, chronic low-grade inflammation, visceral hypersensitivity, and genetics, framing diverticular disease as a complex disorder with overlaps to conditions like irritable bowel syndrome.

Seen whole, the history is a compact lesson in how medical knowledge actually moves. An anatomical curiosity drawn at autopsy (Littré, Cruveilhier) acquired a clinical identity and a name (Klebs, Graser, Beer, Telling and Gruner), then exploded into a common disease of the industrialized world, prompting a sweeping and influential hypothesis (Painter and Burkitt's fibre-deficiency idea) that organized research and dietary advice for a generation — only to be tested, complicated, and partly revised by later evidence. The condition is the same; our explanation for it has grown more careful, more multifactorial, and more honest about uncertainty. For practical guidance on symptoms, diagnosis, diet, and treatment, see the companion Diverticulitis overview.

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Research Papers and References

The references below pair the landmark historical papers in diverticular disease — several available in full through the U.S. National Library of Medicine — with curated PubMed topic-search links into the historical, mechanistic, and dietary literature. Early historical works (Littré, Cruveilhier, Fleischman, Klebs, Graser, Beer, and the Telling–Gruner and Spriggs–Marxer monographs) are named in the article as historical sources; the modern reviews and primary studies below are linked by DOI, PMID, or PubMed search. Each external link opens in a new tab.

  1. Painter NS, Burkitt DP. Diverticular disease of the colon: a deficiency disease of Western civilization. British Medical Journal. 1971 May 22;2(5759):450–454. — doi:10.1136/bmj.2.5759.450 (PMID 4930390)
  2. Painter NS, Truelove SC, Ardran GM, Tuckey M. Segmentation and the localization of intraluminal pressures in the human colon, with special reference to the pathogenesis of colonic diverticula. Gastroenterology. 1965;49(2):169–177. — PubMed: PMID 5653799
  3. Matrana MR, Margolin DA. Epidemiology and pathophysiology of diverticular disease. Clinics in Colon and Rectal Surgery. 2009;22(3):141–146. — doi:10.1055/s-0029-1236157
  4. Peery AF, Barrett PR, Park D, et al. A high-fiber diet does not protect against asymptomatic diverticulosis. Gastroenterology. 2012;142(2):266–272. — PubMed: PMID 22062360
  5. Peery AF, Sandler RS, Ahnen DJ, et al. Constipation and a low-fiber diet are not associated with diverticulosis. Clinical Gastroenterology and Hepatology. 2013;11(12):1622–1627. — PMC: Constipation, low-fiber diet and diverticulosis
  6. Strate LL, Liu YL, Syngal S, Aldoori WH, Giovannucci EL. Nut, corn, and popcorn consumption and the incidence of diverticular disease. JAMA. 2008;300(8):907–914. — PubMed: nuts, corn, popcorn and diverticular disease
  7. Telling WHM, Gruner OC. Acquired diverticula, diverticulitis, and peridiverticulitis of the large intestine. British Journal of Surgery. 1917;4(15):468–530. — PubMed: Telling and Gruner diverticulitis
  8. Diverticular disease: reconsidering conventional wisdom (review of the fibre hypothesis and its revision). Clinical Gastroenterology and Hepatology. — PMC: Diverticular Disease, Reconsidering Conventional Wisdom
  9. History and historical perspective of diverticular disease of the colon — PubMed: history of diverticular disease (Cruveilhier, Graser)
  10. Henri Hartmann and the history of Hartmann's procedure — PubMed: Hartmann's procedure history
  11. Denis Burkitt and the origins of the dietary fibre hypothesis — PubMed: Burkitt and the dietary fibre hypothesis
  12. Dietary fibre intake and risk of diverticular disease (prospective cohort evidence) — PubMed: PMID 24385599
  13. Epidemiology, geography, and the twentieth-century rise of diverticular disease — PubMed: epidemiology of diverticular disease
  14. Modern management of acute diverticulitis: antibiotics, surgery, and diet — PubMed: modern management of acute diverticulitis

External Authoritative Resources

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Connections

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