I said I was going to take a break from writing about bowels and microbiota (I was, I really was), but then my awesome chief resident (the head of my surgery team) distracted me with bowels again. After I revealed my interest in evolutionary medicine (followed by a brief rant on the appendix, gut microbiota, and the general tenets of evolutionary medicine) he said “Cool- let’s see what kinds of patients I can find for you”. He then assigned me a few patients with some thoughts of things I should look up and get back to the team on. I was thrilled. The patients were interesting and the things he suggested I look up were spot-on… He totally ‘gets it’.
Diverticula are out-pouches of the colon, and can either be “true” diverticula, consisting of all layers of the bowel wall, or “false” (AKA pseudodiverticula), where the thin layers of the bowel balloon out through gaps in the muscular layer. Diverticula can occur on the right side of the colon (the part closest to the small intestine) but are much more common (at least in the Western world) on the left side, particularly in the sigmoid colon (the last bit of the colon before the rectum). These are almost always “pseudodiverticula” though are generally referred to as “diverticula” and are the type I will discuss in this post.
Diverticula were once considered so rare that surgical textbooks from the early 1900s didn’t even mention them. It is now thought to be one of the most common colonic conditions in the developed world, though the prevalence is difficult to determine as most cases are asymptomatic. Current estimates, however, are that more than 40% of people in industrialized nations develop diverticula by the age of 60, and more than 60% develop them by the age of 80. As I mentioned, diverticula are frequently asymptomatic, but we become aware of them when they become inflamed, infected, or abscessed, leading to a condition known as diverticulitis (interestingly, diverticula on the right are more prone to bleed, while the ones on the left are more likely to become infected).
The pathogenesis of diverticula is generally believed to be dependent on the intraluminal pressure of the colon, specifically increased pressure during defecation. While straining to ‘perform’, the pressure in the colon greatly increases, especially in the areas closest to the rectum. Exaggerated contractions with spasmodic bowel movements cause increases in bowel pressure that may lead to diverticula. Conventional wisdom would have you believe that increased peristaltic activity is caused by our industrialized low-fiber diet, which leads to low-bulk stool, which cause our colon to work extra hard to expel their payload. You might suspect, however, that I am a little skeptical of conventional wisdom (refreshingly, so is my chief resident!).
The thought process that led to a ‘fiber-deficiency’ model of diverticular disease is actually rather encouraging for those of us who appreciate an ancestral approach to health. The argument was initially made by Burkitt and Painter  who in 1975 compared the stool transit time and volume of native Ugandans (a population virtually devoid of diverticula) with that of native Britons (importantly, while native Africans do not develop diverticula, those of African descent living in the developed world do). Burkitt and Painter realized that Ugandans had much larger (450g/day vs. 110g/day) stools and a much shorter transit time (34 hours vs. 80 hours) than UK natives. It was reasoned that these differences were caused by decreased fiber consumption in the developed world.
Alas, while this argument has gained substantial credence through years of reinforcement, the case for diverticula being a disease of a fiber deficiency fails to hold up. In fact, a paper recently published in the Journal of Gastroenterology is just the most recent take down of the fiber-based model of disease . This paper adds to the library of references that have failed to show a link between low-fiber diets and diverticula. In fact, this paper actually suggests that the inverse is true, with those that consumed the most fiber having the highest incidence of diverticula. This paper also took a look at other factors often implicated in diverticular disease, specifically infrequent bowel movements, high-fat diets, diets with a lot of red meat, and physical inactivity. None of these factors were associated with diverticulosis (indeed, people with few bowel movements had fewer diverticula than those with many!).
So if a lack of fiber doesn’t cause diverticula, what does? In their 1975 paper, Burkitt and Painter focused on the fiber content of the native diet of Ugandans. Their focus on diet, I fear, has led astray those who seek to prevent diverticular disease. While it is true that native Ugandans ate an evolutionary-appropriate diet, they ALSO utilized evolutionary appropriate behavior… For lack of a more tactful explanation- they squat to defecate and only go when they feel the need! Shocking, I know.
The hypothesis that diverticula could be prevented by squatting and urge-driven bowel habits was put forth in a 1988 paper (in one of my favorite journals, Medical Hypotheses), which pointed out that underdeveloped nations (which have an exceptionally low prevalence of left sided diverticular disease) utilize latrine pits. They went on to point out that bowel emptying in a sitting position, as caused by a western toilet, requires multiple straining efforts, while bowel empting upon urge in a squatting position usually only requires one . This suggestion has been followed up with a couple of recent studies that show that straining to defecate is greatest in the standing or lying position and minimized in the squatting position [4, 5]. Anatomically, this is explained by the change in the recto-anal angle, which becomes aligned in the squatting position and is obstructed as the flexion of the hips is decreased.
An interesting aside at this juncture is a quick look at the prevalence of diverticular disease in Japan. As an Asian country, Japan used to have a higher prevalence of right-sided diverticular disease, with left-sided being fairly uncommon. This trend, however, started to change with the westernization of Japan. Following Burkitt and Painter, the increase in left sided diverticular disease has been attributed to a decrease in fiber in the westernized Japanese diet , but is the blame duly placed? My brother has lived in Japan for many years and I’ve visited a number of times, and I’ve often been impressed by the spectrum of toilets available in Japan. They range from the ‘traditional’ Japanese squatting toilet (a ceramic latrine set in the ground) through to the modern toilet which is an amazing feat of engineering (perhaps you’ve seen one on TV somewhere- they come complete with jets that direct warm water and warm air at various body parts, play music to hide unwanted sound effects, and may, in fact, be able to tell you the answer to the ultimate question of life, the universe, and everything). Is it fair to blame a lack of fiber on the increase in diverticular disease in Japan? Or might it actually be due to a conversion from the traditional squatting toilets to westernized seated ones?
“Seated-stooling” has also been implicated in other conditions of the bowel. There’s another Medical Hypotheses paper that names sitting as a mechanism underlying primary constipation , and another communication from the Israel Medical Journal describing a neat little trial conducted on patients with hemorrhoids . This small trial, consisting of only 20 patients, showed interesting results. Of the 20 patients, 17 had tried (with minimal success) conservative treatment for hemorrhoids, including the ‘all-curing’ high-fiber diet, as well as suppositories, salves, and laxative preparations. The remaining 3 patients had undergone ligation for severe hemorroids. Throughout the course of this study (conducted over 1 year) the patients were asked to defecate in a squatting position only and to defecate only in response to a strong urge (no straining to perform!). The result of these interventions was alleviation of symptoms in most patients. Alas, 2 of the 3 who had undergone ligation did not experience significant improvement, which may have been a result of fibrous tissue development at the site of ligation.
The conclusion of this last paper seems particularly fitting in consideration of the overlying evolutionary-based interests of this blog: “that a program may be needed to reacquaint man with his natural habits.”. (No, you don’t need a pit latrine- there are little stools available designed to fit around toilets that allow you to squat over the pot! (Here’s an example, with the option to ‘build your own’)
1. Painter, N.S. and D.P. Burkitt, Diverticular disease of the colon, a 20th century problem. Clin Gastroenterol, 1975. 4(1): p. 3-21.
2. Peery, A.F., P.R. Barrett, D. Park, A.J. Rogers, J.A. Galanko, C.F. Martin, and R.S. Sandler, A high-fiber diet does not protect against asymptomatic diverticulosis. Gastroenterology, 2012. 142(2): p. 266-72 e1.
3. Sikirov, B.A., Etiology and pathogenesis of diverticulosis coli: a new approach. Med Hypotheses, 1988. 26(1): p. 17-20.
4. Sikirov, D., Comparison of straining during defecation in three positions: results and implications for human health. Dig Dis Sci, 2003. 48(7): p. 1201-5.
5. Rao, S.S., R. Kavlock, and S. Rao, Influence of body position and stool characteristics on defecation in humans. Am J Gastroenterol, 2006. 101(12): p. 2790-6.
6. Nakaji, S., K. Sugawara, D. Saito, Y. Yoshioka, D. MacAuley, T. Bradley, G. Kernohan, and D. Baxter, Trends in dietary fiber intake in Japan over the last century. Eur J Nutr, 2002. 41(5): p. 222-7.
7. Sikirov, B.A., Primary constipation: an underlying mechanism. Med Hypotheses, 1989. 28(2): p. 71-3.
8. Sikirov, B.A., Management of hemorrhoids: a new approach. Isr J Med Sci, 1987. 23(4): p. 284-6.