Diverticular Disease: Progression, Smoking and Nicotine


Diverticular disease (DD) can progress from changes in the gut nerves and muscles to formation of diverticula (diverticulosis), to symptoms of colon dysfunction, to infections and inflammation (diverticulitis), to chronic symptoms, and to serious abdominal complications. The number of sufferers along this pathway diminishes greatly at every stage, only a minority ever need surgical treatment. On the other hand, progression and ageing go hand in hand.

The causes and risk factors of progression after diverticulosis are as varied as the people with DD.  Nobody knows what brings on diverticulitis which can be a gateway to problems. Historically, a diet low in fibre was thought to be responsible for all of the disease spectrum and could be easily remedied. This is no longer accepted. In the second half of the 20th century nobody considered an effect of smoking on the gut. Most Western adults smoked despite the risks of lung cancer and heart disease. Cigarettes had calmed the soldiers of the war, they were glamorous and macho, and nicotine was strongly addictive.

Cigarette use was aligned much closer to the appearance of DD in the world than diets which were variable and often assumed. Articles on this website in 2012 and 2013 have details of this epidemiology and also explain the pharmacology of nicotine where chronic use can cause the damage to the colon characteristic of DD.

Diverticula on the colon have to be identified before a diagnosis of the disease can be made. This happens in a hospital setting when symptoms or severe illness leads to investigative scans, x-rays or colonoscopies. Diverticula have already been formed then. The development of diverticula was described by interested pathologists early in the 20th century. Recent genetic and epidemiology research confirms that nerve and collagen changes are involved (1,2). These are the chronic effects of nicotine.

Hospital researchers have used diagnosed patients and their memories to produce “risk factors” and “associations” for DD based mainly on diets. Now, screening for colon cancer by colonoscopy around 50 years of age uncovers symptom-free diverticula. Participants can provide data on their lifestyles. Including smoking is a new opportunity to see if this was relevant to the presence or absence of diverticula. Also, increasing numbers of surveys are providing clinical evidence that cigarette smoking has a major effect on DD and its potential progression.


Data about smoking in 18-20 year old military conscripts in 1969-1970 was compared with Swedish national registers in 2009. Smoking increased the diagnosis of DD (3). The use of tobacco was greater in the 41.7% of colonoscopy outpatients found to have diverticula. The traditional risk factors for the presence of diverticula (low dietary fibre, constipation, red meat intake, low physical activity) were not confirmed (4).These authors thought that diverticula were most certainly present for many years before they were observed. Other American researchers (5) also considered that diverticulosis was longstanding before it was revealed. Two Japanese studies (6,7) related smoking to finding diverticula in outpatients. A history of smoking was revealed in Ulcerative Colitis patients who had diverticulosis (8). Recently in China (9) smoking was associated with diverticula in men (odds ratio = 2.14) and even more so in women (odds ratio = 10.2). Pooling together the data from several surveys (meta-analysis)  increases the validity of results. Two such studies (10,11) implicated smoking with diverticulosis and also increased risk of complications of the disease.


Past and current smokers had increased risk of symptomatic disease in Swedish women (12). In Swedish men, heavy smokers had increased risk of developing symptoms and there was some evidence of a dose/response relationship compared with non-smokers (13). The risk of changing from diverticulosis to diverticulitis was significantly higher in cigarette smokers in a report from Italy (14). Red meat was associated with increased risk of diverticulitis (15) but red meat eaters smoked more, used NSAID drugs and paracetamol, and had less vigorous exercise.


Present and previous smoking increased the risk for women of hospital admission for acute diverticulitis (16) and recurrent episodes (17). Compared with patients with no or minor symptoms, smoking was associated with hospital admissions because of complicated diverticulitis and severe infections (18,19).  Health conscious participants were used in a study by Crowe et al (20) to compare hospital and death records of DD between vegetarians and non-vegetarians. Smoking levels were only between 10% and 15%. Vegetarians and high dietary fibre intake gave a lower risk of hospital admission than meat eaters, but the vegetarians were younger. Compared with non-smokers, the increased risks for former smokers, light and heavy smokers were 31%, 34% and 86% respectively.


A Canadian survey of patients who underwent a partial colectomy found that current and former smokers had increased risk of surgery compared with non-smokers (21). Smoking was a risk factor for leakage of the join in the colon after part of it had been removed (22).

Removal of the sigmoid colon affected by DD was needed at a younger age in smokers compared with non-smokers, and the complications had developed more rapidly in smokers (23).


Some studies have not found any link between smoking and DD (24,25,26,27). These can be difficult to assess with gaps in details such as patient selection and their particulars, and ages. End points can be right sided disease or bleeding. Bleeding has so far not been related to smoking, but age, condition of blood vessels and drug side effects are relevant (28). The most quoted study is that of Aldoori et al (29) and their analysis of US male health professionals followed since 1986. In the 4 years between 1988 and 1992 there were 500 new cases of DD, 382 with symptoms and 118 without. Smoking was positively associated with the risk of symptoms, increasing with the number of cigarettes smoked per day and decreasing with the time since stopping smoking. These results were attenuated when dietary data was included in the analysis. The authors concluded that smoking was not associated with any substantial increased risk of symptomatic DD.  Another recent statistical assessment of the same group of health professionals found that smoking was independently associated with increased risk of diverticulitis (30).


This collection of reports is not exhaustive and more studies are likely. Some reviewers do not include data but an author’s opinion is cited. A mixture of positive and negative results is also found for other risk factors for DD. Bohm (31) emphasises the importance of differentiating risk factors between those for diverticulosis and for the other effects of the disease. This separation has been attempted here. The end point of a study is also relevant. For example, eating nuts, grains, corn and popcorn had no effect on hospital admissions for complications. Dietary avoidance of these foods was dismissed as irrelevant (32), but the long-standing avoidance of these foods for DD was based on pain. Many patients suffer from chronic and severe pain outside the hospital setting which is rarely researched. In fact, information about less serious symptoms and their treatment dealt with at primary care level is largely absent (33).

Age, sex and genetics are risk factors which cannot be changed, but many lifestyle choices, co-existing diseases and drug treatments also affect DD. Increasing opinion is that diverticula take years to form and are evident through symptoms a long time, even decades, after their cause by smoking. The cause of DD is distinct from many other factors which cause symptoms and complications. However, smoking is detrimental to all aspects of the disease and this should be reflected strongly in patient information.

Computer statistical assessments are used to uncover factors relevant to diseases, symptoms and progression, but the data used is subject to human choices and interpretation of results. The effect of smoking on DD was only included as a confounding factoring in studies relatively recently. Are older dietary studies still relevant if this was not included? The article by Labos (34) and its on-line comments are recommended reading on the subject. He considers a result found in several patient populations carries weight when the trials cannot be accurately replicated. In the case of smoking and DD, there is world-wide epidemiology, the pharmacology of chronic nicotine use and now, increasing clinical evidence of its profound effects.

The effect of smoking on DD and other diseases will be more difficult to asses in the future when people replace tobacco cigarettes (smoking) with e-cigarettes (vaping) for their nicotine fix. Many countries have banned e-cigarettes but some official organisations and powerful charities seem to be advising their use. Avoiding the carcinogenic chemicals from tobacco smoke is welcomed to reduce the risks of cancer, but people are then classed as ‘non smokers’ in surveys. The number of smokers will reduce, but the effects of continued use of nicotine should not be dismissed lightly. E-cigarettes are not regulated and long-term effects have still to be revealed. E-cigarettes are not medical devices, they will not overcome addiction to nicotine without commitment, determination and any help available. Retail outlets are increasing to make vaping commonplace and accessible. Its use by under 18s is increasing. Tobacco companies view e-cigarettes as their next generation products and aim to increase promotion and sales, just like they did in the mid 20th century for cigarette smoking.

Déjà vu.

© Mary Griffiths 2019


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