Gut Microbiome – The Basics

March 26th, 2024

A technique using DNA analysis now enables the identification of more types of bacteria that reside in and on the human body. Interest in the organisms found in the gut, known as the microbiome, has exploded in two directions in recent years. Do they have a part in disease and is there a commercial opportunity? The microbiome appears extensively in research papers and in all types of media and ‘health products’. Suddenly, the microbiome might be responsible for many diseases and needs to be controlled. Why do we have the microbiome, where is it, what is it for and what does it do? Is not easy to find among the barrage of ideas and theories.

The caecum is the first part of the large intestine (colon). Its wall is reinforced by immune tissue from the appendix to along the ascending colon to isolate the microorganisms contained within which are known as the gut microbiome. These organisms are acquired from dietary substances and some will survive in the residues of digestion. This is their only source since birth. The liquid ‘chyme’ from digestion enters the caecum from the small intestine (ileum) via a one-way valve (ileocaecal valve). Any reflux here produces small intestine bacterial overload (SIBO). Symptoms of this are not well defined but pain and bloating and IBS are mentioned.

The other import into the caecum microbiome is from the appendix. This is not an evolutionary relic but a safe refuge for the production of live microorganisms to supply and maintain the microbiome if it is depleted. When the output is blocked appendicitis ensues. Being without an appendix appears to increase the risk of infection in diverticular disease.

The liver also uses the food digestion pathway to get rid of detoxification chemicals and those which cannot be passed via the kidneys and urine such as heavy metals and pigments from red blood corpuscles. Bile products from the liver are recycled by the microbiome and returned to the liver for reuse.

When this digestion and body waste enters the caecum it joins the residues of several previous meals and itself will be diluted by several following meals. Colon wall muscles produce mixing movements before slowly advancing the content to the drying phase in the colon and the recycling of water. Because of the slowing of flow in the microbiome, ‘transit time’ from mouth to anus is not related to a complete meal. Similarly, it can take time for the colon to get rid of a toxic organism or irritant.

The array of organisms in the microbiome vary within and between people and are dynamic. They will only be there if they have the right nutrients and conditions to survive. There is an intimate relationship between diet and foodstuffs, and the type of organisms needed to deal with their digestion residues. This system is successful at the extremes of carnivorous or vegetarian diets.

What constitutes an ‘unbalance’ or ‘dysbiosis’ of good and bad bacteria in the microbiome is a human concept, as is the opinion that the microbiome always needs more in number and variety of microorganisms to be effective and healthy. Consider an individual with a restricted diet due to illness found to have a limited range of organisms in their microbiome. This is not dysbiosis but is the microbiome responding to diet. Taking prebiotics, probiotics or fermented food is just changing the diet and too much might not be helpful. Researchers looking for a link between the microbiome and diseases need to consider the effect of the disease on diet. Also, the gut-brain axis is a two-way communication system and neurotransmitter faults in diseases and drugs can also affect colon movement.

There are examples in nature where a lesser species is employed in a symbiotic relationship to solve a problem the host cannot deal with themselves. Powerful enzymes from the pancreas are produced to digest proteins in food but need to be destroyed before they attack the host’s tissues. They cannot be reabsorbed. When a stoma is formed by bringing the end of the small intestine to the outside of the body, the microbiome is not used and the surrounding skin can be attacked by enzymes. A stoma further along the colon, past the microbiome, does not have this problem. Cystic fibrosis patients have to take enzymes to digest their food. Sometimes the microbiome cannot cope with the quantity of enzymes and the ascending colon can be damaged. Only one pancreatic enzyme, elastase, is found in faeces. This is not harmful and is in fact used to show that the pancreas is working.

The microbiome is an integral part of body processes and has self-regulating properties which can be disrupted by pathogenic organisms and antibiotics. The colon itself is controlled by its nerve and blood supply which can change its movements. Not all health problems are caused by the microbiome which is part of an efficient recycling and disposal system which has served mankind for millennia.

© Mary Griffiths 2024

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Diverticular Disease and Nicotine Metabolism

June 13th, 2023

Colon diverticular disease (DD), previously a curiosity, increased in significance in Western countries in the 20th century. The earliest indications of colon abnormality were changes in the sigmoid colon which was shortened, thickened and corrugated. The longitudinal muscles appeared in a contracted  form like after defaecation, unable to relax.

Internal pressure increased, eventually producing blow-out hernia through hardened circular muscle giving grape-like appendages on the outside of the colon – the diverticula. At this stage a diagnosis of diverticulosis could be made when the diverticula were seen by scans, colonoscopy or during surgery. A clinical appraisal alone would not separate easily any symptoms from those of any other bowel disease. An attack of diverticulitis or severe pain however, often lead to diverticula recognition in the hospital setting and it is here where statistics on DD and its ramifications are generated, more often on elderly patients.

Early researchers recognized that the affected colon muscles responded differently to drugs such as acetylcholine, morphine, carbachol and neostigmine, also to physiological stimulation. Parks (1) considered a pharmacological stimulus that would cause such a change, would be uncommon in real life. The ‘nicotinic’ receptors in the autonomic nervous system were a missed clue. Birkitt (2) also recognized an environmental factor was responsible for the diseases in affluent countries compared with Africa. Unfortunately, he attributed non-infective disease of the bowel to diet. DD was supposedly caused by low levels of fibre. Also in the 1970s Painter (3) professed “The factors which cause this acquired disease (DD) are operating more and more effectively and that diverticulitis in young patients will become a greater problem in the future.” In 2023 this has happened (4,5). Hospital admissions continued to endemic proportions and diagnosis in younger people is rising. Diet has never explained the neuromuscular changes in the colon at the beginning of DD which has now been accepted (6,7).

Birkitt’s “geographic medicine” data was in fact the epidemiology in the 1970s which pointed to DD as one of the 20th century ‘Western’ diseases, in time and place these correspond to the use of ‘Western’ cigarettes. Mortality statistics (8) show DD goes hand in hand through the 20th century with lung and other cancers, cardiovascular disease and appendicitis for example. Does Crohn’s disease follow the same pattern? In cigarettes there are the carcinogens and nicotine. Nicotine is the pharmacological stimulus. Globally, DD appearance correlates with the marketing of ‘Western’ cigarettes from the beginning of the 20th century. Firstly, in the USA, UK and Australia, in Europe after WW11 and in eastern countries after the US 1974 Trade Act with a rapid rise of DD in Japan. There is very little in African countries so far. The Japanese smokers merely changed their brands, not diet, as did Japanese immigrants in Hawaii. 

Nicotine is a drug and banned toxic pesticide. Addictive property means nicotine and active metabolites are in the body continuously, often for many years. Chronic effects are predictable. The action of nicotine on post-synaptic neurons is classic pharmacology. It stimulates then blocks normal acetylcholine transmission, leaving muscles contracted for longer. Its effects on the nitric oxide relaxation system may be complicated by nitrate levels in ‘Western’ cigarettes. Nicotine promotes fibrosis and changes to a firmer structure of collagen and elastin in the colon walls, like in the skin with smoker’s wrinkles and rigidity of walls in cardiovascular disease. In the colon walls, these are the neuromuscular precursors of diverticula and DD progression.

Nicotine is metabolized in the liver by enzyme CYP2A6 and its many variants which have ethnic differences in smoking diseases. Faster nicotine metabolism in females increases addiction and smoking habits and gender differences in smoking related diseases. Clinical results suggest that with DD, females have earlier and more extensive colon neuromuscular damage than males. Compared with males, females have more affected colon segments which increase with age (9). They are more at risk of persistent symptoms after sigmoidectomy (10) and diverticula are more scattered along the colon (11). More diverticula results in females having more episodes of diverticulitis and chronic complications and at a younger age (12). They had more chronic diverticulitis and strictures but less bleeding than men (13). Chronic complications such as sepsis, obstruction or pelvic fistula were more likely causes of death in women whose DD mortality rates have exceed men in the UK since WW11 (14,15). Gender differences must question the use and value of male only research cohorts. For example, male health professionals with only 10% smokers have been studied extensively since 1986 and resulted in a significant dietary treatment advice for all with DD irrespective of different disease progression and the basis of no gender differences in DD and diverticulosis rare before the age of 40 (16).

Research data from western countries shows DD usually in the sigmoid area of the colon. Muscles affected by nicotine in colon parts with mixing (ascending) or drying (transverse) movements would have different appearance and symptoms. Right sided disease is found in Eastern countries such as Japan. CYP2A6 polymorphism may be responsible for this difference. CYP2A6*4 variant produces different nicotine metabolic products, far less cotinine and less lung cancer. NakaJima (17) compared the frequency of CYP2A6*4 and other variants with reduced activity, with ethnicity. The table shows some possible association of CYP2A6*4 with the frequency of right-sided DD.

CYP2A6*4 and other liver enzymes have been demonstrated to affect the metabolism of nicotine with ethnic variations in smoking, also in drug and disease research. The long-term damage by nicotine in the autonomic nervous system has had less attention than cancer. How many smokers and non-smokers have DD depends on symptoms bad enough to be investigated. A familial pattern has been recognized which may be genetic or passive smoking. There are many unanswered questions. Nicotine as the cause of colon neuromuscular damage of DD is suggested by epidemiology, pharmacology and the link between genetics and environment. Many research reports show there is no doubt that smoking negatively affects all clinical aspects of DD.

The neuromuscular colon damage in DD is permanent. Lifestyle changes can alleviate some symptoms but there are no drug treatments except antibiotics and surgery. Anticholinergic side effects of drug treatments for other complaints might influence symptoms. Only prevention can make an impact on DD. The current situation with cheap, available, promoted nicotine products to reduce cigarette smoking seems to be producing a new generation of nicotine addicts without knowing long term effects. This is very reminiscent of 70 years ago with cigarettes and a frightening outlook for DD.

% of CYP2A6*4 in ethnic group Ref (17) % with DD in right colon   Reference
JAPANESE   50.5 67 (18)
KOREAN     42.9 85.2 (19)
BLACKS      21.9 18.3 (20)
WHITES        9.1 2.7 (20)

COMPARISON OF THE AMOUNT OF LIVER ENZYME CYP2A6*4 AND DIVERTICULAR DISEASE IN THE RIGHT COLON

© Mary Griffiths 2023

References

  1. Parks T G. The pathogenesis of large bowel diverticula. Ulster Med J. 1971, 41, 45. PMID 5150065.
  2. Birkitt D P. Epidemiology of large bowel diseases: the role of fibre. Proc. Nutr. Soc. 1973, 32, 145.  DOI:  10.1079/pns19730032
  3. Painter N.S. Diverticular disease of the colon- a deficiency disease of Western civilisation. 1975. William Heinemann Medical Books Ltd. London. ISBN 0 433 24660x
  4.  Fialo A. et al. Analysis of the epidemiological trends on inpatient diverticulosis admissions in the USA: a longitudinal analysis from 1997-2018. Cureus. 2023, 15, e34493. DOI:10.7759/cureus.34493
  5. Broad J B. et al. Diverticular disease epidemiology: acute hospitalisations are growing fastest in young men.  Tech Coloproctol. 2019, 23, 713. DOI:10.1007/s10151-019-02040-8
  6. Kupcinskas J. et al. Pathogenesis of diverticulosis and diverticular disease. J Gastrointestin Liver Dis. 2019, 28, suppl.4. DOI:10.15403/jgld-551
  7. Schafmayer C. et al. Genome-wide association analysis of diverticular disease points towards neuromuscular, connective tissue and epithelial pathomechanisms. Gut. 2019, 68 854. DOI:10.1136/gutjnl-2018-317619
  8. National Statistics. Twentieth century mortality. 100 years of mortality data in England and Wales by age, sex, year and underlying cause. Crown Copyright 2003. CD ROM ISBN 0 11 621665 4.
  9. Eide T J. et al. Diverticular disease of the large intestine in Northern Norway. Gut. 1979,20, 609. DOI:10.1136/gut.20.7.609
  10. Choi K K. et al. After elective sigmoid colectomy for divertiulitis, does recurrence-free mean symptom-free? Am Surg. 2020, 86, 49. PMID 32077416
  11. Parks T J. Post mortem studies on the colon with special reference to diverticular disease. Proc R Soc Med. 1968, 61, 932. PMID 5679019
  12. Lightner A L. et al. Use of the Rochester epidemiology project for clinical research in colon and rectal surgery. Clin Colon Rectal Surg. 2019, 32, 8. DOI:1055/s-0038-1673349
  13. McConell EJ et al. Population-based incidence of complicated diverticular disease of the sigmoid colon based on gender and age. Dis Colon Rectum. 2003, 46, 1110. DOI:10.1007/s10350-004-7288-4
  14. Sell N M. et al. Are there variations in mortality from diverticular disease by sex. Dis Colon Rectum. 2020, 63, 1285. DOI:10.1097/DCR0000000000001711
  15. Kang J Y. et al. Diverticular disease of the colon – on the rise: a study of hospital admissions in England between 1989/1990 and 1999/2000. Aliment Pharmacol Ther. 2003, 17, 1189. DOI:10.1046/j.1365-2036.2003.01551.x
  16. Strate L L. et al. Nut, corn and popcorn consumption and the incidence of diverticular disease. JAMA 2008, 300, 907. DOI:10.1001/jama.300.8.907
  17. Nakajima N. et al. Comprehensive evaluation of variability in nicotine metabolism and CYP2A6 polymorphic alleles in four ethnic populations. Clin Pharmacol Ther. 2006, 80, 282. DOI:10.1016/j.clpt.2006.05.012
  18. Takano M. et al. An analysis of the development of colonic diverticulosis in the Japanese. Dis Colon Rectum. 2005, 48, 2111. DOI:10.1007/s10350-005-0111-z
  19. Lee K M. et al. Clinical significance of colonic diverticulosis associated with bowel symptoms and colon polyps. J Korean Med Sci. 2010, 25,1323. DOI:10.3346/jkms.2010.25.9.1323
  20. Golder M. et al. Demographic determinants of risk, colon distribution and density scores of diverticular disease. World J Gastroenterol. 2011, 17 1009. DOI:10.3748/wjg.v17.i8.1009

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Diverticular Disease: Men and Women

February 9th, 2022

 

Diverticular disease (DD) is an acquired disease that was first demonstrated early in the 20th century. Its appearance and increasing importance occurred in cigarette-smoking western countries, particularly the USA and UK, where the habit and nicotine addiction was widespread in the population. These countries are the main source of reports and statistics. DD can no longer be considered the inevitable diet related disease of the elderly. DD can be a long term (26872402), progressive (13444546) and chronic disorder (22777341) as well as the acute infection of diverticulitis and its complications. Differences between males and females have always been apparent in hospital and mortality statistics where females predominate.

Diverticula – the small grape-like hernia – need to be seen on the colon before the disease can be diagnosed. Once they are present they are there for life. The data used to describe DD is in effect a measure of investigations, where and when they took place in the disease progression. For example, the same person could figure in post-mortem, mortality and hospital admission data but the diverticula could have been there for 40 -50 years. Similarly, ‘risk factors’ are for symptoms resulting in investigations revealing DD but are not the cause of DD. The current interpretation of data show DD in more men than women up to the age of 50 – 60 years, then proportions are reversed with more women in surveys measuring investigation of DD. No explanation has been offered for this effect (33727769) except hormone differences which of course cannot be disputed.

Eastwood (873339) considered factors which might influence a decision to investigate symptoms for a diagnosis of DD. Does a complicated selection process operate for a family doctor’s referral to a hospital consultant for an investigation? The presentation of symptoms or the seeking of medical advice, or social or geographical factors may affect data. Other influences mentioned in reports are costs and hospital capacity.

Because of low risk of colon cancer, internal examination, now usually by colonoscopy, are not considered necessary below the age of 50 years unless there are potentially dangerous symptoms. However, both diverticulosis, where diverticula are found without symptoms, and their infection ie diverticulitis, are found before the age of 50 years (15882243, 20604970). CT scanning for suspected appendicitis revealed 14% of the under 20 yrs. And 40% of those between 20 and 39 yrs. had evidence of diverticulosis. (33727769). Anybody with diverticulosis could get diverticulitis infection and nobody knows why. Symptoms of pain and dysfunction in males is more conspicuous than in females where it is part of their biology Males get investigation and diagnosis and earlier surgical treatment for DD than females (9860333).

Women with abdominal pain and bowel dysfunction are diagnosed quickly with Irritable Bowel Syndrome (IBS) (9262978). IBS is based on symptoms, but women have many symptoms peculiar to them that are not included in the research criteria for IBS (9096434). There are many potential causes of abdominal pain unique to females (31943595) that without relief can prompt repeated consultations more than males – a characteristic of IBS. Females can be told they have IBS as young adults, until after the menopause and even in old age. IBS will include people with diverticulosis and diverticulitis (19861955) but if found this does not change the diagnosis of IBS, some researchers think that only infected diverticula can cause pain (16678561). Data on the number of people with DD up to the age of 50 to 60 yrs. will show more males than females because more males are investigated and diagnosed.

Around the age of 50 yrs. screening for colon cancer by colonoscopy occurs. Finding diverticulosis is common and does not show different rates for males and females although females are slightly older. In older patient groups without significant symptoms, there is again no difference between the sexes (22573184). Symptoms such as constipation related to colon ageing at 60 to 70 yrs. old also appear to be the same. Differences between males and females appear if and when symptoms of DD become problematic and potentially serious. Females outnumber males when investigations are needed for episodes of diverticulitis or chronic complications of DD. This can be the first diagnosis of DD and younger age and female gender are independent risk factors (30647541). Frequently the female patients were found to have previously been diagnosed with IBS. Females and a preoperative diagnosis of IBS were also independent risk factors for persistent symptoms after sigmoidectomy (32077416).

For decades since the 1960s DD was considered a diet related disease of the elderly. Eating a low level of dietary fibre for at least 40 years produced diverticula. Adding wheat bran to meals was recommended to prevent the constipation then later any type of dietary fibre. This was supposed to prevent diverticula and diverticulitis development – now disproved. DD research concentrated in detail on diet and on hospital treatment for severe diverticulitis and life – threatening complications needing surgery. If and when dietary fibre was not helpful there were no other effective treatments for persistent, recurring or non-relenting, low grade inflammation symptoms that are now recognized (33727769, 22777341). Such symptoms have been described as ‘smoldering DD’ or ‘SUDD – symptomatic uncomplicated DD’ or the misnomer ‘post-diverticulitis IBS’ More females than males were diagnosed with SUDD in a survey (30023071) and this was a long-term condition (17431721). This is a painful part of some unfortunate patients’ experience of DD affecting quality of life and which does not reach the level of hospital treatment.

There is little information about DD in primary care (22572678). Extensive research at hospital level does not address the problems before patients see the specialists (17681003, 10601059). The number of diverticula can increase with age as can the extent if colon affected. There is no data on this aspect of DD to see if there is a difference between males and females. There are suggestions that more women than men are troubled by long term symptoms. In New Zealand NHS primary care, women had notably more antibiotics prescribed for them than men, particularly those under the age of 60 years, for 5 yrs. before they needed hospital attention for acute or non-acute problems. More antibiotic prescribing for women also continued for the next 5 yrs. of the survey (31314796). Chronic aspects of DD in women also appear in data from hospitals. Females were on average 5 years older than males when seen and had more chronic diverticulitis and strictures, but less bleeding than males (12907908).

This pattern continues in mortality studies. 300 unselected pathology colons found a higher incidence of DD in women and also the onset occurred at an earlier age. Before the age of 50, 21.7% of women and 4.2% of men had DD and diverticula were scattered along the colon in women (5679019). Men were more likely than women to have had surgery and have a surgical complication of diverticulitis as a secondary cause of death and are more likely to die in hospital. Women are more likely than men to die from chronic complications such as sepsis, obstruction or pelvic fistula and are more likely to die at home, in care or in a hospice (33216498, 33216487). Research is not providing reasons for these differences (30046356).

The situation with DD may be like emergency presentation at hospital for colon cancer (30734381). In 2 to 12 months before emergency, twice as many women than men had received a diagnosis of IBS or DD. This increased the risk for women aged 40 – 59 yrs. 20% of women had alarm symptoms before the emergency. These authors cite reports of longer diagnosis intervals, a higher risk of 3 or more consultations before specialist referral of women, different interpretation of symptoms in women compared with men and possible misattribution of symptoms in women to benign causes. New onset of ‘IBS’ in middle aged women was also of concern. Sex differences in health and medicine are increasingly recognized and women are disadvantaged (22699937). This includes DD were women appear to suffer a longer and chronic symptomatic disease which is less acknowledged or treated if and unless it becomes serious.

© Mary Griffiths 2022

REFERENCES

The numbers in the text are PMID references. PubMed is a free resource supporting search and retrieval of biomedical and life science literature with aim of improving health – both globally and personally. It is available at     https://www.pubmed.ncbi.nlm.nih.gov

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Diverticular Disease: Treatments After a Century

July 25th, 2020

THE BEGINNING

Diverticula on the colon were a curiosity until increasing reports lead to official recording of deaths in 1923. This newly discovered disease of the elderly was only seen by surgeons trying to alleviate pain or correct the complications due to infection. Some pathologists were also interested in this phenomenon they found during postmortems. They did not know the patient’s problems which had preceded the serious condition, but their observations gave insight into how diverticula were formed.

Thickened wall muscles, concertina-like shortening of the sigmoid colon and narrowing of the lumen were the precursors of the appearance of diverticula. They did not know why this had happened but they did find that the damaged colon could give rise to pain needing surgery just as severe as the result of complications. The diverticula contained hard pellets of faeces (faecoliths) which could have been responsible for the pain and infection. Their observations appropriately led to recommendations for a diet, not necessarily low fibre, but a “softage” diet without pips, seeds or hard roughage. Only 20% of these patients were constipated.

WORLD WARS

With the advent of radiology, diverticula on the sigmoid colon (diverticulosis) were found in increasing numbers of people in the period between the two wars. There was speculation about the cause but no research was done. Advances in anaesthetics, blood transfusions and antibiotics made surgery safer. After WWII elective surgery was available to 10-20% of patients to remove the affected colon part to avoid future serious complications. How these patients were selected has not been reported. Risk/benefit considerations over the years have seen surgery more used as a treatment rather than a prophylactic.

“How fortunate I am having the opportunity of having this operation while I am fit and healthy”

     “I have seen many doctors and they all refuse me an operation so I am left suffering constant pain and discomfort every day”

In the UK deaths from diverticular disease (DD) increased up to 1939 then the rate was static until the 1950s. There was loss of interest in DD. This pause in mortality was later taken as evidence that the wartime diet in the UK, presumed to have more fibre, would prevent the diseases of the western world including DD. It was in fact due to the recording of deaths of civilians only. In the 1950s DD was beginning to be noticed again. The NHS was in its infancy. People resorted to herbal and traditional medicines. Laxatives were big business, people with or without DD were trying to conform to the daily toileting ideal of that era.

“—it was in 1948 when I first had stomach problems, and our dear old doctor, that we had then, explained to me why I was getting pain and wind, and on occasions blood, these were his words. Once when you were a little girl you ate too much, and your stomach couldn’t take all the food at once, so a part of it stretched a bit like a balloon and now you have a sort of pouch there which sometimes gets a bit packed out with food and causes all your problems, nothing can be done about this, so you must just be careful what you eat.”

     “I was told that I was part of a whole generation brought up during the war with a weekly purging of Syrup of Figs on a Saturday night therefore making a lazy bowel” 

WESTERN DISEASES

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Diverticular Disease: Progression, Smoking and Nicotine

April 14th, 2019

 

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.

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Diverticular disease AND/OR irritable bowel syndrome

June 29th, 2018

Information about diverticular disease (DD) is available in fact sheets on many internet sites, but these should be assessed. Is it up to date, does it help day-to-day problems, is it a charity or a business? Discussions on forums show a variety of experiences of DD and no general approach on what can be done to help. DD is sometimes mentioned by charities which support younger people with, for example, Crohn’s and ulcerative colitis (IBD) or Irritable Bowel Syndrome (IBS). In the last few years some people with DD have been told that they also have IBS. This can be very confusing because DD and IBS are different complaints sometimes with conflicting treatments and certainly different potential outcomes. Some researchers propose that any symptoms without diverticulitis must be IBS. This ignores or denies the colon damage which resulted in diverticula forming. Sources of information about IBS do not cover an IBS/DD diagnosis, never mind any differences which should be considered. Read the rest of this entry »

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Diverticular Disease: The Fibre Story

September 14th, 2017

In the early part of the 20th century constipation was not generally related to any individual illness. The idealised achievement of daily defaecation meant constipation was common particularly in the elderly. Treatment was not free until the NHS came along and natural and herbal laxatives were well used medications. Diverticular disease (DD) became recognised more before WW11. The distinguishing symptoms were pain, fever and diarrhoea. A low residue diet was recommended to reduce diarrhoea and give the bowel rest. Serious pain sometimes resulted in surgery. Infection and inflammation (diverticulitis) were not always present but pieces of food and faeces were trapped in diverticula. Avoidance of coarse fruit and vegetables, seeds and pips was recommended.

Hospital diet sheet for diverticulitis 1961………”forbidden foods – all fried foods, pips and skins of fruits, pastry, suet puddings, coarse stalky vegetables, salads, onions and celery, chunky marmalade, jam with pips or skins, wholemeal or brown bread, coarse biscuits-Ryvita, digestive, Allbran, oatmeal, Weetabix, Shredded Wheat, fruitcake or scones, nuts, dried fruit.”

A significant change in diet started about 1970 when treatment for diverticular disease (DD) was suddenly reversed.

Hospital diet sheet for diverticulis 1982………..”you can eat a normal varied diet but include…… (all of the forbidden foods from 1961 except fried food)….SUPPLEMENT meals with 2 teaspoonfuls of unprocessed bran twice daily. EAT LESS white flour in any form and white and other sugars. DIETARY FIBRE ….by helping to restore normal function of the digestive tract, fibre can be useful in the treatment of constipation and diarrhoea”

  • Who persuaded health professionals that wheat bran was good for diarrhoea?
  • What was the evidence for this complete reversal of treatment?
  • Did anyone ask patients if this helped them?
  • Who was behind this change?

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The Microbiome in Diverticular Disease

November 10th, 2016

New techniques which identify individual species have lead to an explosion of research into the role of bacteria in the colon. The terms ‘microbiota’ (the bacteria) and ‘microbiome’ (the collection of bacteria) are widely used. Some researchers consider the microbiome as equivalent to a body organ. It is certainly a significant, integral and specific part of the digestive system in man and animals. In protein-eating humans the microbiome is in the caecum, the first bag-like part of the large intestine which receives the residues of digestion and has enzymes which degrade amino acids from proteins. In herbivores the microbiome is in an earlier part of the digestive system to deal with large quantities of plant material to extract maximum nutrients for its host with enzymes to synthesise amino acids (1). The microbiome in humans can have both beneficial and unhelpful effects. Its position in the human body and the role of an associated appendix had not been considered apart from the letter on this website (2). The appendix is no longer considered a vestigial organ (3), contains extremely variable bacteria (4) and may be involved in microbiome changes (5).

Differences in the bacteria present in the microbiome have been found in conditions  such as obesity, autoimmune diseases, autism and bowel disease including diverticular disease (DD). The microbiome and its surrounding immune system are linked (6).

  • Is the microbiome content a cause or an effect of a disease?
  • Is the presence of a specific organism significant?
  • Could the microbiome be changed to treat a disease?

These are the questions research is trying to answer. Bacteria will only survive and flourish if the conditions and nutrients are right for the species. There is great variation both between and within people, with age and even with geographical location. So far only diet appears to make a difference (1, 7). Does the microbiome match dietary residues and the disease affect diet? Read the rest of this entry »

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Appendix and Gut Bacteria (Microbiome) PJ 1999

May 12th, 2016

This letter, published in 1999, is not now available on the website of the Pharmaceutical Journal. Only those later than 2000 can be accessed online. The letter has relevance to current interest in the gut microbiome and is published here with permission of the Pharmaceutical Journal.

Ulcerative colitis

More pieces for the jigsaw please

From Dr  Mary Griffiths, MRPharmS, MIBiol

SIR,�The report on the treatment of ulcerative colitis with E coli (PJ, August 28, p303) was another piece in the intriguing jigsaw of what produces the condition and its relapses. The mechanisms of inflammation and treatment and prevention of the damage to the inner surface of the colon by anti-inflammatory, steroid and immunosuppressant preparations are well documented. Dietary changes have little effect on ulcerative colitis, except for omitting milk in some patients. Sometimes, stressful, emotional events are linked with the onset of the disease and episodic symptoms and there may be a hereditary link.
Just suppose that the appendix is not a useless relic of evolution but a culture vessel and inoculating system to deliver actively growing organisms into the caecum. These are added to the chyme, which spurts from the ileocaecal valve, and to the residues of digestion of previous meals which are moved on more slowly when they reach the colon. The segmentation and pendulum movements of the first part of the colon mix its contents and there is fermentation and a rapid increase in the number of micro-organisms.
Why the body encourages this symbiosis is perhaps answered by the question of how does the body get rid of digestive enzymes before they are concentrated in faeces and give rise to self-harm? These enzymes are not normally reabsorbed in any quantity. The capacity of the system can perhaps be exceeded, for example, when single high doses of pancreatic enzymes given for cystic fibrosis damage the ascending colon. The diarrhoea caused by antibiotics is attributed to the ascent of resistant organisms such as Candida albicans, but a lower number of organisms to deal with digestive residues could also be involved. Appendectomy can result in more frequent colon upsets and a higher risk of certain cancers. In active ulcerative colitis, the colon walls are smooth and tubular and reduced segmentation means less effective mixing of its contents. E coli organisms surviving digestion could supplement the reduced numbers for the deactivation of digestive residues. Short-chain fatty acids normally produced by caecum fermentation have a beneficial effect in ulcerative colitis and the protection of mucous lining from enzyme action has explained the effectiveness of bismuth enemas.
I remember reading somewhere that there is an excess of acetylcholinesterase in ulcerative colitis which could be either a cause or effect of the lack of colon mixing movements and might be genetically determined; certainly, sympathetic stimulation would compound such an effect. Lack of movement causes toxic megacolon, which can be relieved by neostigmine injection. Nicotine stimulates acetylcholine release from postsynaptic neurones in the “gut brain” in the colon wall and would increase segmentation and caecum mixing. This explains why ulcerative colitis is less common in smokers, can relapse if smoking is stopped and symptoms can be reduced by nicotine patches.
Does anyone know of any other pieces of this jigsaw? Have any other anticholinesterase or cholinergic drugs ever been tried in ulcerative colitis to increase colon mixing? Do more readily available probiotics, eg, Lactobacillus species have any benefits? Are there any differences in enzyme activity in the faeces of patients when the disease is active or in remission. Many articles are not specific about which type of colon movement is involved in diseases and treatments, and ulcerative colitis is not always considered separately from Crohn’s disease.
Any comments on this speculative jigsaw puzzle would be appreciated.

Mary Griffiths
Macclesfield, Cheshire

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Diverticular Disease: Genetics and Collagen

July 9th, 2015

Compared with other diseases, advancements in science and technology left diverticular disease (DD) behind decades ago. Worldwide occurrence, poor quality of life, level of mortality and healthcare costs should have generated far more research effort. Preoccupation with dietary fibre levels, constipation and ageing has and still is stunting research. Fibre levels have benefits for constipation and symptoms but research into cause, prevention and other treatments has been overtaken by the necessary investigations into the surgical rescue of DD effects. Recently valid trials and surveys have disputed traditional thinking about a dietary cause and revealed a genetic factor. Read the rest of this entry »

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Posted in Associated illnesses, Cause of DD, Diverticular disease information | Comments Off on Diverticular Disease: Genetics and Collagen

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