What is the cause of IBD?
There are several factors which are now understood to be important in the development of Inflammatory Bowel Disease (IBD). These include:
- Genetic factors
- Immunological factors
- Psychological factors
- Non-Steroidal Anti-Inflammatory Drugs (NSAIDs).
Genetics & IBD
Both genetic and environmental factors play a significant role in causing IBD. It has long been known that IBD is more frequent in certain races, and that it may run in families. Recently, as scientists have examined the human genome, the genetic basis of the development of IBD has been intensively explored and it is known that people who develop it are susceptible because they possess certain genes.
A positive family history is the strongest known risk factor in the development of IBD. Individuals who have a first degree relative with these problems have approximately 1 in 10 chance of developing IBD themselves whereas the incidence in the general population is 1 in 10,000. This is a not a reason to decide not to have a family as it means that there is a 90% chance that a child from an affected family will never develop the condition.
Very rapid progress has recently been made in the identification of genes which increase susceptibility to IBD, and for an up-to-date review it is necessary to consult the scientific literature. The current challenge, however, is to translate this scientific progress into real clinical benefit. It is not expected that it will be possible in the foreseeable future to change an individual’s established genetic make-up. Indeed, as many genes are known to have more than one function, that may be undesirable. It is hoped that prediction of drug effects will result from these studies and that it may be possible to decide the optimal treatment for each patient in the light of his or her genetic make-up.
If this topic is of interest and you would like to read further about genetics and IBD, it is discussed in more detail in ‘Inflammatory Bowel Disease: The essential guide to controlling Crohn’s Disease, Colitis and Other IBDs’ by Professor John Hunter
IBD is NOT contagious. Partners of those with IBD, or people close to them are not at any increased risk of getting the condition. IBD may arise, however, after certain infections particularly gastroenteritis. It appears that in some way infections in the gut may trigger in susceptible persons an immune response not only against the bacteria causing the infection but also against other harmless bacteria which live in the intestines of us all.
The body’s own defence mechanism (the immune system), which provides protection against infection, is activated by intestinal bacteria in IBD and the reaction between the immune attack and the bacteria living in the bowel is believed to be the cause of damage to the lining of the gut. In IBD, bacteria in the bowel, even harmless ones, are coated with antibodies, showing that they are under attack. It seems likely that this happens because they are causing the production of toxic chemicals which activate the immune system. When the disease is controlled, these antibodies disappear. Many drugs used to control IBD e.g. corticosteroids and azathioprine, are effective because they suppress the immune system.
Some patients find that their Crohn’s disease is better if they avoid certain foods such as wheat, yeast or milk. However, many other patients with the disease are able to eat these foods without difficulty and it would be a mistake to believe that the foods themselves are dangerous. It seems that the breakdown of food residues by bacteria in the intestine to produce toxic chemicals plays a part in Crohn’s disease. Current research is starting to show exactly what the nature of these chemicals may be.
In Ulcerative Colitis (UC), however, there is accumulating evidence that the bacteria producing these toxic chemicals may not live off food residues, but instead use substances found naturally in the intestine, such as mucus, as a source of energy. Mucus is the lubricant produced by the body to ease the passage of faeces along the bowel and cannot be altered by dietary means. It is believed that this may be the reason why diet is not effective in controlling inflammation in UC, in the way that it is in Crohn’s disease (CD). For further information, please visit the ‘Diet in UC’ section
Although not a proven cause, periods of emotional stress have been linked with flare-ups of IBD and can make it worse.
Crohn’s disease is always much worse in people who smoke. They are more likely to need surgery and suffer more frequent relapses. The reason that smoking makes CD worse is poorly understood, but it is a great mistake for people suffering from CD to continue to smoke as it reduces the chances of successful treatment.
UC, on the other hand, seems to improve after smoking, or may get worse when people decide to quit. The reasons for this are not clearly understood, but smoking appears to protect against the development of colitis. It has been suggested that nicotine in cigarettes is helpful in healing UC. Others have suggested that smoking is helpful because smoking a cigarette is known to have a mild laxative effect, preventing the development of proximal constipation. However, for numerous crucial health reasons, it is not recommended that people with UC continue smoking even if it does seem to help their colitis!
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)
Although probably not a direct cause of IBD, NSAIDs are well known to provoke an attack once the disease has developed. This may be because they block the effects of chemicals called prostaglandins, which are produced in the body, and which are known to be important in protecting the cells in the lining of the stomach and intestine from damage – an effect known as ‘cytoprotection’. If you have IBD, avoid taking NSAIDs as far as possible.
Anti-inflammatory drugs that may upset IBD.
- Aceclofenac (Preservex)
- Acemetacin (Emflex)
- Aspririn (many preparations – check on packet)
- Celecoxib (Celebrex)
- Dexibruprofen (Seractil)
- Dexketoprofen (Keral)
- Diclofenac Sodium (Voltarol, Diclomax, Arthrotec)
- Diflunisal (Dolobid)
- Etodolac (Lodine)
- Etoricoxib (Arcoxia)
- Fenbufen (Lederfen)
- Fenoprofen (Fenopron)
- Flurbiprofen (Froben)
- Ibruprofen (Brufen, Fenbid, Nurofen)
- Indometacin (Indomethacin, Flexin Continus)
- Ketoprofen (Orudis, Orovail)
- Lumiracoxib (Prexige)
- Mefenamic Acid (Ponstan)
- Meloxicam (Mobic)
- Nabumetone (Relifex)
- Naproxen (Naprosyn, Synflex, Napratec)
- Piroxicam (Brexidol, Feldene)
- Sulindac (Clinoril)
- Tenoxicam (Mobiflex)
- Tiaprofenic Acid (Surgam)