Around 2-4 in 1,000 people in Northern Europe have ulcerative colitis or Crohn's disease (Rubin 2000). Both are chronic, relapsing, inflammatory disorders of the gastrointestinal tract with several shared clinical features, but with largely distinct risk factors, genetic, immunological, anatomical and histological features, and response to therapy (DTB 2003). Their treatment, which includes medical and surgical approaches, is usually considered in two phases: the induction of remission in an acute attack, and the long-term maintenance of remission (DTB 2003).
Gastritis is an inflammation, irritation, or erosion of the lining of the stomach, which can be acute or chronic. Causes include irritation due to excessive alcohol use, chronic vomiting, stress, or the use of certain drugs (e.g. NSAIDs), Helicobacter pylori infection and pernicious anaemia. Symptoms of gastritis vary among individuals, and many have no symptoms. However, the most common symptoms include nausea, vomiting (possibly with blood), abdominal pain and bloating, indigestion, loss of appetite, and blood in the stools. Treatment usually involves drug therapy.
Gastro-oesophageal reflux is a common (affecting up to 25% of adults) relapsing condition caused by repeated exposure of the lower oesophagus to refluxed gastric contents (Moayyedi 2007). It presents in various ways: some patients just have symptoms, some have endoscopic evidence of mucosal damage (oesophagitis), with or without symptoms, and an important minority have complications such as bleeding, stricture or columnar epithelial (Barrett's) transformation of the lower oesophageal mucosa which predisposes to adenocarcinoma. Conventional treatment options include drugs and surgery.
About 20% of people in the UK have functional gastrointestinal disorders such as functional dyspepsia and irritable bowel syndrome (Jones 1990; Jones 1992). The latter condition is the subject of another professional information backgrounder, and will not be discussed further here. Functional gastrointestinal disorders are characterised by persisting gastrointestinal symptoms (e.g. pain, bloating) in the absence of any identifiable underlying structural or biochemical explanation (Drossman 2000). They are conventionally treated with drugs or with psychological treatments such as cognitive behavioural therapy, brief psychotherapy and gut-directed hypnotherapy (DTB 2005).
Drossman DA (Ed). Diagnostic Criteria for the Functional Gastrointestinal Disorders. Second edition. Kansas: Degnon Associates, 2000: 659-69.
Hypnotherapy for functional gastrointestinal disorders. DTB 2005; 43: 45-8.
Inducing remission in inflammatory bowel disease. DTB 2003; 41: 30-2.
Jones RH et al. Dyspepsia in England and Scotland. Gut 1990; 31: 401-5.
Jones R, Lydeard S. Irritable bowel syndrome in the general population. BMJ 1992; 304: 87-90.
Moayyedi P, Delaney B. GORD in adults. Clinical Evidence. Search date July 2007.
Rubin GP et al. Inflammatory bowel disease: epidemiology and management in an English general practice population. Aliment Pharmacol Ther 2000; 14: 1553-9.
How acupuncture can help
Acupuncture has been found superior to sham acupuncture for disease activity scores in Chrohns Disease and Ulcerative Colitis (Joos 2006; Joos 2006; Schneider 2007). Other 'placebo' comparisons have tended to show no statistical effect; however, there is as yet no satisfactory placebo intervention for acupuncture so the interpretation of such data is difficult and controversial. In comparisons with Western drug treatments acupuncture has been found beneficial for a variety of gastrointestinal diseases: dyspepsia (Chen 2005), gastritis (Ren 2009; Gu 2009), ulcerative colitis (Mu 2007; Lee 2009), reflux (Journal of the National Medical Association 2008; Zhang 2010) and pancreatitis (Wang 2007). Nevertheless most systematic reviews have been reluctant to endorse acupuncture because of the generally poor quality, and hence unreliability, of the studies to date (Schneider 2007; Lee 2009). (see Table overleaf).
Acupuncture may help in the treatment of GI tract disorders, by:
- inhibiting gastric and duodenal motility by activating sympathetic nerves via spinal reflexes, and increasing motility via the vagus nerve and supraspinal reflexes (Chang 2001; Takahashi 2006; Sehn 2006; Yao 2006; Noguchi 2008);
- altering acid secretion, and visceral pain (Takahashi 2006)
- improving delayed gastric emptying (Xu 2006)
- reducing inflammation, by promoting release of vascular and immunomodulatory factors (Zijlstra 2003)
- stimulating areas in the brain that are involved in gastric perception (Zeng 2009)
- inhibiting stress-induced pro-opiomelanocortin expression in the hypothalamus (Sun 2008)
- increasing vasoactive intestinal peptide and nitric oxide in plasma, gastric mucosal and bulb tissues, and elevating expression of vasoactive intestinal peptide in antral smooth muscle (Shen 2006);
- decreasing permeability of intestinal mucosa in patients with acute pancreatitis, and reducing accumulation of endogenous inflammatory mediators and vascular active substance in intestinal mucosa (Wang 2007).