Chocolate and reflux - the evidence

(also: onions and chilli)

 It has been well known for over 30 years that chocolate reduces the pressure in the Lower Oesphageal Sphincter (LOS) and furthermore, this effect is not abolished by alkalinisation of the stomach. This lowering of LOS pressure has also been shown to lead to an increase in oesophageal exposure to refluxed acid for at least an hour after ingestion.

 Not many studies have looked at onions specifically with in GORD but one study from Oklahoma specifically did. Volunteers with and without reflux were given a plain hamburger one day and a hamburger with onion on another day and patients with reflux experienced an increased number of reflux episodes, percentage of the time pH < 4, heartburn episodes and belches. Normal controls were unaffected.

 The active ingredient in chillis is called capsaicin. Depending on the type of chilli this is of variable perceived 'heat' and is measured by a subjective scale in what are called Scoville Heat Units. Again, not much literature exists that examines the effects of chilli on reflux. There is evidence that chronic ingestion of chillies can predispose to reflux and the severity depends in part on the type of chilli eaten.

There is a paradox here however, insofar as capsaicin has also been shown to improve oesophageal body motility by increasing the amplitute of the 'stripping' waves that are integral to clearing the oesophagus of acid. How can this circle be squared? One study showed that, even in the absence of endoscopic mucosal injury, the number of capsaicin receptor (TRPV1) fibres in the lamina propria (present in normal controls) increased with increasing levels of oesophageal acid exposure. This numerical upregulation would then begin to explain reflux symptoms seen in NERD and it is thought that it is the excess acid exposure that causes increased expression of the TRPV1 receptor, not the other way round.

Nociception in the oesphagus is triggered, at least in part, by the activation of the capsaicin receptor with consequent release of neuropeptides that in turn trigger the release of pro-inflammatory cytokines leading to increased vasodilatation, leucocyte infiltration and mast cell degranulation. As these neuronal endings lie in the lamina propria then the Dilated Inter-cellular Spaces seen in NERD would help explain the excess stimulation of these receptors as acid permeates beneath the epithelial layer. Mucosal breaches however cannot be caused through this mechanism and it is likely that factors such as Epidermal Growth Factor (EGF), which is present in the endothelial cells of the capillaries of the normal oesophageal mucosa and reduced in cases of inflamed oesophageal epithelium, play a role in the initial mucosal breach to allow penetration of the refluxate into the lamina propria. Oesophageal EGF is also found in the mucous layer covering the epithelium and is reduced in patients with erosive disease and hence again can be implicated in the development of, or delay the healing of, any mucosal injury.