After reading last night’s post on spices and IBS, Joan Ransley sent me the following, published in Cooking for The Sensitive Gut .
‘Have you ever eaten fresh mint after chilli has burned your mouth? If you have you will have been relieved. Both capsaicin a compound that gives chilli its heat and menthol contained on the outer surface of mint act on the same receptor in the mouth – but in different ways.
The neurologist Professor Anand of the Imperial College London Pain Centre explains why:
The active component of chilli, capsaicin stimulates nerves in the mouth to feel heat and pain via a receptor known as TRPV1. It also makes nerves grow. Capsaicin is an ingenious compound because it deceives the body into thinking it is hot when it is not. Interestingly mint does the opposite. Menthol blocks the receptor and induces a cool sensation in the mouth. South East Asian cooks know this all too well and use minty aromatic herbs in their delicious salads to accompany hot spicy dishes and relishes.’
So does this action of menthol explain why enteric coated peppermint oil (marketed as Apercap, Colpermin or Mintec) is said to help people with IBS? I must admit when it was first released, I was sceptical, and suggested that the most beneficial action of delayed release peppermint oil might be the fact that it disguised the odour of intestinal gas by replacing it with a delicate aroma of mint. Peppermint was originally marketed as an antispasmodic, but a recent study from Adelaide suggests that it’s mode of action might be on pain receptors in the colon. The most recent study on chilli, from Thailand, suggested that it’s major effect was on the sensation of burning, not necessarily crampy pain. So how relevant is the action of chilli and menthol in IBS?
One piece of research has found an over-expression of the TRPV1 receptor in the sigmoid colon of IBS patients compared to controls – http://gut.bmj.com/content/57/7/923
Great. Thank you for that.
I was thinking about this today. Could there be bacterial metabolites that interact with vanilloid receptors? Hypothesis: the low FODMAP diet works by minimising the production of metabolites that interact with vanilloid and other receptors that regulate pain, motility and secretion in the gut.
A quick bit of searching and I came across a literature review – http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367209/ – that cited a specific piece of research – http://www.ncbi.nlm.nih.gov/pubmed/17101327.
The research (I can only view the abstract and need to learn more about the physiology and biochemistry it discussed) suggested that hydrogen sulphide might activate nerve signalling via the vanilloid receptor. The review went one step further to claim that Lactobacillus could produce hydrogen sulphide from nitrates and nitrites which in turn led to increased gut motility via the vanilloid receptor (not sure how much it was overemphasising results there).