As gluten-sensitives, inflammation is the bane of our lives. There are two main pathways that can occur, and you can have both, but experts on the recent Gluten Summit suggested that whilst autoimmunity is rife in coeliacs, inflammation is the main issue with non-coeliac gluten sensitives. I’m not sure I totally agree with that, having seen both in both groups, but either way inflammation is known to continue long after the start of a gluten free diet EVEN if you do it strictly. That’s why mortality levels show higher in the first year on a gluten free diet. Ooer.
When I asked Dr Tom O’Bryan about that, he said it was because of the inflammation levels. People tend to get diagnosed when they are most poorly, of course, which means that their body is under attack most at that time. You remove the trigger – gluten – but no-one is really doing anything about the inflammatory processes that continue unchecked. That’s why I have alluded to it in the new Gluten Testing Protocol:
Gut Status and Inflammation
Next, check the state of your gut environment (eg bacteria, candida, parasites etc) to make sure you are not harbouring chronic infections that would scupper healing. Do the Doctor’s Data Stool Test, which will also give an indication of digestive ability and gut inflammation. It is also a good idea to check whole body levels of inflammation, so ask your doctor to test your ESR and CRP levels, or do this Inflammation Test. If anything is positive do an appropriate Gut Detox or Candida Plan and use a natural anti-inflammatory.
I will be putting details of the anti-inflammatories etc in the Gluten Sensitivity factsheet shortly for you, but it will involve curcumin, from turmeric, as it’s one of my favourite anti-inflammatories.
I was interested to see a new study on this very subject this morning too. The researchers, publishing in the Journal International Immunopharmacology, concluded:
…curcumin can effectively suppress inflammatory response by inhibiting pro-inflammatory mediators and regulating humoral and cellular immune responses.
In other words, it helps slow down the processes that lead to inflammation. That’s what we need.
Here is the write-up about it from Life Extension for you. Don;t like the fact it is an animal study, of course, for several reasons, but there are a lot of studies about curcumin coming to the same conclusions:
Curcumin attenuates inflammatory response in IL-1beta-induced human synovial fibroblasts and collagen-induced arthritis in mouse model.
Curcumin, a major component of turmeric, has been shown to exhibit anti-oxidant and anti-inflammatory activities. The present study was performed to determine whether curcumin is efficacious against both collagen-induced arthritis (CIA) in mice and IL-1beta-induced activation in fibroblast-like synoviocytes (FLSs). DBA/1 mice were immunized with bovine type II collagen (CII) and treated with curcumin every other day for 2weeks after the initial immunization. For arthritis, we evaluated the incidence of disease and used an arthritis index based on paw thickness. In vitro proliferation of CII- or concanavalin A-induced splenic T cells was examined using IFN-gamma production. Pro-inflammatory cytokines TNF-alpha and IL-1beta were examined in the mouse ankle joint and serum IgG1 and IgG2a isotypes were analyzed. The expression levels of prostaglandin E(2) (PGE(2)), cyclooxygenase-2 (COX-2), and matrix metalloproteinases (MMPs) in human FLSs were also determined. The results showed that compared with untreated CIA mice, curcumin-treated mice downregulated clinical arthritis score, the proliferation of splenic T cells, expression levels of TNF-alpha and IL-1beta in the ankle joint, and expression levels of IgG2a in serum. Additionally, by altering nuclear factor (NF)-kappaB transcription activity in FLSs, curcumin inhibited PGE(2) production, COX-2 expression, and MMP secretion. These results suggest that curcumin can effectively suppress inflammatory response by inhibiting pro-inflammatory mediators and regulating humoral and cellular immune responses.
Int Immunopharmacol. 2010 May;10(5):605-10