There are a number of reasons why the AIP protocol is effective for auto-immune disease including rheumatoid arthritis (RA). However it is important to point out that not all will respond to AIP, there are many factors that contribute to auto-immune disease apart from diet. AIP is not the only diet that works, in fact for some it may make their disease worse. This is due to consuming more of a food that the individual reacts to – for example mammal meats. An example of this is that many people with Hashimotos (auto-immune thyroid disease) have increased levels of an antibody against a carbohydrate Neu5Gc found in red meats (Eleftheriou, P et al, 2014).
With respect to RA; fasting, both water and fruit and vegetable juice fasts typically reduce symptoms and improve clinical markers in as few as 7 days, this leads us to conclude that food has an effect in RA (Skoldstam et al., 1979, Skoldstam, 1986, Kjeldsen-Kragh et al., 1991). A diet which removes foods that exacerbate the disease process and increasing foods that improve health would theoretically be effective.
When I looked at a large number of research studies about RA the following aspects appear to be of importance with respect to a diet that improves the symptoms and clinical markers of RA:
It reduces inflammatory markers – for example ESR and CRP. An anti-inflammatory diet is low in saturated fat and arachidonic acid, low in refined grains and sugar, high in fruit & vegetables, and high in seafood for omega 3 (Adam et al., 2003)
It reduce or eliminates exacerbating foods, which may act as possible antigens. An appropriately structured elimination, re-introduction protocol is critical to success(Kjeldsen-Kragh, 1999). Certain anti-body tests may show some food intolerances such as gliadin or ß-lactalbumin (Hafstrom et al., 2001). I looked at over 20 elimination diet and case studies which when taken together show the most problematic foods are: wheat, corn, dairy, beef, pork, grains/ cereals, eggs, oranges/ citrus, coffee, sugar, tomatoes, peanuts, chicken. It is interesting to note that AIP does not remove foods which appear to be problematic for some people.
It improves gut microbiome by reducing bacterial flora linked with RA, which may be acting as antigens. A diet high in plant fibre and polyphenols with the addition of fermented foods may offer the best solution( T. Nenonen et al., 1998). Changing from acellular carbohydrates such as grain starch and sugars to cellular starches found in root vegetables is theorised to provide a better substrate for gut bacteria, as well as reduce inflammation (Spreadbury, 2012).
It improves gut epithelial integrity, reducing the intestinal permeability that allows antigens to cross the gut barrier in intact sequences of amino acids (Sundqvist et al., 1982).
A diet that improves gut microbiome, as well as removing foods which are shown to increase intestinal inflammation and permeability, for example gluten grains and dairy (for some). Cordain suggests all grains and legumes have certain lectins contributing to intestinal permeability ( Cordain, Toohey, Smith, & Hickey, 2000) and should be avoided.
It decreases red cell membrane ratio of arachidonic acid to omega 3 EPA ratio; this reduces inflammatory eicosanoid hormones and increases anti-inflammatory ones. This is achieved by reducing dietary sources of AA such as egg yolks and fatty meat, and increasing EPA by eating seafood or adding supplemental marine omega 3 (Adam et al., 2003).
A diet that reduces the support of the growth of urinary bacteria proteus mirabilis linked with RA, possibly a diet high in plant foods (Kjeldsen-Kragh, Rashid, et al., 1995).
Adam, O., Beringer, C., Kless, T., Lemmen, C., Adam, A., Wiseman, M., . . . Forth, W. (2003). Anti-inflammatory effects of a low arachidonic acid diet and fish oil in patients with rheumatoid arthritis. Rheumatology International, 23(1), 27-36. doi: 10.1007/s00296-002-0234-7
Cordain, L., Toohey, L., Smith, M. J., & Hickey, M. S. (2000). Modulation of immune function by dietary lectins in rheumatoid arthritis. British Journal of Nutrition, 83(3), 207-217.
Eleftheriou, P., Kynigopoulos, S., Giovou, A., Mazmanidi, A., Yovos, J., Skepastianos, P., … Efterpiou, M. (2014). Prevalence of Anti-Neu5Gc Antibodies in Patients with Hypothyroidism. BioMed Research International, 2014, 963230. http://doi.org/10.1155/2014/963230
Hafström, I., Ringertz, B., Spångberg, A., Von Zweigbergk, L., Brannemark, S., Nylander, I., . . . Klareskog, L. (2001). A vegan diet free of gluten improves the signs and symptoms of rheumatoid arthritis: The effects on arthritis correlate with a reduction in antibodies to food antigens. Rheumatology, 40(10), 1175-1179.
Kjeldsen-Kragh, J., Borchgrevink, C. F., Laerum, E., Haugen, M., Eek, M., Fo̸rre, O., . . . Hovi, K. (1991). Controlled trial of fasting and one-year vegetarian diet in rheumatoid arthritis. The Lancet, 338(8772), 899-902. doi: http://dx.doi.org/10.1016/0140-6736(91)91770-U
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Nenonen, M. T., Helve, T. A., Rauma, A. L., & Hanninen, O. O. (1998). Uncooked, lactobacilli-rich, vegan food and rheumatoid arthritis. British Journal of Rheumatology, 37(3), 274-281.
Skoldstam, L. (1986). Fasting and Vegan Diet in Rheumatoid-Arthritis. Scandinavian Journal of Rheumatology, 15(2), 219-221.
Skoldstam, L., Hagfors, L., & Johansson, G. (2003). An experimental study of a Mediterranean diet intervention for patients with rheumatoid arthritis. Annals of the Rheumatic Diseases, 62(3), 208-214. doi: 10.1136/ard.62.3.208
Skoldstam, L., Larsson, L., & Lindstrom, F. D. (1979). Effects of Fasting and Lacto-Vegetarian Diet on Rheumatoid-Arthritis. Scandinavian Journal of Rheumatology, 8(4), 249-255.
Spreadbury, I. (2012). Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity. Diabetes Metab Syndr Obes., 5, 175-189.
Sundqvist, T., Lindstrom, F., Magnusson, K. E., Skoldstam, L., Stjernstrom, I., & Tagesson, C. (1982). Influence of Fasting on Intestinal Permeability and Disease-Activity in Patients with Rheumatoid-Arthritis. Scandinavian Journal of Rheumatology, 11(1), 33-38.