european crystal network workshop



    T. Major, R. K Topless, E. Sanchez Lopez, J. Harrè Hindmarsh, N. Dalbeth, L. K Stamp, M. Guma, R. Terkeltaub, T. R Merriman

    University of Otago, University of Otago, University of California San Diego, NgaTi Porou Hauora, University Of Auckland, University of Otago, University of California San Diego, University of California San Diego, University of Otago


    Introduction: A wide variety of foods are anecdotally reported by patients to be triggers of gout. Some of these foods have been associated with serum urate levels and onset of gout, and their possible mechanism for involvement in gout explained through their high purine content and the subsequent influence this has on the purine metabolism pathway (e.g. red meat and seafood). However, not all reported gout flare trigger foods have a high purine content and acute increases in serum urate are not thought to be the primary mechanism leading to acute inflammation. This study aimed to assess which nutrients are commonly found within gout flare trigger foods.


    Methods: Gout patients recruited across New Zealand (n = 2,106) were asked to list their dietary triggers of gout flares in an open-text format. Their open-text answers were aligned with a list of 115 foods commonly included in food frequency questionnaire forms. The nutrient content (per 100 g) of these 115 foods was estimated using the USDA Food Central database (70 different nutrients, vitamins, and minerals). The proportion of gout patients who included each of the 115 foods as a gout flare trigger was calculated and this proportion was associated with the estimated nutrient content across these foods using a linear regression. The 115 foods were also dichotomised into those that were reported by more than 20 patients and those reported by 20 or fewer patients (17 foods were not listed as a trigger by any patient) and the analysis was repeated using this dichotomised variable in a logistic regression.


    Results: Nine of the food nutrients analysed were more likely to be present (in large quantities) within foods listed as gout flare triggers. These nine nutrients were; protein (ß = 4.28 g, P = 0.005), vitamin D (ß = 45.70 µg, P = 1.1x10-4), ethyl alcohol (ß = 12.60 g, P = 1.34x10-4), selenium (ß = 2.43 µg, P = 0.001), the monounsaturated fatty acid C22:1 (ß = 1.40 mg, P = 4.5x10-4), and four omega 3 polyunsaturated fatty acids C18:4 (ß = 7.97 mg, P = 1.4x10-8), C20:5 (ß = 2.50 mg, P = 8.0x10-14), C22:5 (ß = 8.84 mg, P = 5.7x10-9), and C22:6 (ß = 1.30 mg, P = 8.4x10-12). Three of the food nutrients analysed were less likely to be present (in large quantities) within foods listed as gout flare triggers by gout patients. These three nutrients were; carbohydrates (ß = -1.39 g, P = 0.005), dietary fibre (ß = -10.08 g, P = 0.011), and sugars (all types combined; ß = -1.48 g, P = 0.044). The carbohydrate, dietary fibre, sugar, protein, and C22:5 results maintained their significant results (P < 0.05) when assessed using gout flare trigger foods as a dichotomised variable.


    Conclusions: This study identified twelve nutrients that correlate with foods reported by gout patients to trigger their flares. The association of ethyl alcohol and several fatty acids aligns with current knowledge of pathways involved in gout development and flare onset. The protein association may represent the influence of purines in gout development. Purine-content was not directly estimated. The reduced carbohydrate, dietary fibre, and sugar content of foods listed as gout flare triggers is a novel finding, as is the link between increased vitamin D and selenium content of foods listed as gout flare triggers. This work is the first step toward gaining greater insight into the mechanisms involved in the triggering of a gout flare.