Nutrition and rheumatic disease: are we really what we eat?

Nutrition and rheumatic disease: are we really what we eat?

Speaker: Elena Philippou PhD

Purpose: To explore which foods and/or dietary patterns are associated with the risk of rheumatic and musculoskeletal diseases (RMDs).

Methods: Research studies associating diet and RMDs were identified through MEDLINE.

Results: A number of dietary factors might act as environmental triggers in disease development.  Overall, a ‘Western’ type diet rich in energy intake, total and saturated fat, an unbalanced ratio of n-3 to n-6 fatty acids, high in sugar and low in fiber and antioxidants might increase the risk of RMDs both directly through increasing inflammation (Minihane et al. 2015) and indirectly through increasing insulin resistance, obesity and associated co-morbidities, with obesity being a known risk factor for RD (Qin et al. 2015).

High consumption of foods characteristic of the ‘Western-type’ diet such as red meat, meat and meat products combined, or total protein have been shown to increase the risk of inflammatory polyarthritis suggesting a role of advanced glycation end products (AGEs) (Pattison et al. 2004).  This is supported by findings of regular consumption of sugar-sweetened soda, but not diet soda, being associated with an increased risk of seropositive rheumatoid arthritis (RA) in women (Hu et al. 2014), and of high-fructose corn-syrup sweetened soft drinks, fruit drinks and apple juice being associated with arthritis in young US adults (DeChristopher et al. 2016).  It is hypothesized that regular consumption of excess free fructose and HFCS contributes to fructose reactivity in the gastrointestinal tract and intestinal in situ formation of enFruAGEs, which once absorbed, travel beyond the intestinal boundaries to other tissues and promote inflammation (DeChristopher et al. 2016).    Individual biomarkers of antioxidant intake have also been previously investigated in relation to RA with some evidence that low serum levels of selenium and alpha tocopherol (Knekt et al. 2000) and beta carotene (Comstock et al. 1997) are associated with an increased disease risk.  Interestingly, a meta-analysis also suggests that coffee consumption of ≥ four cups per day is associated with an elevated risk of seropositive RA but not seronegative RA (Lee et al. 2014).  However, the results should be interpreted with caution due to other potential confounders.  The same meta-analysis found no association between tea consumption and risk of RA (Lee et al. 2014).

On the contrary, consumption of long-chain omega-3 polyunsaturated fatty acids, derived from fish and fish oil, is associated with a reduced risk of RA (Di et al. 2014) probably due to their anti-inflammatory properties.  The  Mediterranean diet (MD), rich in plant-based foods such as wholegrains, legumes, fruit, vegetables, extra-virgin olive oil and low in red meat consumption, might have the potential to reduce the risk of RA.  It has been shown that greater adherence to the MD is associated with lower concentrations of inflammatory biomarkers (Fung et al. 2005), while daily consumption of monounsaturated fatty acids from olive oil is thought to be the key factor in suppressing RA disease activity (Matsumoto et al. 2017).

Conclusions: Based on current research evidence, it is suggested that adherence to the MD  with an increased consumption of fatty fish, reduced consumption of sugar-sweetened drinks and maintenance of a normal body weight, contributes to reducing the risk of RA.  Further research on RA susceptibility will allow more specific dietary recommendations.

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