The place of omega-3 and omega-6 acids in supplementary treatment of inflammatory joint diseases

Feb 28, 2020
Brygida Kwiatkowska and Maria Maślińska

Abstract

Eating habits have been analysed for years as a factor influencing the development of autoimmune diseases and susceptibility to infections. On the basis of research, observational studies and meta-analyses, special attention was paid to omega-3 and omega-6 acids.

The purpose of the review is to show the importance of omega-3 and omega-6 acids as important ingredients in the healthy diet and as factors protecting against the development of the most common inflammatory rheumatic diseases. The influence of these omega-3 and -6 acids on the course of rheumatic diseases and arguments for their use as complementary therapy are also presented.

Keywords: rheumatic diseases, omega-3, omega-6 acids

Introduction

Inflammatory joint diseases are enumerated among chronic autoimmune diseases, which mostly affect young people and result in changes within multiple organs and lead to limited mobility.

Both genetic factors (not modifiable) and environmental factors (some of which can be modified) may have an influence on the development of these diseases. Current scientific research focuses on testing genetic factors increasing the risk related to the development of the disease in people who are still healthy. In the future this could possibly allow implementation of prophylactic therapy and analysis of environmental factors, as well as enabling an attempt to modify them in order to reduce the likelihood of being affected by the disease or modify the course of the existing inflammatory joint disease.

Smoking is one of the environmental factors posing a recognised and considerable influence on the development or the course of inflammatory joint diseases such as rheumatoid arthritis (RA) and psoriatic arthritis (PsA). Active smokers are at 20% higher risk of development of RA than non-smokers [1].

As far as PsA is concerned, smoking increases the risk of being affected by this disease in the general population, whereas the majority of trials indicate a reduced risk of suffering from PsA within the population of patients with psoriasis. This phenomenon is known as the “smoking paradox” [2].

Body weight is yet another environmental factor influencing the development and the course of inflammatory joint diseases. Psoriatic arthritis reveals clear correlations between obesity and the risk related to the development of the disease and its course. What concerns patients with psoriasis, the frequency associated with the prevalence of PsA increases along with the growing body mass index (BMI) [3]. What is more, obesity in patients suffering from PsA also results in worsened efficiency of administered treatment, even one based on biological medications [4, 5]. Positive correlations between the activity of the disease and obesity have also been observed in patients suffering from RA [6].

Physical activity is indicated as the next environmental factor which could possibly influence the development of RA. It has been reported that physical activity (> 20 minutes a day/hour a week) such as working at home, walking, strolling, riding a bicycle, swimming, doing aerobics, jogging and playing tennis can reduce the risk of developing RA [7, 8].

Many reports indicate that there is a causal link between infections and the development of inflammatory rheumatism.

There is currently a discussion about the importance of infection caused by Porphyromonas gingivalis, resulting in protein citrullination and hence leading to chronic periodontal disease as a triggering factor of RA development. De Smith et al. [9] studied seropositive patients with arthralgia and seropositivity of antibodies against P. gingivalis and concluded that these antibodies do not predict RA development, but another study by Johansson et al. [10] showed that antibodies against. P. gingivalis were increased in RA patients and may emerge years before the disease onset.

Nevertheless, infections with this particular bacterium are more frequently observed in patients with RA and they impact the activity of the disease in the DAS28 assessment [11].

Recent studies have shown that a change in human microflora, especially the intestinal microbiota, plays a crucial role in the pathogenesis underlying many inflammatory rheumatic diseases including RA, spondyloarthropathies (SpA), systemic lupus erythematosus (SLE), systemic sclerosis (SS), antiphospholipid syndrome (APS) and Sjögren’s syndrome (SS) [12].

The human microbiota is filled not only with commensal microorganisms, but also with clearly pathogenic ones. There are 3 main mechanisms related to how these microorganisms act in rheumatic diseases.

Firstly, commensal microorganisms may deplete nutrients and thereby limit the growth of new bacteria, which impacts the immune defence mechanisms [13].

Secondly, microorganisms may activate the immune system directly by the fact that their products cross the intestinal lamina propria and adhere to the specific receptors on the surface of the antigen-presenting cells, such as dendritic cells and macrophages. This, in turn, activates the T cells and initiates the production of pro-inflammatory cytokines such as IL-1, IL-6, IL-17, TNF-a, as well as stimulating the production of various antibodies [14].

Thirdly, overgrowth of certain intestinal microorganisms may cause the excessive production of metabolites – short-chain fatty acids (SCFAs) such as acetate, butyrate or propionate, which contribute to the development of comorbidities. These metabolites may lead to obesity by signalling pathways coupled with the G protein (GPR41, GPR43), which then impacts not only the course, but also the treatment of diseases such as RA or PsA [15].